Textbook of ORAL MEDICINE
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DISCLAIMER NOTICE The information in this book should not be used by unqualified personnel to do any self diagnosis. All dental surgeons are requested to kindly verify the latest prescribing practices prior to making decision. Most values are indicative and have been checked against latest reliable sources, but the publisher and author do not have any direct or indirect liability to the use or misuse of this information. Prior to prescribing any medication please check that they are from ethical drug manufactures following sound quality control practice. Follow the manufacture direction in most prescription and please confirm side effect, safety in children and pregnancy. Author
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Textbook of ORAL MEDICINE Second Edition
Anil Govindrao Ghom MDS (Oral Medicine and Radiology)
Professor and Head Department of Oral Medicine and Radiology Chhattisgarh Dental College and Research Institute Rajnandgaon, Chhattisgarh, India Formerly Rural Dental College, Loni VSPM Dental College, Nagpur
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[email protected] Central America Office Jaypee-Highlights Medical Publishers Inc. City of Knowledge, Bld. 237, Clayton, Panama City, Panama Ph: 507-317-0160 Textbook of Oral Medicine © 2010, Anil Govindrao Ghom All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted in any form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the author and the publisher. This book has been published in good faith that the material provided by author is original. Every effort is made to ensure accuracy of material, but the publisher, printer and author will not be held responsible for any inadvertent error(s). In case of any dispute, all legal matters to be settled under Delhi jurisdiction only.
First Edition: 2005 Reprint: 2006, 2007 Second Edition: 2010 ISBN 978-81-8448-700-8
Typeset at JPBMP typesetting unit Printed at Nutech
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To My Mother, My Daughter Milini, My Son Sanvil, My Wife Savita and My Family
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Contributors Vikas Meshram Reader, Chhattisgarh Dental College and Research Institute, Rajnandgaon, Chhattisgarh Ch 48: Emergency Drugs used in Dentistry
Sachin Manglekar Reader, School of Dental Science, Krishna Institute of Medical Science University, Karad, Maharashtra Ch 46: Desensitizing Agents, Gum Paints and Mouthwashes
Savita Ghom Lecturer, Chhattisgarh Dental College and Research Institute, Rajnandgaon, Chhattisgarh Ch 43: Anticancer Drugs Ch 47: Drugs used in Pregnancy
Raghvendra Shetty Reader, Chhattisgarh Dental College and Research Institute, Rajnandgaon, Chhattisgarh Ch 40: Antibiotics
Amit Parate Lecturer, Government Dental College and Hospital, Nagpur, Maharashtra Ch 20: Oral Pigmentation
Vaishali Gawande Lecturer, Chhattisgarh Dental College and Research Institute, Rajnandgaon, Chhattisgarh Ch 42: Antifungal Drugs Ch 44: Antiviral Drugs
Abhishek Soni Reader, VSPM Dental College and Research Institute, Nagpur, Maharashtra Ch 24: Gingival and Periodontal Diseases
Anjusha Ganar Ex-lecturer, Chhattisgarh Dental College and Research Institute, Rajnandgaon, Chhattisgarh Ch 45: Corticosteroids
Neeta Wasnik Lecturer, Chhattisgarh Dental College and Research Institute, Rajnandgaon, Chhattisgarh Ch 41: Analgesic and Anti-inflammatory Drugs
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Foreword “Enthusiasm is a driving force that overcomes all obstacles” It is my proud privilege to write a foreword for second edition of this book by Dr Anil Ghom. In short time, this book has become most popular among undergraduates and postgraduates all over the country. In the second edition, numbers of chapters have been presented in a better organized manner. This book carries updated information of the subject in this rapidly changing world of science. A new chapter “Controversial Diseases and Terminologies” is incorporated, also there are large number of new photographs, radiographs, MCQs and references. I am sure this new updated second edition will be more beneficial for the undergraduate and postgraduate students for reference and regular reading. RN Mody Professor and Head Department of Oral Medicine and Radiology Hitkarini Dental College Jabalpur, MP
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Preface to the Second Edition ‘We become strong only after we have acknowledged our weakness. Gather knowledge, insight, and experience and then make your own decision’ This is the second edition of the textbook and I am gratified by the acceptance and support that the book has received over the years from educators, students and practitioners. The purpose of second edition of this book is two-fold. First, to include what is new and recent knowledge and the second is correct shortcoming of the first edition. I have evaluated and utilized suggestions from all the critical reviews and recommendations from the faculty members. Obviously, each successive edition of textbook finds the edition with more information. So in this edition I have attempted to solidify and include recent knowledge. This book also includes a new Chapter Controversial Diseases and Terminologies. Purpose of this chapter is that as knowledge is changing everyday with advanced diagnostic techniques, many old terminologies are discarded and new one are introduced. My first book was criticized a lot for not including references and not having enough photographs in the book. So in this second edition I have included references and around 1000 photographs/illustrations for easy understanding of the diseases. MCQs chapter is completely revised and all the new MCQs are added at the end of chapter. I have also included diagnosis of each lesion in diseases, so that students can understand key point in disease and they can easily remember it. Again, as a human being, mistakes are bound to happen. I tried this second edition to best of my efforts, still there can be shortcoming and I request readers to make note of it and I will try to rectify it in the next edition. Anil Govindrao Ghom
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Preface to the First Edition
“You must not be discouraged if the world does not rush to you, demanding what you have; neither must you quietly sit down to let world wonder and then seek you; you must be aggressive, you must carry your truths to people and cause them to see them so clearly that they must accept them” The student looked for a reference on which to build an educational foundation with regard to basic principle. A few years ago much of the information offered in this text was not available. Since the principle and treatment modalities offered herein will continue to evolve, it behooves the student to be fully informed of the state-of-art to be able to critically evaluate the worthiness or applicability of any future development. I have endeavored to ensure that a consistent style has emerged and is in harmony where appropriate with the diseases of oral region along with the differential diagnoses which are covered in detail. The purpose of this book is to correlate the gross and microscopic pathological features with the radiographic appearance of oral diseases and systemic diseases manifested in the jaw. In our increasingly litigious society, it is vital that the dentist understands the law as it relates to dentistry. The Chapter on Medicolegal Issue is Essential Reading, along with the Consumer Protection Act. Diseases can be understood best when the interpreter understands not only the disease process but also the basic science associated with it. For this reason, I have included separate section for basic science. Recently, as exam pattern is changing and MCQs are getting importance, MCQs are added in separate chapter. I tried my best, to cover all the aspects of oral diseases in my book. If this goal is achieved, then this textbook may contribute, in a small way to better care of patients who suffer from these diseases. Anil Govindrao Ghom
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Acknowledgements ‘The man who really wants to do something finds a way, the other finds an excuse’ No work will be complete without help of your friends and well wishers and I am lucky to have them with me in this venture. First of all, I am immensely thankful to Dr Vaishali Gawande for her untiredly help in completion of this project. My special thanks to Dr Neeta Wasnik and Dr Anjusha Ganar who helped me a lot. I am also thankful to Dr Swapnil Diwakirti for her help in preparation of diagrams in the book. I am thankful to all the contributors for their contribution in this book. My sincere thanks to Dr Pravin Lambade, Dr Jitendra Sachdeo, Dr Vikas Meshram, Dr Bhaskar Patle, Dr Revant Chole, Dr Amit Parate, Dr Sanjay Pincha, Dr Milind Chandurkar, Dr Ashok L, Dr Umaraji, Dr Tapasya Karemore, Dr Avinash Kshar, Dr M Shimizu, Dr Fusun Yasar, Dr Iswar, Dr Bande, Dr Kadam, Dr R Kamikawa, Dr FM Debta and Dr Suwas Darvekar for providing clinical and radiological photographs in the book. Beauty is God’s gift but to utilize it in proper direction is in your hand. I am thankful to all those beautiful faces in book— Dr Gagandeep Chawala, Dr Smiriti Goswami, Dr Uma Rohra, Dr Swapnil Dewakirti, and Dr Pragya Jaiswal. I would like to thank Dr Ranit Chhabra, Dr Priyanka Aggarwal, Dr Shaheen Hamdani, Dr Payal Tapadiya, and Dr Vivek Lath for their help in proofreading. I offer my humble gratitude to my guide Dr RN Mody for his guidance during my postgraduation and after postgraduation. Friends are always big supporters so I am grateful to Dr Pravin Sundarkar, Dr Neeraj Alladwar and Dr Ravindra Govindwar for heartily wishes. I am also thankful to my brothers and sisters especially elder brother Sadanand for their moral support in my life. I am thankful to Shri Jitendar P Vij (Chairman and Managing Director) and Mr Tarun Duneja (Director-Publishing) of M/s Jaypee Brothers Medical Publishers (P) Ltd., for publishing this book. Commendable type setting, proofreading and improvement in illustrations have been done respectively by Ms Sunita Katla, Md Shakiluzzaman & Ms Geeta Srivastava and Mr Sumit Kumar. Whenever I think who completely changes my life is my wife Savita, who is there in my thick and thin. Whenever I am down, she is there to uplift me with her prayer and support. She is a person with generous heart and I am thankful to God to give gift like her to me in my life. Lastly, I offer my earnest prayers to the Almighty for endowing me the strength and confidence in accomplishing to the best of my abilities.
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Contents Section 1
Basics 1. Oral Diseases: An Introduction .....................................................................................................................3 2. Development and Eruption of Teeth ............................................................................................................5 3. Development and Anatomy of Craniofacial Region ................................................................................9 4. Immunity, Antigen-Antibody Reaction .................................................................................................... 18 5. Neoplasm ........................................................................................................................................................ 24 6. Infection Control in Dental Office ............................................................................................................. 35
Section 2
Diagnostic Procedures 7. Case History .................................................................................................................................................... 45 8. Investigation in Dentistry ............................................................................................................................ 86
Section 3
Diseases of Oral Structure 9. Teeth Anomalies .......................................................................................................................................... 111 10. Developmental Defect of Craniofacial Structure ................................................................................ 153 11. Keratotic and Nonkeratotic Lesions ........................................................................................................ 171 12. Oral Premalignant Lesions and Conditions .......................................................................................... 194 13. Cysts of Jaw ................................................................................................................................................. 230 14. Odontogenic Tumor of Jaw ........................................................................................................................ 266 15. Benign Tumor of Jaw .................................................................................................................................. 293 16. Malignant Tumor of Jaw ............................................................................................................................ 336 17. Vesicular Bullous and Erosive Lesions .................................................................................................. 387 18. Orofacial Pain ............................................................................................................................................... 414
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xvi Textbook of Oral Medicine 19. Infections of Oral Cavity ............................................................................................................................ 440 20. Oral Pigmentation ........................................................................................................................................ 489 21. Dental Caries ................................................................................................................................................ 516 22. Diseases of Tongue ..................................................................................................................................... 533 23. Diseases of Lip ............................................................................................................................................. 557 24. Gingival and Periodontal Diseases ......................................................................................................... 572 25. TMJ Disorders .............................................................................................................................................. 602 26. Salivary Gland Disorders .......................................................................................................................... 638 27. Disorders of Maxillary Sinus .................................................................................................................... 677 28. Traumatic Injuries of Oral Cavity ........................................................................................................... 697 29. Soft Tissue Calcifications .......................................................................................................................... 721
Section 4
Systemic Diseases Manifested in Jaw 30. Bacterial Infections ..................................................................................................................................... 733 31. Viral Infections ............................................................................................................................................ 757 32. Fungal Infections ......................................................................................................................................... 775 33. Specific System Disorders ......................................................................................................................... 784 34. Diseases of Bone Manifested in Jaw ...................................................................................................... 828 35. AIDS ................................................................................................................................................................ 859 36. Endocrine Disorders .................................................................................................................................... 874 37. Blood Disorders ............................................................................................................................................ 894 38. Vitamins ......................................................................................................................................................... 926 39. Metabolic Disorders .................................................................................................................................... 944
Section 5
Drugs used in Dentistry 40. Antibiotics ..................................................................................................................................................... 959 41. Analgesic and Anti-inflammatory Drugs .............................................................................................. 972 42. Antifungal Drugs ......................................................................................................................................... 980 43. Anticancer Drugs ......................................................................................................................................... 988 44. Antiviral Drugs ............................................................................................................................................. 995 45. Corticosteroids ............................................................................................................................................ 1002 46. Desensitizing Agents, Gum Paints and Mouthwashes .................................................................... 1010 47. Drugs used in Pregnancy ......................................................................................................................... 1021 48. Emergency Drugs used in Dentistry ..................................................................................................... 1025
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Contents xvii
Section 6
Miscellaneous 49. Professional Hazards of Dentistry ........................................................................................................ 1035 50. Forensic Dentistry ...................................................................................................................................... 1040 51. Controversial Diseases and Terminologies ........................................................................................ 1051
Appendices Appendix 1: Causes and Classifications ............................................................................................... 1063 Appendix 2: Syndromes of Oral Cavity ................................................................................................. 1103 Appendix 3: Glossary ................................................................................................................................. 1114 Appendix 4: Multiple Choice Questions ............................................................................................... 1133
Index ................................................................................................................................................. 1149
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Meeting Nutritional Needs/Nutrition in Nursing
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3
Oral Diseases: An Introduction
The ultimate aim of entire dental education is to see how well it prepares the practitioners to serve patients. If one has to be a good practitioner it is essential to have a thorough understanding of the basic sciences related to dentistry. Stomatology is the science of structure, function, and disease of the oral cavity. Study methods include examination of related histories, evaluation of clinical signs and symptoms and use of biochemical, microscopic and radiological procedures to establish a diagnosis and a plan for therapeutic management. Diagnosis is the process of evaluating patient’s health as well as the resulting opinions formulated by the clinician. Oral diagnosis is the art of using scientific knowledge to identify oral disease processes and to distinguish one disease from another. History of oral medicine starts when William Gies of Columbia University in 1926 recommend that oral medicine topics should be covered in dental curriculum. In 1945, the American Academy of Oral Medicine was formed. Oral medicine definition accepted in 1993 by international association of oral medicine. It states that — ‘Oral medicine is that area of special competence in dentistry concerned with diseases involving the oral and paraoral structures. It includes the principles of medicine that relate to the mouth as well as research in biological, pathological, and clinical spheres. Oral medicine also includes the diagnosis and medical management of diseases specific to the orofacial tissues and oral manifestations of systemic diseases. It further includes the management of behavioral disorders, the oral and dental treatment of medically compromised patients’. It can also be defined as ‘diagnosis and treatment of oral lesions as well as non-surgical management of temporomandibular joint disorders and facial pain and dental treatment for medically compromised patients in an outpatient sitting, or in an inpatient sitting under general
anesthesia, including specialty care in periodontics and endodontic’. The goal and objective of oral medicine are discussed below. The goal is to provide education, research and service for health care professionals and the public. • Education—it consists of predoctoral, postdoctoral and continuing education training for the health care professional. • Research—it includes activities in the field of biology as it is related to oral disease. • Service—service to society and health care professionals is the objective of oral medicine. Oral medicine will train the professional to provide current and future patient care. As nowadays, epidemiology is changing, in the future, oral medicine person has to come across many oral diseases and he has to diagnose them. World Health Organization in 1989 study called ‘trends in oral health care, a global perspective’ told that in future greater role is required by the oral medicine professional. In the field of oral medicine, you should have a basic understanding of various diseases and their impact on oral tissue, so that it is easy for a practitioner to recognize the presence of any major systemic diseases and then accordingly make the correct diagnosis and treatment plan so as to do thorough justice of what is happening to him. The field of oral medicine consists chiefly of the diagnosis and medical management of the patients with complex medical disorders involving the oral mucosa and salivary glands as well as orofacial pain and temporomandibular joint disorders. Specialists trained in oral medicine also provide dental and oral health care for patients with medical diseases that affect dental treatment, including patients receiving treatment for cancer, diabetes, cardiovascular diseases, and infectious diseases (Fig. 1-1). Oral medicine practice provides physical and medical evaluation, head and neck examination, laboratory
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4 Textbook of Oral Medicine
1
analysis, oral diagnosis and oral therapeutics for such conditions as: vesiculobullous, ulcerative mucosal diseases, painful and burning mucosa, infectious oral diseases, oral conditions arising from medical treatment, oral manifestations of systemic diseases and salivary gland dysfunction. The specialist will perform a comprehensive and/or specialized examination, provide consultation, possibly perform and interpret laboratory tests and perform or prescribe treatments or make the appropriate referrals.
Fig. 1-1: Diagrammatic representation of different areas of oral medicine showing branches and goal of oral medicine.
Dental management of medically compromised patients is becoming a routine and increasingly important part of dental practice. Several factors contribute to this phenomenon. First, the population continues to age. Many older patients have multiple medical conditions. Second, as medical care becomes more effective and cost issues are emphasized, many patients are being treated on an ambulatory basis to avoid hospitalization. Consequently, these individuals are in the community and readily seek dental care. Third, the sophistication of medical treatment is prolonging life. And fourth, the level of and access to available dental care has improved, resulting in more patients (regardless of medical status) wanting dental treatment. Therefore, behavior disorders and diseases of the mouth as manifestations of systemic disease are seen at an increasing rate, and require prompt and adequate care by experienced specialists. Philosophically and in practice, dentistry is similar to one of the various specialties of medicine and consequently,
it is imperative that the dentist understands the medical background of patients before beginning dental therapy, which might fail because of the patients compromised medical status or result in morbidity or death of the patients. The dentist trained in oral medicine should be philosophically atuned to the patient and have knowledge of medically important diseases as well as of dental problems. The dentist should be well versed in the use of rational approaches in diagnosis, medical risk assessment and treatment. The hospital is frequently the setting for the most complex cases in oral medicine. Hospitalized patients are most likely to have oral or dental complications of bone marrow transplantation, hematological malignancies, poorly controlled diabetes, major bleeding disorders, and advanced heart disease. The hospital that wishes to provide the highest level of care for its patients must have a dental department. The hospital dental department should serve as a community referral center by providing the highest level of dental treatment for patients with severe systemic disease and management of the most medically complex patients is best performed in the hospital because of the availability of sophisticated, diagnostic and life-sustaining equipment and the proximity of expert consultants in all areas of health care. Most difficult and unusual problems evaluated by the dentist are seen as consultations. To handle consultations properly, the dentist must be familiar with the proper method of requesting and answering consultations. The role of imaging in oral medicine varies greatly with the type of problem being evaluated. Certain problems, such as pain in the orofacial region, frequently require imaging to determine the origin of the pain. For other conditions, however, such as soft-tissue lesions of the oral mucosa, imaging offers no new diagnostic information. Thus, to conclude oral medicine expert is an important professional in dental and medical team of nations health care scheme to public. Oral medicine personal is also expert in studying, diagnosing and treating the mouth disease.
Suggested Reading 1. Geis WJ. Dental education in the United States and Canada: A report to the Carnegie Foundation for the Advancement of Teaching. Carnegie Foundation: New York, Bulletin 19.1926. 2. Gnanasundaram N. Nine gems of the speciality and ten commandments for specialists in oral medicine and radiology. JIAOMR 2006:18(4):196-201. 3. Millard HD, Mason DK. Perspectives on 1988 World Workshop in Oral Medicine. Chicago: Year Book Publishers, 1989. 4. Millard HD, Mason DK. Perspectives on 1993 World Workshop in Oral Medicine. Ann Arbor: University of Michigan, 1995. 5. Knapp MI. Oral disease in 181,338 consecutive oral examinations. J Am Dent Assoc 1971; 83:1288-93. 6. Pilot T. Trends in oral health care, a global perspective. World Health Organization: Geneva, 6-23 November 1989.
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Development and Eruption of Teeth 5
2
Development and Eruption of Teeth
Introduction Development of tooth is a result of complex process occurring between oral epithelium and underlying mesenchymal tissue. The primitive cavity is lined by stratified squamous epithelium, i.e. oral ectoderm, which contacts the endoderm of foregut to form the buccopharyngeal membrane. At 27th day of gestation, this membrane ruptures and primitive oral cavity establishes a connection with the foregut. The scale of human tooth development: • 42-48 days—dental lamina formation. • 55-56 days—bud stage-deciduous incisor, canine and molar. • 14th week—bell stage for deciduous bud for permanent. • 18th week—dentin and functional ameloblast. • 32nd week—dentin and functional ameloblasts of permanent 1st molar.
Stages of Tooth Development Dental Lamina Formation • Proliferation of basal cells—proliferation of certain areas of basal cells of the oral ectoderm occurs more rapidly than cells of adjacent area. This will result in formation of dental lamina. Dental lamina is a band of epithelium which has invaded underlying ectomesenchyme along each of the horseshoe shaped future dental arch (Fig. 2-1). • Time taken for dental lamina formation—total activity of dental lamina formation extends at least over a period of 5 years. The remnants of dental lamina persist as epithelial pearls or islands within the jaw as well as in the gingiva. • Successional lamina—the lingual extension of dental lamina is called as successional lamina.
Fig. 2-1: Schematic diagram showing initiation of dental lamina by some proliferating basal cells.
Bud Stage (Initiation) • Primordia of enamel organ—after the differentiation of dental lamina, round or ovoid swellings arises from basement membrane. This arises at 10 different points which corresponds to the future position of deciduous teeth. These are primordia of the enamel organs, the tooth bud. • Enamel organ—the enamel organ consists of peripherally located low columnar cells and centrally located polygonal cells. • Dental papilla—the area of ectomesenchymal condensation immediately adjacent to enamel organ is called as ‘dental papilla’. Cells of dental papilla form future tooth pulp and dentin (Fig. 2-2). • Dental sac—the condensed ectomesenchyme that surrounds the tooth bud and dental papilla is called as a ‘dental sac’. Cells of dental sac form cementum and periodontal ligament.
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6 Textbook of Oral Medicine Bell Stage (Histodifferentiation and Morphodifferentiation)
1
Fig. 2-2: Diagram of bud stage showing dental lamina and dental papilla formation (ectomesenchyme condensation).
Cap Stage (Proliferation) • Proliferation—as the tooth bud continues to proliferate, there is unequal growth in different parts of the tooth bud, which leads to cap stage, which is characterized by shallow invagination on the deep surface of bud. • Enamel epithelium—the peripheral cells of the cap, which cover the convexity is called as ‘outer enamel epithelium’ which is cuboidal cells and cells of concavity are called ‘inner enamel epithelium’ which is tall columnar cells (Fig. 2-3). • Stellate reticulum—stellate reticulum is located between outer and inner enamel epithelium, which assume a reticular form. The space in this reticular network is filled with mucoid fluid (rich in albumin) which gives it a ‘cushion-like’ consistency. Due to this, stellate reticulum supports and protects the delicate enamel-forming cells.
• Types of cell present—as the invagination of epithelium deepens and its margins continue to grow; the enamel organ assumes ‘a bell shape’. Four different types of cell i.e. cells of inner enamel epithelium, stratum intermedium, stellate reticulum and outer enamel epithelium are present (Fig. 2-4). • Cells of inner enamel epithelium—it is single layer of tall columnar cells. The cells of inner enamel epithelium differentiate into ameloblast prior to amelogenesis. The cells of inner enamel epithelium exert an organizing influence on the underlying mesenchymal cells in dental papilla, which then differentiate into odontoblasts. • Stratum intermedium—it is the squamous cells occurring between inner enamel epithelium and stellate reticulum. • Stellate reticulum—these cells are star shaped. It has long process and it anastomoses with process of adjacent cells. • Outer enamel epithelium—these are single layered cuboidal cells. • Enamel knot—the cells in the center of the enamel organ are densely packed and form the enamel knot. • Enamel cord—this is the vertical extension of the enamel knot. These cells are attached to one another by junctional complex laterally and to cells in stratum intermedium by desmosomes. • Membrana preformativa—the basement membrane that separates the enamel organ and dental papilla just before dentin formation is called as ‘membrana preformativa’.
Fig. 2-4: Bell stage showing four different types of cells.
Advanced Bell Stage
Fig. 2-3: Inner enamel epithelium cells further differentiate into ameloblasts. It also shows outer enamel epithelium (red arrow) and stellate reticulum (yellow arrow).
• Dentinoenamel junction—during the advanced bell stage, the boundary between inner enamel epithelium and odontoblasts outline the future dentino-enamel junction. • Epithelial root sheath of Hertwig’s—in addition, cervical portion of enamel organ gives rise to epithelial root sheath of Hertwig’s (Fig. 2-5).
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Development and Eruption of Teeth 7
1 Fig. 2-5: Advanced bell stage showing root sheath of Hertwig’s.
Eruption of Teeth The axial or occlusal movement of tooth from its developmental position within the jaw to its functional position in the occlusal plane is known as eruption of teeth. There are 3 types of movements which are described as follows:
Pre-eruptive • Crowding of teeth—when deciduous tooth germ first differentiates, there is good deal of space between them. But due to their rapid growth, this available space is utilized and developing teeth become crowded together, especially in incisor and canine region (Fig. 2-6). • Drifting of deciduous molar—crowding is relieved by growth in length of infant’s jaws, which provides room for second deciduous molars to drift backward and anterior teeth to drift forward. At the same time, the tooth germ also moves outward as jaw increases in width and height (Fig. 2-6). • Movement of permanent teeth—permanent teeth with deciduous predecessors also undergo complete movement before they reach the position from which they will erupt (Fig. 2-6). • Eruption of deciduous predecessor teeth—as their deciduous predecessors erupt, they move to a more apical position and occupy their own bony crypt. • Permanent premolars—premolars begin their development lingual to their predecessors at the level of occlusal surface. They are situated beneath the divergent roots of deciduous molars. • Permanent molar—the permanent molars which do not have predecessors also move from the site of their initial differentiation.
Fig. 2-6: Diagrammatic representation of pre-eruptive phase of eruption.
its final functional position in the occlusal plane. It is important to recognize that jaw growth is normally occurring while most of the teeth are erupting, so that movement in plane other than axial is superimposed on eruptive movement (Figs 2-7 and 2-8).
Fig. 2-7: Diagrammatic representation of eruptive phase of eruption.
Fig. 2-8: Eruptive phase of eruption of teeth showing root resorption of deciduous molar.
Eruptive
Posteruptive
• Axial movement—there is axial or occlusal movement of tooth from its developmental position within the jaw to
• Maintenance—it maintain the position of the erupted tooth while the jaw continued to grow.
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8 Textbook of Oral Medicine Chronology of eruption of teeth
1
Deciduous dentition
Tooth
Formation of enamel matrix and dentin begins
Enamel completed
Eruption
Root completed
4 months in utero 4½ months in utero 5 months in utero 5 months in utero 6 months in utero
1½ months 2½ months 9 months 6 months 11 months
7½ months 9 months 18 months 14 months 24 months
1½ years 2 years 3½ years 2½ years 3 years
4½ months in utero 4½ months in utero 5 months in utero 5 months in utero 6 months in utero
2½ months 3 months 9 months 5½ months 10 months
6 months 7 months 16 months 12 months 20 months
1½ years 1½ years 3¼ years 2¼ years 3 years
Upper Central incisor Lateral incisor Cuspid First molar Second molar Lower Central incisor Lateral incisor Cuspid First molar Second molar
Permanent dentition
Tooth
First evidence of calcification
Crown completed
Eruption
Root completed
3-4 months 10 months 3 years 1½ - 1¾ years 2-2¼ years At birth 2½- 3years 7-9 years
4-5 years 4-5 years 6-7 years 5-6 years 6-7 years 2½ -3 years 7-8 years 12-16 years
7-8 years 8-9 years 11-12 years 10-11 years 10-12 years 6-7 years 12-13 years 17-21 years
10 years 11years 13-15 years 12-13 years 12-14 years 9-10 years 14-16 years 18-25 years
3-4 months 3-4 months 4-5 months 1¾ - 2 years 2¼ - 2½ years At birth 2½ -3 years 8-10 years
4-5 years 4-5 years 6-7 years 5-6 years 6-7 years 2½ - 3 years 7-8 years 12-16 years
6-7 years 7-8 years 9-10 years 10-12 years 10-12 years 6-7 years 11-13 years 12-21 years
9 years 10 years 12-14 years 12-13 years 13-14 years 9-10 years 13-15 years 18-25 years
Upper Central incisor Lateral incisor Canine First premolar Second premolar 1st molar 2nd molar 3rd molar Lower Central incisor Lateral incisor Canine 1st pre molar 2nd pre molar 1st molar 2nd molar 3rd molar
• Compensatory growth—it compensates for proximal and occlusal wear (Fig. 2-9).
Fig. 2-9: Diagrammatic representation of posteruptive phase of eruption.
Suggested Reading 1. Avery JK.Oral Development and Histology (1st edn), BC Decker Inc, Philadelphia, 1988. 2. Avery JK. Embryology of the Teeth. J Dental Research 1951;30: 490. 3. Bhaskar SN. Oraban’s Histology and Embryology (11th edn), Mosby, 1997. 4. Johnson PL, Bevelander G. The Role of the Stratum Intermedium in Tooth Development. Oral Surg 1957;10:437. 5. Mina M, Kollar E. The Induction of Odontogenesis in Non-dental Mesenchymal Combine with Early Murine Mandibular Arch Epithelium. Archive of Oral Biology 1987;32:123. 6. Thesleff I, Vaahtokari A. A Role of Growth Factors in the Determination of Odontoblastic Cell Lineage. Proc Finn Dent Soc 1992;88:357-68. 7. Ten Cate A. Oral Histology Development: Structure and Function (2nd edn), St. Louis CV Mosby, 1986.
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Development and Anatomy of Craniofacial Region
Oral Cavity Development The primitive oral cavity is seen in third prenatal week. There is formation of pit in the tissue which underlies the forebrain. This pit is the future oral cavity. The formation of branchial arches occurs on either side of fetal neck, between the oral pit and developing heart. The process of development of oral cavity is as follows: • Invagination—it occurs between forebrain and heart. Oral cavity forms under the forebrain. • Formation of oropharyngeal membrane—this is wall formed between oral and pharyngeal cavity. It separates the stomodium from first part of foregut. Foregut will develop into pharynx. • Disintegration of oropharyngeal membrane—in fourth week of intrauterine life, oropharyngeal membrane disintegrates. This will lead to continuity between oral and pharyngeal cavity. • Formation of endocrine gland—endocrine glands can develop from roof and floor of oral cavity. Roof gives rise to Rathke’s pouch, which results in the formation of anterior pituitary. Floor can give rise to second epithelial pouch which results in formation of endocrine tissues of the thyroid gland. • Formation of branchial arch—tissues which surround the oral pit give rise to five to six pairs of branchial arch. The mandibular branchial arch is first arch to develop. The hyoid is second arch to develop. Other three archs are not so important in dental point of view.
Anatomy of Oral Cavity The oral cavity is incompletely bounded by bones. Its lateral and anterior walls are formed by the inner surface of the alveolar processes, which join at the midline. The lingual surface of the teeth completes these walls. Oral cavity is divided into:
• Vestibule—it is outer smaller portions of oral cavity. Vestibule of the mouth is a narrow space bounded externally by lips and cheeks and internally by teeth and gums. • Oral cavity proper—it is inner larger part of oral cavity. It is bounded anterolaterally by the teeth, the gums and the alveolar arches of the jaws. The roof is formed by the hard and soft palate. The floor is occupied by the tongue posteriorly and sublingual region anteriorly, below the tip of tongue. Posteriorly, the cavity communicates with the pharynx through the oropharyngeal isthmus which is bounded superiorly by the soft palate, inferiorly by the tongue and on each side by the palatoglossal arches. • Arterial and venous supply of face—arterial and venous supply is showing in Figs 3-1 and 3-2.
Vestibule Lips It is described in the Chapter 23: Disease of Lip.
Cheeks • Content—cheeks are the fleshy flaps, forming a large part of the sides of the face. Mobile portion of cheeks is formed by the buccinator muscle. Intraorally, it is covered by the mucous membrane, and extraorally by the skin. The mucous membrane of the cheeks is fixed to the inner fascia of the buccinator muscle by tight strands of connective tissue. • Posterior part—posterior part consist of masseter muscle and the parotid gland which are interposed between the mucous membrane and buccinator muscle on one side and the skin on the other side. • Nasolabial sulcus—cheek are continuous infront with the lips and the junction is indicated by the nasolabial sulcus which extends from the side of nose to the angle of the mouth.
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• Buccal fat pad of Bichet—the cheek contains a peculiar body of fat tissue called as buccal fat pad of Bichet. It is rounded biconvex structure limited by a thin but distinctive capsule. • Blood supply—it is supplied by the branches of the maxillary artery (Fig. 3-1). • Lymphatic drainage—drain into the submandibular and pre-auricular lymph nodes and partly to the buccal and mandibular nodes.
Fig. 3-1: Arterial supply of the face.
Oral Cavity Proper
Hard Palate • Development—this is the tissue which is interposed between oral and nasal cavity. Palate develops from medial and lateral palatine process. Development of palate starts in sixth week. It develops as intermaxillary segment, between maxillary process of upper jaw. This is called as primary palate. At the end of sixth week, secondary palate develops from lateral palatine process. Lateral palatine process grows medially downward or vertically on either side of tongue. • Boundaries—it is a partition between the nasal and oral cavities. Anterolateral margins are limited by alveolar arches and gingiva. Posterior margin is continuous with the soft palate. Superior surface forms the floor of the nose and inferior surface forms the roof of the oral cavity. • Nerve supply—it is supplied by greater palatine nerves from the greater palatine foramen and nasopalatine nerve from the incisive foramen. • Blood supply—it is supplied by greater palatine branch of the maxillary artery and nasopalatine artery. • Venous drainage—palatine vessels go to the pterygoid plexus of veins. • Lymphatic drainage—it drains mostly into the upper cervical and partly into the retropharyngeal groups of nodes.
Soft Palate
Gingiva It is described in the Chapter 24: Gingival and Periodontal Diseases.
Teeth • Structure—the teeth form a part of the masticatory apparatus and are fixed to the jaws. In man, the teeth are replaced only once (diphyodont) in contrast with nonmammalian vertebrates where teeth are constantly replaced throughout life (polyphyodont). Each tooth has three parts, i.e. crown (projection above the gums), root (embedded in the jaw beneath the gum) and neck (between the crown and root and surrounded by the gums). • Nerve supply—it is supplied by anterior superior alveolar (upper incisor and canine teeth), middle superior alveolar (upper premolar teeth), posterior superior alveolar (molar teeth) and inferior alveolar nerve (lower teeth). • Blood supply—it is supplied by posterior superior alveolar artery (molar and premolar maxillary teeth), anterior superior alveolar (It is branch of infraorbital artery and supplies incisor and canine maxillary teeth) and inferior alveolar artery (it enters the mandibular canal and gives branches to the mandible and to the roots of each teeth attached to the bone).
• Content—it is a movable fold suspended from the posterior border of the hard palate. It separates the nasopharynx from the oropharynx. It has two surfaces, i.e. anterior and posterior and two borders, i.e. superior and inferior. • Anterior surface—it is concave and is marked by median raphe. • Posterior surface—it is convex and is continuous superiorly with the floor of the nasal cavity. • Superior border—it is attached to the posterior border of the hard palate, blending on each side with pharynx. • Inferior border—it is free and bounds with pharyngeal isthmus. • Muscle of the soft palate—these are tensor palati, levator palati, musculus uvula, palatoglossal and palatopharyngeus. • Nerve supply—all muscle of the soft palate except the tensor palati are supplied by the pharyngeal plexus. The fibers of the plexus are derived from the cranial part of the accessory nerve. The tensor palati is supplied by mandibular nerve. General sensory nerves are derived from lesser palatine nerve. • Blood supply—greater palatine branch of the maxillary artery, ascending palatine branch of facial and palatine branch of ascending pharyngeal arteries.
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Development and Anatomy of Craniofacial Region • Venous drainage—veins pass to the pterygoid and tonsillar plexus of veins. • Lymphatic drainage—lymphatics drain into upper cervical and retropharyngeal lymph nodes.
•
Tongue It is described in the Chapter 22: Diseases of Tongue.
Floor of Mouth • Content—it is a crescent shaped area between the lower gingiva and undersurface of the tongue which composes the inferior most portion of the oral cavity overlying the mylohyoid and thyroglossal muscles. • Nerve supply—it is supplied by the branches of trigeminal nerve. • Arterial supply—it is supplied by facial artery. • Venous drainage—drains into facial or lingual vein (Fig. 3-2). • Lymphatic drainage—from the anterior portion of mouth, lymphatics may pass into the deep cervical nodes or laterally to the periosteal lymphatics and then to the submandibular nodes and goes to the deep internal jugular nodes.
•
•
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cell of third and fourth arches. It forms the stylopharyngeal, cricothyroid, levator palatine and constrictor muscle of the pharynx. Content—it is a wide muscular tube situated behind the nose, mouth and larynx. Clinically, it is a part of upper respiratory tract. It is divided into three parts, i.e. nasopharynx (nasal part of pharynx), laryngopharynx (laryngeal part of pharynx) and oropharynx (oral part of pharynx). Oropharynx is the middle part of the pharynx situated behind the oral cavity. Blood supply—it is supplied by ascending pharyngeal branch of the external carotid artery, ascending palatine and tonsillar branch of the facial artery, dorsal lingual branch of lingual artery and greater palatine, pharyngeal and pterygoid branch of the maxillary artery. Venous drainage—it is supplied by a plexus which receives blood from the pharynx and soft palate and prevertebral region and drains into the internal jugular and facial veins. Lymphatic drainage—it drains into the retropharyngeal and deep cervical lymph nodes. Nerve supply—it is supplied by the pharyngeal plexus of nerves which lies chiefly on the middle constrictor.
Muscles of Mastication The muscles of mastication move the mandible during mastication and speech. They are the masseter, the temporalis, the lateral pterygoid and the medial pterygoid.
Development
Fig. 3-2: Venous supply of the face.
Maxillary Sinus It is described in the Chapter 27: Disorders of Maxillary Sinus.
Salivary Glands It is described in the Chapter 26: Disorders of Salivary Glands.
Pharynx • Development—muscles of pharynx are formed at about 7th week of intrauterine life. It forms from the muscle
• Proliferation of myoblasts—muscles of mastication are derived from mandibular arch, i.e. first branchial arch. In fifth and sixth week of intrauterine life, proliferation of myoblasts occurs. • Orientation of muscle cells—muscle cells become oriented to the sites of origin and insertion. • Migration—enlargement of muscle mass occurs and it will migrate into the areas of differentiation. • Formation of muscles—after this, it will be differentiated into masseter, medial and lateral pterygoid and temporal muscle. By tenth prenatal week, muscle mass becomes well organized. Muscle cells of masseter and medial pterygoid form vertical lob which is inserted at angle of mandible. Fibers of lateral pterygoid go horizontally and insert in the articular disc. The temporalis muscle has differentiated in the infratemporal fossa and is inserted in the coronoid process (Fig. 3-3). • Innervations of facial muscle—in seventh week, fifth nerve enters the mandibular arch and seventh nerve in second branchial arch.
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Textbook of Oral Medicine • Functions—its main function is elevation of mandible, its superficial layer may also aid in protruding the mandible. When the mandible is protruded and biting force is applied, the fibers of the deep portion stabilize the condyle against the articular eminence.
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The Temporalis Muscle
Fig. 3-3: Muscle of mastication—A diagrammatic representation.
Masseter Muscle • Site—it is the most superficial to the masticatory muscle, stretches as a rectangular plate from the zygomatic arch to the outer surface of the mandible. It has three layers i.e. superficial, middle and deep. • Superficial layer—it arises by thick aponeurosis from the zygomatic process of the maxilla and from the anterior two-third of the lower border of zygomatic arch. Its fibers pass downward and backward to be inserted into the angle and lower half of lateral surface of ramus of mandible (Fig. 3-4). • Middle layer— it arises from the deep surface of the anterior two-third of the zygomatic arch and posterior one-third of lower border of zygomatic arch and is inserted into middle of ramus of mandible. • Deep layer—it arises from deep surface of the zygomatic arch and is inserted into upper part of the ramus of the mandible and into the coronoid process. • Nerve supply—it is supplied by masseteric nerve which is a branch of anterior division of the mandibular nerve. • Blood supply—the masseteric artery which is a branch of internal maxillary artery and the masseteric vein follow the course of the nerve.
• Origin and insertion—it is fan shaped and arises from whole of the temporal fossa and from the deep surface of temporal fascia. Its fibers converge and descend into tendon which passes through the gap between the zygomatic arch and the side of the skull to be attached to the medial surface, apex, anterior and posterior borders of the coronoid process and the anterior border of the ramus of mandible nearly as far as the last molar teeth (Fig. 3-5). • Nerve supply—it is supplied by the two deep temporal branches of anterior trunk of the mandibular nerve. • Blood supply—it is supplied by middle and deep temporal arteries. The middle temporal artery is a branch of the superficial temporal artery. The deep temporal artery is a branch of internal maxillary artery. • Function • When the entire temporalis contract, it elevates the mandible. • Its middle fibers have a retracting component because of their oblique direction downward and forward. • Its posterior fibers retract the protruded mandible.
Fig. 3-5: Origin and insertion of temporalis muscle.
Lateral Pterygoid
Fig. 3-4: Origin and insertion of masseter muscle.
• Origin and insertion—It is a short thick muscle with two heads. Upper arises from the infratemporal surface and infratemporal crest of the greater wing of sphenoid bone and lower from the lateral surface of lateral pterygoid plate. Its fibers pass backward and laterally to be inserted into the pterygoid fovea on the anterior surface of the neck of the mandible and into the articular capsule and disc of temporomandibular joint (Fig. 3-6).
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Development and Anatomy of Craniofacial Region • Nerve supply—it is supplied by a branch of the anterior trunk of mandibular nerve. • Blood supply—branch of maxillary artery. • Function • It assists in opening the mouth by pulling forward the condylar process of the mandible and the articular disc, while the head of the mandible rotates on the articular disc. • During closure of mouth, backward gliding of the articular disc and condyle of the mandible are controlled by slow elongation of lateral pterygoid with medial pterygoid of the same side. • The medial and lateral pterygoid muscle of both sides contract alternately to produce side-to-side movement of the mandible. • When medial and lateral pterygoid of both sides act together, they protrude the mandible.
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1 Fig. 3-7: Origin and insertion of medial pterygoid muscle.
Bones The skull consists of the 22 bones. Out of which, 8 are paired and 6 are unpaired. Paired bones are parietal, temporal, maxilla, zygomatic, nasal, lacrimal, palatine and inferior nasal concha. Unpaired bones are frontal, occipital, sphenoid, ethmoid, mandible and vomer. From dental point of view, maxilla and mandible are the most important and they are described below:
Maxilla
Fig. 3-6: Origin and insertion of lateral pterygoid muscle.
Medial Pterygoid • Origin and insertion—it is a thick quadrilateral muscle attached to the medial surface of lateral pterygoid plate and the grooved surface of the pyramidal process of the palatine bone above. It has a superficial head which originates from the tuberosity of the maxilla and adjoining bone. Its deep head originates from the medial surface of medial pterygoid plate and the lateral surfaces of pyramidal process of palatine bone. Its fibers pass downward, laterally and backward and are attached by strong tendinous lamina to the posterior inferior part of the medial surfaces of the ramus and the angle of mandible as high as mandibular foramen and as forward as mylohyoid groove (Fig. 3-7). • Nerve supply—it is supplied by branch of the mandibular nerve. • Blood supply—it is supplied by the branch of maxillary artery. • Functions—it helps in the elevation of mandible. Acting with the lateral pterygoid, they protrude the mandible.
The maxilla consists of a central body, which is hollowed out forming the maxillary sinus and four processes (Fig. 3-8). • Frontal process —it ascends from the anteromedial corner of the body, serves as the connection with the frontal bone. • Zygomatic process—it forms in the lateral corner of the body, connects with the zygomatic bone. • Palatine process—it is horizontal and arises from the lower edge of the medial surface of the body. • Alveolar process—it extends downwards and carries the socket for the maxillary teeth.
Fig. 3-8: Maxilla showing frontal process (red arrow) zygomatic process (green arrow) and alveolar process (yellow arrow).
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• Body of maxilla—the body of maxilla is three side pyramid with its base facing the nasal cavity (Fig. 3-9). It lies in an almost horizontal axis with its apex being elongated into the zygomatic process.
tubercle, which often contains a single large marrow process. The lateral and external alveolar plate continues upward into the anterolateral and posterolateral surface of the maxillary body. The internal alveolar plate continues into the palatine process and behind the posterior end of the latter into the nasal surface of the maxillary body. The deep furrow between the two alveolar plates is divided by radial bony plates into the sockets of the individual teeth. • Incisive foramina—at the boundary between two portions of the nasal crest, a canal commences in the nasal floor close to the midline and extends downwards, anteriorly and medially to unite with the canal of the other side in a common opening which is called as incisive or nasopalatine canal (Fig. 3-10). On the anterior surface of maxilla, there is canine fossa situated lateral to the canine eminence.
Mandible
• Side of maxilla—the three sides are superior or orbital (it forms greater part of the orbital floor), an anterolateral or malar (surface forming part of the skeleton of the cheek and face) and posterolateral or infra-temporal (surface turned towards the infra-temporal fossa). • Base—the base is rimmed on its inferior edge by the alveolar process housing the teeth row. • Alveolar process—alveolar process consists of two roughly parallel plates of bone that unite behind the last tooth to form a small rough prominence, the alveolar
It is the largest and strongest bone of the face. It consists of a horseshoe shaped body continuous upward and backward on either side with the mandibular rami. • Body—the body is thick, has a rounded lower border and carries the alveolar process on its upper border. It extends backward from the chin at the midline symphysis to the anterior limit of the ramus. • Ramus—it is a thick quadrilateral plate which extends backward from the groove for the facial artery (antegonial notch) to include the region called the mandibular angle (Fig. 3-11). The anterior border of the ramus continues along the body lateral to the alveolar process as a blunt ridge, the oblique line, running downward and forward to disappear at about the level of the 1st molar.
Fig. 3-10: Palatal view of maxilla showing incisive foramen (red arrow).
Fig. 3-11: Overview of mandible showing body and ramus of mandible.
Fig. 3-9: Front view of maxilla.
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Development and Anatomy of Craniofacial Region • Mental protuberance—in the midline of anterior surface of the body projects a triangular prominence called mental protuberance. • Symphysis menti—it is the line at which the right and left halves of the bone meet each other. • The mental foramen, through which the mental nerve and blood vessels pass, is located on the lateral surface of body between the roots of the 1st and 2nd premolars. In the vertical dimension, the foramen lies halfway between the lower border of mandible and the alveolar margin. • Genial tubercle—slightly above the lower border on its inner surface the mandibular symphysis is elevated in more or less sharply defined projection called as genial tubercle. • Mylohyoid line—it is a prominent ridge that runs obliquely downward and forward from below 3rd molar tooth to the medial area below the genial tubercle. Below the mylohyoid line, the surface is slightly hollowed out to form submandibular fossa, which lodges the submandibular gland. • Mandibular canal—the mandibular canal which houses the inferior alveolar nerve and blood vessels begins at the mandibular foramen, curves downward and forward and turns into a horizontal course below the roots of the molars. In the region of the premolars, the mandibular canal splits into two canals of unequal width; the narrower incisive canal continues the course of mandibular canal toward the midline and the wider branch, the mental, turns laterally, superiorly and posteriorly to open at the mental foramen (Fig. 3-12).
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• Digastric fossa—the lower border of the mandible is also called as base. Near the midline, the base shows an oval depression called digastric fossa.
Trigeminal Nerve The trigeminal nerve is the 5th cranial nerve and is also the largest. It has a large sensory root and a small motor root. It is attached to lateral part of pons by its two roots. It conveys both exteroceptive and proprioceptive impulses. Exteroceptive impulses of touch, pain and thermal senses are transmitted from skin of face, forehead, mucous membrane of nasal and oral cavity, sinus, and floor of mouth, teeth and anterior 2/3rd of tongue. Proprioceptive impulses of deep pressure are conveyed from teeth, periodontium, hard palate and temporomandibular joint receptors.
Branches of Trigeminal Nerve (Fig. 3-13) Ophthalmic division It is the smallest branch of semilunar ganglion and passes forward in the lateral wall of cavernous sinus. • Lacrimal nerve—it supplies sensory fibers to the gland and the adjacent conjunctiva. • Frontal nerve—it divides into supraorbital nerve (supplies the skin of the upper eyelid, forehead and the anterior scalp region to the vertex of skull), and supratrochlear nerve (supplies skin of the upper eyelid and lower medial portion of forehead). • Nasociliary nerve —it gives numerous branches. It include branches in orbit (Long ciliary nerves, posterior ethmoid nerve, anterior ethmoid nerve, external nasal branches), branches arising in nasal cavity and terminal branches on the face.
Fig. 3-12: Side view of mandible showing mental foramina (red arrow).
• Alveolar bone—the alveolar plates consist of two compact bony plates, the external and internal alveolar plate. These two plates are joined to each other by radial interdental and in the molar region, by inter-radicular septa, thus forming the sockets for the teeth in the same manner as in the upper jaw.
Fig. 3-13: Different branches of trigeminal nerve supplying to face.
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Maxillary division It is intermediate division, and entirely sensory. It enters the orbit through inferior orbital fissure. It is now named infraorbital nerve and having traversed the infraorbital groove and canal in floor of orbit, it appears on face through infraorbital foramen. Branches are divided into 4 groups • Middle meningeal nerve—supplies the dura with sensory fibers. • Ganglionic branches—they contain secretometer fibers for the lacrimal gland and sensory fibers for orbital periosteum and mucous membranes of the nose, palate and pharynx. • Zygomatic nerve—it is divided into two branches, i.e. zygomaticofacial (supplies sensory fiber to skin over the prominence of zygomatic bone) and zyomaticotemporal (it supplies sensory fibers to skin over anterior temporal fossa region). • Posterior superior alveolar nerve—it gives sensory branches to mucous membrane of sinus. It also supplies the maxillary molars and their gingivae. • Middle superior alveolar nerve—it supplies upper premolar and mesiobuccal root of upper first molar. • Anterior superior alveolar nerve—it supplies roots of maxillary central and lateral incisors. They also send branches to superior dental plexus of nerves within maxilla. They also supply mucous membrane of anterior part of maxillary sinus as well as labial gingivae of incisors and cuspid teeth. • Inferior palpebral branches—they supply sensory fibers to skin of lower eyelid and its conjunctiva. • External or lateral nasal branches—they supply skin of side of nose.
• Superior labial branches - three or more in number and supply skin and mucous membrane of upper lip and labial glands.
Mandibular Nerve It is the largest of the three divisions. It is divided into following branches: • Nervus spinosus—it supplies dura and mastoid cells. • Nerve to internal pterygoid muscle—it supplies internal pterygoid muscle. • Pterygoid nerve—it enters medial side of external pterygoid muscle to provide motor nerve supply. • Masseter nerve—it supplies masseter muscle. • Anterior deep temporal nerve—it ends in deep part of anterior portion of temporal muscle. • Posterior deep temporal nerve—it passes upward to deep part of temporal muscle. • Long buccal nerve—it supplies mandibular 2nd and 3rd molars. It then sends fibers to mucous membrane and skin of cheek, retromolar triangle, and buccal gingivae of mandibular molars and mucous membrane of lower part of buccal vestibule. • Auriculotemporal nerve—it traverses upper deep part of parotid gland and then crosses the posterior root of zygomatic arch. It passes with superficial temporal artery in its upward course and then divides with numerous branches to tragus of external ear, to scalp, to the ear and as for upward as vertex of skull. • Parotid branches—they are sensory, secretory and vasomotor fibers to the gland. • Articular branches—it enter the posterior part of the temporomandibular joint.
TABLE 3-1: Lymphatic drainage of head and neck
Nodes
Sites
Occipital
Scalp, posterior to the ear and occipital region
Posterior auricular
External ear, scalp above and behind the ear.
Anterior auricular (pre-auricular/parotid )
Skin anterior to the temple, external meatus, lateral forehead, lateral eyelids, infraorbital nodes, posterior cheek, part of the outer ear, parotid gland
Inferior auricular (infra-auricular)
Pre- and post-auricular nodes
Infra-orbital
Skin of inner corner of the eye, skin of anterior face, and superficial aspect of the nose
Buccal
Skin over the anterior face, mucous membrane of the lips and cheeks, occasionally mandibular and maxillary teeth and gingivae
Submental
Tip of the tongue, midportion of the lower lips, chin, lower incisors and gingivae
Mandibular (supra-mandibular)
Skin over the mandible, mucous membrane of the lips and cheeks. Occasionally, maxillary and mandibular teeth and gingivae.
Submandibular (sub-maxillary)
Upper and lower teeth and gingivae except mandibular incisor, anterior nasal cavity, palate, body of tongue, upper lip, lateral angle of eye, submental nodes
Superficial cervical
Pinna and adjacent skin, pre- and post-auricular nodes
Deep cervical
Submandibular, submental, inferior auricular, tonsillar and tongue nodes
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Fig. 3-14: Lymphatic drainage of face.
• Auricular branches—it supplies the skin of helix and tragus. • Meatal branches—two small branches which supply skin lining the meatus and tympanic membrane. • Terminal branches—they supply scalp and temporal region. • Lingual nerve—It gives off small branches that are sensory to part of tonsil and mucous membrane of posterior part of oral cavity. It is sensory to mucous membrane of oral cavity, anterior 2/3rd of tongue (along with chorda tympani nerve), floor of mouth and gingivae on lingual surface of the mandible. • Inferior alveolar nerve—it is the largest branch of posterior division of mandibular nerve. It sends motor branches to mylohyoid muscle and anterior belly of digastric muscle. It then enters mandibular foramen and descends in the mandible in the inferior dental canal as inferior alveolar nerve. It is sensory to mandibular teeth, body of mandible and labial gingiva anterior to bicuspid teeth. • Mental nerve—it passes through mental foramen on lateral surface of mandible. It is sensory to skin of chin, lower lip, and mucous membrane lining of lower lip.
• Incisive nerve—it continues anteriorly in the inferior dental canal to midline. It is sensory to anterior teeth and labial gingivae.
Lymphatic Drainage of Head and Neck It is described in Table 3-1 and Fig. 3-14.
Suggested Reading 1. Avery JK. Oral Development and Histology (1st edn), BC Decker Inc, Philadelphia, 1988. 2. Bhaskar SN. Oraban’s Histology and Embryology (11th edn), Mosby, 1997. 3. Gasser RF. The Development of Facial Muscle in Man. American Journal of Anatomy 1967;120:357. 4. Gray’s Anatomy (38th edn), Churchill Livingstone, 1995. 5. Hall BK. The Embryonic Development of Bone. Amer Scientist 1988;76(2):174. 6. Poswillo D. The Pathogenesis of the First and Second Branchial Arch Syndrome. Oral Surg 1973;35:302. 7. Ten Cate A. Oral Histology Development: Structure and Function (2nd edn), St. Louis CV Mosby, 1986.
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Immunity, AntigenAntibody Reaction
Immunity The word immunology derived from Latin word ‘immunis’ meaning ‘free of burden’. “It is the resistance exhibited by the host towards injury caused by microorganisms and their products”. It is a reaction of body against any foreign antigens. Immunity against infectious diseases consists of two main types, each with humoral and cellular components and their effective cells. The importance of immune system occurs in life-threatening infection suffer by patient with immune defect.
Uses of Immunity • Understanding the disease—it helps to understand the etiology and pathogenesis of many diseases. • Vaccine—development of vaccine can be done with the help of immunity. • Treatment—treatment of many diseases can be done with antibodies. • Future susceptibility—it helps to find with future susceptibility to disease with the help of HLA typing system.
Classification (Fig. 4-1) • Innate immunity • Non-specific • Specific • Acquired • Active — Natural — Artificial • Passive — Natural — Artificial • Local • Herd
Fig. 4-1: Different types of immunity— A diagrammatic representation.
Innate Immunity This is also called as natural immunity. This compromise of preexisting non-specific defences. It is the resistance to infection, which an individual possesses by virtue of his genetic and constitutional make up. It does not depend upon the prior contact with microorganisms or immunization. Innate immunity can be considered at the level of race, species or at individual’s levels.
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Immunity, Antigen-Antibody Reaction 19 Types of Innate Immunity
Acquired Immunity
• Specific and non-specific—it may be non-specific when it indicates degree of resistance to infection in general or specific when resistance to particular pathogen is concerned. • Species immunity—it refers to total or relative refractoriness to a pathogen shown by all members of a species e.g. all human beings are totally unsusceptible to plant pathogens and to many pathogens of animals, such as rinderpest or distemper. It may be due to physiological and biochemical differences between the tissues of different host species, which determine whether a pathogen can multiply or not. • Racial immunity—within species, different races may show differences in susceptibility to infection. This is called as ‘racial immunity’ e.g. high resistance of Algerian sheep to anthrax. Such racial differences are known to be genetic in origin. • Individual immunity—the differences in individual immunity exhibited by different individuals in a race is called as ‘individual immunity’ e.g. homozygous twins exhibit similar degree of resistance or susceptibility to lepromatous leprosy and tuberculosis. Such correlation is not seen in heterozygous twins.
The resistance that an individual acquires during life is known as ‘acquired immunity’. It is of two types.
Factors Affecting Innate Immunity • Age—the two extremes of life carry higher susceptibility to infection as compared to adults. The fetus in utero however is protected from maternal infection by the placental barrier. • Hormonal influence—endocrine disorders such as diabetes mellitus, hypothyroidism and adrenal dysfunction are associated with an enhanced susceptibility to infection. Corticosteroids exert an important influence on response to infection. The elevated steroid levels during pregnancy may have a relation to heightened susceptibility of pregnant women to many infections. • Nutrition—in general, both humoral and cell mediated responses are reduced in malnutrition. Cell mediated immune response such as Mantoux test becomes negative in severe protein deficiency. Certain infections may not become clinically apparent in severely malnourished patients.
Mechanism of Innate Immunity • Epithelial surface—skin and mucous membrane covering the body gives protection against bacteria. They act as mechanical barrier. • Humoral factors—it consists of lysozyme, properdin, betalysin, C-reactive protein, bactericidin etc. • Cellular factors—it includes phagocytosis, and inflammation.
Active Immunity It is resistance developed by an individual because of antigenic stimulus. This involves active functioning of host’s immune apparatus leading to synthesis of antibodies or production of immunologically active cells. Once the active immunity develops, it is long lasting. It is also of two types. • Natural—it results from either a clinical or an inapparent infection with the parasite, e.g. a person who has recovered from an attack of smallpox develops natural immunity to it. The immunity following bacterial infection is generally less permanent than that following a viral infection. • Artificial—it is the resistance induced by vaccines, which are preparations of live or killed microorganisms or their product.
Passive Immunity The resistance that is transmitted to a person in readymade fashion is known as passive immunity. There is no antigenic stimulant, instead preformed antibodies are administered. There is no latent period, protection being effective immediately after passive immunization. It is less effective and inferior to active immunization, but it is immediate in action and can be employed when instant immunity is needed. It is also of two types. • Natural—it is the resistance passively transferred from mother to baby. By active immunization of mothers during pregnancy, it is possible to improve the quality of passive immunity in the infants. • Artificial—it is passively transferred to the recipient by the administration of antibodies. The agent used is hyperimmune sera of animal or human origin, convalescent sera and pooled human gamma globulin.
Local Immunity It is important in treatment of infection, which is either localized or due to surgeries (postoperative infection), in combating infections at the site of primary entry of the pathogen. Natural infection or the live virus vaccine administered provides local immunity.
Herd Immunity This refers to the overall level of immunity in a community and is relevant in the control of epidemic diseases. When a large proportion of individuals in a community (herd)
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is immune to a pathogen, herd immunity to a pathogen is satisfactory. When herd immunity is low, epidemics are likely to occur on the introduction of a suitable pathogen.
Antigen-Antibody Reaction Antigen • Definition—any substance which when introduced parenterally into a body stimulates the production of an antibody, with which it reacts specifically and in an observable manner. The immune system can respond to antigen either by cell mediated immunity or by humoral immunity. • Size—most antigens are large molecules (over 1000 molecular weight). Smaller molecules do not provoke an immune response unless bound to large carrier molecules. The complete antigen is able to induce antibody formation and produces a specific and observable reaction with the antibody so produced. • Haptens—these are substances which are incapable of inducing antibody formation by themselves, but can react specifically with antibodies. • Epitope—the smallest unit to antigenicity is known as an epitope or antigenic determinant.
7S molecule found on mucosal surfaces and in secretions. It is a dimer formed by two monomer units joined together at their carboxyterminals by glycopeptides termed the ‘J chain’. This is called as secretory IgA. It can activate complement by the alternative pathway.
IgM It is formed by J chains into pentamers of the Ig molecules and these attain very high molecular weight of 9000,000. The large molecular size prevents it from leaving the plasma, except when permitted by increased vascular permeability in inflammatory lesions. As it has antigen combining sites, it has good agglutinating and complement fixing properties. It is the first class of antibodies to be formed in immune response.
IgE It binds selectively to mast cells and to basophils by its Fc fragment. The binding of antigen to its Fab fragment triggers reflex of histamine and other substances which are important in anaphylactic type of hypersensitivity.
IgD The function of IgD is largely unknown, but it may act as an antigen receptor on the lymphocyte surface.
Antibody Antibody is produced by plasma cells in the lymph nodes, bone marrow and spleen. The cells are ovoid with an eccentrically placed nucleus. The cytoplasm is basophilic. One plasma cell produces antibody of one class, reactive with only one antigen. There are five classes of immunoglobulins which are as follows:
Antigen–Antibody Reaction Mechanism Antigen-antibody reaction in vitro is known as serological reaction (Fig. 4-2).
IgG It is the most abundant immunoglobulin in the plasma and extracellular fluid. It can cross placenta and is important in passive transfer of immunity to the fetus. It is capable of neutralizing toxins and may be cytolytic through the activation of a complement. Polymorphs and macrophages have surface receptors for Fc fragment of IgG, thus binding of IgG to particular antigens promotes adhesion of these cells and subsequent phagocytosis of antigen.
IgA It is secreted locally by plasma cells in the respiratory passages, salivary and lacrimal glands and intestinal mucosa. It is an important constituent of breast milk. IgA occurs in two forms, serum IgA is principally a monomeric
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Fig. 4-2: Diagrammatic representation of antigen-antibody reaction.
Immunity, Antigen-Antibody Reaction 21 • Primary state —In this, there is initial interaction between the two without any visible effect. This reaction is rapid and occurs even at low temperature and also is reversible because inter-molecular forces between Ag and Ab are weaker. • Secondary state—it leads to precipitation, agglutination, lysis of cells, killing of live antigens, neutralization of motile organisms and enhancement of phagocytosis. An antigen can stimulate production of different types of immunoglobulins, which differ in their reaction capability and other properties. • Tertiary state—some antigen-antibody reactions occurring in vivo initiate chain reactions that leads to neutralization or destruction of injurious antigens or tissue damage. These are tertiary reactions and include humoral immunity against infectious diseases, clinical allergy and other immunological diseases.
1 Fig. 4-3: Precipitation reaction—A diagrammatic representation.
General Features of an Antigen-Antibody Reaction • Specific—the reaction is specific; an antigen combines only with its homologous antibody and vice versa. Entire molecule reacts and not its fragments. • Non-degenerative—there is no degeneration of the antigen or antibody during the reaction. • Combination—the combination occurs at the surface, which is firm and reversible. Antigen and antibody can combine in varying proportions.
Precipitation Reaction • Formation of insoluble precipitate—when a soluble antigen combines with antibody in the presence of electrolyte (NaCl) at a suitable temperature and pH, the antigenantibody complex forms an insoluble precipitate which is greatly influenced by the relative proportions of antigens or antibodies. • Results—if into the same amount of antiserum in different tubes, increasing quantities of antigens are added, precipitation will be found to occur most rapidly and abundantly in one of the middle tubes in which Ag and Ab are present in optimal or equivalent proportion. The precipitation will be weak in proceeding or later tubes (Fig. 4-3).
Fig. 4-4: Agglutination reaction.
when an antigen and antibody react in equivalent proportions. Better agglutination reaction takes place with IgM antibody than with IgG antibody (Fig. 4-4).
Complement Fixation Test Agglutination Reaction • Mechanism—when the particulate antigen is mixed with its antibody in the presence of the electrolyte at a suitable temperature and pH, the particles are clumped or agglutinated. It is more sensitive than precipitation for the detection of an antibody. It occurs optimally
• Mechanism—complement takes part in many immunological reactions and is absorbed during the combination of antigens with their antibodies. The ability of antigen-antibody complexes to fix complement is made to use in the complement fixation test. This is a very sensitive and a versatile test.
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• Component—it consists of five reagents which are antigen, antibody, complement, sheep erythrocytes, and amboceptor. Each of these has to be separately standardized. • One unit or minimum hemolytic dose of complement is defined as the highest dilution of guinea pig serum that lyses one unit volume of washed sheep erythrocyte in the presence of excess of hemolysin (amboceptor) within a fixed time (usually 30 or 60 minutes) and at a fixed temperature (37°C) (Figs 4-5 and 4-6).
Fig. 4-5: Positive complement fixation test.
Fig. 4-6: Negative complement fixation test.
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Immunity, Antigen-Antibody Reaction 23 Virus Neutralization Test Neutralization of viruses by their antibodies can be demonstrated in various systems. Neutralization of bacteriophages can be demonstrated by the plaque inhibition test. Neutralization of animal viruses can be seen in three systems: animal, eggs and tissue culture.
Immunofluorescence • Mechanism—fluorescence is a property of absorbing light rays of one particular wavelength and emitting rays with different wavelengths. Fluorescence dye can be conjugated to antibodies and such labelled antibodies can be used to locate and identify antigen in tissue.
• Use—this test can be used for identification of bacteria, viruses or other antigens using specific antisera labelled with fluorescence dyes. • Dye use—commonly used dye is fluorescein isothiocynate and lissamine rhodamine exhibiting blue-green and orange-red fluorescence respectively.
Suggested Reading 1. Gupte S. A Short Textbook of Medical Microbiology (9th edn), Jaypee Brothers, New Delhi, 2006. 2. Roitt I, Brostoff J, Male D. Immunology (5th edn), Mosby, London, 1997. 3. Samaranayake LP. Essential Microbiology for Dentistry (2nd edn), Churchill Livingstone, 2002.
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Neoplasm
Definition It is an abnormal mass of tissue, growth of which exceeds and is uncoordinated with that of normal tissues and persists in the same excessive manner, after cessation of the stimuli that evokes the changes. Oncology is the study of neoplasm.
Nomenclature There are mainly of two types neoplasm: benign and malignant. Benign tumors are designated by attaching ‘oma’ to cell of the organ. Malignant tumors arising from mesenchymal tissues are known as ‘sarcomas’, like osteosarcoma. Malignant tumors of epithelial origin are called ‘carcinoma’, like adenocarcinoma and squamous cell carcinoma.
Normal Cell Cycle All renewing cells go through a series of events known as cell cycle. Successive phases of progression of cell cycle are described below (Fig. 5-1). • G1 phase—after mitosis (M phase), cells spend a variable period of resting (G1 phase) where DNA synthesis is absent but the synthesis of RNA and protein continues. • S phase—at the end of G1 phase, unknown signals continuously institute a burst of RNA synthesis which is followed by DNA synthesis (S phase). Then the cells undergo replication or remain polypoid and eventually die. • G2 phase—the cells cease DNA synthesis during G2 phase and DNA content is fairly constant in the growing normal cells. The proportion of cells population undergoes active proliferation in the cycle is termed as growth fraction.
Fig. 5-1: Normal cell cycle—A diagrammatic representation.
• G0 phase—daughter cells may continue to remain in cell cycle and divide further or may go out at the cell cycle in resting phase.
Predisposing Epidemiologic Factor for Development of Neoplasm Hereditary Predisposition The risk of developing cancer in relatives of a known cancer patient is three times higher than control study. Genetic cancers comprise not greater than 5% of all cancers, e.g. retinoblastoma, familial polyposis coli, cancer of breast etc.
Racial and Geographic Factors Cancers are largely due to the influence of environment and geographic differences affecting whole population such as climate, water, diet, habit. For example— • Black Africans commonly have cancers of skin, penis, cervix, and liver. Europeans and Americans commonly develop malignancies of lung, breast, and colon.
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Neoplasm • Carcinoma of stomach is five times higher in Japanese than in Americans. • Nasopharyngeal cancer is common in south East Asians.
Environmental and Cultural Factors We are surrounded by an environment of carcinogens which we eat, drink, inhale and touch (Fig. 5-2). For example— • Cigarette smoking is the etiology of cancer of oral cavity, pharynx, larynx, esophagus, lung, pancreas and urinary bladder. • Alcohol causes cancer of esophagus and liver. • Alcohol and tobacco together accelerate the risk of developing cancer of upper aerodigestive tract. • Betel nut chewing causes cancer of cheek and tongue. • Industrial and environmental materials are carcinogenic. This includes exposure to substances like arsenic, asbestos, benzene, and naphthylamine. • Overweight individuals, deficiency of vitamin A, people consuming foods rich in animal fats and low in fiber content have more risk of developing cancers like colonic cancer.
Age Generally, it occurs in older individuals past 5th decade of life but, there is variation in age groups. For example, acute leukemia occurs in children, neuroblastoma in infancy.
Fig. 5-2: Different types of etiological factors responsible for formation of neoplasm.
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Sex It is generally more common in men except cancer of breast, gallbladder, and thyroid.
Acquired Preneoplastic Conditions These may be inflammatory, hyperplastic conditions or may be certain benign tumors. It includes chronic atrophic glossitis, leukoplakia of oral cavity, vulva and penis, cirrhosis of liver, chronic irritation and multiple neurofibromas.
Carcinogenesis Carcinogenesis or oncogenesis or tumorigenesis means induction of tumors; agents which can induce tumors are called carcinogens. Carcinogens are broadly divided into four groups (Fig. 5-3): • Chemical carcinogens • Physical carcinogens (radiation) • Hormonal carcinogens • Biologic carcinogens (virus)
Fig. 5-3: Types of carcinogenesis.
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Chemical Carcinogenesis
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Chemical carcinogens are divided into two broad groups:
Initiators of Carcinogenesis • Direct-acting carcinogens—these require no metabolic conversion to become carcinogens. • Alkylating agents —it includes, various chemotherapeutic drugs that have successfully cured, controlled or delayed recurrence of certain types of cancers only to later evoke a second form of cancer usually leukemia. Various agents used are cyclophosphamide, chlorambucil, busulfan, melphalan, nitrosourea, β-propiolactone and epoxides. This tragic consequence is called as “Pyrrhic victory” which becomes less of a victory when their initial use has been converted to cause later on second form of cancer. • Acylating agents—substances like acetyl imidazole. • Indirect-acting carcinogens or procarcinogens—these are chemical substances requiring metabolic activation for becoming potent initial carcinogens. • Polycyclic aromatic hydrocarbons (in tobacco, smoke, animal foods, industrial oil, and atmospheric pollutants). Important chemical compounds included are benzanthracene, benzapyrene, methylcholanthrene. They may cause lung cancer, skin cancer, cancer of oral cavity, and sarcoma. • Aromatic amines and azo dyes—These are β-naphthylamine, benzidine, azo dyes used for coloring foods, and acetyl aminofluorene. They may cause bladder cancer and hepatocellular carcinoma. • Naturally occurring product—Aflatoxin, actinomycin-D, mitomycin-C, safrole, and betel nut. It can cause hepatocellular carcinoma. • Miscellaneous—nitroso compounds, vinyl chloride monomer, asbestos, arsenical compounds, metals like nickel, lead, chromium, and insecticides, fungicides can cause gastric carcinoma, hemangiosarcoma of liver, bronchogenic carcinoma, epidermal hyperplasia, basal cell carcinoma, and lung cancer.
molecule inducing miscoding error during transcription and replication. • Factors affecting a carcinogenicity • Dose dependent—the carcinogenicity of chemical agents is dose dependent and multiple traditional doses have same oncogenicity as a single comparative dose. • Administration of promoters—the carcinogenicity of chemical agents can be significantly enhanced by the subsequent administration of promoters. To be effective, the promoter must follow the initiator.
Stage of Chemical Carcinogen The phenomenon of cellular transformation by chemical carcinogenesis is a progressive process involving two different stages. These are initiation and promotion. Initiation In this initiator carcinogen interact with DNA of target cell to induce mutation that is more or less irreversible to transform it into initiated cell. • Metabolic activation—only indirect acting carcinogen or procarcinogens require metabolic activation chiefly by mixed oxidases of cytochrome P-450 system located in microsomal compounds of the endoplasmic reticulum or in the nucleus. • Reactive electrophiles—they are electron deficient protons, which bind to electron rich portions of other molecules of cell such as DNA, RNA or other protein. • Target molecules—the primary target is DNA, producing mutagenesis. • Initiated cell—the unrepaired damage produced in the DNA of the cell becomes permanent, only if the altered cell undergoes at least one cycle of proliferation. Promotion It does not damage the DNA but enhances the effect of direct-acting carcinogen or procarcinogens. The ultimate effect is further clonal proliferation of the initiated cell. Two or more initiators may be chemical, oncogenic virus or radiant energy may act in concert to induce malignant transformation referred to as cocarcinogens.
Promoters of Carcinogenesis
Physical Carcinogenesis
Certain chemical substances lacking the intrinsic carcinogenic potential but helping the initiated cell to proliferate further are called promoter of carcinogenesis. E.g. phorbol, phenols, drugs like phenobarbital, and artificial sweetener like saccharine.
It is divided into two groups.
Mechanism of Action • Binding to DNA and RNA—the great majority of chemical carcinogens are mutagens. They bind directly to DNA and RNA or cytoplasmic proteins to specific sites within
Radiation Carcinogenesis • Forms of radiation—radiation whenever in the form of UV light from sunlight, UV lamp, welder’s arc, or ionizing radiation like X-ray, α, β and γ ray, radioactive isotopes, protons and neutrons are established carcinogens. • Example of radiation induced cancers—most frequent radiation induced cancers are leukemia, cancer of
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Neoplasm thyroid, skin, breast, lung, and salivary gland. Therapeutic irradiation can also induce carcinogenesis. • Facts about radiation causing cancer—radiant energy have potential of producing mutation and even killing cells. It can affect carcinogenesis by the following facts: • Few tumors appear only after long latent period during which successive generation of clones are developed. • The radiation initiation is generally irreversible, but at a low dosage level is amenable to repair. • The effect of radiation depends upon a number of factors such as type of radiation, dose, length of interval between the doses, capability of cells to repair in intervals and various host factors such as age, individual susceptibility, immune competence, hormonal influence and type of cell irradiated. • Mechanism—it induces cancer by following mechanism; • Radiation may directly alter the cellular DNA and it may dislodge ions from water and other molecules of cell and result in the formation of highly reactive free radicals that may bring about the damage. • Radiation mutation may render cell vulnerable to other carcinogenic influence, i.e. acting as cocarcinogen. • Inhibition of cell division and inactivation of enzymes. • Radiation might cause cell killing; permitting survivors to proliferate and thereby, become vulnerable to oncogenic influence.
Non-radiation Physical Carcinogenesis Mechanical injury to tissues such as from stones in the gall bladder, stones in the urinary tract, and healed scars following burns or trauma has been suggested as causes of increased risk of carcinoma. Implants of inert materials such as plastic, glass, etc. in prosthesis and foreign bodies like metal foils observe to cause tumor development in experimental animals.
Hormonal Carcinogenesis Carcinoma is most likely to develop in organs and tissues which undergo proliferation under influence of excessive hormonal stimulation. Hormone sensitive tissues developing tumors are breast, endometrium, myometrium, vagina, thyroid, liver, prostate, and testis. • Estrogen—in experimental animals, estrogen can cause induction of breast cancer in mice. Other cancers which can be induced in mice by estrogens are squamous cell carcinoma of cervix, connective tissue tumor of myometrium, tumor of kidney in hamsters, and benign and malignant tumors of liver in rats. In case of human women receiving estrogen therapy and women with estrogen secreting granulosa cell, tumor of the ovary have
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increased risk of developing endometrial carcinoma. Adenocarcinoma of the vagina is seen with increased frequency in adolescent daughter of mother who had received estrogen therapy during pregnancy. • Contraceptive hormones—there is increased risk of developing breast cancer, benign tumors of the liver and few patients have developed hepatocellular carcinoma. • Anabolic steroids—consumption of anabolic steroids by athletes to increase the muscle mass also increases the risk of developing benign and malignant tumor of the liver. • Hormone dependent tumors—it has been shown in experimental animals that induction of hyperfunction of adenohypophysis is associated with increased risk of developing neoplasia of the target organs following preceding functional hyperplasia.
Biologic Carcinogenesis The epidemiological studies on different types of cancer indicate the involvement of transmissible biologic agents in their development, chiefly viruses. It has been estimated that about 20% of all cancers worldwide are virus associated cancers. Therefore biological carcinogenesis is largely viral oncogenesis. A large number of viruses have been proved to be oncogenic in wide variety of animals and in certain types of cancers in humans. The association of oncogenic virus with neoplasia was observed by an Italian physician Sanarelli in 1889 who noted association between myxomatosis of rabbit with poxvirus. Oncogenic viruses fall into 2 broad groups, i.e. those containing ribonucleic acid are termed as RNA oncogenic viruses and those containing deoxyribonucleic acid are termed as DNA oncogenic viruses.
RNA Oncogenic Viruses These are retroviruses, i.e. they contain the enzyme reverse transcriptase, which is required for reverse transcription of viral RNA to synthesize viral DNA strands. Based on their activity to transplant target cells into neoplastic cells, they all are divided into three subgroups: • Acute transforming viruses—it includes Rous sarcoma virus in chickens, leukemia-sarcoma viruses of avian, feline, bovine and primate. • Slow transforming tumor viruses—mouse mammary tumor virus (MMTV) that causes breast cancer in daughter mice. • Human T-cell Lymphotropic viruses (HTLV)—it can cause adult T-cell leukemia-lymphoma syndrome and AIDS.
DNA Oncogenic Viruses They are divided into five groups • Papovavirus group—human papilloma virus, polyoma virus, SV-40 (simian vacuolating) virus.
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• Herpes virus—Epstein Barr virus, Human herpesvirus, cytomegalovirus, Lucke’s frog virus, Marek’s disease virus. • Adenoviruses—it can cause upper respiratory infections and pharyngitis. In man, they are not known to be involved in tumors but in hamsters they may induce sarcomas. • Poxvirus—in rabbits, it can cause myxomatosis and in humans, it can cause molluscum contagiosum and may induce squamous cell papilloma. • Hepadnaviruses—hepatitis B virus is a member of this family and it can cause acute hepatitis and is responsible for carrier state which can result chronic hepatitis. In some cases, to progressing to hepatic cirrhosis and into hepatocellular carcinoma.
Mechanism of Biological Carcinogenesis RNA viral oncogenesis: Reverse transcriptase acts as a template to synthesize a single strand of matching viral DNA. • Single strand of viral DNA is then copied by DNA dependent DNA synthetase to form another strand of complementary DNA resulting in double stranded viral DNA or provirus. • The provirus is then integrated into the DNA of the host cell genome and may transform the cell into a neoplastic cell. • Virus replication begins after integration of provirus into host cell genome. Integration results in transcription of proviral genes or progenes into messenger RNA which then forms components of the virus particle, i.e. virion core proteins from gag gene, enveloped glycoprotein from env gene and reverse transcriptase from pol gene. • The three components of virus particles are then assembled at the plasma membrane of host cells and virus particles released by budding off from plasma membrane, thus completing the process of replication.
carcinogen exposure and under conditions of stress. Free radicals may therefore contribute widely to cancer development in humans. Free radicals scavenging vitamins C and E have been shown to protect against cancer development in animal models.
Biology of Tumor Growth The life cycle of malignant tumors can be divided into four phases.
Induction of Malignant Changes in the Target Cell (Transformation) (Fig. 5-4) • Effect on genes—large number of carcinogen agents induce neoplastic transformation of cells in vivo and in experimental animals. All etiologic factors ultimately affect the function of two sets of genes, one is protooncogenes or oncogenes and another one is antioncogenes or cancer suppressor genes. • Binding with DNA—the majority of carcinogens are mutagenes which bind the DNA directly or indirectly by undergoing enzymatic activation, inducing miscoding errors during transcription and replication. • Production of growth factors—oncogenes may code for growth promoting factors and as a result, the tumor cells produce large amount of growth factors to which, only they can respond.
DNA viral oncogenesis: • Replication—The virus may replicate in the host cell with consequent lysis of infected cell and release of virions. • Integration—The viral DNA may integrate into the host cell DNA. This results in neoplastic transformation of the host cell.
Oxidative Mechanism of Carcinogenesis Active oxygen species and other free radicals have long known to be mutagenic. Further, these agents have emerged as mediators of the other phenotypic and genotypic changes that lead to form mutation to neoplasia. Free radicals production is ubiquitous in all respiring organism and is enhanced by many disease states, by
Fig. 5-4: Biology of tumor growth (induction phase).
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Neoplasm • Encoding—oncogenes may encode a defective receptor that send stimulating signals to the cells, even in the absence of growth factors. • Multiple mutations—cancer is a genetic disease that results when multiple mutations accumulate in the DNA of a cell and specific chromosomal abnormalities predispose to cancer.
Growth of Transformed Cells (Kinetics of Tumor Cell Growth) (Fig. 5-5) • Doubling—the monoclonal cancer cell (10 µm in diameter) has to undergo about 30 population doublings to produce 109 cells weighing approximately 1 gm, which is the smallest clinical detectable mass. To produce a tumor of 1012 cells, weighing 1 kg approximately, which is usually the maximum size compatible with life, the tumor cells have to undergo 10 further population doublings. So by the time the tumor is clinically detectable, it has already complete a major portion of its life cycle. • Factors affecting growth of cells—in tumor cells, there is an imbalance between cell production and cell loss, therefore, the tumor grows progressively. The rate of tumor growth depends upon the growth fraction and the degree of imbalance between cell production and cell loss.
Fig. 5-5: Biology of tumor growth (kinetic of tumor cell growth).
Mechanism of Local Invasion and Distant Metastases • Routes of metastasis—there are three routes through which metastases of tumor cells occur, i.e. local invasion, via blood vessels and via lymphatics. • Local invasion—the local invasion takes the path of least resistance and the tumor cells invade the surrounding tissue spaces.
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• Lymphatics spread—in case of oral malignancies, distant metastasis is mainly via lymphatics, either by lymphatic permeation or by lymphatic embolism. • Blood vessels—rarely, it spreads through blood vessels and if this occurs, the tumor cells invade the lumen of blood vessels, the tumor emboli form, which are fragmented and the tumor cells are lodged into distant tissues.
Theories of Carcinogenesis The Epigenetic Theory According to this theory, the carcinogenic agents act on the activators or suppressors of genes and not on the genes themselves and result in the abnormal expression of genes.
Genetic Theory • Concept—this is the most popular theory which suggests that cells become neoplastic because of alteration in the DNA. It is suggested that, the secret of cancer lies within the normal cells themselves in the form of protooncogenes (C-oncs). The mutated cells transmit their characters to the next progeny of cells. Inappropriate over expression of the gene or point mutation cause the cell to produce stimulating growth factors or in some way damages normal regulatory control. The qualitative and quantitative changes in the expression of genome may be brought about by carcinogenic influence, i.e. chemical, viruses, radiation or spontaneous random mutations. • Oncogenes—Oncogenes are the transforming genes present in many tumor cells. Closely related genes are detected on normal animal and human cells and are called as ‘proto-oncogenes’ or ‘cellular oncogenes’, abbreviated as ‘c-oncs’ • ‘Cellular oncogenes’ of the host cells can transcribe its copies in the viral genome of acute transforming oncogenic retroviruses called as viral oncogenes or ‘v-oncs’. An alternate mechanism is by anti-oncogenes in which, there is inactivation or deletion of genes that normally perform the function of suppressing cell proliferation, thus allowing them to proliferate. • Feedback deletion—according to genetic regulatory mechanism theory, primary change in the cell consists of a modification of repressor molecule which controls the functions of the gene. The repressor molecules are either RNA or protein. The modification of repressor molecules removes their orderly inhibitory control, which is responsible for normal morphogenesis and differentiation, and unearths the cell genetic potentiality for unrestricted growth. This concept of loss of growth control is described as ‘feedback deletion’.
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Virus Theory
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At some stage, it participates in the development of cancer. The concept of mode of action of virus has taken many forms• Act as parasite—virus is present as a parasite in all tumor cells and it is transmitted from cell-to-cell and stimulates extreme hyperplasia without affecting the genome cell. • Act as biologic carcinogen—it acts as a biologic carcinogen on some cellular constituents to release or activate neoplastic potentialities normally present in cells. • Auto synthesis—carcinogens of all kinds ultimately act by creating some new auto-synthesizing cytoplasmic constituents, probably an auto-catalytic protein, which can excite the cell to unlimited growth.
Immune Surveillance Theory It suggests that an immune-competent host mounts an attack on developing tumor cells so as to destroy them while an immune-incompetent host fails to do so. According to original immunological theory, normal cells contain specific ‘self-marker’ (identity proteins) which is recognized by the normal growth regulating mechanism. These proteins serve as receptor for chemical carcinogens (hapten) and the resulting complex is self-replicating. The complex (complex antigen) triggers off an immune response and the antibody (free or cell bound) combines with the self-marker carcinogen complex and eliminates it. The new race of cells produced is deleted with selfmarkers and goes unrecognized by growth regulatory mechanism. The high incidence of cancer in AIDS patients is in support of this theory.
Monoclonal Hypothesis Currently, there is strong evidence on studies of human and experimental animals that most of the cancers arise from single clone of transformed cell. The best documentation of monoclonal origin of cancer cells come from the study of G6PD in women who are heterozygous for its two isoenzymes A and B. It is observed that all tumor cells in benign uterine tumor (leiomyoma) contain either A or B genotype of G6PD—i.e. the tumor cells is derived from a single progenitor cell.
Multistep Theory According to this theory, carcinogenesis is a multistep process which is substantiated in vitro by changes in experimental animals as well as in vivo by changes in human cancers. In chemical carcinogenesis, there are two essential features, i.e. initiation and promotion. Many tumors arise from combination of activation or growth promoting
oncogenes and inactivation of growth suppressing antioncogenes. In some cancers, there is initial dysplastic change that may progress into carcinoma in situ and then into invasive carcinoma.
Metastasis ‘Metastasis is defined as spread of tumor by invasion in such a way that discontinuous secondary tumor mass/masses are formed at the site of lodgment’. This metastasis is the transfer of the disease from one organ or part to another not directly connected with it. If malignant cells did not metastasize, the surgical removal of primary neoplasm would completely cure the patient. Metastasis is fundamentally an embolic process. The invasiveness of malignant cells involves motility, which requires change in shape and adhesiveness and ability to degrade the matrix in order to penetrate it. Thus, a definition of the behavior of the metastatic tumor cells is the tendency to cross the tissue compartment / boundary and intermix with other cell types. The metastatic process can be divided into several sequential steps although these steps are interconnected. Factors which control metastasis are proteolysis, cell adhesion, tumor angiogenesis, cell mediated immunity and genetic factor.
Steps of Metastasis • Breaking of cells—the breaking of loose neoplastic cells from the parent tumor. • Invasion—invasion of the matrix (sarcoma), penetration of the basement membrane and invasion of connective tissue (carcinoma). • Entering the blood vessels—it then entering the wall of blood and lymphatic vessels. • Survival—survival of malignant cells in the bloodstream. Survival in the compatible tissue environment and induction of growth factor to stimulate new vessel formation to obtain nutrition. • Emergence of cells—emergence of the malignant cells from the blood vessels in the form of the emboli and lodgment in other tissues. • Multiplication—multiplication of neoplastic cells and growth to form secondary neoplasm at the new site. • Control mechanism—each of these steps is probably controlled by different molecular mechanism and this may explain the differences in the behavior with reference to tumor metastasis. Neoplastic cells within a single tumor might differ in their ability to metastasize. A sub-population of cells preexists within the heterogeneous primary tumor. The relative size of this subpopulation in the primary tumor may vary with time between the neoplasms.
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Neoplasm Routes of Metastasis (Fig. 5-6)
Grading and Staging of Tumors
• Lymphatics—particularly for carcinoma and lymphosarcoma. For example, mouth-to-neck nodes and breastto-axillary nodes. • Bloodstream—particularly veins from gut via portal circulation to liver, from systemic sites through right heart to lung, from left heart to any systemic sites. • Cavities—along epithelium lined cavities, for example: respiratory tract, gut, urinogenital tract etc. • Others—transcelomic spread, cerebrospinal fluid, tissue planes and through nerve sheath.
Grading
Pattern of Metastatic Spread • Mechanistic theory—the capillary bed of the first organ which encounter viable neoplastic cells is the preferred site of metastasis. • Seed and soil hypothesis—it suggests that availability of fertile environment (the soil) in which compatible tumor cells (the seed) can grow is important. Ewing suggested that varying pattern of metastasis is due to fact that different tumor cells thrive in certain biological sites (soils) but not in the other sites. • Cell interaction—interaction between cell surface protein of malignant cells and organ specific protein, e.g. fibronectin receptor.
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The grading features are those indicative of proliferation and differentiation. It is defined as, ‘macroscopic and microscopic degree of differentiation of tumor’. Grading depends mainly on two histologic features, the degree of anaplasia and the rate of growth. Different types of grading systems are as follows:
Broder’s Classification System (Fig. 5-7) • Grade I (well differentiated, i.e. less than 25% anaplastic cells)—it is characterized by the presence of relatively mature cell with few nuclear aberration and with the presence of keratin pearls and individual cell keratinization. • Grade II—(Moderately differentiated, i.e. 25 to 50% anaplastic cells)—it is characterized by the presence of tumor cell exhibiting a wide range of differentiation, keratinization is occasionally present, and nuclear aberrations are moderately abundant. Usually, the invasion is poorly delineated from the stroma. • Grade III—(Moderately differentiated, i.e. 50 to 75% anaplastic cells)—it is characterized by disorderly and poorly differentiated cells with no tendency towards keratinization, nuclear aberrations are abundant.
Fig. 5-6: Different routes of metastasis in the human body.
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Fig. 5-7: Broader’s classification (Grading System)—A diagrammatic representation
• Grade IV—(Poorly differentiated, i.e. more than 75% anaplastic cells)—in it, cells are so poorly differentiated that they cannot be identified as epithelial origin on the basis of histology alone, nuclear aberrations are abundant and no keratinization is found.
CIN Grading Alternative classification for grading of dysplasia and carcinoma in situ together is cervical intraepithelial neoplasia (CIN). According to this grading, the criteria are as follows: • CIN I—it represents less than 1/3rd involvement of the thickness of the epithelium. • CIN II—in it, there is 1/3rd to 2/3rd involvement. • CIN III—it is full thickness or equivalent to carcinoma in situ. Depending on thickness of squamous epithelium involved by atypical cells According to this, grading of dysplasia is as follows: • Mild • Moderate • Severe
Staging It is the extent of spread of tumor within patients.
Assessment It is assessed by following ways: • Clinical examination—staging can be assessed clinically by the size and extent of primary lesion. • Investigation—investigation like radiology, sonography can lead to staging of disease. • Pathological examination—this is very important part while staging of neoplastic process is done. Mainly biopsy, cytology are used. • Infiltration—degree of infiltration of primary lesion should be carried out. • Metastasis—presence or absence of metastasis to regional lymph nodes. Presence and absence of distant metastasis. Involvement of contralateral or ipsilateral node. Whether node are fixed or not. Objectives • Treatment planning—it aids clinician in the planning of treatment. • Prognosis—to give some indication of prognosis. • Evaluation of treatment—to assist in evaluation of the result of treatment. • Exchange of information—to facilitate the exchange of information between treatment centers. • Investigation—to contribute to the continuing investigations of human cancer.
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Neoplasm
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TNM Staging
AJC (American Joint Committee)
It is universally accepted system which is developed by UICC (Union Internationale Contre of Cancer). • Primary tumor (T): local extent is major factor contributing to prognosis. • Tx: primary tumor cannot be assessed. • T0: no evidence of primary tumor. • Tis: carcinoma in situ. • T1: tumor 2 cm or less in diameter. • T2: tumor 2-4 cm in diameter. • T3: tumor more than 4 cm in greatest diameter. • T4: tumor of any size in which tumor invades adjacent structure (e.g.: cortical bone, inferior alveolar nerve, floor of mouth, skin of face etc). • Regional lymph nodes (N) • Nx: regional lymph node cannot be assessed. • N0: no regional lymph node metastasis. • N1: metastasis in single ipsilateral lymph node less than 3 cm in diameter. • N1a: nodes considered not contain to tumor growth. • N1b: nodes considered to contain growth • N2: single lymph node, no more than 6 cm in greatest dimension, of bilateral/contralateral lymph node, no more than 6 cm. • N2a: Single ipsilateral lymph node more than 3 but less than 6 cm. • N2b: multiple ipsilateral lymph nodes less than 6 cm. • N2c: Bilateral or contralateral lymph node less than 6 cm in greatest dimension. • N3: metastasis in lymph node more than 6 cm and it is fixed. • N3a—ipsilateral nodes at least one greater than 6 cm. • N3b—bilateral nodes greater than 6 cm. • N3c—contralateral nodes at least one greater than 6 cm. • Distant metastasis (M) • Mx: Distant metastasis cannot be assessed. • M0: No distant metastasis. • M1: Distant metastasis. • Category M1 may be further specified according to the notation. • Pulmonary—PUL • Osseous—OSS • Hepatic—HEP • Brain—BRA • Lymph nodes—LYM • Bone marrow—MAR • Pleura—PLE • Peritoneum—PER • Skin—SKI • Other—OTH
It divides all cancers into stage 0 to 4, and takes into account all three previous TNM systems. • Stage 0—T0 N0 M0 • Stage 1—T1 N0 M0 • Stage 2—T2 N0 M0 • Stage 3—T3 N0 M0, T1 N1 M0, T2 N1 M0, and T3 N1 M0 • Stage 4A—T4 N0 M0, T4 N1 M0, any T N2 M0 • Stage 4 B—Any T N3 M0 • Stage 4 C—Any T, Any N, M1
Dukes ABC Staging It is used in cancers of bowel • Stage A—when tumor is confined to submucosa and muscle and cure rate is 100%. • Stage B—tumor penetrates the entire thickness of bowel wall into pericolic or perirectal tissues and cure rate is 70%. • Stage C—it is characterized by lymph node metastasis and reduces the cure rate to 30%.
STNMP Staging System • S—site of primary tumor • S1—lip and skin. • S2—lip mucosa. • S3—tongue. • S4—cheek. • S5—palate. • S6—floor of mouth. • S7—alveolar process. • S8—antrum. • S9—central carcinoma of bone. • Size of tumor—it is denoted by T • T1—less than 2 cm in diameter. • T2—between 2 cm and 4 cm in diameter. • T3—between 4 cm and 6 cm in diameter and extending beyond the primary region and extending through adjacent periosteum. • T4—greater than 6 cm in diameter and extending to involve adjacent structures. • Regional nodes were grouped as • N0—no palpable nodes. • N1—equifocal node enlargement. • N2—clinically palpable homolateral regional nodes, not fixed. • N3—same as N2 but fixed. • N 4—clinically palpable contralateral or bilateral nodes, not fixed. • N5—same as N4 but fixed. • Metastasis • M0—no distant metastasis.
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Features
Benign tumors
Malignant tumors
Boundaries
Encapsulated or well circumscribed
Poorly circumscribed and irregular
Surrounding tissues
Often compressed
Usually invaded
Size
Usually small
Often large
Growth
Slow and expanding
Rapid and infiltrating
Capsule
Present
Absent
Degeneration
Rare
Common
Recurrence
Not common
Common
Fixity
Absent
Present
Secondary changes
Occur less often
Occur more often
End of growth
May come to standstill
Growth rarely ceases
Pattern
Usually resemble tissue of origin
Have poor resemblance to tissue of origin
Basal polarity
Retained
Lost
Pleomorphism
Usually not present
Often present
Nucleo-cytoplasmic ratio
Normal
Increased
Anisonucleosis
Absent
Present
Hyperchromatism
Absent
Often present
Mitosis
May be present but always with typical mitosis
Mitotic figures are increased and are generally atypical and abnormal
Tumor giant cells
May be present but without nuclear atypia
Present with nuclear atypia
Cytoplasm
May show normal constituents
Normal cytoplasmic elements are decreased or lost
Function
Well maintained
May be retained, lost or become abnormal
Growth rate
Usually slow
Usually rapid
Local invasion
Often compresses the surrounding tissue without invading or infiltrating
Usually infiltrates and invades the adjacent tissue
Metastasis
Absent
Present frequently
Macroscopic Features
Microscopic features
• M1—clinical evidence of distant metastasis without definite histological or radiographic conformation. • M2—proven evidence of metastasis beyond regional nodes. • Pathology of lesion • P0—hyperkeratotic lesion showing atypia. • P1—carcinoma in situ. • P2—basal cell carcinoma. • P3—verrucous carcinoma. • Well differentiated sq. cell carcinoma.
• Moderately differentiated sq. cell carcinoma. • Poorly differentiated sq. cell carcinoma.
Suggested Reading 1. Franks LM, Teich NM. Introduction to the Cellular and Molecular Biology of Cancer (3rd edn), Oxford University Press, 1997. 2. Howaldt HP, Kainz M, et al. Proposal for Modification the TNM Staging Classification for Caner of the Oral Cavity: DOSAK. J Craniomaxillofac Surg 1999;27:275-88. 3. Underwood JCE. General and Systematic Pathology (3rd edn), Churchill Livingstone, 2000.
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Infection Control in Dental Office
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Infection Control in Dental Office
Introduction In dental practice, the risk of infection is a high priority issue, considering the nature of oral environment which is rich in diverse aerobic and anaerobic bacterial flora and more hazardous viral pathogens. Dental personnel and patients are at increased risk of acquiring many diseases which can get transferred from patient to doctor and vice versa. With changing times, risk associated with viral pathogens such as herpes, hepatitis and HIV are increased. The common goal of infection control is to eliminate or reduce the number of microbes shared between people. Many objects in the dental office are potential source of infection. These are called as ‘vectors’. For examples; saliva, blood, nasal secretion, dust, hands, hair, clothing, films, X-ray machine, dental instrument and dental chairs. Cross infection occurs when these vectors transmit pathogenic organisms from one patient to another or to dental personnel. All patients should be treated using universal precaution. There should be no exception and no extra precaution for specific patients. By practicing infection control, patients as well as operator can be protected. High standard of dental infection control and occupational safety must be followed by dental personnel; for the safety of patient and dental health care workers. The word infection control does not mean total prevention of iatrogenic, nosocomial or occupational exposure, but it means to reduce the risk of disease transmission.
General Consideration Every person working in hospital or general practitioner has a legal duty to ensure that all necessary steps are taken to prevent cross infection protect themselves, their colleagues and the patients.
Effective infection control measures are required in dental radiography even though most investigations are non-invasive or non-exposure prone and they do not involve breaches of the mucosa or skin. Every patient in the department should have current medical history. Information gained by the history will alert the dental team about high risk situation. In dentistry, infection can occur due to any of the following: • Salivary contamination—the main risk from cross infection is due to salivary contamination from one patient to another or from working areas and equipments. • Contaminated object—indirect contact with contaminated objects or instrument can occur. • Airborne infection—direct contact with airborne contaminant present in spatter or aerosols or oral and respiratory fluids. Identification of the risk and the presence of these infections is achieved by recording and keeping updated medical history. But, this cannot be relied on as: • Patient may be unaware that they are infected. 50% of hepatitis B cases are asymptomatic and up to 10% become carrier. • Patients may not have understood the diagnosis given to them by their medical practitioner. • Patient may be incubating the infection. • Information may be deliberately withheld. It is therefore safer for HCW (health care worker) to accept that all patients can be infectious and age or class of the patient is no excuse.
Routes of Infection Transfer (Fig. 6-1) • Percutaneous—this is high risk route. In this, transfer of microbes from saliva and blood can occur through needles and sharp instruments.
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• Contact—this is also high risk transmission. In this, touching or exposing non-intact skin to infective oral lesion, infected tissue surface or infected fluids, splash and spatter of infected fluids. • Inhalation—this is moderate risk transmission. In this, inhalation of aerosol or droplet containing pathogen can occur. Pathogens suspended in air from handpiece and droplet nuclei from coughing. • Through fomites—it is low risk. It is very rare to touch contaminated inanimate surface in dental room or operation.
• Patients who are HBs antigen positive and HBe antigen negative. • Established cases of AIDS or AIDS related diseases like hairy leukoplakia, atypical ulceration and Kaposi’s sarcoma. • Patients who are HIV antibody positive. • Patients who use IV drugs or other risk activities.
Methods of Decontamination • Sanitization—this is first level of decontamination. This is process of physical cleaning to reduce quantity of microbes. This is done by cleaning the surface with soap and water or with detergent. • Disinfection—this is next level of decontamination. It kills all vegetative microorganisms, fungi. This uses chemical germicides, radiation, ultraviolet rays or heat. • Sterilization—this is third level. Sterilization kills all bacteria, fungi, virus and bacterial endospores. It uses chemical methods and physical methods.
Classification of Surface for Infection Control Fig. 6-1: Different routes of infection transfer
Infection of Main Concern • Infective hepatitis—it includes mainly hepatitis B or hepatitis C. Risk group include IV drug user, heterosexual with multiple partners, homosexual, mentally subnormal patients and hemodialysis patient. 2% of the populations are known carriers of HBV which can be transmitted by saliva. • HIV and AIDS—It is caused by HIV virus. Risk group include homosexuals, heterosexual with multiple partners, IV drug users, and patient with hemophilia. Most people are not aware of it at the time of infection and it may take 10 years or longer for AIDS to develop. • Herpes simplex infection—Cold sores caused by herpes simplex infection are very infectious. There are chances of contracting herpetic whitlow, i.e. painful finger infection. • Tuberculosis—it is caused by mycobacterium tuberculosis. If there is active infection, it may get transfer from saliva to the dentist.
Infection Risk Patients • Patients with clinical sign of oral and systemic infection.
According to Spaulding’s classification in dental radiography is as follows: • Critical surface—this is a surface that penetrates the tissue and contact blood. Examples are, scalpel blades, burs, extraction forceps, files, periodontal instruments, surgical drains, dental explorer, periodontal probes, biopsy punch, surgical drains, endodontic file reamer and implants. In this case, sterilization is done with the help of autoclave, chemical, dry heat. • Semi-critical surface—this is the surface which does not penetrate tissue but contact with mucous membrane. It includes mouth mirrors, handpiece, anaesthetics syringe, chip syringes, amalgam condenser, impression trays, air/water syringe tips and high volume evacuator tips. In this case, high level disinfection and sterilization is required or barrier should be used. • Non-critical—this includes the surface which penetrates neither tissue nor contact with mucous membrane. There is only contact with intact skin. It includes chair light handles, instrument trays, high touch work surface, bracket tales, chair control and dental chairs. In this case intermediated level of disinfection and sterilization is required. It is done by hydrogen peroxide bases, phenols, idophores. • Environmental surface—this does not contact with patient directly. They can be contaminated by the care provider. It includes floor and door handles. In this case, sanitization should be properly done.
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Infection Control in Dental Office
Working Area
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The best method to reduce microorganism transfer is, to touch as few areas as possible. • Preparation of area—the entire surface that is touched during radiography, should be covered with plastic wrap, plastic backed paper or aluminum foil. Covering eliminates the need for surface disinfectant after radiography. • After treatment—if working area is not covered by protective covering, then after treatment of each patient, dental unit surface can become contaminated with blood and saliva. Operator should avoid touching walls and other surfaces with contaminated gloves. This area should be thoroughly cleaned with disposable towel. • Material used—to clean working surface disinfecting solution is sprayed and allowed to dry. Most commonly used disinfectant is phenolic, idophores and chlorine containing compounds.
Sterilization Sterilization is the process of destroying all the microbial life from an article or surface inclusive of bacterial spores. It can be achieved by:-
Dry Heat
Fig. 6-2: Ultraviolet sterilizer.
It denatures the proteins of a microorganism rendering them non-viable. This principle is applied in the hot air oven. The instruments are packed loosely inside the oven and a temperature of 160°C is achieved with a holding time of 1 hour. The hot air oven is exclusively used for sterilizing glass articles, oils, greases and powders. The other physical methods include microwave and ultraviolet methods (Fig. 6-2).
Moist Heat Moist heat denatures and coagulates the proteins of a microorganism and is a better method of sterilization due to a higher efficiency of penetration than dry heat and a faster killing rate. This is due to latent heat of vaporization which is present in moist heat. This principle is used in the autoclave (Fig. 6-3). Various methods of autoclaving are available base on the same principle. The temperature required for this is 121°C with a minimum holding time of 20 minutes. For practical consideration, vacuum models are operated at a temperature of 139°C, 332lb pressure and holding time of 5 minutes.
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Fig. 6-3: Autoclave used in dentistry.
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Infection Control Procedures
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The basis for infection control lies in the fact that, as dentist are more prone to acquire many infectious diseases; including blood borne diseases such as AIDS and hepatitis B. The procedure for infection control can be grouped into six major areas:
Training All the staff members should be given training of infection control procedure. They should be told about the hazards due to infection which can occur to them or get transferred from them to patients. Continued education programme about infection control measures should be held regularly.
Fig. 6-4: Formalin chamber.
For gravity displacement models, a temperature of 121°C, 20lb pressure and a holding time of 30 minutes are used. Root canal instruments and burs can be washed and thereafter sterilized in a glass bead sterilizer at a temperature of 210-230°C. The specific disadvantage of this sterilizer is that the handle portion is not sterilized and therefore, these articles are not entirely sterile.
Chemical (Fig. 6-4) Ethylene oxide—this is a toxic gas that can be used to sterilize heat sensitive equipments. The articles are to be packed dry prior to sterilization otherwise a thin film of toxic ethylene glycol is formed. After sterilization, the articles should be aerated for at least 24 hours before use for dissipation of residue of the gas which could cause haematological complications. These are suited for large institutions and may not be a feasible option where small establishments are involved. Glutaraldehyde—it is being marketed as a 2% solution which has to be activated with an alkali which is provided with the product as an activator, as only the alkaline solution is effective. The solution should have a contact time of at least 6 hours. A lesser contact time is employed for disinfection will not be effective against spores.
Disinfection This is the process by which pathogenic microorganisms are removed from the surface without removing bacterial spores. This process is used to treat articles which do not penetrate mucous membrane or skin. Examples of disinfectants are formaldehyde, halogens, phenols and chlorhexidine.
Vaccination This is very important in infection control procedure. All clinical staff should be vaccinated against hepatitis B, etc. and regularly get it checked.
Covering of Wound Open wound on the hand should be covered with waterproof dressing. Hand injuries during dental procedure should be avoided.
Hand Washing It provides protection to both the patients and the dental team. Hand washing continues to be an important means for personal protection and of disease prevention. Washing hands before gloving reduces the skin microbial flora and helps to prevent skin irritation by waste products of bacterial growth under gloves. Gloved hands should be washed under running water before and after taking radiograph of patient and a disinfectant like povidone iodine and 7.5% surgical scrubs or chlorhexidine gluconate 4% surgical scrub should be used. Hand washing should be done at the start of treatment and after removing the gloves. Hand washing after using gloves is required to reduce the bacterial count that build on the skin during glove used. Specific step should be taken to hand wash. They are as follows (Fig. 6-5). • Wet hands with warm water. • Dispense an adequate amount of soap. • Thoroughly rub the hands including area around the thumb and finger for 30 seconds. • Wash hand with warm water to remove the soap. • Dry hands with proper towel.
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Protection against Aerosol and Spatter It involves the use of a pre-procedural rinsing of the patient’s mouth with an anti-microbial solution, use of rubber dam, high volume evacuation, protective clothing and eyewear. Reduce the amount of spray and spatter that exist in a patient’s mouth during care, which in turn reduce the number of microbes contaminating the dental team. Rubber dam (Fig. 6-7) has been shown to reduce the number of microbes in dental aerosols generated during operative procedures and saliva ejection minimizes saliva form accumulating in the mouth.
Fig. 6-5: Hand should be properly washed before gloving.
Gloves Gloves used for patient care protect the dental team members from direct contact with patient microbes and they protect patients from contact with microbes on the hands of dental team member. Gloves need to be changed between patients and are to be washed with detergent. Gloves should be inspected periodically during patient care and torn or punched gloves should be removed as soon as possible and the hands should be washed. Although some of these types, i.e. utility gloves can be autoclaved (nitrile type) through washing with an antimicrobial hand washing agent followed by rinsing and towel drying is adequate between routine uses. Exam gloves are made from latex, vinyl, nitrile and polyurethane. While wearing the gloves, you should look for breaches in the integrity of gloves. Gloves should never be washed before use or disinfected for reuse. Grubby gloves and cleaning swabs should be placed in suitable disposable bags and sealed for incineration.
Fig. 6-6: Doctor should always wear double gloves while examination of the patient.
Fig. 6-7: Rubber dam should be used to control dental aerosols generated during operative procedure.
Having patient rinse their mouth with an antimicrobial mouth rinse just before care, will reduce the number of bacteria that exist in the mouth. Eyewear and face shield—eyewear and face shields with adequate side protection prevent spatter from patient’s mouth or splashes of contaminated solution and chemicals from contacting eyes (Figs 6-8 and 6-9).
Fig. 6-8: Dental professional should wore eyewear to prevent spatter from patient mouth.
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Masks—face masks prevent spatter from patient’s mouth or splashes of contaminated solution and chemicals from contacting the mucous membrane of mouth and nose. A secondary protective aspect of a mask is the reduction in the inhalation of airborne particles. Thus, masks should be worn whenever there is a risk of aerosol generation, spraying, spattering, or splashing of patient’s oral fluid or chemicals used (Fig. 6-10).
Fig. 6-9: Complete face shield also help to protect from aerosols from patient oral cavity.
Protective clothing—as with eyewear and masks, protective clothing is also worn under conditions generating sprays, spatters, splashes or spills of body fluids, contaminated solutions. Protective clothing is the outer layer covering the garment that would first be contacted by the contaminating droplets. Such fluid resistant garments for use at chair side in dentistry may be reusable or disposable but it should protect the skin and underlying clothes from
exposure to potentially infectious material. This protection can be provided by high-neck, long sleeved, knee length garments.
Instrument Asepsis You should provide instruments that are safe for patient’s use. Pre-soaking of contaminated instruments keeps them wet until thorough cleaning can occur. This procedure prevents blood and saliva from drying on the instrument which facilitate cleaning. A cleaning solution manufactured for use in ultrasonic cleaners should be used and it needs to be changed daily. Protection against splashing and direct contact with this contaminated solution is important. Usually 2 to 20 minutes are needed to clean instruments ultrasonically as determined by observing the cleanliness of the processed instruments and making appropriate adjustments. After cleaned instruments have been rinsed and dried, they are to be packaged in functional sets before sterilization. Instrument packages sterilized in steam becomes wet and must be allowed to dry before handling so that the packing does not tear.
Surface Asepsis It eliminates the involvement of surface in the spread of diseased agents. There are two general approaches to surface asepsis. One is to clean and disinfect contaminated surface and the other is to prevent the surface from becoming contaminated by use of surface covers. Disinfection of surfaces involves the cleaning of surface after every patient and application of a disinfectant chemical. These chemicals include alcohol, phenols, glutaraldehyde, chlorine etc. Spittoons should be flushed with water.
Management of Sharp and Other Waste Products It reduces the chances for sharp injuries and contact with potentially infectious materials. There should be safe handling of needles and safe removal of needles. Needles should not be recapped instead, should be disposed off directly. Handpiece should not be left in position with burs; instead the bur should be removed after use. Infectious waste is preferably done by incineration.
Aseptic Technique Fig. 6-10: While examining the patient, dental professional should wear mask, gloves.
It includes aseptic retrieval of supplies, reducing contamination from dental unit water supplies, aseptic radiographic procedures.
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Infection Control in Dental Office
Suggested Reading 1. American Dental Association, infection control recommendation for the dental office and dental laboratory. J American Dental Association, 1992;123(8), suppl 1. 2. Bachman CE, White JM, Goodis HE, et al. Bacterial adherence and contamination during radiolgic processing. Oral Surg Oral Med Oral Pathol 1990;76;112-9. 3. Ciola B. A readily adaptable, cost effective method of infection control for dental radiography. JADA 1988;117:349-52.
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4. Kartz JO, Geist JR, Melanuria JA, et al. Potential for bacterial and mycotic growth in developer and fixer solutions; J Dentomaxillo-facial Radiol 1988; (suppl); 52. 5. Kohli A, Puttaiah R. Infection control and occupational safety recommendation for oral health professional, Dental council of India, 2007. 6. Miller CH. Sterilization and disinfection, why every dentist needs to know; JADA 1992;123: 46. 7. Stranczyk DA, Paunovich ED Broome JC, et al. Microbiological contamination drig dental radiographic film processing. Oral Surg Oral Med Oral Pathol 1993;76;112-9.
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Case History
Introduction
Diagnostic Procedure (Fig. 7-2)
A case history can be considered to be a planned professional conversation that enables the patient to communicate his symptoms, feeling and fears to the clinician so that the nature of the patient’s real and suspected illness and mental attitudes may be determined. The interest, warmth and compassion exhibited by the dentist are important factors in establishing patient rapport and in obtaining meaningful history. A kind and considerate approach is most important in securing and gaining the confidence of the patient. Indicate the patient that you are a friend who is keenly interested in him/her as a person. Ideally the patient’s history should be taken in a consultation room or a private office in which the décor and the furnishing are quite different from those of the dental operatory. The friendly atmosphere is an important factor in helping the patient to talk freely about his problems (Fig. 7-1).
The procedure can be divided into:• Personal information. • Taking and recording history. • Examining the patient. • Establishing a provisional diagnosis on the basis of history and examination. • Conducting the necessary investigation. • Formulation of final diagnosis on the basis of the results of the investigations. • Making a plan of treatment and medical risk assessment for dental patient
Personal Information Name A patient usually likes to be called by name. This will help to elicit the history properly, but it will also be of psychological benefit to the patients. In case of pediatric patients, addressing the patient by his/her name or pet name will encourage him/her to talk freely. Advantage of knowing the patient names are identification, to maintain record, communication and psychological benefit
Age Knowing the patient’s age is beneficial to the clinician in more ways than one.
Diagnosis Certain diseases are more common at certain ages (Tables 7-1 to 7-4).
Treatment Planning Fig. 7-1: Taking and recording history of the patient is important part in diagnostic sequence.
• Absence of teeth—if there is complete absence of teeth (i.e. true anodontia) even at the age of 4-5 years; it is most
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Fig. 7-2: Diagrammatic representation of diagnostic procedure of case history.
frequently in association with hereditary ectodermal dysplasia. • Delayed eruption—delayed eruption of teeth may be associated with rickets, cretinism or certain local factors such as fibromatous gingivae. If the permanent tooth does not erupt in its eruption period, we have to check by radiograph whether the permanent tooth bud is present or not. If the bud is present, deciduous tooth should be extracted. • Ankylosed deciduous teeth—ankylosed deciduous teeth prevent the eruption of permanent teeth; in such cases,
ankylosed teeth should be removed surgically to prevent the development of malocclusion, local periodontal disturbances and dental caries. • Behavior management technique—it differs according to the age of the patient. In case of pediatric patients, the dentist has to deal with the child as well as with the parent; hence in pediatric dentistry, the approach is 1:2; while in case of adults, the approach is 1:1. In talking to a child, the dentist must get down to the patient’s own level, in position and in conversation. Child patients may be intelligent or retarded.
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Case History Table 7-1: Disease present at/since birth DENTAL DISEASES
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Table 7-2: Diseases more commonly seen in infancy Dental/oral/systemic diseases with oral manifestations • Palatal cyst of the newborn • Heterotrophic oral gastrointestinal cyst • Hemangioma • Fibrosarcoma • Hemangioendothelioma • Hemangiopericytoma • Embryonic rhabdomyosarcoma • Melanotic ameloblastoma • Dental lamina cyst of the newborn • Hurler’s syndrome • Acute suppurative osteomyelitis of the jaw • Letterer-Siwe disease • Progeria • Infantile cortical hyperostosis of the jaw • Fibrous dysplasia of the jaw • Sprue • Thalassemia
Related to jaw • Agnathia • Facial hemihypertrophy • Macrognathia • Cleft palate • Facial hemiatrophy Related to lip • Commissural pits and fistulae • Double lip • Cleft lip • Hereditary intestinal polyposis syndrome Related to gingiva • Congenital epulis of the newborn • Fibromatosis gingiva Related to rest of oral mucosa • Pigmented cellular nevus • Cystic hygroma • Fordyce’s granule
Systemic diseases • Congenital heart diseases • Bronchiectasis • Pneumonia
Related to tongue • Microglossia • Macroglossia • Aglossia • Ankyloglossia • Cleft tongue • Fissured tongue • Median rhomboidal glossitis • Lingual thyroid nodule
• Child dose Child’s age Young rule = ————— ×adult dose Age+12 Child age at next birth day Clark rule = ————————————– × adult dose 24
Related to salivary glands • Aplasia • Atresia • Aberrancy • Developmental lingual salivary gland depression
Age Dilling rule = ——— × adult dose 20
Related to teeth • Pre-deciduous dentition Related to TMJ • Aplasia or congenital hypoplasia of the mandibular condyle Others • Teratoma • Erythroblastosis fetalis • Hemophilia SYSTEMIC DISEASES Related to heart • Atrial septal defect • Patent ductus arteriosus • Ventricular septal defect • Pulmonary stenosis • Aortic stenosis • Tetralogy of Fallot Related to respiratory system • Bronchiolitis • Cystic fibrosis Related to CNS • Congenital myopathy • Aqueduct stenosis Related to alimentary tract • Meckel’s diverticulum (it is common congenital anomaly. It is a small hollow wide mouthed sac protruding from ileum) • Annular pancreas (pancreas encircle the 2nd and 3rd part of duodenum leading to gastric outlet obstruction )
Sex • Diagnosis—certain diseases are more common in a certain sex (Tables 7-5 and 7-6). • Gifting—in case of pediatric patients, gifting varies according to the sex of the child. • Esthetics—females are much conscious about esthetics. • Emotion—females are emotional and sensitive hence one must be very careful during treatment. Failure to thrive, educational and emotional abuse are most common in case of female patients. • Child abuse—sexual abuse or exploitation is more common in case of females. • Dose—females have smaller body weight and require lower dose as compare to males. • Drug interaction—in females, consideration must be given to menstruation, pregnancy and lactation. Drugs given during pregnancy can affect the fetus. Antihypertensive drugs interfere with sexual function in males but not in females. Gynecomastia is a side effect of ketoconazole, metronidazole, chlorpromazine and digitalis administrations that occur in males. Ketoconazole causes loss of libido in men but not in women.
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Table 7-3: Diseases frequently seen in children and young adults
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Dental/oral/systemic diseases with oral manifestations • Focal epithelial hyperplasia • Retrocuspid papilla • Fissured tongue • Benign migratory glossitis • Benign cervical lymphoepithelial cyst • Epidermoid and dermoid cyst • Papilloma • Papillon-Lefèvre syndrome • Peripheral ossifying fibroma • Juvenile periodontitis • Naso-alveolar cyst (12-75 years) • Thyroglossal duct cyst • Oral submucus fibrosis (20-40 years) • Osteoid osteoma of the jaw • Benign osteoblastoma of the jaw • Torus palatinus • Kaposi’s sarcoma • Ewing’s sarcoma • Osteosarcoma of the jaw • Primary lymphoma of bone • Burkitt’s lymphoma • Hodgkin’s disease • Rhabdomyosarcoma • Alveolar (soft part) sarcoma • Pleomorphic adenoma • Central odontogenic fibroma • Odontogenic myxoma (2nd and 3rd decade) • Peripheral cemental dysplasia • Benign cementoblastoma • Dentinoma • Ameloblastic fibro-odontoma • Reiter’s syndrome (20-30 years) • Chronic focal sclerosing osteomyelitis of the jaw • Chronic osteomyelitis with proliferative periostitis of the jaw • Basal cell carcinoma • Lymphoepithelial cyst • Lingual varices • Sq. cell carcinoma • Scarlet fever • Diphtheria • Sarcoidosis • Nasopharyngeal angiofibroma (16 years) • Chondromyxoid fibroma (under 25 years) • Benign chondroblastoma of the jaw (5 to 25 years) • Osteoma of the jaw (young adult) • Rickets • Sickle cell anemia • Infectious mononucleosis • Acute leukemia • Pemphigus • Noma • Primary herpetic stomatitis • Recurrent aphthous stomatitis • Acute lymphonodular pharyngitis • Dental caries • Nursing bottle caries (children) • Pulp polyp • Eruption cyst • Dentigerous cyst (2nd decade) Systemic diseases • Congenital heart diseases • Rheumatoid heart diseases • Asthma • Acquired bronchiectasis • Pneumonia • Jaundice • Smallpox • Juvenile diabetes • Typhoid • Cretinism
Table 7-4: Diseases frequently seen in adults and older patients Dental/oral/systemic disease with oral manifestation • Attrition • Abrasion • Gingival recession • Periodontitis • Acute necrotizing • Dentinal sclerosis ulcerative gingivitis • Cementicles • Pulp stone and fibrosis • Atrophic diffuse sclerosing • Root resorption osteomyelitis of the jaw • Lichen planus • Leukoplakia • Leukoedema • Erythroplakia • Carcinoma in situ • Sjogren’s syndrome • Adenoid cystic carcinoma (over 40 years) • Acinic cell carcinoma • Mucoepidermoid carcinoma • Necrotizing sialometaplasia • Gingival cyst of the adult • Ameloblastoma (30-50 years) • Primary intra-osseous • Adenoameloblastoma carcinoma of the jaw • Sq. odontogenic tumor • Macroglobulinemia • Peripheral odontogenic fibroma • Ameloblastic fibrosarcoma • Trigeminal neuralgia • Carcinoma of gingiva • Verrucous carcinoma • Spindle cell carcinoma • Adenoid sq. cell carcinoma • Orolingual paresthesia • Sphenopalatine neuralgia • Glossopharyngeal neuralgia • Temporal arteritis • Malignant melanoma • Fibroma • Peripheral giant cell granuloma • Carcinoma of lip, tongue, floor (30 years) of mouth and buccal mucosa • Median anterior maxillary • Keratoacanthoma (50-70 years) cyst (40-60 years) • Lymphoepithelial cyst • Nasoalveolar cyst (15-65 years) • Lingual cyst (7-99 years) • Basal cell carcinoma • Herpes zoster • Chronic leukemia • Pernicious anemia • Iron deficiency anemia • Osteomalacia • Pleomorphic adenoma • Canicular adenoma • Oxyphilic adenoma • Adenolymphoma • Lipoma • Hereditary hemorrhagic • Myxoma of jaw bone telangiectasia • Chondroma of jaw bone • Osteoma of jaw bone • Torus mandibularis • Fibrosarcoma of jaw bone • Liposarcoma of jaw bone • Hodgkin’s disease • Multiple myeloma • Solitary plasma cell myeloma • Leiomyoma • Malignant schwannoma • Olfactory neuroblastoma Systemic diseases • Diabetes • Hypotension • Renal failure • Atherosclerotic diseases like angina pectoris and coronary heart disease • Peptic ulcer
• Hypertension • Congestive cardiac failure and myocardial infarction • Chronic valvular heart disease • Hepatitis • Asthma
Table 7-5: Diseases more common in females • • • • • • • • • •
Iron deficiency anemia Diseases of thyroid Sjogren’s syndrome Central cementifying fibroma Torus palatinus Sickle cell anemia Cicatricial pemphigoid Malignant melanoma Central giant cell granuloma Nasoalveolar cyst
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Caries Pleomorphic adenoma Adenoameloblastoma Myasthenia gravis Peripheral cemental dysplasia Juvenile periodontitis Recurrent aphthous stomatitis Peripheral giant cell granuloma Peripheral ossifying fibroma Idiopathic thrombocytopenic purpura
Case History Table 7-6: Diseases more common in males • • • • • • • • • • • • • •
Attrition Carcinoma in situ Keratoacanthoma Leukoplakia Verrucous carcinoma Liposarcoma Hodgkin’s disease Solitary plasma cell myeloma Wegener’s granulomatosis Osteoid fibroma Benign osteoblastoma Reiter’s syndrome Adenolymphoma Pernicious anemia
• Caries in deciduous teeth • Carcinoma of the buccal mucosa • Basal cell carcinoma • Adenoid cystic sq. cell carcinoma • Multiple myeloma • Chondrosarcoma • Herpes simplex • Ewing’s sarcoma • Ameloblastic fibro-odontoma • Basal cell adenoma • North American blastomycosis
Address (Residence) • Correspondence—it is necessary for future correspondence. Full postal address of the patient should be taken for future communication. • Geographical prevalence of dental/oral diseases—a few diseases have got geographical distribution. Dental caries and mottled enamel are dependent on the fluoride content of the domestic water. In India, cancer of the lip is very rare and cancer of tongue and buccal mucosa constitute the bulk of oral cancers. In cancer patients from Mumbai, common site affected is the tongue and in Chennai, it is the buccal mucosa. Dental caries is more common in modern industrialized areas while periodontal diseases are more common in rural areas. Habits also vary according to residence. Chutta, a form of tobacco, is common in Tamilnadu, gutkha in Bihar, hukli in Bhavnagar district of Gujarat. Bajjar is a dry snuff used by women in Gujarat. • Geographical prevalence of medical disease—there are many medical diseases which have got geographical prevalence. For example filariasis (Orissa), leprosy (Bankura district of West Bengal), gall bladder disease (West Bengal and Bangladesh), peptic ulcer (North Western and Southern parts of India), sleeping sickness (South Africa), hydatid disease (Australia), tropical disease (tropical countries), kangri cancer (Kashmir), anemia and malnourishment (rural areas) obesity, arthrosclerosis (urban area) and other industry related diseases (urban areas).
Registration Number It is good to give each and every patient a unique registration number and to maintain his/her records under that number so that when the patient visits the doctor at a later date, the doctor can know the details of the patient and the treatment done before.
Occupation • Financial status—treatment varies according to the financial status of the patient. Expensive treatment
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cannot be given to the patient with low socio-economic status. • Disease—some diseases are peculiar to certain occupations: • Attrition—Certain occupations, in which the worker is exposed to an atmosphere of abrasive dust and cannot avoid getting the material into his mouth, causes severe attrition. Habitual opening of the pins may result in notching of the incisal edge. • Abrasion—it is commonly noted in carpenters, shoemakers or tailors who hold pins, nails or tacks between their teeth. • Gingival staining—the strange dark stippling of the marginal gingiva is seen in patient works with lead, bismuth or cadmium. • Erosion—undue erosion of teeth is seen in sandblaster, who should be promptly referred to his physician for pulmonary silicosis. • Hepatitis-B—dentists, surgeons, blood bank personnel etc. are very prone to hepatitis –B. • Chelitis glandularis—in occupations where there is chronic exposure to sun, wind and dust can cause cheilitis glandularis. • Varicose veins—it is common in bus conductors and traffic policemen. • Urinary bladder neoplasm—it is common in aniline dye workers. • Carcinoma of scrotum—it is common in chimney sweepers or those who work in tar and oil companies. • Medial semilunar cartilage injury—injury to the medial semilunar cartilage of the knee occurs in football players and miners. • Student elbow—enlargement of certain bursae may occur from repeated friction of the skin over the bursae like in ‘student’s elbow’, ‘tennis elbow’ and ‘house-maid knee’. • Mesothelioma—an ice cream vendor may have mesothelioma due to exposure to asbestos for many years. • Stress disease—certain occupational hazards are associated with office work, e.g. repetitive strain injury and migraine induced by stress of inappropriate lighting. • Cirrhosis of liver—barmen who have ready access to alcohol have high mortality for cirrhosis of liver and tuberculosis. • Countryman’s lip—carcinoma of lip is commonly seen in persons who have to do outdoor work and that’s why, it is called as ‘countryman’s lip’ • Time—In case of pediatric patients, if both the parents are working and even if they are aware of the importance of dental health, they cannot properly attend the appointments given by the dentist.
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Religion
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• Carcinoma of penis—it is hardly seen in Jews and Muslims owing to their religious custom of compulsory circumcisions of penis. • Phimosis—for the same reason phimosis, subprepucial infection etc are not seen in them. • Intussusception—on the other hand intussusception is sometimes seen after the month long fast in Ramjan in Muslims.
• Relapse and remission—this should be noted. If patient has got any similar complaint in the past and then again it relapse. • Treatment—if the patient has taken any treatment for the same problems, the mode of treatment and doctor who has treated the patient should be recorded. • Negative history—e.g. in case of sinus on the cheek absence of the history of watery discharge at the time of meals excludes the possibility of the parotid fistula.
History with Particular Reference
Taking and Recording History Chief Complaint • Definition—it is the patient’s response to the dentist’s questions. Chief complaint is the reason for which the patient has come to doctor or the reason for seeking the treatment. The chief complaint should be recorded in the patient’s own words and first attention should be given to it. • Chronological recording—each of these complaints should be recorded in chronological order. If few complaints start simultaneously, record them in the order of severity. • Do not interrupt—do not interrupt the patient if possible. • Significance—chief complaint aids in the diagnosis and treatment planning. • Most common chief complaints and their causes are described in Table 7-7.
Pain (Fig. 7-3) • Anatomical location where the pain is felt—the patient should be asked to point to the area affected and outline the way in which the pain may spread to affect other areas. He should be asked whether the pain is deep or superficial. • Origin and mode of onset—the onset may be wholly spontaneous. It may be induced by certain activities like yawning, chewing, drinking hot and cold liquids etc. It may be triggered by minor stimulation such as touch or movement of skin, lip and tongue.
History of Present Illness • Collecting information—the history commences from the beginning of the first symptom and extends to the time of examination. Information should be collected by asking the following questions: • When did the problem start? • What did you notice first? • Did you have any problems or symptoms related to this? • Did the symptoms get better or worse at any time? • What you done to treat these symptoms? • Have you consulted anyone else for this problem? • Mode of onset—it can be sudden or gradual. It should be in terms of time, in days, weeks, months, before the current appointment. • Cause of onset—one has to determine whether if any thing that the patient has experienced may have precipitated the signs and symptoms. • Duration—it should be noted that, since how many days complaint was present. • Progress—it may be described as intermittent, recurrent, constant, increasing or decreasing in severity. Aggravating and alleviating factors should be noted.
Fig. 7-3: History of the patient in particular reference to pain.
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Case History
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Table 7-7: Most common complaints and their causes Pain • Gingival and periodontal disease • Pulpal disease • Mucous membrane disease • Salivary gland infection • Lesions of jaw bones • Lymph node inflammation • TMJ disorder • Maxillary sinus disease • Ear disease • Psychosis • Angina pectoris • Tonsillar disease • CNS disease • Neuralgia • Neuritis • Esophageal diverticulum • Eagle’s syndrome • Trotter’s syndrome Burning sensation • Idiopathic burning tongue • Psychosis • Neurosis • Viral infection • Fungal infection • Chronic bacterial infection • Geographic tongue • Xerostomic condition • Fissured tongue • Generalized oral mucosal disease • Anemia • Achlorhydria • Multiple sclerosis • Vitamin deficiency Bleeding • Gingivitis • Periodontal disease • Inflammatory hyperplasia • Allergy • Traumatized tumor • Hemangioma • Traumatic injury • Deficiency of coagulation factors Loose teeth • Periodontal disease
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Trauma Normal resorption of deciduous teeth Pulpoperiodontal disease Malignant tumor Chondroma Myxoma Hemangioma Histiocytosis X Familial hypophosphatemia Papillon-Lefèvre syndrome AIDS
Recent occlusal problems • Periodontal disease • Traumatic injury • Periapical abscess • Cyst and tumor of tooth bearing region of jaw • Fibrous dysplasia Delayed tooth eruption • Malposed or impacted teeth • Cyst • Odontoma • Sclerosed bone • Tumor • Mal-development • Cleidocranial dysplasia • Hypothyroidism Xerostomia • Local inflammation • Infection and fibrosis of major salivary gland • Dehydration state • Drugs like tranquilizers and antihistaminic • Autoimmune diseases like Sjogren’s syndrome and Mikulicz’s disease • Chemotherapy • Post radiation changes • Psychosis Swelling • Inflammation and infection • Cyst • Retention phenomenon • Inflammatory hyperplasia • Benign tumor • Malignant tumor
• Intensity of pain—the intensity of pain should be established by differentiating between mild and severe pain. This will show how patient reacts to his suffering. Intensity can recorded verbally or by some scaling method. • Nature of the pain—the general quality of the pain complaint should be classified as how it makes the patient feel. It can be burning, throbbing, scalding, shooting, stabbing, vague aching pain, splitting, dull, aching, lacinating, cutting, boring, constricting, gripping, scorching, pounding, heavy, pressing, sharp, bright, gnawing, cramping, squeezing, or searing. • Progression of the pain—the progression of pain should be noted.
Bad taste • Aging changes • Heavy smoking • Poor oral hygiene • Dental caries • Periodontal disease • ANUG
Diabetes • Hypertension • Medication • Psychosis • Neurological disorder • Decreased salivary flow • Uremia • Intraoral malignancy
Paresthesia and anesthesia • Injury to regional nerve—anesthetic needle and jaw bone fracture • Malignancy • Medications like those used in sedation, hypnosis • Diabetes • Pernicious anemia • Multiple sclerosis • Acute infection of jaw bones • Psychosis
Halitosis • Poor oral hygiene • Periodontal disease • Third molar opercula • Decayed tooth • ANUG • Oral cancer • Spicy foods • Tobacco use • Nasal infection • Tonsillitis • Pharyngeal infection and tumor • Gastric problems • Diabetes • Uremia
• Duration of pain—the duration of an individual pain episode is an important descriptive feature that aids in pain identification. A pain is said to be momentary if its duration is expressed in seconds. The pain that continues from one day to the next is said to be protracted. • Movement of pain—radiation of pain, referred pain and shifting or migration of pain. • Localization behavior—a determination of pain localization should be made in the description of the behavior. This includes whether the pain is localized or diffuse, radiating or spreading and enlarging or migrating. • Effect of functional activities—the effect of various activities such as talking, brushing of teeth, shaving, washing the face, turning the head, lying down, etc. should be noted.
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The effect of tension, fatigue and the time of the day should also be noted. Concomitant neurological signs—the description of pain cannot be completed unless other sensory, motor and autonomic effects are included. Accompanying sensation of hyperesthesia, anesthesia or dysesthesia should be mentioned. Any concomitant change in the special senses affecting vision, hearing, smell or taste should be noted. Motor changes such as muscular weakness, muscular contraction should be described; likewise ocular signs, nasal signs, and cutaneous signs should be described. Temporal behavior—the temporal behavior of pain should be evaluated, whether the pain is intermittent or continuous. It should not be confused with the effect of medication that induces a period of comfort by analgesic action. Others—other point like special time of occurrence, periodicity of pain and precipitating factors and relieving factors should be noted. Questions to be asked to the patient• Is the pain sharp and lacinating or dull aching and throbbing? • Does pain occur spontaneously or do certain activities cause it? • Is the pain constant or periodic? • Does the pain gradually build in intensity or it is paroxysmal? • Is the pain worse at any time of the day? • Is the pain of short duration or long?
• Associated features—fever, presence of other swellings and loss of body weight should be asked and noted. • Secondary changes—like softening, ulceration, inflammatory changes. • Impairment of function—nature of loss of movement and intensity. • Recurrence of the swelling—if the swelling recurs after removal, it may indicate malignant changes. Cystic swelling may recur if the cyst wall is not completely removed.
Swelling (Fig. 7-4) • Duration—since how many days swelling is present should be noted as it will determine its acute or chronic nature. • Mode of onset • Masses that increase in size just before eating—salivary gland retention phenomenon. • Slow growth—reactive hyperplasia, chronic infection, cysts and benign tumors. • Moderately rapid growing mass (week to about 2 months)—chronic infection, cysts and malignancy. • Rapidly growing mass—abscess, infected cyst, aneurysm, salivary retention phenomenon and hematoma. • Mass with accompanying fever—infection and lymphoma. • Symptoms—symptoms associated with swelling like pain, difficulty in respiration, swallowing or any other movement; disfiguring etc. In case of pain; nature, site and time of onset should be noted. • Progress of swelling—swelling can increase gradually in size or rapidly.
Fig. 7.4: History of swelling should be taken properly.
Ulcer • Mode of onset—mode of onset and duration of the ulcer should be asked and recorded. • Pain—ulcers associated with inflammation are painful; ulcers associated with epithelial or basal cell carcinoma are painless. • Discharge—serum, blood and pus. • Associated diseases—tuberculosis, nephritis, diabetes, and syphilis.
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Case History Past Dental History • Patient attitude—in addition to chief complaint and history of the present illness, it is necessary to elicit a past dental history. It is necessary to obtain description of the details of previous dental treatment and his reaction to his dentist and the treatment. By noting this, you may get accurate idea of the importance he gives to good dental treatment and how conscious he has been in pursuing a goal of good oral health. • Component of past dental history—significant component of past dental history include previous restorative, periodontic, endodontic or oral surgical treatments, reasons for loss of teeth, untoward complication of dental treatment, experience with orthodontic appliance and dental prostheses; and radiation or other treatment for past oral and facial lesions.
Past Medical History Obtaining the patient medical history is very important as it can assess the patient health status and also it can facilitate for the better diagnosis for the orofacial complaint of the patient. By taking proper medical history, following goal are achieved. • Assess in diagnosis of oral disease—there are many systemic problems which have oral manifestation. So by taking medical history, we can come to diagnosis of many orofacial complaints. For example, in HSV infection, negative history of recurrent herpes labialis and positive history of close contact with patient with primary and recurrent herpes is helpful in making the diagnosis. • Detection of underlying systemic problems—many times, patient is not aware of systemic problems due to his negligence. So by taking proper medical history, we can detect many systemic problems in the patient. • Management of patient—by assessing the patient general status, we can determine our plan of treatment. As many systemic diseases can change our line of treatment while treating the dental complaint. So we can modify our treatment according to need. • Consultation with other professional—by assessing the medical status, we can also determine whether any additional information is necessary to assess the patient medical status. Dentist may require consultation in following conditions: • Known medical problems—consultation is required in patients who have known medical problems and schedule for stressful dental procedure. • Unknown medical problems—in some patients abnormalities are detected while history taking or physical examination or laboratory studies. Patient is unaware of this problem.
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• High risk patient—some patient have high risk for development of particular problems. For example, obese patient may have hypertension. • Additional information—in patient who require additional information which may alter dental care and assist in the diagnosis of orofacial problems.
Consultation letter Place Date Patient Name Referral doctor name To Dr X I am referring the patient ———— who has to undergo stressful procedure. We have to use local anesthesia for this patient. Medical history of patient reveals that he is suffering from ————. Please advice us about the status of the patient whether he can undergo stressful dental procedure, which type of local anesthesia should we use and what precaution should we take. Patient signature
Date
Doctor signature
Date
Please return this consultation to ———————— • Medical questionnaire—one should ask the following particulars to the patient. • Systemic problems—whether the patient was suffering from any medical problems before? If yes, what was the duration and treatment? Whether the treatment was beneficial or not? Whether he had taken any medication for that? Patient must be reminded that medicine may include anything taken into the body that is not food. All diseases suffered, by the patient, previous to the present one should be recorded. These diseases may not have any relation with present disease; particular attention must be given to diseases like diabetes, asthma, bleeding disorders, hypertension, myocardial infarction, hepatitis B, diphtheria, rheumatoid heart disease, tuberculosis, and gonorrhea. • Chest pain—history of chest pain should be asked. As we will come to know the cardiological status of the patient. • Allergy—whether he has any allergy? (According to that the treatment plan may be adjusted). Allergy can be due to any drug or food. Patient should be asked
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Textbook of Oral Medicine about asthma, eczema and hay fever, urticaria, angioedema etc. Previous hospitalization—ask the patient to enumerate all previous hospitalizations and indicate the purpose. Blood transfusion—history of blood transfusion should be asked. Accident and operation—Previous operations, fractures, and accidents should also be noted. Drug history—you should ask patient to tell the medication that they are presently taking.
• Bruxism—it may lead to attrition. • Tobacco—tobacco preparations such as khaini, manipuri tobacco, mawa, mishri, pan, snuff, zarda etc should be ask. • Smoking—smoking habits such as bidi, chutta, cigarette, dhumti, hookah, etc. • Drinking habit—drinking alcohol, charas, ganja, marijuana etc.
Personal History (Fig. 7-7) • Habits and addiction—it is important aspect of history taking. There are many diseases which can correlate with particular habit of the patient. The most important habit you should ask about the tobacco, smoking and alcohol. You should note down frequency per day and length of time that patient had habit in years. • Oral hygiene and brushing technique—bad oral hygiene and improper brushing technique may lead to dental caries and periodontal disease. Horizontal brushing technique may lead to cervical abrasion of the teeth. • Pressure habits—thumb sucking, lip sucking, and finger sucking may lead to anterior proclination of maxillary anterior teeth. • Tongue thrusting—it may lead to anterior and posterior open bite and proclination of anterior teeth. • Mouth breathing—it may lead to anterior marginal gingivitis and caries (Fig. 7-5).
Fig. 7-5: Mouth breathing habit may lead to gingivitis (Courtesy Dr Abhishek Soni).
• Bobby pin opening—seen in teenage girls who open bobby pin with anterior incisors to place them in the hair. This results in notching of incisors and denudation of labial enamel. • Other habits—nail biting, pencil and lip biting (Fig. 7-6), lead to proclination of upper anterior and retroclination of lower anterior teeth.
Fig. 7-6: Lip biting habit of patient (Courtesy Dr Shetty).
• Patient’s appetite—whether it is regular or irregular? You should ask the type of diet (vegetarian, mixed, spicy food) to the patient. • Soft diet—soft refined diet adheres tenaciously to the teeth and is not removed because of lack of rough edges leading to more dental caries than coarse diet. • Coarse diet—in persons, having coarse diet, there is more evidence of attrition. • Carbohydrate content—increased carbohydrate contents leads to increased prevalence of dental caries. Phosphate diet prevents dental caries. • Vitamin deficiency diet—diet having deficiency of vitamins may cause enamel hypoplasia. Deficiency of calcium and phosphorus during period of tooth formation results in enamel hypoplasia and defects of dentin. Vitamin D can reduce the caries incidence. • Fluoride content—fluoride content may influence the caries process. • Bowel and micturition habit—Is it regular or irregular? • Sleep—insomnia occurs in cases of primary thyrotoxicosis. • Social status—caries, arteriosclerosis, heart disease, and acute appendicitis are more common in middle and high
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• Masochistic habit—some children use the finger nail to strip away the gingival tissue from the labial surface of a lower cuspid. If not discontinued, the marginal and attached gingival tissue will be stripped away exposing the alveolar bone.
Family History This is very important for many hereditary diseases. Many diseases recur in families like hemophilia, diabetes mellitus, hypertension and heart diseases.
Other Past History • Past laboratory investigations—this will aid in diagnosis of the disease. • Previous hospitalizations and operations—this is important as it can affect the treatment plan of the patient. • History of immunization—you should ask history of immunization regarding chickenpox, mumps and measles. The reason behind this is that, many oral manifestations may mimic above disease. • History of allergy—this is very important. You should ask history of allergy to the drug, specific allergen or any other specific allergy. Fig. 7-7: Diagrammatic representation of personal history.
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social status individual. Periodontitis, tuberculosis, anemia due to malnourishment is more common in low social status individual. Menstrual and obstetric history—you should ask about premenstrual tension, presence or absence of pain with periods, whether the patient is taking oral contraceptives, obstetric history, miscarriage, therapeutic abortion. Excessive bleeding may occur during childbirth in cases of hematological disorders. Endocrine diseases may be accompanied by abnormalities of pregnancy, labor and lactation. Cardiac failure may be triggered by circulatory demand of pregnancy and labor. Domestic and marital relationship—ascertain feelings about other members of family. Interest, hobbies, hopes, fears, the amount of exercise taken. Interest in games and sports. In males, particularly, if unmarried consider the possibility of homosexuality which may be associated with personal and social stresses that may culminate in mental illness. Home surrounding—whether the surrounding is overcrowded or there is loneliness? What pets are kept? Travel abroad—whether the patient has lived abroad and if so whether he/she was ill there? Recent travel- e.g., patient may suffer from malaria if he has recently traveled from or even through malaria prone area.
Examination Steps of Clinical Examination • Inspection—it is referred to as passive visualization of the lesion. Intraorally mirror can be used for visualization of structure. • Palpation—this will help for evaluation of structure and to know their consistency, fixity etc. • Bilateral palpation—this is done to differentiate between symmetrical structures on both side of face (Fig. 7-8). • Bidigital palpation—in this, two fingers are used to manipulate the tissue. It is used for thinner structure (Fig. 7-9). • Bimanual palpation—it is done by palms of both hands. In this, one hand is used to support the structure hand and another is used to manipulated the structure. This type of palpation is used in floor of mouth (Fig. 7-10). • Auscultation—it is used to study the movement of TMJ and also used for examination of venous malformation (Fig. 7-11). • Probing—this is used to detect carious lesion. • Percussion—this is used to check whether patient is having periapical infection.
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2 Fig. 7-11: Auscultation of TMJ is done to examine the movement of TMJ.
Fig. 7-8: Bilateral palpation is done to palate the TMJ.
General Examination Build It can be described as poorly built, moderately built and well built. • Asthenic—it appears as lean and underweight. • Sthenic—they are athletic in appearance. • Hypersthenic—persons have thick muscular and heavy bone structure. • Pyknic—they appear as heavy and rounded. • Cachexia—there is abnormally low tissue mass, occur due to malnutrition.
Pulse Fig. 7-9: Bidigital palpation is done in case of thinner structure.
Fig. 7-10: Bimanual palpation done in case of floor of mouth.
• Significance—it is an important index for severity of illness, abnormalities of heart and the vascular system e.g. hypertension and hypotension, shock, fever and thyrotoxicosis. • Types of pulse—pulse can be radial pulse (located on ventral aspect of wrist), branchial pulse (located medial to biceps tendon in the antecubital fossa) and carotid pulse (medial to sternocleidomastoid muscle, inferior and medial to the angle of mandible). • Technique –Assuming that the radial pulse is to be examined, the examiner should take the opportunity to note the warmth of the hand. Find the radial artery a few centimeters proximal to the wrist and just medial to the radius. Palpate the artery wall with the tips of the index and middle fingers. The tips are very sensitive. Avoid the thumb for fear of misinterpreting your own radial pulse. Do not press too hard for fear of obliterating the pulse (Fig. 7-12).
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Case History
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Fig. 7-12: Palpation of radial artery for the examination of pulse of the patient.
• Points to be noted—following are particularly noted in pulse: • Rate—fast or slow (normal 60-100 beats/min). • Rhythm—regular or irregular, irregularly irregular in arterial fibrillation and regularly irregular in ventricular ectopic. • Volume—high, low and normal volume indicate pulse pressure (normal pulse pressure is 40-60 mm/Hg). Narrow pulse pressure is in left ventricular failure, obstruction to left ventricle like mitral stenosis, aortic stenosis. Wide pulse pressure in aortic and mitral regurgitation, high output states like pregnancy, anemia etc. • Tension and force—it indicates diastolic and systolic pressures. • Character—water hammer pulse of aortic regurgitation, pulsus paradoxus of pericardial effusion, anaerotic pulse (it is a slow rising twice beating pulse where both waves are felt during systole in carotid artery) in aortic stenosis, pulsus bisferingus (it is a rapid rising twice beating pulse where both waves are felt during systole) in idiopathic hypertrophied subaortic stenosis, dicrotic pulse (it is twice beating pulse where the first percussion wave is felt during systole and second dicrotic is felt during diastole) in fever like typhoid, congestive cardiac failure, cardiac temponade following open heart surgery. • Other factors—other factors like condition of arterial wall, peripheral pulsations of radial artery, carotid artery, brachial artery should also be seen. Delay of the left temporal pulse compared with right pulse is found in coarctation of aorta.
Blood Pressure • Normal blood pressure—Systolic 120–140 mm Hg and diastolic 80 mm Hg (any above 90 is abnormal). Normal—
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120/80 mm Hg. The stroke volume of the heart and stiffness of the arterial vessels control systolic blood pressure. Peripheral resistance controls diastolic blood pressure. Blood pressure variation—blood pressure varies with emotion, exercise, meal, alcohol, tobacco, bladder distension, temperature and pain. Conditions diagnosed by blood pressure—conditions diagnosed by blood pressure are hypertension, hypotension and aortic incompetence. Unequal blood pressure—unequal blood pressure in 2 arms may be due to supravalvular aortic stenosis (right side higher blood pressure), preductal coarctation of aorta (same) and unilateral occlusive disease of aorta. Procedure for blood pressure determination—blood pressure determination is easily accomplished and is well within the capabilities of every dentist. The procedure is as follows. • Equipment—the equipment required is stethoscope and sphygmomanometer. • Patient position—seat the patient and place his right arm on a table or desk so that the forearm is adequately supported at elbow level about the level of heart. • Placement of cuff—center the rubber balloon of the cuff over the brachial artery (Fig. 7-13). The artery is usually palpable about three quarters of the way across the arm going in a lateral to medial direction. Wrap the pressure cuff smoothly and snugly around the upper arm with its lower border 1 to 2 inches above the elbow crease in the antecubital fossa.
Fig. 7-13: Measurement of blood pressure with the help of stethoscope and sphygmomanometer.
• Pumping of cuff—palpate the patient’s radial pulse and pump the cuff up to above 20 to 30 mm Hg, the point at which the pulse is no longer palpable. It is essential to always record the systolic pressure by palpation to avoid missing the occasional occurrence of silent gap in hypertensive patients.
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• Measurement of systolic pressure—applies either the bell or the diaphragm of the stethoscope over the artery just distal to the elbow crease and slowly deflates the cuff about 3 mm Hg per heart beat until the first sound appears. Record this first sound as a systolic pressure. • Measurement of diastolic pressure—further lower the pressure in the cuff until the sound disappears. Record this point as the diastolic pressure. • Errors—faulty technique in taking the blood pressure may induce error. If the cuff is applied too loosely and if it is not completely deflated before applying or it is too small for the patient’s arm size, the pressure reading obtained will be inaccurately high and will not represent the pressure in the artery at the time of determination. Anxiety and pain are factors that may cause an elevation of the blood pressure of the patient above his true resting level.
Temperature • Procedure—this is normally taken in the mouth or in the axilla by keeping mercury thermometer (Fig. 7-14) for a minute. The temperature of mouth is about 1 degree higher than that of axilla. The normal body temperature varies from 36 degree Celsius to 37.5 degree Celsius. The lowest temperature being between 2-4 am and highest in the afternoon. The normal oral temperature is 37oC. Fever or pyrexia is more than 1 degree or any rise above the maximum normal temperature. • Conversion of Fahrenheit to Celsius—temperatures usually taken in Fahrenheit and to convert Fahrenheit into Celsius subtract 32 and multiply by 5/9.
‘tertian’, and when every 3rd day it is ‘quatrian’ e .g. malaria, kala azar, pyemia and septicemia. • Septic fever—the temperature variation between peak and nadir is very large and exceeds 5 degrees e.g. in septicemia. • Low grade fever—temperature is present daily especially in the evening for several days but does not exceed 37.8 degree at any time, like in tuberculosis. • Hyperpyrexia—tetanus, malaria, septicemia, heat stroke, encephalitis, and hemorrhage. • Benefit of fever—in some diseases, fever is beneficial. Fever is associated with release of endogenous pyrogen, which activates T cells and thus enhances the host defense mechanism. • Harmful effects—there is hypercatabolism—N2 wastage and weight loss, fluid and electrolyte imbalance due to sweating, convulsions, brain damage, circulatory overload and arrhythmias. • Hypothermia—hypothermia may be caused by endocrine disorders like hypothyroidism, hypopituitarism hypoglycemia, toxicity like alcohol intoxication, barbiturate poisoning, ketoacidosis, and exposure to cold and autonomic dysfunction.
Respiration • Significance—it is used to assess the condition of the patient under anesthesia and in early postoperative days. • Procedure—you should always check the respiration while checking the pulse of the patient. You should look at the patient abdomen and see how many times he breath. One complete cycle of inspiration and expiration is counted as one. Normal rate—14-18 cycles/minute (Fig. 7-15). • Tachypnoea (fast breathing)—it occurs in fever, shock, hypoxia, cerebral disturbances, metabolic acidosis, tetany, and hysteria.
Fig. 7-14: Temperature should be recorded with the help of thermometer.
• Types of fever • Continuous fever—the temperature remains above normal throughout the day and does not fluctuate more than 1 degree in 24 hours. E.g. lobar pneumonia, typhoid and infective endocarditis. • Remittent fever—The temperature remains above normal throughout the day and fluctuates more than 1 degree in 24 hours e.g. typhoid. • Intermittent fever—the temperature is present only for some hours in a day and remits to normal for the remaining hours. When the spike occurs daily, it is called as ‘quotidian’, when every alternate day it is
Fig. 7-15: Respiration rate of the patient should be counted while examining the pulse of the patient by looking at the abdomen.
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Case History • Bradypnoea—slow and deep respiration is seen in cerebral compression. • Snoring noise—paralysis of the soft palate causes an inspiratory snoring noise. • Expiratory wheezing—expiratory wheezing is heard in bronchitis and asthma.
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• Endocrine causes—like myxedema and acromegaly. • Miscellaneous causes—like hereditary, idiopathic and only in upper limb in heroin addicts due to chronic obstructive phlebitis. • Pseudoclubbing—in hyperthyroidism due to excessive bone resorption there is ‘drumstick appearance’ of the finger resembling clubbing.
Clubbing • Definition—clubbing is bulbous enlargement of soft part of the terminal phalanges of the nail (Figs 7-16 and 7-17).
Fig. 7-16: Lateral view of clubbing showing bulbous enlargement of soft part terminal phalanges on nail (Courtesy Dr Milind Chandurkar).
Cyanosis • Definition—cyanosis is the bluish discoloration due to increased amount of reduced Hb (more than 5 mg%) in capillary blood. • Types—it can be central, peripheral, cyanosis due to abnormal pigment or mixed. • Sites where peripheral cyanosis is looked for—nailbed, tip of the nose, skin of the palm and toes. • Sites where central cyanosis is looked for—tongue and other sites mentioned above. Tongue is unaffected in peripheral cyanosis. • Causes • Central—cardiac causes like congenital cyanotic heart disease and congestive cardiac failure, pulmonary causes like chronic obstructive lung disease (Fig. 7-18), collapse and fibrosis of lung, pulmonary obstruction, and high altitude due to low pressure of O2. • Peripheral—it includes cold, increased viscosity of blood and shock. • Mixed—it includes acute left ventricular failure, mitral stenosis and cyanosis due to abnormal pigments like sulfonamides and aniline dye.
Fig. 7-17: Clubbing seen in nails of leg of patient (Courtesy Dr Milind Chandurkar).
• Causes—it includes: • Pulmonary causes—like bronchogenic carcinoma, lung abscess, bronchiectasis, and tuberculosis with secondary infection. • Cardiac causes—like infective endocarditis and cyanotic congenital heart disease. • Alimentary causes—like ulcerative colitis, Crohn’s disease and biliary cirrhosis.
Fig. 7-18: Central cyanosis seen in tongue showing bluish discoloration of tongue due to chronic obstructive lung disease.
Icterus • Definition—in jaundice, there is icteric tint of the skin, due to presence of bilirubin, which varies from faint
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yellow of viral hepatitis to dark olive greenish yellow color of obstructive jaundice. • Site where you should look of Icterus—the places where one should look for Icterus are sclera of the eyeball (Fig. 7-19), nailbed, lobule of ear, tip of the nose and under surface of tongue. • Hypercarotenemia—jaundice may be confused with hypercarotenemia in which yellow pigment of carotene is unequally distributed and is particularly seen in the face, palm and soles but not in the sclera. It occurs mostly in vegetarians.
• Signs—such as petechial hemorrhage indicating blood dyscrasias. • Eruptions—any eruption such as macule, papule, vesicle or bulla. • Pigmentation—pigmentation of Addison’s disease affects buccal mucous membrane as well as skin in regions subjected to friction. In Von Recklinghausen’s disease, milky coffee pigmentation on the limbs, trunk and face. • Edema—in acute nephritis, edema of face is marked when patient rises in the morning. Dependent edema with pallor and glossy appearance over the swollen part, doughy consistency, and pitting on pressure is characteristic.
Head
Fig. 7-19: Icterus seen in eyes of patient who is suffering from jaundice (Courtesy Dr Bhaskar Patle).
Extraoral Examination Skin • Appearance—changes in appearance, rashes, sores, lumps or itching is looked for and history of sun exposure is questioned. • Color—it is seen for anemia and jaundice. • Generalized pallor—it is seen in severe anemia. Pallor can be seen in hypopituitarism, shock, syncope, left heart failure and Raynaud’s disease. • Lemon yellow tint—a pale lemon yellow tint in hemolytic jaundice and dark yellow or orange tint in obstructive jaundice is seen. • Yellowness of skin—yellowness of skin is seen in carotenemia. • Texture—it is thickened, greasy and loose in acromegaly. In dehydration, skin is dry and inelastic so that it can be pinched into ridge. Skin is atrophied with age and sometimes after treatment with glucocorticoids.
• Headache—important symptoms like headache should be noted. Following point should be noted in headache. • Nature of headache—persistent or intermittent and localized or generalized. Unilateral or bilateral or frontal. Associated with unusual disturbances. Familial disorder or induced by stress. • Site—the exact location of headache. • Radiation—does it stay in its place or does it move or spread? • Severity—does it interfere with daily activity or keep you awake at night? • Timing and duration—when did it start, when does it come and when does it go, has it changed since it began? • Character—shooting or pricking etc. • Occurrence or aggravation—what brings it on, and what makes it worse. • Relief—what makes it better? • Head circumference—hydrocephalus should be suspected when the rate of growth of the head is greater than normal for the sex, age and size of the infant.
Jaws • Normal landmark—normal anatomic landmarks to be identified include mandibular border, angle of mandible, condyle and coronoid process, maxillary bone, lingual notch and maxillary sinus. • Tenderness over the jaws—note any tenderness over the joint or masticatory muscles (temporalis, masseter) while palpating externally over lateral pterygoid and buccinator muscles (distal and lateral to upper molar teeth) and medial pterygoid muscle (pterygomandibular ligament and medial aspect of anterior faucial pillars) with the mouth open. • Trauma—any trauma to head and neck such as injury from motor vehicle or bicycle accident, injury to the side of face and chin should be looked for.
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Case History
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Temporomandibular Joint The clinical examination for a patient with possible temporomandibular disorder supplements the routine regional head and neck examination. Following point should be noted while examining the temporomandibular joint. • History—medical history about illness, particularly rheumatoid arthritis, degenerative joint disease, osteoarthritis should be asked. Before treatment of temporomandibular joint disorder is initiated, it is necessary to exclude other disorders that might present with similar symptoms like trigeminal neuralgia, multiple sclerosis, glossopharyngeal neuralgia, temporal arteritis, migraine headache, angina pectoris, pulpoperiodontal disease, salivary gland inflammation, duct blockage, otitis, sinusitis and psychogenic pain. • Symmetry of face—the symmetry of the face should be assessed. Gross asymmetry reflects growth disturbances. • Interincisal opening—the maximum interincisal opening of the mouth should be determined, which is, normally, in an adult, 35-50 mm. Measurement also should be recorded for the degree of opening where pain begins. • Mandibular movement—any deviation of the mandible during opening should be noted, along with its severity. The lateral mandibular range of motion is determined by having the patient to occlude the teeth and then slide the jaw in both directions. The range of movement from the midline is measured in mm and any pain along with location and severity is recorded. Normal lateral movement is usually 8-10 mm. • Question to be asked to patient—jaw and joint symptoms should also be discussed with the patient: • Does the TMJ click or pop on opening or closing? • Has there been limitation in the movement or deviation of the lower jaw on opening? • Has the jaw ever locked or dislocated on opening? • Has the patient experienced pain and dysfunction in other joints of the body? • Palpation of joint—palpate the joint and listen for clicking and crepitus during the opening and closing of the jaw. Use stethoscope to characterize and locate this sound accurately. Explore the anterior wall of external auditory meatus for tenderness and pain that are usually associated with arthritic changes. • Methods of palpation • Pretragus palpation—the patient should be requested to slowly open and close the mouth while the doctor bilaterally palpates the pretragus depression with his/her index fingers (Fig. 7-20). • Intra-auricular palpation—it is also performed by inserting the small finger into the ear canal and pressing anteriorly (Fig. 7-21).
2 Fig. 7-20: Examination of TMJ with pretragus palpation method.
Fig. 7-21: Intraarticular palpation method showing finger inserted in the articular area.
• Significance of palpation—it is important to perceive, during the pretragus and intra-auricular palpation, whether the condyle moves symmetrically, with the rotation and translation phase being evident. Palpation is also used to detect the tenderness, clicking and crepitus. Subluxation of the joint is also recorded.
Masticatory Muscle • Digital palpation—regional muscles are examined for the tenderness and trigger points using the digital palpation. • Masseter muscles—the masseter muscles are most effectively examined by simultaneously pressing them from inside and outside the mouth in the process of bimanual palpation. • Lateral pterygoid muscle—the lateral pterygoid muscles are evaluated by inserting a finger each behind the maxillary tuberosities, whereas the medial pterygoid is checked by running a finger in an anteroposterior
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direction along the medial aspect of the mandible in the floor of mouth.
Lymph Nodes
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• Significance—normal lymph nodes are difficult to palpate. Nodes draining area of active infection are usually tender; the overlying skin may be warm and red. Gradually enlarging group of nodes in the absence of local infection and inflammation is a significant finding that suggests either systemic disease (infectious mononucleosis, generalized lymphadenopathy associated with HIV infection, lymphoma) and justifies examination for lymphoid enlargement at distant sites such as axilla, inguinal region and spleen to confirm the generalized nature of the process. • Inspection of lymph node swelling • Position—position is important, as it will not only give an idea as to which group of lymph nodes is affected but also help in diagnosis. • Number—it is important since in some diseases there is generalized involvement of the lymph nodes like Hodgkin’s disease, lymphatic leukemia and lymphosarcoma. • Pressure effect—swelling and venous engorgement of the face and neck may occur due to pressure effect of the lymph nodes at the root of the neck. • Palpation—the swelling is palpated for number, situation, local temperature, surface, margin and consistency. Enlarged lymph nodes should be carefully palpated with palmar aspect of the fingers. While rolling the finger against the swelling slight pressure is maintained to know the actual consistency. • Fixity to underlying tissues—the lymph nodes of the neck should be examined by standing behind the patient with the patient’s neck slightly flexed.
• Palpation of superficial lymph nodes—palpation of the lymph nodes of the neck is commonly begun with most superior nodes and worked down the clavicle for supraclavicular nodes, anterior to the tragus of ear for preauricular nodes, mastoid and base of skull for posterior auricular and occipital nodes, under the chin for submental nodes (Fig. 7-22) and further posteriorly for submandibular and sublingual lymph nodes. • Examination of deep cervical nodes—to examine the deep cervical nodes ask the patient to sit erect and turn the head to one side to relax the sternomastoid muscle (Fig. 7-23). Use thumb and finger to palpate under the anterior and posterior borders of the relaxed muscle and repeat the procedure on the opposite side. Palpate the posterior cervical nodes in the posterior triangle close to the anterior border of the trapezius muscle. Finally, check for supraclavicular nodes just above the clavicle, lateral to the attachment of the sternomastoid.
Fig. 7-23: Examination of deep cervical lymph nodes is done by relaxing the sternomastoid muscle.
Fig. 7-22: Palpation of submental lymph node is done by standing in front of the patient and patient neck flexed.
• Causes of lymph nodes enlargement • Inflammatory—acute lymphadenitis, chronic lymphadenitis, septic, tuberculosis, syphilis, filariasis, and lymphogranuloma inguinale. • Neoplastic—primary (lymphosarcoma), secondary (carcinoma, sarcoma, malignant melanoma). • Hematological—Hodgkin’s disease, non-Hodgkin lymphoma, chronic lymphatic leukemia. • Immunological—AIDS, serum sickness, drug reaction, SLE and rheumatoid arthritis.
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Case History Examination of Other Parts • Nose—severe nasal obstruction leads to breathing through mouth which leads to dryness of mouth which results in persistent sore throat. Infection from nose may spread to the orbit from the adjacent paranasal sinus. Longstanding nasal obstruction suggests a deviated nasal septum. Epistaxis (nasal bleeding) may indicate life threatening conditions like cerebral hemorrhage. Nasal discharge may be purulent, bloody, watery or mucoid. • Paranasal sinus—an apical tooth abscess of the upper jaw may drain into the maxillary sinus causing acute sinusitis. • Eyes—visual disturbances, color of the sclera and conjunctivae are looked for anemia and liver diseases. Ocular pain, diplopia and edema of eyelid etc. are also looked for. • Ears—impaired hearing, loss of hearing, discharge from ears, tinnitus. • Neck—check for movement in neck, lump in the neck, cervical lymphadenopathy. If thyroid enlargement is suspected, check if the mass moves up and down with trachea when the patient swallows. • External jugular vein—observe the external jugular vein as it crosses the sternomastoid muscle and with the patient at an angle, approximately 45 degree to the horizontal, note any distension and/or pulsation in the vein. Distension more than 2 cm above the sternal notch is abnormal and is seen in severe right side heart failure.
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try to directly visualize upper teeth in the patient mouth (Fig. 7-24).
Doctor’s Position Position of doctors is very important while intraoral examination. As there are many professional hazards which occur due to improper position of the doctors. • Basic position—doctor should be either low seated or in standing position. In cases of examining while doctors in standing position, he should stand erect without bending of spinal cord. Patient head should be at elbow level of the doctor. The ideal position is 10 o’ clock or 11 o’ clock position. • Guideline for examination—you should avoid resting arms over patient shoulder, and maintain comfortable distance from the patient. Eye contact should be maintained with the patient. Drape the patient and avoid keeping instrument on the patient chest. • Upper left posterior region—In this case doctors should stand behind the patient with his left hand going around the patient head (Fig. 7-25).
Intraoral Examination Intraoral examination is the most important part in dental point of view.
Diagnostic Set of Instrument Basic diagnostic set which require for intraoral examination are mouth mirror, tweezers, probe, explorer. The use of mirror is mainly for the retraction and indirect vision. Never
Fig. 7-25: Doctor’s position of upper left posterior region.
• Upper right posterior region—doctors should stand at side of patient (Fig. 7-26). • Lower right posterior region—in this case, doctors should stand at side of the patient (Fig. 7-27). • Lower left posterior region—in this case, doctor should stand behind the patient (Fig. 7-28).
Examination of Nondental Structures Tongue Fig. 7-24: Basic diagnostic set of instrument consist of mouth mirror, probe, tweezers, explorer.
Inspection • The volume of the tongue—massive tongue due to lymphangioma, hemangioma and neurofibroma.
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Textbook of Oral Medicine • Papillae of tongue—observe and note the distribution of filiform and fungiform papillae, margins of the tongue, crenation and fasciculation, depapillated areas, fissures, ulcers and keratotic areas. • Color—the white color of leukoplakia, candidiasis (Fig. 7-29) the red color tongue when the leukoplakic plaque gets desquamated, blue color of venous hemangioma. Black hairy tongue due to hyperkeratosis of the mucous membrane in heavy smoker or caused by fungus aspergillus are very characteristic. In jaundice, yellowish tint to the tongue may be seen.
2 Fig. 7-26: Doctor’s position for upper right posterior region.
Fig. 7-29: One should note the color of tongue. In this case, color is white due to candidiasis
Fig. 7-27: Doctor’s position for lower right posterior region.
Fig. 7-28: Doctor’s position for lower left posterior region.
• Any crack or fissure—note the direction of fissure; congenital fissures are mainly transverse whereas syphilitic fissures are usually longitudinal. • Swelling and ulcer—examine the tongue for any swelling or ulcer. If there is a swelling or an ulcer, note the size, shape, extent, margin etc. Also note whether it has extended to the floor of mouth, to the jaw or tonsil. The site of the ulcer is usually characteristic; like the dental ulcer appears on the side of the tongue where it comes in contact with sharp teeth or dentures, tuberculosis ulcer on the lip and side of tongue, gummatous ulcer on the dorsum and carcinomatous ulcer occurs usually on the margin of the tongue. • Mobility of the tongue—ask the patient to put the tongue out and move it side ways (Fig. 7-30). Inability to put the tongue out completely is due to ankyloglossia. If the tongue deviates to one side during the protrusion it indicates impairment of nerve supply to that half of the tongue. This is noticed in carcinoma of the tongue, which has damaged the nerve supply of consequent side. If the child with impaired speech fails to protrude the tongue, it is possibly due to tongue-tie; look for short frenum linguae.
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Case History
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2 Fig. 7-31: Note for any cleft in the palate while examining. In this case, cleft is due to cleft palate. Fig. 7-30: Mobility of tongue can be checked by holding it with the hand.
• Tongue thrusting—note tongue thrust on swallowing. • Central cyanosis—look for central cyanosis. Palpation • Procedure—while palpating for induration of the base of an ulcer, tongue should be relaxed and at rest within the mouth. If it is kept protruded, the contracted muscles may give a false impression to induration and lead to error in diagnosis. Induration is an important clinical sign of epithelioma. It may be present in gummatous ulcer but is absent in tubercular ulcer. • Points to be noted—note whether ulcer bleeds during palpation. This usually occurs in malignant ulcer. Palpate carefully for a sharp tooth or tooth placed against an ulcer in the tongue. Palpate the back of the tongue for any ulcer or swelling.
Palate Inspection • Point to look for—congenital cleft, perforation, ulceration, swelling, fistulae, papillary hyperplasia, tori, recent burns and hyperkeratinization. • Cleft examination—in case of congenital cleft, note the extent of the cleft (involving only the uvula, only the soft palate or part or whole of the hard palate). Whether the nasal septum is hanging free or attached to one side of the cleft (Fig. 7-31). • Perforation—perforation of the hard palate is usually caused by gumma. • Scar of operation—any scar of the operation around or history of operation, as sometime a hole may persist after an operation for closure of congenital cleft. Palpation • Point to look for—tender, fluctuating swelling close to alveolar process is an alveolar abscess. Soft swelling in the midline of the hard palate is gumma.
Lip Inspection • Point to be noted—note lip color, texture and any surface abnormalities, angular or vertical fissures. • Cleft—cleft lip (Fig. 7-32), either complete or incomplete, bilateral complete cleft lip in which there is also cleft palate and protuberant pre-maxilla. Cleft between maxilla and side of the nose. • Pigmentation—pigmentation of lip and buccal mucosa in Addison’s disease. In Peutz Jeghers syndrome, melanin pigmentation of the lip and oral mucosa occurs. • Chancre—chancre on lip is a painless ulcer with dull red color. • Ectopic salivary neoplasm—ectopic salivary neoplasm is seen in upper lip as slow growing, lobulated tumor. • Macrochelia—thickening of the lip which often involves the upper lip. • Cheilitis—in cheilitis glandularis, lower lip becomes enlarged, firm and everted. In cheilitis granulomatosa, there is diffuse swelling of the lower lip.
Fig. 7-32: Cleft lip should be properly examined in patient.
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Palpation • Point to be noted—benign neoplasm is firm and lobulated while carcinoma of the lip is hard in consistency. Chancre is rubbery hard whereas carcinoma is stony hard. Mucous retention cyst is seen on the inner surface of the lip. In cheilitis granulomatosa, the swelling is soft usually exhibiting no pitting on pressure.
lipoma, mixed salivary tumor, papilloma and carcinoma. • Pigmented patches—pigmented patches are seen in Addison’s disease and in Peutz Jegher’s syndrome. • White lesion—it can be seen in pronounced linea alba, leukoedema, hyperkeratotic patches. • Red lesion—it can be present in ulcer, nodule, scar, and malignancy.
Floor of Mouth Inspection • Procedure—ask the patient to open his mouth and to keep the tip of tongue upward to touch the palate. This will expose the floor of mouth. • Point to be noted—any swelling, red-white patches in the floor of mouth should be noted. • Color of swelling—when a swelling is present note its color. A ranula appears as a unilateral bluish translucent cyst over which Wharton’s duct can be seen. In hemangioma swelling is red in color (Fig. 7-33). • Site of lesion—a sublingual dermoid lies exactly in the midline and may extend into the submental region. A deeper plunging ranula may have cervical prolongation into the submandibular region. • Ankyloglossia—in ankyloglossia there is fusion between the tongue and floor of mouth. Fig. 7-34: White patch seen on cheek mucosa due to leukoplakia
Palpation • Point to be noted—mucous cysts have smooth surface and are movable over the deeper structures. Fluctuation can be elicited by pressing on the top of the cyst while the sides are palpated by other 2 fingers. Papilloma is a solid tumor with irregular surface and is mobile over the deeper structures. Carcinoma is fixed and indurated. Palpate the muscles of cheek.
Tonsil and Pharynx Fig. 7-33: Swelling in floor of mouth is due to hemangioma.
Palpation • Point to be noted—Ranula is a fluctuant swelling with positive translucence. Sublingual dermoid which is not translucent but tense and fluctuant swelling is seen on the midline. Carcinoma of the floor of mouth is revealed by its indurated base and probable fixation to the underlying structures.
Cheek Inspection • Point to be noted—examine the inside of the cheek for aphthous ulcer, leukoplakia (Fig. 7-34), and mucous cyst,
• Point to be noted—note the color, size and surface abnormalities of the tonsil. Palpate tonsil for discharge and tenderness. Note restriction of oropharyngeal airway. Observe the faucial pillars for nodules, red and white patches (Fig. 7-35), lymphoid aggregates and deformities. Observe the postpharyngeal wall for swelling, nodules, lymphoid hyperplasia, hyperplastic adenoid, and postnasal discharge.
Salivary Glands—Parotid Gland Inspection and palpation • Swelling—keep in mind the position of the parotid gland, which is below, behind and slightly in front of the lobule of the ear. A swelling of the parotid gland thus obliterates
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Case History
• • • • Fig. 7-35: Redness in tonsillar area should be noted.
the normal hollow just below the lobule of the ear. Position is important since many of the lymph node swellings are mistaken for parotid gland tumor and vice versa. Note the extent, size, shape and consistency. Whether the swelling is fixed to the masseter muscle or not, is confirmed by asking the patient to clench his teeth and mobility is tested over the contracted masseter muscle. • Skin over the parotid gland—in case of parotid abscess, the skin becomes edematous with pitting on pressure. Fluctuation is a very late feature of parotid abscess as there is strong parotid fascia over the parotid gland. The skin is warm and tender. Any scar or fistula should be looked for. If there is malignancy check if there is infiltration of the skin by the tumor. • Duct—Stensen’s duct on the buccal surface of the cheek is opposite to the crown of the upper second molar
Fig. 7-36: Stensen’s duct opening seen in upper second molar region as a papilla.
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(Fig. 7-36). For its proper inspection, retract the cheek with spatula. If there is suppurative parotitis gentle pressure over the gland will cause purulent saliva to come out of the orifice of the duct. Blood will come out in case of malignant growth of the gland. The terminal part of the duct is best palpated bidigitally between the index finger inside the mouth and the thumb over the cheek. Fistula—if there is parotid fistula, note its position and whether it is in relation to the gland or duct. Examination of facial nerve—facial nerve is not involved in benign tumor but is involved in malignant growth. Lymph nodes—preauricular, parotid and submandibular groups of lymph nodes are mostly involved. Movement of the jaw—it may become restricted if the growth is malignant and has involved the pre-articular tissue of TMJ.
Submandibular Salivary Gland • History—swelling with colicky pain at the time of meals suggests obstruction in submandibular duct. It is tense and painful. Swelling is more often due to lymph node enlargement rather than salivary gland enlargement. If the patient gives the history which is suggestive of a stone in the duct ask the patient to suck a little lemon or lime juice. The swelling will appear at once. • Mikulicz’s disease—in Mikulicz’s disease; submandibular, parotid as well as lacrimal glands are enlarged. • Wharton’s duct—inspection of the Wharton’s duct is made by means of torch on the floor of mouth which is situated on either side of lingual frenum. Whether the orifice is inflamed or swollen? If the gland is infected, slight pressure on the gland will exude pus through the respective orifice. If stone is suspected in one duct, saliva will be seen coming out with normal flow from the other orifice while the affected duct orifice remains dry. This is tested by putting dry sweets one on each orifice and some lemon juice is given on the dorsum of the tongue, 2 minutes later the sweets are taken out. The sweet on the orifice of the duct where the stone is suspected will remain dry. • Bimanual palpation—patient is asked to open the mouth; one finger of one hand is placed on the floor of mouth medial to the alveolus and lateral to the tongue and pressed on the floor of mouth as far as possible. The finger of the other hand on the exterior are placed just medial to the inferior margin of the mandible. These fingers are pushed upward; this will help to palpate both the superficial and deep lobes of submandibular salivary gland. This also differentiates an enlarged salivary gland from enlarged submandibular lymph nodes.
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Mucobuccal Fold
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• Point to be noted—observe color, texture, any swelling, and fistulae. Palpate the swelling and tenderness over roots of the teeth and look for tenderness of the buccinator insertion by pressing laterally with finger over roots of the upper molar teeth.
Examination of Dental Structures Teeth • Teeth nomenclature—various nomenclature systems used are as follows • Zsingmondy’s and palmar method—it is the oldest method of recording teeth. The oral cavity is divided into four quadrants. For deciduous teeth and permanent teeth dental formula is as follows Deciduous teeth EDCBA ABCDE EDCBA ABCDE
Permanent teeth 87654321 12345678 87654321 12345678
• Universal system—the primary teeth in the maxillary arch are designated by letter A through J, beginning with the right second molar. The teeth in mandibular arch are designated by letter K through T beginning from the left second molar. Similarly for the permanent teeth numbers 1 to 32 are used. Permanent teeth – 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 32 31 30 29 28 27 26 25 24 23 22 21 20 19 18 17
Deciduous teeth – +05+04+03+02+01 +01+02+03+04+05 –05–04 –03–02 –01 –01 –02–03–04–05 • Point to look for—you should look for caries (pit and fissure, smooth surface caries, cervical caries), defective restoration or recurrent caries. You should also note missing and supernumerary teeth (Mesiodens, paramolar, distomolar). Presence of root piece of badly carious fractured teeth. You should also look for overretained deciduous teeth, impacted teeth, ankylosed teeth, fusion of teeth, Talon’s cusp, dens evaginatus, taurodontism, and anodontia, enamel hypoplasia, mottled enamel, neonatal teeth, eruption sequestra, delay eruption, attrition, abrasion, erosion, sclerosis, pulp calcification, resorption of teeth, hypercementosis, plaque, calculus and stains. • Difference between deciduous and permanent teeth—it is described in Table 7-8. • Stains and calculus—stains and calculus should be recorded in the finding. If calculus is present, there are always chance that gingival inflammation is present as calculus act as local irritant. Different grading for stains and calculus is as follows • +—stain and calculus involving only cervical portion of teeth (Fig. 7-37). • ++—stains and calculus extending upto the middle third of teeth (Fig. 7-38). • +++—stains and calculus involving whole of the facial or lingual surface (Fig. 7-39).
Deciduous teeth— A B C D E FG H I J T S R Q P ON MLK • F.D.I (two digit system)—in it first digit indicates the quadrant as 1 to 4 of the permanent teeth and 5-8 for primary teeth. The second digit indicates the tooth in the quadrant. Thus, deciduous upper right second molar is denoted as 55 and pronounced as five-five and not fifty five and first mandibular left permanent molar is denoted as 36. Permanent teeth— 18 17 16 15 14 13 12 11 21 22 23 24 25 26 27 28 48 47 46 45 44 43 42 41 31 32 33 34 35 36 37 38 Deciduous teeth—
Fig. 7-37: Stains showing involvement of cervical portion only.
55 54 53 52 51 61 62 63 64 65 85 84 83 82 81 71 72 73 74 75 • Dane system Permanent teeth— +8+7+6+5+4+3+2+1 +1+2+3+4+5+6+7+8 –8 –7–6–5 –4–3–2 –1 –1–2 –3–4 –5–6–7–8
• Percussion test—this test enables to evaluate the status of the periodontium surrounding a tooth. There are two types of percussion tests carried out i.e. vertical percussion and horizontal percussion test. • Vertical percussion test—if vertical percussion test is positive, it indicates periapical pathology. To carry
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2 Fig. 7-38: Stains ++ showing involvement upto middle third of the patient. In this patient there is also calculus + on the lingual surface.
Fig. 7-40: Vertical percussion test showing tapping of teeth in vertical direction.
Fig. 7-39:Stains +++ and calculus ++ in this patient.
Fig. 7-41: Horizontal blow should be given in horizontal percussion test.
out vertical percussion test the tooth is struck a quick, moderate blow, initially with low intensity by the finger and then with increasing intensity by using the handle of an instrument, to determine whether the tooth is tender. First you have to tap adjacent teeth first and then tap an affected one. The patient response should be taken from patient body movement, reflex reaction of eye. If tooth is tender patient will blink his eyes due to pain (Fig. 7-40). • Horizontal percussion test—if horizontal test is positive it indicates periodontium associated problems. In case of horizontal percussion test, the procedure is same but direction of blow is in horizontal direction (Fig. 7-41). • Mobility and depressibility test—it is used to evaluate the integrity of the attachment apparatus surrounding the tooth.
• Mobility test—the test consists of moving a tooth laterally in its socket by using the finger or preferably in the handles to two instruments. The objective of this test is to determine whether the tooth is firmly or loosely attached to its alveolus. • Depressibility test—similarly, the test for depressibility consist of moving a tooth vertically in its socket. When depressibility test is positive chances of retaining the tooth range from poor to hopeless. • Pathologic mobility—it results from inflammatory process, parafunctional habits or iatrogenic induced situation. • Adaptive mobility—occurs due to anatomic factors such as short roots and/or poor crown to root ratios that are normally directly contributory to mobility. • Measurement of tooth mobility—there are different ways to measure tooth mobility. They are as follows:
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Textbook of Oral Medicine Table 7-8: Difference between primary and permanent teeth Primary teeth
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The primary teeth are 20 in number
The permanent teeth are 32 in number
The crowns of primary anterior teeth are wider mesiodistally than the cervicoincisally
The cervicoincisal dimension of the permanent teeth are more as compared to mesiodistal dimension
The crown of the primary teeth have prominent cervical ridge on the buccal surface
The buccal surface of the permanent teeth do not have marked cervical ridge as that of the primary teeth
The roots of the primary teeth are narrow and thin
The roots of permanent teeth are more bulky as compared to that of the primary teeth
The crown and roots of the primary teeth show marked cervical constriction The roots of the primary molar flare out from the cervical third The furcation is close to the cervical line resulting is a short root trunk The primary teeth are lighter in color because of thinner enamel and different refractive index of the enamel Both enamel and dentin thickness is less as compared to the permanent teeth
The permanent teeth do not have such as marked cervical constriction The roots of the permanent molars do not possess flare as that of the primary teeth The furcation is at a distance from the cervical line resulting in longer root trunk The permanent teeth are yellowish in color because of thicker and more translucent enamel Both enamel and dentin are thicker as compared to the primary teeth
Pulp chambers are larger in size
Pulp chambers are smaller in size
Pulp horns are at higher level
Pulp horns are at a lower level as compared to the primary teeth
Enamel rods are inclined occlusally in the cervical third
Enamel rods are inclined cervically in the cervical third
Number of accessory canals are more
Accessory canals are less in number
Broader and flatter contact areas
Contact areas are less broad
• According to Glickman • Grade-I—slightly more than normal. • Grade II-—moderately more than normal. • Grade III—severe mobility faciolingually and/or mesiodistally combined with vertical displacement. • According to Millar—2nd method was developed by Millar (1950) in which tooth is held firmly between 2 instruments and move back and forth and mobility score is noted (Fig. 7-42) as follows • 0—it denotes no detectable movement when force is applied other than what is considered normal (physiologic) motion.
Fig. 7-42: Mobility of tooth is checked by handles of two instruments.
• 1—it indicates mobility greater than normal. • 2—mobility up to 1 mm in buccolingual direction. • 3—mobility greater than 1 mm in a buccolingual direction combined with the ability to depress the tooth. • Dental arch irregularities—it classified by Angle as follows • Class I—arch in normal mesiodistal relationship, i.e. mesiobuccal cusp of the maxillary first permanent molar occludes in the buccal groove of mandibular first permanent molar (Fig. 7-43). Dewey’s modification of class I Angle classification is as follows. • Type I—crowded anterior teeth. • Type II—proclinated maxillary incisors. • Type III—anterior cross bite (Fig. 7-44). • Type IV—posterior cross bite. • Type V—the permanent molar has drifted mesially due to early extraction of second deciduous molar or second premolar. • Class II—mandibular arch distal to normal in its relation to the maxillary arch, i.e. distobuccal cusp of upper first permanent molar occludes in the buccal groove of lower first permanent molar (Fig. 7-45). • Div I—proclination of upper incisors, abnormal muscular activity. • Div II—lingually inclined upper central incisors and labially tipped upper lateral incisors overlapping the central incisors. • Class II subdivision—Class II molar relationship on one side and class I on other side. • Class III—mandibular arch mesial to normal in its relation to the maxillary arch, i.e. mesiobuccal cusp
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of maxillary first permanent molar occluding in interdental space between mandibular first and second molar (Fig. 7-46). • Class III subdivision—class III on one side and class I on other side.
2 Fig. 7-43: Class I molar relationship showing mesiobuccal cusp of maxillary permanent molar occlude in buccal groove of mandibular first molar.
Fig. 7-46: Class III malocclusion showing mandibular arch mesial to normal.
Fig. 7-44: Anterior cross bite seen in patient (Courtesy Dr Shetty).
Fig. 7-45: Class II molar relationship showing mandibular arch distal to its normal relationship.
• Occlusion in deciduous dentition—it is evaluated by following ways • Flush terminal plane—the distal surface of maxillary and mandibular second molar are in straight plane. • Mesial step—distal surface of mandibular second molar is more mesial to maxillary second molar. • Distal step—distal surface of mandibular second molar is more distal to maxillary second molar. • Point to look for in dental arch—orthodontic anomalies, abnormal jaw relationship. Occlusal interference. • Presence of periodontal pocket—it can be true or false pocket. The probe should be inserted parallel to the vertical axis of the tooth and ‘walked’ circumferentially around each surface of each tooth to detect the areas of deepest penetration (Fig. 7-47). • Furcation involvement—the term furcation involvement refers to the invasion of the bifurcation and trifurcation of multirooted teeth by the periodontal disease. The extent of involvement is determined by exploration with Naber’s probe, along with simultaneous blast of warm air to facilitate visualization. There are different grade of furcation involvement which are as follows: • Grade I—it is incipient bone loss. Clinically only slight catch occurs in furcation area while probing. • Grade II—partial bone loss. In this case probe can pass in the furcation area upto middle. • Grade III—total bone loss with through and through opening of the furcation. Probe can pass through and through. • Grade IV—it is similar to grade III but with gingival recession exposing the furcation to view (Fig. 7-48A).
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2 Fig. 7-47: Probe should be inserted parallel to the vertical axis of tooth in periodontal pocket examination.
• Apply the electrolyte—apply an electrolyte (toothpaste) on the tooth electrode, and place it against the dried enamel to the crown’s occlusobuccal or incisobuccal surface. It is important to avoid contacting any restoration on the tooth or the adjacent gingival tissue with the electrolyte or the electrode; this will cause a false and misleading response. • Retract the patient’s cheek—retract the patient’s cheek away from the tooth electrode with the free hand. This hand contact with the patient’s cheek completes the electrical circuit. • Turn the rheostat—turn the rheostat slowly to introduce minimal current into the tooth and then slowly increase it and ask the patient to indicate when sensation occurs by using words as “tingling” or ‘warmth’. Record the results according to the numeric scale on the pulp tester (Fig. 7-48B).
Fig. 7-48B: Electric pulp tester is used for vitality testing of pulp. Fig. 7-48A: Grade IV furcation involvement winch is associated with gingival recession.
• Pulp testing or vitality testing—there are four types of pulp testing: • Electric pulp testing—the electric tester, when testing for pulp vitality uses nerve stimulation. The objective is to stimulate pulpal response by subjecting the tooth to an increasing degree of electric current. A positive response is an indication of pulp vitality and helps in determining the normality or abnormality of that pulp. No response to the electrical stimulus can be an indication of pulp necrosis. The procedure is as follows: • Describe test to patient—describe the test to the patient in a way that will reduce anxiety and will eliminate bias response. • Isolation of teeth—isolate the area of teeth to be tested with cotton rolls and saliva ejector and air dry all teeth.
• Thermal testing—these tests involve the application of cold or heat to a tooth, to determine sensitivity to thermal changes. A response to cold indicates a vital pulp, regardless of whether that pulp is normal or abnormal. An abnormal response to heat usually indicates the presence of a pulpal or periapical disorder requiring endodontic treatment. • Heat testing—the area to be tested is isolated and dried, warm air is directed at the exposed surface of the tooth and the patient’s response is noted. If a higher temperature is required then one should use a hot burnisher or hot gutta purcha. • Cold testing—cold air can be directed against the crown of the previously dried tooth and also at the gingival margin. If no reaction occurs the tooth can be isolated under the rubber dam and sprayed with ethyl chloride, which evaporates so rapidly that it absorbs heat and thereby cools the tooth. A more common method is using cotton pellet saturated with
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Case History ethyl chloride on the tooth being tested. Another simple method is to wrap a sliver of ice in wet gauze, and to place it against the facial surface of the tooth and to compare to reaction of control tooth. • Anesthetic testing • When it is required—this test is restricted to patient which is in pain at the time of the test, when the usual test has failed to enable one to identify the tooth. The objective is to anesthetize a single tooth at a time until the pain disappears and is localized to specific tooth. • Infiltration of teeth—using either infiltration or the intraligament injection injects the most posterior tooth in the area suspected of being the cause of pain. If pain persists when the tooth has been fully anesthetized, anesthetize the next tooth mesial to it and continue to do so until the pain disappear. • Inferior alveolar nerve block—if the source of the pain cannot be determined, whether in maxillary or mandibular teeth, an inferior alveolar injection should be given. • Test cavity—it is performed when other method of diagnosis have failed. It is made by drilling through the enamel and dentin junction of an unanesthetized tooth. The drilling should be done at slow speed and without a water coolant. Sensitivity and pain felt by the patient is an indication of pulp vitality. Sedative cement is placed in the cavity and search for the source of infection continues. If no pain is felt, cavity preparation continues until the pulp chamber is reached. If the pulp is completely necrotic, endodontic treatment can be continued in many cases without anesthesia.
Gingiva • Color—normal is coral pink; physiological pigmentation of melanin may be seen. • Size—it corresponds to the sum total of the bulk of cellular and intercellular elements and their vascular supply. Alteration in size is a common feature of gingival disease. • Contour—it depends upon shape of the teeth and their alignment in the arch, location and size of the area of proximal contact and dimension of the facial and lingual gingival embrasures (Fig. 7-49). • Shape—it is governed by the contour of proximal tooth surface and the location and shape of gingival embrasures. • Consistency—firm and resilient with exception of free margin. • Surface texture—orange peels appearance or stippled. • Position—the level at which the gingival margin is placed on the tooth.
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2 Fig. 7-49: Irregular shaped contour of gingiva in the patient who has got misalignment of teeth. Gingiva is of normal color.
• Earliest sign of periodontics—earliest sign of periodontitis is a deep red line along the free edge of gum. Vincent stomatitis is an inflammatory condition of the gingiva. • Cancrum oris—cancrum oris starts with painful, purple red indurated papule found on the alveolar margin in the region of the molar or premolar teeth which later on ulcerates to rapidly expose the underlying bone and extends to the cheek and lip. Swollen gums, dental abscess and blue line are seen in lead poisoning. • Bleeding gums—as the age advances, there is recession of the gingiva. The gums may bleed, be swollen, spongy and tender in scurvy. Gums may bleed in uremia but may not as spongy as in scurvy. Epulis is the swelling of the alveolar margins of the gums. • Gingivitis—if there is inflammation of the gingiva, it is called as gingivitis. It may be acute or chronic, localized or generalized. Signs of gingivitis are bleeding on slight probing, red, spongy, swollen and edematous gingivae. • Periodontitis—if there is inflammation of the periodontium, that is gingiva, alveolar bone, cementum, and periodontal ligament, it is called as periodontitis. Signs of it include all the sign of gingivitis, gingival recession and alveolar bone loss, foul smell, pocket formation.
Examination of Swelling Inspection • Situation—a few swellings are peculiar in their position such as dermoid swelling which is mostly seen in the midline of the body or on the line of fusion of the embryonic process. Nasopalatine cyst is common in maxillary anterior region. • Color—the color of swelling should be noted. Color of swelling lead to some clue in the diagnosis. • Black color—it is of benign nevus and melanoma; red purple color of hemangioma.
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• Pink—normal color is pink as healthy stratified squamous epithelium is semitransparent and hence, the red color of blood in the extensive capillary bed beneath although somewhat muted shows through. Transitory pink color to whiter appearance is caused due to increased thickness of epithelium layer which occurs due to increased retention of keratin. Masticatory mucosa which is subjected to greatest mechanical stimulation appears light pink, e.g. buccal mucosa, vestibule, floor of mouth and ventral surface of tongue. • White—many pathological variations will impart white color to mucosa. Clinician must be familiar with it. • Red—mucosa changes from pink to red because of thinning of epithelial covering, increased vascularity, and dissolution of part of the collagen content of subepithelial tissue. • Yellow—it is due moderate distribution of adipose tissue contained in connective tissue just beneath the basement membrane e.g. Fordyce’s granule. • Brownish, bluish or black—it is induced by melanin, hemosiderin or heavy metal. • Contour—diagnostician must be familiar with normal tissue contour in and around the oral cavity to be able to detect any disorder that might alter the usual configuration of the area (Fig. 7-50).
Fig. 7-50: Swelling should be observed for contour, extension, shape.
• Shape—the shape of the swelling must be noted, whether it is ovoid, pear or kidney shaped, spherical or irregular. Sometimes, student by mistake utter the term circular to describe the shape of the swelling. A swelling cannot be circular as we do not know about the deeper dimension of the swelling. So it is wiser to say spherical to describe the swelling.
• Size—on inspection, we can miss the deeper dimension but we can mention vertical and horizontal extension approximately. • Surface—normal mucosa is smooth and glistening except for area of rugae and attached gingiva which demonstrate stippling and pebbling. Surface of pathological mass may be smooth, ulcerated, papillomatous, eroded, keratinized, necrotic, and bosselated. • Smooth surface—masses that arise beneath stratified squamous epithelium are smooth like fibroma, osteoma, chondroma, hemangioma, intradermal and compound nevus, minor salivary gland tumor, cyst, retention phenomenon, lipoma, schwannoma, neuroblastoma, space abscess and bullous pemphigoid. • Ulcerated surface—malignant counterparts of above lesions are smooth in early phase but after repeated trauma, they become ulcerated and necrotic. • Cauliflower surface—it is seen in sq. cell carcinoma, irregular numerous branches on the surface of a papilloma. • Corrugated or papillomatous surface—masses that originate in the stratified squamous epithelium have ‘corrugated’ or ‘papillomatous’ surface like papilloma, verruca vulgaris, seborrheic keratosis, keratoacanthoma, verrucous carcinoma and exophytic growth. • Edges—it may be clearly defined or indistinct, sessile or pedunculated. • Skin over swelling • Red or edematous skin—it will be red or edematous when the swelling is an inflammatory one. • Tense and glossy skin—the skin becomes tense, glossy with venous prominence when the swelling is a sarcoma with rapid growth. • Black punctum on skin—presence of black punctum over a cutaneous swelling indicates sebaceous cyst. • Scar—presence of scar indicates previous operation, injury or previous suppuration. • Peau d orange skin—sometimes, the skin over a growth looks like the peel of an orange (peau d’orange), which is due to edematous swelling from blockage of small lymphatics draining the skin. • Number—number of swelling should be noted. Multiple swelling (neuro-fibromatosis), solitary swelling (lipoma, dermoid cyst, etc). • Pulsation—the swellings arising from the arteries are pulsatile like aneurysms and vascular growths such as carotid body tumor. The swellings which lie just superficial to the artery in close relation with it will pulsate. It is called as ‘transmitted pulsation’. The pulsations which originate in the arterial wall will give rise to ‘expansible pulsation’. • Movement with respiration—this is observed if you are examining the swelling in neck and abdominal area. Swellings arising from the upper abdominal viscera move with respiration.
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• Impulse on coughing—the swellings which are in continuity with abdominal cavity, pleural cavity, spinal canal or cranial cavity, will give rise to impulse on coughing. • Movement on deglutition—few swellings which are fixed to the larynx or trachea move during deglutition like thyroid swelling, thyroglossal cyst, subhyoid bursitis, pre- or paratracheal lymph node enlargement etc. • Movement with protrusion of tongue—there are some swellings which move with the protrusion of tongue like thyroglossal cyst. • Pressure effect—an axillary swelling with edema of the upper limb means the swelling is probably arising from the lymph nodes. Wasting of distal limb indicates the swelling to be a traumatic one. Sometimes a swelling may be seen in the neck with venous engorgement.
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Palpation • Temperature—temperature of the swelling is best felt by the dorsal aspect of the hand. First, note systemic temperature. Place finger of the hand on skin in the area of concern and finger of other hand on skin on contralateral part of body. It is increased in inflammation as there is increased metabolic rate and increased vascularity of area. It is increased in superficial aneurysm, arteriovenous shunt and large recent hematoma. • Tenderness—inflammatory swellings are mostly tender whereas neoplastic swellings are non-tender. When the patient complains of pain due to the pressure exerted by the clinician, the swelling is said to be tender. • Size, shape and extent—deeper dimensions of the swelling remain unknown during inspection. The vertical and horizontal dimensions are better clarified by palpation. Tissue surrounding and underlying bases should be carefully palpated to determine the maximum extension of lesion into the surrounding tissue. Whether the mass is poorly defined or moderately defined or well define should be ascertained (Fig. 7-51). • Surface—with the palmar surface of the fingers the clinician should palpate the surface of the swelling. It can be smooth (cyst), lobular with smooth bumps (lipoma), nodular (matted lymph nodes) and irregular and rough (carcinoma). • Edges and border—Margins are palpated with the help of tip of the finger. Border of firm process in loose connective tissue is readily determined than soft process in loose connective tissue. If the surrounding normal tissue is of same consistency as the pathological tissue, the border cannot be determined. • Benign swellings—it has smooth margins whereas malignant growth has irregular margins.
Fig. 7-51: Swelling should be palpated for the consistency, margin and extension of swelling.
• Acute inflammatory swelling—acute inflammatory swellings have ill-defined or indistinct margins. • Malignancies—malignancies have ill-defined borders that are extremely difficult to palpate as malignant tumors infiltrate adjacent tissue by extending many processes of the tumor into surrounding tissue. • Tumor with extension—tumor with its extension elicits inflammatory reaction in adjacent tissue which results in sequelae of fibrosis which in turn reveal irregular and diffuse areas that are inflamed and result in more tenacious binding of tumor to the adjacent tissue by an ill-defined border, fibrous attachment whose limit is impossible to perceive by manipulation. • Consistency—the consistency or degree of firmness of the lesion in contrast to that of its surrounding tissue will also affect the ease with which the lesion itself or its border may be identified (Tables 7.9 and 7.10). Following terms are used to describe consistency: • Soft—easily compressible tissue such as lipoma or mucocele and cyst. • Cheesy—indicates a somewhat finer tissue that has granular sensation but no rebound. • Rubbery—tissue that is firm but can be compressed slightly and rebound to normal contour as soon as pressure is withdrawn. • Firm—tissue such as fiber tissue that cannot be readily compressed. • Bony hard • Modifying factors • Thick layer of overlying tissue especially muscle or fibrous tissue.
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Textbook of Oral Medicine Table 7-9: Consistency of normal tissue or organ
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Soft • Adipose tissue • Fascia • Veins • Loose connective tissue • Glandular connective tissue • Minor salivary gland • Sublingual salivary gland Firm • Fibrous tissue • Tensed muscle • Large muscle • Cartilage
Cheesy • Brain tissue Rubbery • Skin • Relaxed muscle • Glandular tissue with capsule • Arteries and arteriole • Liver Bony hard • Bone • Enamel • Dentin • Cementum • Cartilage
• Technique—this test can be carried out by one finger of each hand (Fig. 7-52). Sudden pressure is applied on one pole of swelling. This will increase pressure within the cavity of the swelling and will be transmitted equally at right angle to every part of its wall. If another finger is placed on the other side of the swelling the finger will raise passively due to increased pressure within the swelling. This means that swelling is fluctuating. This test is always performed in two planes at right angle to each other. The two fingers should be kept as far as apart as the size of swelling will allow.
Table 7-10: Consistency of pathological mass Soft • Cyst • Warthin’s tumor • Papillary cystic adenoma • Vascular tumor • Varicosity’s • Cystic hygroma • Fatty tumor • Myxoma • Plexiform neuroblastoma • Inflammatory hyperplasia • Emphysema • Retention phenomenon (mucocele and ranula) Cheesy • Cyst (sebaceous, dermoid and epidermoid) • Tubercular node Rubbery • Cyst under tension • Lymphoma • Myxoma • Myoblastoma • Aneurysm • Pyogenic space infection • Edentulous tissue • Early hematoma Firm • Infection • Benign tumor of soft tissue • Malignancy of soft tissue • Osteosarcoma • Chondrosarcoma • Metastatic carcinoma • Inflammation and infection of parotid and submaxillary salivary gland • Inflammation and infection of lymph node Bony hard • Osteoma • Exostosis • Osteogenic sarcoma • Chondroma • Chondrosarcoma
• Soft glandular tissue surrounded by dense connective tissue capsule will be perceived more firm. • Depth in tissue will alter consistency. • Fluctuation—swelling fluctuates when it contains liquid or gas.
Fig. 7-52: Fluctuation test is carried out in patient by using two fingers.
• Paget’s test—in case of very small swelling which can not accommodate two fingers this test can be performed by simply pressing the swelling at the centre (Fig. 7-53). The swelling containing fluid will be softer at the center than its periphery while solid swelling will be firmer at the centre than its periphery. It is called as ‘Paget’s test’. • Fluid thrill—in case of swellings containing fluid, a percussion wave is seen to be conducted to its other poles when one pole of it is tapped as done in percussion. In case of big swelling, it can be demonstrated by tapping the swelling on one side with two finger while percussion wave is felt on the other side of the swelling with palmer aspect of the hand (Fig. 7-54). In case of small swelling three fingers are placed on the swelling and middle finger is tapped with a finger of the other hand, the percussion wave is felt by other two fingers on each side.
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Case History
Fig. 7-53: Paget’s test is performed in case of small swelling.
Fig. 7-54: Fluid thrill is felt by tapping the swelling.
• Translucency—the swelling can transmit light through it. For this it must contain clear fluid like water, serum, lymph or plasma. For this test, darkness is essential. In day time this can be done by using roll of paper which is held on one side of the swelling while a torch light is held on the other side of the swelling. The swelling will transmit the light if it is translucent. The torch light should not be kept on the surface of the swelling, but on one side of the swelling, while roll of paper on the other side so that the whole swelling intervenes between the light and the roll of paper. • Impulse on coughing—on palpation, this test corroborates the finding detected in inspection. The swelling is grasped and the patient is asked to cough. An impulse is felt by the grasping hand. Due to coughing, pressure is increased within the abdominal, pleural, spinal and cranial cavities. This increase in pressure is transmitted to the swelling, where it is felt.
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• Reducibility—this means that the swelling can be reduced and ultimately disappear as soon as it is pressed upon. This is a feature of hernia, varicocele, meningocele etc. • Compressibility—the swelling can be compressed but would not disappear completely like arterial, capillary or venous hemangioma. The most differentiating features between a compressible swelling and a reducible swelling is that in case of latter the swelling completely disappear as the content are displaced within the said cavities and may not come back until and unless an opposite force such as coughing or gravity is applied, but in the case of the former the content are not actually displaced so the swelling immediately reappears as soon as the pressure is taken off. • Pulsatility—a swelling may be pulsatile if it arises from the wall of an artery or lies close to an artery or if the swelling is a vascular one. Two fingers one from each hand are placed on the swelling as far apart as possible. If the two fingers are raised with each throb of the artery, the swelling is a ‘pulsatile’ one. When the two fingers are not only raised but also separated with each beat of pulse the pulsation is said to be ‘expansile’. When the two fingers are only raised but not separated the pulsation is said to be ‘transmitted’. • Fixity to the overlying skin—for this the skin is made to move over the swelling. If it is fixed to the skin, the skin will not move. The skin over the swelling is pinched up in different parts, when the skin is not fixed it can be easily pinched up which may not be possible when the swelling is fixed to the skin. Next attempt is made to move the mass independent of underlying tissue. • Benign lesion—if it is freely movable then it is benign, possibly encapsulated mass originating in loose subcutaneous tissue or submucosal tissue. • Sebaceous cyst—sebaceous cyst is freely movable over the underlying tissue but is bound to skin. • Fixed swelling—swelling may be fixed in fibrosis after previous inflammation episode, infiltrating malignant tumor that originated in skin or mucous membrane and has invaded deep structure, malignancy that originates in deep structure and invade the subcutaneous or submucosal tissue and skin or mucosa and malignancy that originates in loose connective tissue and invade both superficial and deep layer. • Mass in neck—if fluent mass in neck moves up and down as patient swallows then it must be partly attached to hyoid bone, larynx, trachea, thyroid or parathyroid gland. If it is elevated on protrusive movements of the tongue then it is thyroglossal duct cyst. • Relation to the surrounding structures—The tumor arising from the subcutaneous tissue is free from the overlying
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skin and from the underlying contracted muscles. In case of tumor arising from the muscle the swelling can be moved when the muscle is relaxed. Swelling about a bone is absolutely fixed even when the overlying muscle is absolutely relaxed, and cannot be moved apart from the bone.
Aspiration The preoperative aspiration of a fluid-filled mass is worthwhile precautionary procedure, as it should eliminate an unpleasant surprise of opening of an innocuous lesion that may be proved to be a dangerous vascular tumor. Usually it should be carried out before surgery to avoid bacterial infection. • Straw colored fluid—it contain cholesterol crystals in wall that are frequently seen as small shiny particles when syringe is transilluminated. It is seen in some odontogenic and fissural cyst. • Thick yellowish white and granular fluid—it is seen in epidermoid and keratocyst in which lamina is filled with keratin. • Yellowish cheesy material—dermoid cyst contains most of dermal appendage and the aspirate is thickest and fills of yellowish cheesy substance. • Sebum—sebaceous cyst yields sebum which is thick homogenous and yellowish cheesy substance. • Amber colored fluid—dark amber colored fluid of thyroglossal duct cyst. • Lymph fluid—it is colorless with high lipid content, appears cloudy and frothy. It is seen in hygroma and lymphoma. • Blue blood—it is seen in early hematoma, hemangioma and varicosities. • Brighter red blood—aneurysm and arteriovenous fistula. • Pus—aspiration of painful warm fluctuant swelling yield pus. • Sulfur granules—in actinomycosis, it yield pus with few yellow granule in it. These are sulfur granule. • Clear viscous fluid—sticky clear viscous fluid yielded in retention phenomenon.
Other Examination Other examinations of swelling which are not frequently done in dental office: • Percussion—its role is to find gaseous content within the swelling like resonant note over the hernia or to elicit slight tenderness like Brodie’s abscess. Hydatid thrills in case of hydatid cyst. • Auscultation—all pulsatile swellings are auscultated to exclude presence of any bruit or murmur. • Measurement—it is done to find out increase in swelling size at definite intervals but is also to find out if there is any wasting distal to the swelling.
• Movement of nearby joint—movement of nearby joint to exclude any impairment. • Examination of pressure effect—nerve may be involved by the pressure of swelling. This will cause wasting, paresis or paralysis of the muscle supplied by the nerve with or without sensory disturbance. The arterial pulse distal to swelling is felt. Sometimes swelling may press on the main artery of the limb and cause weak pulse distally. Swelling may even exert pressure on the adjacent bone by eroding it. It is sometimes seen in aneurysm and dermoid cyst on the skull.
Examination of Ulcer An ulcer is a break in continuity of the skin and epithelium.
Inspection • Size and shape—the size and shape of the ulcer should be noted. This will yield in diagnosis of the ulcer. The size of an ulcer is important in deciding the time which will be required for healing. A bigger ulcer will definitely take longer time to heal than smaller ulcer. To record exactly the size and shape of an ulcer sterile gauze may be pressed on to the ulcer to get measurement. • Tuberculosis ulcers—they are generally oval in shape but their coalescence may give an irregular crescentic border. • Syphilitic ulcers—syphilitic ulcers are similarly circular or semilunar to start with but may unite to form serpiginous ulcer. • Carcinomatous ulcers—carcinomatous ulcers are irregular in size and shape. • Number—tuberculosis, gummatous, varicose and soft chancre may be more than one in number. • Position—it is very important and often gives clue to the diagnosis. Rodent ulcers are usually confined to the upper part of the face above a line joining the angle of the mouth to the lobule of the ear, occurring frequently near the inner canthus of the eye. Malignant ulcers are more commonly seen on the lips, tongue, breast and penis. • Edges—edges of the ulcer should be properly examined (Fig. 7-55). • Spreading ulcer—in a spreading ulcer the edges are inflamed and edematous whereas in a healing ulcer the edges, if traced from the red granulation tissue in the center towards periphery, will show blue zone (due to thin growing epithelium) and a white zone (due to fibrosis of the scar). • Undermined edge—it is mostly seen in tuberculosis. The disease causing the ulcer spreads in and destroys the subcutaneous tissue faster than it destroys the skin. The overhanging skin is thin friable, reddish blue and unhealthy.
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Fig. 7-55: Different types of edges of the ulcer—A diagrammatic representation.
• Punched out edges—it is mostly seen in a gummatous ulcer or in a deep trophic ulcer. The edges drop down at right angle to the skin surface as if it has been cut out a punch. It is seen in diseases in which activity is limited to the ulcer itself and does not tend to spread to the surrounding tissues. • Sloping edge—it is seen mostly in healing traumatic or venous ulcers. Every healing ulcer has a sloping edge, which is reddish purple in color and consists of new healthy epithelium. • Raised and pearly white beaded edge—it is a feature of rodent ulcer which develops in invasive cellular diseases and becomes necrotic at the center. • Rolled (everted) edge—it is characteristic feature of squamous cell carcinoma or an ulcerated adenocarcinoma. This ulcer is caused by fast growing cellular disease, the growing portion at the edge of the ulcer heaps up and spills over the normal skin to produce an everted edge (Fig. 7-56).
• Floor—this is the exposed surface of the ulcer. One must be very careful to note what is there at the floor of an ulcer. When floor is covered with red granulation tissue, the ulcer seems to be healthy and healing. Pale and smooth granulation tissue indicates a healing ulcer. Wash leather slough on the floor of ulcer is pathognomonic of gummatous ulcer. A black mass at the floor suggests malignant melanoma. • Discharge—the character of the discharge should be noted, its amount and smell. A healing ulcer will show scanty serous discharge, but the spreading and inflamed ulcer will show purulent discharge. Serosanguineous discharge is often seen in a tuberculosis ulcer or a malignant ulcer. • Surrounding area—if the surrounding area of an ulcer is glossy, red and edematous, the ulcer is acutely inflamed. Very often the surrounding skin of varicose ulcer is eczematous and pigmented. A scar or wrinkling in the surrounding skin of an ulcer may well indicate an old case of tuberculosis.
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•
2 Fig. 7-56: Edges, margins and floor of ulcer should be properly examined. In this case, it has got rolled and everted edges of malignancy.
•
Palpation • Tenderness—an acutely inflamed ulcer is always exquisitely tender. Chronic ulcers are slightly tender. Neoplastic ulcers are never tender. • Edges—in palpation different types of the edge of the ulcer are corroborated with the finding of the inspection. Marked induration of the edge is characteristic feature of a carcinoma. • Base—the student must understand the difference between the floor (exposed surface within the ulcer) and base (on which ulcer rests and it is better felt than seen). If an attempt is made to pick up the ulcer between thumb and the index finger, the base will be felt. Marked induration of the base is an important feature of squamous cell carcinoma and hunterian chancre. • Depth—you should make assessment regarding depth of the ulcer. It can be recorded in the examination sheet in millimeters. • Bleeding—whether the ulcer bleeds on touch should be checked as it is a common feature of malignant ulcer. • Relation with deeper structure—the ulcer is made to move over the deeper structures to know whether it is fixed to any of these structures. A gummatous ulcer over a subcutaneous tissue or bone is often fixed to it. Malignant ulcer will be fixed to the deeper structure by infiltration.
• •
sometimes ulcerative colitis may produce multiple fistulae. Position—diagnosis of sinuses and fistulae can be made only by looking at the position of these sinuses and fistulae. • Preauricular sinus (due to failure of fusion of the ear tubercles) is situated at the roots of the helix or on the tragus of the pinna, direction of the sinus being upwards and backwards. • Branchial fistula (due to failure of the fusion of second branchial arch with the fifth) brachial arch is almost always situated at the lower third of the neck in front of sternocleidomastoid muscle. • Osteomyelitis—a single sinus over an irregular lower jaw is mostly due to osteomyelitis. Opening of sinus—sprouting granulation tissue at the opening of the sinus suggests presence of foreign body at the depth. The opening of tuberculous sinus is often wide and the margins are thin blue and undermined. Discharge—in osteomyelitis the discharge is often pus while in actinomycosis discharge is of sulfur granules. Surrounding skin—there may be scar in the surrounding tissue which may indicate chronic osteomyelitis or previously healed tuberculous sinus. There may be surrounding dermatitis and pigmentation, which are characteristic features of Crohn’s disease.
Palpation • Tenderness—is the sinus tender? The sinus from inflammatory source will be tender. • Wall of sinus—it is palpated to note any thickening there. Chronic sinus will have thick wall due to presence of fibrosis surrounding the wall of the sinus.
Examination of Sinus or a Fistula A sinus is a blind track leading from the surface down to the tissue. Fistula is communicating tract between two epithelial surfaces. Both sinus and fistula are lined by granulation tissue which later may become epithelialized.
Inspection • Number—the majority of fistulae which occur in the body are single. Actinomycosis has multiple sinuses and
Fig. 7-57: Gutta percha is used to locate the depth of sinus.
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Case History • Mobility—is the sinus mobile over the deep structure? Sinuses resulting from osteomyelitis are fixed to the bone, which becomes irregular, thickened and tender. • Lump—presence of lump in the neighborhood of a sinus often indicates tuberculosis lymphadenitis. • Probe examination—this will inform the clinician about the direction and the depth of the sinus. It will also detect presence of any foreign body which will be movable at the depth of the wound and whether fistula is communicating with a hollow viscous or not and whether fresh discharge comes out on withdrawal of the probe or not. • Depth of sinus—it is done with the help of radiograph. A gutta percha point is inserted in the sinus and radiograph is taken (Fig. 7-57). As gutta percha points are radiopaque it will locate the exact direction and depth of the sinus.
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• Precaution—such a procedure tests for olfactory nerve function only when the nasal airway is patent to the olfactory receptors and when the substance being tested does not produce a response from the patient solely on the basis of chemical irritation of non-specific somatic sensory receptors in the nasal mucosa.
Optic Nerve • Ophthalmoscope—it is tested by investigation of visual acuity and the visual fields and those trained in the use of the ophthalmoscope can use this instrument to examine the ocular fundus directly for lesions. • Wall chart—visual activity can be tested with the familiar wall chart but can also be evaluated by asking the patient to read print of various sizes in a book or newspaper held at various distance from the patient eye.
Trigeminal Nerve
Examination of Cranial Nerves In evaluating patients with oral sensory or motor complaint, it is important to know whether there is any objective evidence of abnormality of cranial nerve function that might relate to the patients oral symptoms. The routine cranial nerve evaluation is systematically carried out according to the sequence of cranial nerve from I to XII.
Olfactory Nerve • Procedure—it is traditionally tested by closing one of the patient nostrils with a finger and asking him if he can smell a strongly scented volatile substance such as coffee or lemon extract. The test is then repeated with other nostril. The patient should sniff strongly to draw the volatile molecules well into the nose (Fig. 7-58).
Fig. 7-58: Smelling of volatile substance from nostril will test for olfactory nerve.
• Significance—it is tested for both motor and sensory functions. A small motor branch of this nerve supplies the muscle of mastication, and strength of these muscles is used as measure of the intactness of their motor supply. • Palpation while patient clenches—the force of contraction and muscle bulk of the masseter and temporal muscles are noted by external palpation of these muscles bilaterally while the patient clenches (Fig. 7-59). Lateral movement of the jaw against the examiner’s finger is one test of pterygoid functions. • Displacement against resistance—another useful test of motor power of the masticator muscles is to check their ability to carry out voluntary displacement of the jaw against the imposed resistance of the examiner’s hand. Place your thumb on molar table with fingers externally about the body and ramus of mandible. The patient
Fig. 7-59: Test for motor function of trigeminal nerve, patient clenches and doctor palpate masticator muscle.
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moves the jaw forward, sideways and upward his head steadied by your other hand. • Percussion hammer test—abnormalities of the jaw jerk may indicate muscular weakness or an abnormality of the proprioceptive reflex arc controlling jaw movement. Press your index finger downward and posteriorly above the mental eminence and lightly strike the finger with a percussion hammer or with one or two finger of the other hand. • Graded von Frey hairs—for testing of trigeminal sensory function ‘graded von Frey hairs’, a series of fine hairs or nylon fibers calibrated according to the force required to bend the filament when it is placed against skin, mucosa or tooth, esthesiometers often designed with a pistol grip to facilitate placement of the points of the instrument on the oral mucosa and calibrated thermal device for application of hot and cold can be used. Fig. 7-60: Patient is asked to wrinkle his forehead for motor function test of facial nerve.
Facial Nerve • Significance—the facial nerve is tested for abnormalities of motor function involving the ‘mimetic’ muscle of facial expression and also gustatory disorders. A gustosalivary reflex involves facial nerve gustatory stimuli and increase salivary function. • Lemon juice application—Affected chorda tympani may be associated with failure of salivary flow to increase following application of lemon juice or citric acid to the affected side of the mouth. • Motor function test—motor function of facial nerve is tested by observing facial muscle function in response to request to wrinkle (Fig. 7-60) the forehead, frown, close the eyelid tightly, open the mouth, retract the mouth, blow out the cheek, pucker the lips, screw up the nose, whistle and speak.
Glossopharyngeal Nerve It provides taste fibers to the posterior aspect of the tongue, somatic sensory fibers to the same area of the tongue as well as pharynx and soft palate and motor fibers to the stylopharyngeal muscle that plays only minor role in palatal function, preventing any accurate testing of 9th cranial nerve functions.
Vagus Nerve • Significance—the vagus nerve is the chief motor nerve of the pharynx and larynx and also provides sensory fibers to the pharyngeal and faucial mucous membrane • Pharyngeal movement observation—routine testing is carried out by observation of pharyngeal movements’ i.e. symmetrical elevation of the soft palate and shortening of the uvula when the patient says ‘ah’ and
pharyngeal and gag reflex, i.e. contraction of the palate and faucial muscles in response to touching the mucous membrane of the posterior pharynx.
Hypoglossal Nerve It provides motor supply to the tongue; hypoglossal paralysis causes deviation of the tongue when patient extrudes it. Atrophy of tongue musculature may be noted on oral examination and its muscular tonus by the force with which the patient can push the tongue against either cheek or by evaluation of the tongue jerk.
Establishing the Diagnosis Provisional Diagnosis All the records and clinical findings clubbed together, clinician should be able to frame a provisional diagnosis. Clinician should keep in mind the differential diagnosis of the lesion. In provisional diagnosis you should list all those items that either indicate an abnormality or suggest the possibility of significant health problems requiring further evaluation.
Investigations Laboratory investigations help to come to the final diagnosis, e.g. in case of caries (proximal) the provisional diagnosis will be mesial or distal caries. Radiograph will confirm the diagnosis and help us to differentiate it into incipient, moderate, advanced and severe. To confirm the
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Case History
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Table 7-11: Case history format Personal information Name Age / sex Case No Occupation Religion Address Date Chief complaint : History of present illness History of past illness Past medical history Past dental history Personal history : • Marital status • Educational status • Oral hygiene habits • Other habits Family history : General examination : • Patients attitude • Built • Gait • Vital signs : • Temperature • Pulse • Respiratory rate • Blood pressure • Pallor • Icterus
• Clubbing • Cyanosis Extra oral examination • Facial symmetry • Lip seal • TMJ movements • Lymph node • Ear • Nose Intraoral examination Hard tissue examination • Teeth present • Dental arch irregularities • Caries • Fractured tooth • Tenderness • Wasting disease • Discolored tooth • Calculus and stains • Occlusal facets • Mobility • Furcation involvement Soft tissue examination Tongue • Size • Dorsum • Ventral surface • Margin • Frenal attachment • Distribution of papilla
diagnosis, one should proceed with available methods of investigation. The common methods are radiological, hematological investigations, urine analysis, biochemical investigations, histopathological investigations, microbiological investigations and special investigations like sialography, MRI etc.
Final Diagnosis The final diagnosis can usually be reached following chronologic organization and critical evaluation of the information obtained from the patient history, physical examination and the result of radiological and laboratory examination. The final diagnosis usually identifies the diagnosis for the patient’s primary complaint first, with subsidiary diagnosis of concurrent problems. Previously diagnosed conditions that remain as actual or potential problems are also included, with comment by ‘history’ ‘previously diagnosed’. In case of no definite diagnosis is made diagnosis should be written as idiopathic, unexplained, functional and symptomatic. The patient should be informed of the diagnosis, results of tests and examination.
Cheek • Color • Any ulcer Lips • Color • Vermillion border • Commissures • Ulcer and lesion Hard and soft palate • Discoloration • Papillary hyperplasia • Swelling • Ulcer • Any recent burns • Any lesion Floor of mouth Gingiva • Color • Contour • Consistency • Surface texture • Position • Size • Bleeding on probing • Exudate/suppuration • Frenal attachment Provisional diagnosis Investigation Final diagnosis Treatment planning : • Medical / emergency phase • Planned treatment
Making a Treatment Plan and Medical Risk Assessment The formulation of an appropriate treatment plan will depend on both knowledgeable, experienced, competent clinician and nature and extent of treatment facilities available. Details of medical or surgical treatment, which the patient has received, should be known. Evaluation of any special risks posed by the patient’s compromised medical status in the circumstance of the planned anesthetic diagnostic or surgical procedure. Medical risk assessment is also needed to identify the need of medical consultation and to recognize significant deviation from normal health status that may affect dental management.
American Society of Anesthesiologists Physical Status Classification P1—a normal healthy patient P2—a patient with mild disease P3—a patient with severe systemic disease that limits activity but no incapacitating P4—a patient with an incapacitating systemic disease that is a constant threat to life P5—a Mir bund patient who is not expected to survive without operation P6—a declared brain dead patient whose organs are being removed for donor purpose
Adapted from American Society of Anesthesiologists
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Textbook of Oral Medicine Table 7-12: Medical questionnaire to be asked to the patient in medical examination
System
Question to be asked
General
• • • •
Cardiovascular system
• • • • • • • •
Respiratory system
• Dyspnea on exertion • Wheezing, coughing, excessive sputum production • Coughing up blood.
Blood disorders
• • • • •
Prolonged bleeding during cut, tooth extraction or other injury Do you bruise easily Required a blood transfusion Have frequent infections Have ever been told that you were anemic.
Nervous system
• • • • •
Head-injury or concussion Seizures/black-outs/fits Frequent headaches Experienced any pain, numbness, or tingling in your face , arms or legs Had any paralysis.
Metabolic-endocrine system
• • • •
Any recent loss or gain of weight Hyperthyroidism or hypothyroidism Do your hands sweat excessively Are you easily fatigued?
Gastrointestinal, hepatic, biliary tracts
• • • • • • • •
Difficulty in swallowing Heart-burn or belching Episodes of nausea and vomiting Vomited blood Frequent stomach or abdominal pain Recently had a change in bowel habits Frequent episodes of diarrhea Ever noticed bright-red, or black colored stools.
Genitourinary system
• • • •
Urinate frequently Difficulty or pain during urination Ever passed brown or red urine (for females) had abnormal or irregular menstrual period
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Are you now or recently been under a physicians care? if so, what is the condition being treated? Have you been hospitalized during past 2 years? Do you take prescription or non-prescription medicines on a permanent or non-permanent basis? Do you have any allergies, if so to what? • Aspirin • Sulphur containing drugs • Penicillin or any other antibiotics • Codeine or any narcotic • Dental anesthetic or • Any specific drug • Does dental treatment make you nervous? Chest discomfort on exertion, when eating or at rest Tightness of the chest Palpitation Fainting Ankle edema Shortness of breath High or low blood pressure Heart murmur.
• Drugs given to the patient, dose and duration of treatment—the drug can be prescribed in following formats. • OD—Omni Die • B.I.D.—Bis in Die • B.D.S.—Bis in die summendus • T.I.D.—Ter in Die • T.D.S.—Ter die sumendum • Q.I.D.—Quater in die
• Q.D.S—Quater die sumendum • S.O.S—as and when required (si. opus sit) • H.S—Hora somni • Rx—Take though • Prescription writing • Superscription—general background information regarding the dentist (name, address and telephone number), the patient (name, address, age) and the date the prescription is written.
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Case History • Inscription—specific information regarding the drug (generic or proprietary name or both) and the dosage. • Subscription—direction to the pharmacist for filling the inscription (number of capsules or tablets to be dispensed or the volume of liquid), the number of refills allowed and time constraints, directions to be listed on the container label. • Transcription—instruction to the patient, to be listed on the container label. • Signature and educational degree of prescribing doctor- a signature is required by law only for certain controlled substance (schedule II drug). • Guidelines for prescription writing • Obtain an accurate and complete patient history, including whether the patient is taking any drugs prescribed by other doctors or any over the counter drugs; both can affect the dosage or effects of the drug being prescribed. • Use separate prescription blank for each drug ordered. Avoid using prescription blank with trade names printed on them. • Never presign prescription blank and always store blank prescription pads in a secure place. • Write out number than using digits so that prescription cannot be altered. • Prescribe sufficient drug and at adequate dosing intervals to maintain therapeutic blood level. • Keep the record of all drugs prescribed for each patient. • Instruction listed on the drug container for the patient must be specific. Full disclosure is verbally given regarding the prescription before the patient leave
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the office. Stress the need to consume all of the prescribed medication, as in taking the antibiotics even if the patient is feeing better before the prescribed amount is taken. • Instruction regarding anticipated side effect as well as the use of alcohol with taking the prescribed drugs should be explained to the patient verbally. Advise the patient to call the office when side effects develop. • Cost factor should be considered when prescribing medication. • In surgical treatment • Types of anesthesia; local or general anesthesia • Anesthetics used • Name of the anesthetist • Name of the surgeon • Closure • Drainage given or not • Follow up—these resume when the patient is discharged from the hospital and extends till he starts his normal active life.
Suggested Reading 1. Glick M. Did you take your medication? The dentist role in helping patient adhere to their drug regimen. JADA 2006;137:1636-8. 2. Glick M. Screening for traditional risk factors for cardiovascular disease. JADA 2002;133:291-300. 3. Greenberg, Glick, Ship. Burket’s Oral Medicine: BC Decker Inc: 2008. 4. Kay E, Nuttal N. Clinical decision making—an art or a science. Br Dental J 1995;190-3. 5. McCarthy FM, Malamad SF. Physical evaluation system to determine medical risk and indicated dental therapy modification. JADA 1979;99:181-4.
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Investigation in Dentistry
Introduction There are various important investigations which are required for the diagnosis and treatment plan of various disorders related to the oral cavity. Laboratory studies are an extension of physical examination in which tissue, blood, urine or other specimens are obtained from patients and subjected to histological, bio-examination, microbiological or immunological examination. Information obtained from these investigations help in identifying the nature of the disease.
Diagnostic Test for Cancer Detection The earliest is the diagnosis of the oral cancer, best is the prognosis of the cancer. In cancer, cellular and tissue alteration occurs. This fact is kept in mind for the entire diagnostics test for cancer detection.
• Molecular methods • Quantification of nuclear DNA content • Tumors markers • Microsatellite markers.
Clinical Method Toluidine Blue Staining The use of Toluidine blue (tolonium chloride) dye as a mouthwash or topical application is currently receiving much attention as an aid to the diagnosis of oral cancer and potentially malignant lesions. The method has good sensitivity with a very low false negative rate. The dorsum of the tongue always stains positively, due to the retention of dye in crevice between the papillae. It is effective in demonstrating dysplasia and early malignant lesion which is not clinically recognizable.
Mechanism Classification • Clinical method • Vital staining—toluidine blue method and Lugol’s iodine method • Vizilite • Acridine binding method • Photodiagnosis • 5-Aminolevulinic acid mediated fluorescence endoscopic imaging • 5-Aminolevulinic acid mediated digitized fluorescence endoscopic imaging • Autofluorescence spectroscopy • Fluorescence photography • Histopathological methods • Biopsy • Exfoliative cytology • Oral CDx system
• Binding with DNA—it is an acidophilic, metachromatic nuclear dye of thiazine group that selectively stains acidic tissue components particularly nucleic acid such as DNA and RNA. Dysplastic and anaplastic areas which contains more DNA than normal cells. • Intracellular canal—malignant epithelium contains intracellular canals that are wider than normal epithelium, which also facilitates the penetration of dye. • Effect on normal epithelium—most of the epithelial surfaces stain blue after the application of 1% toluidine blue solution but the stain is lost after application of 1% acetic acid solution to normal epithelial surface or benign erythematous lesions on oral mucosa. • Effect on benign ulceration—benign ulceration has well defined uptake of dye at the margins whereas, diffuse marginal pattern is characteristic of dysplasia or malignancy.
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Investigation in Dentistry 87 Availability
Lugol’s Iodine Test
It is readily available to use kit as 3 component system. First contain 1% toluidine blue 10 ml solution. Second and third kit contains 1% acetic acid as pre- and post-rinse solution.
It is retained in normal squamous epithelial cells but not in dysplastic or malignant cells of the squamous epithelium. The use of Toluidine blue application in combination with Lugol’s iodine solution may offer potential advantage. The Toluidine blue will stain the abnormal (reactive and dysplastic) epithelium whereas, Lugol’s iodine solution will bind to glycogen present in normal epithelium. In the oral tissues, Lugol’s iodine has less sensitivity in identifying oral premalignant and dysplastic diseases. But, is of greater specificity.
Contents • • • • •
Toluidine blue—1 gm Acetic acid—10 cc Absolute alcohol—4.19 cc Distilled water—86 cc pH adjusted to 4.5
Contents
Technique • Rinsing—initially you ask the patient to rinse the mouth twice with water (20 seconds each). After rinsing with water, ask patient to rinse with 1% acetic acid (20 seconds). • Drying of area—you should gently dry suspicious mucosal areas with gauze. You have to take care not to abrade the tissue while drying. • Application of toluidine blue solution—apply 1% toluidine blue solution to the lesion with a cotton swab. • Rinsing—ask patient to rinse again with acetic acid (approximately 150 ml for one minute). After rinsing with acetic acid, then ask patient to rinse with water. • Positive staining—if the mucosa is stained positive (Fig. 8-1), you have to repeat the procedure in one to two weeks. Biopsy of all sites is advised, which stain positive on two successive visits.
• Iodine—2 gm • Potassium iodide—4 gm • Distilled water—100 cc
Mechanisms • Reaction with glycogen—Lugol’s iodine solution produces a brown black stain by reaction of iodine with glycogen. Iodine is removed by fixation in alcohol and formaldehyde. • Effect on proliferating epithelium—glycogen content is inversely related to the degree of keratosis, suggesting a role of glycogen in keratinization. So when proliferating epithelium is present it is usually poorly stained or unstained. • Effect on inflammatory tissue—there is relationship between the degree of inflammation and glycogen content. So in this case, tissue will stain dark brown.
Vizilite Vizilite is non-toxic chemiluminescent light that is shined in the mouth. Tissue which are not normal, they glows differently, as compared to normal tissue. This will make them more visible. Vizilite will be more useful for the detection of biopsy proven squamous cell dysplasia which is not seen with naked eye.
Contents • Vizilite rinse—1% acetic acid solution • Vizilite capsule—chemiluminescent light stick • Vizilite retractor—sheath and handle
Mechanism
Fig. 8-1: Positive toludine blue staining showing uptake toludine blue by dysplastic mucosa (Courtesy Zila Pharmaceutical).
• Physics—normal tissue absorb Vizilite and as a reason they appear dark. This is not the case with dysplastic cells. In case of dysplastic cells nucleus become larger, resulting in reflection of light and gives white appearance.
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Technique
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• Application of Vizilite rinse—acetic acid solution should be applied first. This will result in change in refractile properties of lesion like leukoplakia. The change will occur in the cells as acetic acid is cytoplasmic dehydration agent and there is increased nuclear-cytoplasmic ratio in atypical keratinized mucosa. • Visualizing the mucosa with Vizilite—then chemiluminescent capsule is projected on the mucosa. The abnormal mucosa like dysplastic mucosa will show more reflection of light and will appear whiter as compared to normal mucosa (Fig. 8-2).
5-aminolevulinic Acid (ALA) Mediated Fluorescence Endoscopic Imaging • Source—aminolevulinic acid is precursor in biosynthesis of heme and it induces the production of endogenous photosensitizer protoporphyrin. • Mechanism—after oral administration of ALA, synthesis of protoporphyrin occurs in dysplastic cells. This will result in fluorescence and can be easily detected.
5-aminolevulinic Acid Mediated Digitized Fluorescence Endoscopic Imaging It is same method as above with digitalization facility. It has capability of high quality images and it can measure the fluorescence effect of diseased oral tissue.
Autofluorescence Spectroscopy • Use—autofluorescence spectroscopy is non-invasive method. It is used for detection for alteration in the structural and chemical composition of cells. It is also useful for optimal location of biopsy. • Mechanism—autofluorescence occurs due to endogenous fluorophores. It consists of fluorophores from tissue matrix molecule, intercellular molecules like collagen, elastin and nicotinamide adenine dinucleotide phosphate.
Fluorescence Photography
Fig. 8-2: In Vizilite testing, dysplastic mucosa will show appearing whiter as compared to adjacent mucosa (Courtesy Zila pharmaceutical).
The basic principle behind this is that, by repeated fluorescence photography, it will show reduction and diminution of positive fluorescence associated with cancer regression and vice versa. This is useful as an adjunct aid in the diagnosis of squamous cell carcinoma.
Acridine Binding Method In this method, the uptake of acriflavine by desquamated buccal cells is measured. Since the DNA content of the dysplastic cells are more, they will stain more intensely than normal cells.
Photodiagnosis This optic method is used for the early diagnosis. It is based on fluorescence measurement. Light induced fluorescence (LIF) spectroscopy is useful for the early cancer detection in oral cavity. The principle is that there is endogenous tissue fluorescence of photosensitizer which is accumulated in tumor tissue. Photosensitizer which can be used are m-THPC and delta aminolevulinic acid.
Histopathological Examination Biopsy It is a process of surgically removing tissue from a patient for histopathological examination. It is the removal of sample tissue from living individuals. It provides valuable information in determining the prognosis and type of treatment required.
Indications • Undiagnosed clinical condition—after careful clinical examination, if any alteration from normal is seen and it is not possible to identify the condition clinically, a histopathological investigation is necessary.
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Investigation in Dentistry 89 • Nature of lesion—to evaluate the exact histological nature of any soft tissue or intra-osseous lesion. • Screening test—to screen abnormal tissues removed from oral cavity including granuloma and cyst. • Detection of malignancy—to confirm the existence and nature of directly apparent malignancy so that the treatment can be undertaken immediately. • Diagnostic test—diagnostic tests for evaluation of nonneoplastic lesions such as mucosal nodules, papilloma, erosive lichen planus, erythema multiforme, lupus erythematosus, pemphigus, pemphigoid and desquamative gingivitis.
Avoidance of Delay for Biopsy Biopsy should not be delayed when following feature are present. • Rapid growth—rapid increase in size of the lesion that cannot be explained by inflammation, edema and opening of new vascular channels. • Absent local factors—absence of any recognized irritant, particularly when the lesion is chronically ulcerated or bleeds spontaneously. • Fixed lymph node enlargement—presence of firm regional lymph nodes, especially when they are seen to be fixed to surrounding tissues. • Root resorption with loosening—destruction of tooth roots and loosening of teeth with evidence of rapid expansion of the jaw. • History of malignancy—history of cancer elsewhere in the body, previous history of oral cancer and radiation therapy.
How to Submit Biopsy Specimen • Information written on specimen—the submission of specimen should be accompanied by the date of biopsy, name, age and sex of the patient, the area from where biopsy specimen is taken and brief description of clinical appearance of lesion and associated symptoms, along with tentative clinical diagnosis. The biopsy specimen should not only include the lesion but also the adjacent clinically normal tissue. • Sectioning of biopsy specimen—as soon as possible after the surgical procedure, carefully section the biopsy specimen with a fresh scalpel or razor blades into pieces. Pieces should not be larger than 0.5 cm in diameter, identifying each fragment in relation to the overall specimen and lesion. • Avoid surface with iodine—iodine containing antiseptics should be avoided with surface since they have a tendency to stain certain tissue cells permanently. • Fixing solution—the portion of the biopsy specimen to be used for routine histological study should be placed at once in a suitable fixing solution. Fixative which is used is Karnovsky’s fixative (4% paraformaldehyde) and 5% glutaraldehyde in 0.1 M solution for 2 to 4 hours and delivers promptly to the laboratory. • Stains—many different types of stains are used in diagnostic pathology (Fig. 8-3).
Uses • Diagnosis—biopsy is useful for the diagnosis of pathologic lesions. It also helps in determining neoplastic and non-neoplastic lesions of oral cavity. • Grading of tumors—it aid in determining the grading of tumor. • Metastatic lesion—it is also useful for the diagnosis of metastatic lesions. • Recurrence—for the evaluation of recurrence. • Management assessment—it is useful for the therapeutic assessment of the lesion by differentiating between benign and malignant lesion.
Types of Biopsy More commonly used biopsies are excisional, incisional, fine needle, punch, scrape and trephine. Some biopsy like bite, cone, core, endoscopic, irrigation, pressure, shave and sponge are less commonly used.
Fig. 8-3: Different types of stains used in diagnostic pathology.
• Submission of teeth—for the histologic examination of teeth, the apex of tooth should be clipped with a pair of pliers or a small hole should be drilled into the radicular pulp with dental burr to allow penetration of the fixative. • Preservation—the excellent preservation of cellular detail required is obtained by following methods. • Cutting the specimen into tiny blocks before fixation. • Use of special fixatives that preserve cellular detail with minimum disruption from rapid dehydration or osmotic shock.
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• Post-fixation and processing of tissues in the laboratory after the initial period of prefixation (Fig. 8-4).
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attached at the edge of specimen. Care must be taken not to crush the specimen. • Dissection of tissue—the specimen is now gently dissected out with either a scalpel or a pair of surgical scissors. • Keeping in formalin solution—the tissue must be immediately submerged in 10% formalin solution. • Suturing—surgical site is closed with either silk or absorbable sutures placed approximately 5 mm apart.
Incisional Biopsy Fig. 8-4: Biopsy slide is prepared and stored properly.
Instrument and Materials • Excisional and incisional—Local anesthesia with vasoconstrictor, scalpel holder and blade. Pointed surgical scissors, tissue forceps and surgical hemostat. Sterile sponge, curved needles and suture, needle holder. Wide mouthed bottle containing 10% formalin. • Intraosseous biopsy—periosteal elevator, bone bur, curette. • Aspiration biopsy—large syringe (10 –20 cc) with a large needle.
Incisional biopsy can be performed by removing a wedge shaped specimen of the pathological tissue along with surrounding normal zone.
Indications • Large lesion—if the lesion is large and diffuse and extends deeply into the surrounding tissue so that total removal cannot be obtained easily with local anesthesia, an incisional biopsy is indicated. • To determine nature of treatment—lesions in which diagnosis will determine whether the treatment should be conservative or radical.
Procedure
Excisional Biopsy Total excision of a small lesion for microscopic examination is called as ‘excisional biopsy’. It is a therapeutic as well as a diagnostic procedure. Normal tissue on the margins of the lesion should be included.
Indications • Small lesion—it is the preferred treatment if, the size of lesion is such that it may be removed along with the margins of normal tissue and wound can be closed primarily. It is usually done in case of lesion smaller than 1 cm. • Sessile lesion—when the lesion is sessile or pedunculated, excisional biopsy can be done. • Movable tissue—tissues which are freely movable and located above the mucosa or just beneath the surface.
Procedure • Local anesthesia—anesthetize the lesion with 2% local anesthetic containing vasoconstrictor. Care is taken not to inject directly into the lesion that is to be removed. • Elliptical incision—with the scalpel, make an elliptical incision on either side of the base of the lesion so that incision line intersected. The blade should be at an angle of 45° towards the center of the lesion. • Pulling of tissue—outward tension is placed on the lesion by means of suture or with the help of tissue forceps
• Selection of site—the selection of site is important. It is best to select the site away from an obvious ulceration or area of necrosis, as these are areas of intense inflammation which make interpretation difficult. • Local anesthesia—the tissue around the specimen is infiltrate with 2% local anesthetic. • Elliptical incision—with a scalpel, make an elliptical incision encompassing the selected area of the lesion. The incisional lines must be deep enough to include underlying connective tissue to the level of muscle or bone. • Suturing—suture is inserted through the end; upward tension is applied while tissue sample is dissected out.
Intraosseous Biopsy It is less frequently performed. It may be in the form of exploratory curettage in which the representative tissue is obtained to determine the nature of large radiological alterations.
Procedure • Selection of site—after correlating the radiographs with overlying anatomical structures, the site of which the mucoperiosteal flap is to be raised is selected. • Local anesthesia—anesthesia to the area is accomplished by block injection to the area and with local infiltration
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with a 2% solution of local anesthetic along with vasoconstrictor. Incision lines—with a scalpel, press firmly against the cortical bone, outline the flap using the periosteal elevator and strip the tissue from the bone. Drilling by bur—using a small bone bur in low speed drill, make a small square window through cortical plate; using a water spray as a coolant. Removal of cortical plate—remove the cortical plate of bone and with curette, obtain deep sample of the underlying lesion and place the sample in 10% formalin. Closing of flap—the surgical site is closed by replacing the flap.
microscopic examination of the cells shed from an epithelium. The appreciation of the fact that some cancer cells are so typical that they can be recognized individually has allowed the development of this diagnostic technique, which is developed by Dr. George Papanicolaou Who is also known as the ‘father of cytology’ and the technique is called as Pap smear (Fig. 8-6).
Punch Biopsy It is rarely necessary in the oral cavity as most of the oral lesions are easily accessible. With this technique the surgical defect that is produced is small and does not require suturing. In this technique, a sharpened hollow tube (Fig. 8-5); several millimeters in diameter is rotated until underlying bone or muscle is reached. The tissue is then removed in the same manner as in incisional or excisional biopsy.
Fig. 8-6: Pap smear ( Courtesy Dr Akshay Dhoble).
Principle of Pap Smear
Fig. 8-5: Different types of punch of different diameter are used in punch biopsy.
• Normal cells—individual cells can often be diagnosed as such microscopically by their large size, their pleomorphism, increased nucleo-cytoplasmic ratio, hyperchromatism and prominence of nuclei and their abnormal mitosis. • Dysplastic cells—cancer cells exfoliate more easily than normal cells most likely due to their lowered cohesiveness as a result of either decrease in number of tight junctions or lower calcium content.
Advantages Frozen Section Biopsy It is performed in order to get an immediate histological report of a lesion. It is done to determine whether a lesion is malignant or not. It is also used to evaluate the margins of an excised cancer, to ascertain that the entire lesion is removed at the time of surgery. The tissue is obtained from lesion and it is kept in deep freeze and then frozen tissue is sectioned and stained to get a prompt diagnosis. In this type of biopsy, the slides cannot be preserved for future reference.
Exfoliative Cytology In this, the surface of the lesion is either wiped with some sponge material or scraped to make a smear. It is the
• Time saving—cytology is quick procedure so it saves lot of time. It is simple procedure. • Painless—as it is painless, it causes minimum discomfort to the patient. • Low cost—cost of performing cytology is less as compared to cost of biopsy. • No anesthesia—it does not require anesthesia. • False negative biopsy—it helps to check against false negative biopsy. • Follow up—it is especially helpful in a follow up detection of recurrent carcinoma. • Screening test—it is valuable for screening lesions whose gross appearance is such that biopsy is not warranted. • Safety—it is a safe procedure as complications are rare. • Rapid diagnosis—it enables a rapid diagnosis.
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• Bloodless procedure—as it is bloodless procedure there is less risk of delayed wound healing and infection. • Accuracy—there are report of 100% accuracy in lymph node aspiration from metastatic carcinoma, melanoma, Hodgkin’s and Non-Hodgkin’s lymphoma.
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Disadvantages • Firm tumors—firm tumors may prevent a proper cytodiagnosis due to paucity of cells in the aspirate. • False negative results—oral cytology can give false –ve findings due to inadequate sampling. Another reason for this is many lesion have a thick keratinized surface layer and contain subtle change of dysplasia. • Non-assessment—some specimens cannot be assessed due to poor cellularity.
Indications • Patient preference—as a compromise, when the patient refuses for biopsy. • Follow-up—as a means of follow-up for recurrence in patients who had radiation therapy for the lesion that was superficial or adjacent to bone, periodic recall of high risk patient. • Debilitated patients—in place of biopsy, when dealing with extremely debilitated patients possessing problems to determine a suitable biopsy site. • Adjunct test—as an aid to the diagnosis of some dermatological diseases such as Pemphigus, White sponge nevus, oral malignant and pre-malignant lesions. • Periodic review—periodic review of oral lesion like leukoplakia, lichen planus should be carried out by this method. • Rapid evaluation—for rapid evaluation of an oral lesion that on clinical grounds, is thought to be malignant or pre-malignant and for which, the dentist is unable to obtain permission for a biopsy. • Sequential laboratory evaluation—for sequential laboratory evaluation of an area of the mucosa that has previously been treated by radiation or by excisional biopsies to remove malignancy. • Vesicular lesion—for evaluation of vesicular lesions where facilities for rapid evaluation of Tzanck smears are not available. • Population screening—when population screening is done for the detection of oral caner exfoliative cytology is the recommended method.
Instruments Used Instrument which are used in exfoliative cytology are glass microscopic slide, lead pencil, cement spatula or wax carver, wooden tongue depressor, toothpick, canister of cytospray and 95% isopropyl alcohol or ethyl alcohol.
Procedure • Information to written on slide—use of two slides for each site to be sampled. With lead pencil print the patient’s name, date when the slide is prepared and the site of the lesion on frosted end of glass microscopic slide. • Instrument—the instrument selected to remove the superficial cell must have a square edge with a contour sufficient to scrape off the superficial layer of cells. When the lesion is very small, the edge of toothpick is effective. • Clearing of surface—clear the surface of oral lesions with debris and mucus. • Scraping the tissue—while the tissue is stretched, the squared edge of the collection instrument is positioned at the back of the lesion and is firmly held and brought forward and pressure applied until visible material is collected. Vigorous scraping of the entire surface of the lesion several times is done with a metal cement spatula or a moistened tongue blade. • Spreading of material on microscopic slide—collected material is then quickly spread evenly over the microscopic slide. • Fixing of tissue—fix it in commercial preparation such as spraycyte, 95% alcohol or equal part of alcohol and ether, immediately before it dries. Then allow it to stand for thirty minutes so that it air dried. • Repeat—repeat the procedure and prepare a second smear.
Interpretation It is reported by a cytologist as follows into one of the following five classes: • Class I (normal)—it indicates that only normal cells are observed. • Class II (atypical)—presence of minor atypia but no evidence of malignant changes. • Class III (indeterminate)—this is a stage in between that of class II and IV and separates non-cancer cells from cancer cells displaying wider atypia that may be suggestive of cancer but they are not clear-cut and may represent pre-cancerous lesion or carcinoma in situ and a biopsy is recommended in such cases. • Class IV (suggestive of cancer)—few cells with malignant characteristic or many cells with borderline features. Biopsy is mandatory in such cases. • Class V (positive of cancer)—cells that are obviously malignant. Biopsy is mandatory in such cases.
Fine-Needle Aspiration Cytology It is the microscopic examination of an aspirate obtained by inserting a fine needle into the lesion. It is a painless
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Investigation in Dentistry 93 and a safe procedure for rapid diagnosis. First discovered by Kun in 1847 and reintroduced in 1930 by Martin and Ellis.
• Image processor—this is specially designed to detect as few as two abnormal epithelial cells scattered among more than thousand cells on each biopsy specimen.
Indications
Interpretation
• Salivary gland pathology—FNAC of salivary glands is a useful procedure for evaluation of salivary gland tumors. • As replacement for extensive biopsy—it is indicated in lesions in which open biopsy require extensive procedures. • Suspicious lymph nodes—for examination of enlarged clinically suspicious lymph nodes. • Recurrence—to check against recurrence or local extension. • Metastatic lesion—detection of metastatic sq. cell carcinoma within cervical nodes.
The specimen is reviewed by a pathologist for final diagnosis. • Negative results—it indicated no epithelial abnormality. • Positive results—it indicated definitive cellular evidence of epithelial dysplasia. Patient should be referred to scalpel biopsy. • Atypical results—it indicates abnormal epithelial changes. This should be referred to scalpel biopsy.
Procedure • Needle positioning—first you have to position the needle within the target tissue. • Application of negative pressure—plunger is pulled to apply negative pressure. Needle is moved back and forth within the target tissue to obtain a greater field. • Releasing of negative pressure—negative pressure is then released while the needle remains within the target tissue. • Withdrawing the needle—needle is withdrawn and then the defumed air drawn in the syringe and the aspirate is blown onto the slide. • Fixing—fixing is done in 95% alcohol for 1 hour for Pap stain and a little prolonged for HE stain.
Fig. 8-7: Use of disposable brush to collect sampling of cells in oral brush biopsy.
Molecular Methods
ORALCDX Test It is highly specialized computer assists analysis of an oral brush biopsy performed on oral tissue. It is the most recent development in oral biopsy technique. This technique is ideal for determining the need for scalpel biopsy in benignappearing oral mucosal leukoplakia.
Procedure • Collection of sample cells—this technique utilizes a disposable brush to collect a transepithelial sampling of cells (Fig. 8-7). • Computer screening—the sample is screened by computer which is programmed to detect cytologic changes associated with premalignancy and squamous cell carcinoma. The computer consists of neural network based image processing system specially designed to detect oral epithelial precancerous and cancerous cells.
Quantification of Nuclear DNA Content Principle The DNA content of nucleus is dependent upon the number of chromosomes. In case of epithelial dysplasia and malignancy there can be polyploidy (more number of chromosomes) or aneuploidy (abnormal number of chromosome). So quantitative analysis of DNA content reflects the total chromosomal content.
Procedure It is done by flow cytometer analysis. Flow cytometer is automated, precise, reproducible, reliable and objective measuring device of cellular DNA content. Limitation of flow cytometer analysis is that it scans only severe dysplasia of detectable oral premalignancy.
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Tumors Markers
Indirect Immunofluorescence
Tumor markers are defined as biochemical substances synthesized and released by cancer cells. Tumor markers may be produced by host in response to cancerous substances. Tumors markers can be seen in blood circulation, body cavity fluids, cell membrane and cell cytoplasm. In oral cavity no markers are found there in cases of oral cancer. In some cases of leukoplakia tumor marker like PCNA, Ki-67 are found which can be value predicting lesion behavior.
• Application of unlabeled specific antiserum and FITC conjugated anti-globulin antiserum—it is directed against a particular tissue component. Applied directly to the smear or tissue section, allowed to react and followed by a FITC conjugated anti-globulin antiserum. • Examination under ultraviolet microscope—following incubation and washing to remove unreacted reagent, the slide is examined in the ultraviolet microscope. • Advantages • Brighter fluorescence—the fluorescence is brighter because several fluorescent anti-globulin molecules bind onto each of the antibody molecules in the specific antiserum (Fig. 8-8). • Cost effective—because the process of conjugation is lengthy, there is considerable cost saving and versatility to the indirect technique, which requires only one labelled antiserum. • More staining—staining of more than one tissue component per slide can also be accomplished.
Microsatellite Markers It is one of sensitive method for studying clonal changes in tumors and premalignant lesion. This requires small quantities of DNA. It is done by polymerase chain based Microsatellite analysis. In oral premalignant lesion loss of heterozygosity is seen.
Immunofluorescence Procedure Fluorescent dyes such as fluorescein isothiocyanate (FITC) and rhodamine can be chemically linked (conjugated) with antibody globulin without destroying the specificity of the antibody. Such fluorescent labeled antibodies used to detect specific antigen-antibody reaction can be used to locate either antigens or antibodies of known specificity in tissue sections. When tissue sections labeled in this fashion are illuminated with ultraviolet light in an ultraviolet microscope, specific labeled tissue component can be identified by their bright apple green fluorescence against a dark or counter stained background. The technique is used to identify a number of tissue structures and abnormal deposits of antibody globulin and other macromolecules as well as bacteria and viruses in infected tissues and smears. It is carried out in the following three ways.
Direct Immunofluorescence • Application of fluorescent labeled antiserum—fluorescent labeled antiserum directed against a particular tissue component is applied directly to a thin, unfixed smear or tissue section mounted on a slide. • Incubation of slide—the slide is incubated at 37°C to allow the antigen and the labeled antibody to react. • Washing of slide in buffered normal saline—following incubation, the slide is washed in buffered normal saline to remove un-reacted labeled antibody. • Examination under ultraviolet microscope—the slide is examined in ultraviolet microscope.
Fig. 8-8: Positive immunofluorescence in case of HSV infection.
Sandwich Technique of Immunofluorescence • Why called sandwich—the name sandwich technique refers to the fact that antigen is sandwiched between two layers of the same specific antibody, one labeled and one not. • Reaction of solution of antigen with antibody—appropriately fixed tissue sections are reacted with a solution of the antigen for which specific antibody is to be identified in the section. • Application of FITC labeled antiserum—following incubation and washing, FITC labeled antiserum with the same specificity as that to be identified in the section, is applied to the section. The labeled antiserum again identifies the location of the tissue component.
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Investigation in Dentistry 95
Caries Activity Tests (Fig. 8-9) Caries activity can be defined as the occurrence and rate at which teeth are destroyed by the acid produced by plaque bacteria or it can also be defined as the sum total of new carious lesions and the enlargement of existing carious cavities during the given time.
Uses • Preventive measures—to determine the need and extent of preventive measures. • Success of therapeutic measure—to determine the success of therapeutic measures. • Diet counseling and oral hygiene procedure—to motivate and monitor the effect of education programs related to diet counseling and oral hygiene procedures. • Identification of high risk group—to identify high risk groups and individuals.
Lactobacillus Count Test It was introduced by Hadley in 1933. It estimates the number of bacteria in the patient’s saliva by counting the number
of colonies appearing on tomato Peptone Agar or L.B.B. Agar. Although it is quick and easy, the results are not available for several days and counting colonies is a tedious and complex process.
Technique • Collection of saliva—stimulated saliva is collected before breakfast by chewing paraffin. • Spreading on agar plate—this is shaken and 1:10 and 1:100 dilutions are spread on the surface of agar plate. • Incubation—these are incubated at 37°C for a period of 3-4 days. The number of colonies is then counted in a Quebec counter. • Results—the count expressed as the average number of colonies per milliliter of the original saliva sample.
Interpretation • Immune—if the count is less than 103 then the patient is immune. • Slight—if the count is between 103 —5000, caries activity is slight. • Medium—if the count is between 5000—104 , caries activity is medium. • High—if it is more than 104 then caries activity is high.
Snyder Test This test measures the ability of microorganisms in saliva responsible for formation of acids from carbohydrate media.
Technique • Collection of saliva—the saliva sample is collected in a manner similar to the Lactobacillus colony count test. • Snyder media—the media contains bactopeptone (20 gm), dextrose (20 gm), sodium chloride (5 gm), agar (16 gm) and bromocresol green (0.02 gm). • Mixing of media with saliva—then 0.2 cc of saliva is pipette into the media which is incubated at 37°C for a period of 72 hours. • Results—bromocresol green, being an indicator, changes the color from blue green to yellow in the range of pH of 5.4-3.8. The color change is then correlated with the caries activity.
Interpretation
Fig. 8-9: Diagrammatic representation of caries activity test.
• High—if color changes in 24 hours, caries activity are high. • Medium—if the color changes in 48 hours, it is medium. • Slight—if color changes in 72 hours, it is slight. • Immune—if there are no color change patient is immune to caries.
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Alban’s Test
Buffer Capacity Test
It is a modification of Snyder’s test. It uses less quantity of agar i.e. 5 ml per tube. Because of its simplicity and its low cost it is recommended for all patients prone to caries. The main feature of Alban’s test is the use of a softer medium that permits the diffusion of saliva and acids without the necessity of melting the medium and use of a simpler sampling procedure in which the patient expectorates directly into the tubes that contain the medium.
Technique
Technique • Preparation of Alban medium—60 gm of Snyder test agar is placed in 1 liter of water and the suspension is brought to boil over a low flame or a hot plate at medium heat (excessive heating should be avoided to prevent scorching of medium). When thoroughly melted, agar is distributed, using about 5 ml per tube. The tube should be autoclaved for 15 minutes, allowed to cool and stored in a refrigerator. • Mixing and incubation of saliva with Alban medium—two tubes of Alban medium are taken from the refrigerator and saliva is drooled directly into the tubes and tubes are incubated for 4 days at 37° Celsius. • Results—the tubes are observed daily for change in color. The color change is noted from bluish green to yellow and the depth to which change has occurred is noted.
Interpretation • Negative—no color changes. • + beginning of color change (from top of the medium towards bottom). • ++ one-half color changes. • +++ three-fourth color changes. • ++++ total color change.
• Collection of saliva—10 ml of stimulated saliva is collected under oil at least one hour after eating; 4 ml of this is measured into a beaker. • Adjusting pH of saliva to 7—after collecting the pH meter, the pH of saliva is adjusted to 7.0 by addition of lactic acid or base at room temperature. • Results—the level of lactic acid in the graduated cylinder is re-recorded. Lactic acid is then added to the sample until a pH of 6.0 is reached. The number of millimeter of lactic acid needed to reduce pH from 7.0 to 6.0 is a measure of buffer capacity of saliva.
Interpretation • Low buffer capacity—saliva sample requiring less than 0.45 ml of standard hydrochloride acid to reduce the pH to 5 has low buffer capacity. • High buffering capacity—saliva sample requiring 0.45 ml or more has high buffering capacity.
Fosdick Calcium Dissolution Test Technique • Collection of saliva—twenty five milliliters of gum stimulated saliva is collected. • Keeping powdered enamel with saliva—part of this is analyzed for calcium content and the rest is placed in an eight inch sterile test tube with about 0.1 gm of powdered human enamel. • Shaking of tube—the tube is sealed and shaken for four hours at body temperature after which, it is again analyzed for calcium content. If paraffin is used, a concentration of about 5% glucose is added.
Interpretation Streptococcus Mutans Level in Saliva Saliva samples are obtained by using tongue blades (after air drying the tooth for plaque samples). These are then incubated on M.S.B. agar (Mitis Salivarius Bacitracin Agar). The number of colonies is then used to estimate the caries activity and more than 105 colonies per ml of saliva is indicative of high caries activity.
• The amount of enamel dissolution increases as the caries activity increases which is indicated by an increase in the calcium content of saliva.
Dewar Test Technique • Collection of plaque sample—plaque samples are collected from the gingival third of buccal tooth surfaces and placed in Ringer’s solution. • Mitis Salivarius agar plate—the sample is shaken until homogenized. The plaque suspension is streaked across a Mitis-Salivarius agar plate. • Incubation—after aerobic incubation at 37° C for 72 hours, the culture is examined under a low power microscope and the total colonies in 10 fields are recorded.
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Investigation in Dentistry 97 Interpretation • This test is an attempt to semi-quantitatively screens the dental plaque for a specific group of caries causative organisms including streptococci.
Swab Test The swab test involves sampling of the oral flora by swabbing the buccal surface of teeth and placing it in Snyder media. This is incubated for 48 hours and the pH changes are read and correlated with caries activity.
• Puncturing the finger with blood lancet—the prepared area is rapidly punctured with a blood lancet taking care not to squeeze the finger (Fig. 8-10). • Collection of blood sample—the patient’s hand is at about the waist level and the first drop of the blood that wells up is wiped out with dry sponge. The next drop that appears allows to flow into a capillary tube or is collected on a glass slide.
Reductase Test This test measures the activity of salivary enzyme reductase.
Technique • Collection of saliva and mixing with diazoresorcinol—saliva is collected and the sample is mixed with a diazoresorcinol, which colors the saliva blue. • Results—the change in color from blue to red is measured after 30 seconds and 15 minutes and this is taken as measure of caries activity. Fig. 8-10: Collection of capillary blood specimen is done by finger prinking.
Interpretation • Non-conductive—if it remains blue after 15 minutes it is non-conductive. • Slightly conductive—if it changes to orchid after 15 minutes, it is slightly conductive. • Moderately conductive—if it changes to red after 15 minutes, moderately conductive. • Highly conductive—if it changes immediately to red, it is highly conductive. • Extremely conductive—if it changes to pink or white immediately, it is extremely conductive.
• Venous blood specimen—venous blood specimens are used for majority of tests that are to be performed in clinical diagnostic laboratory. Venipuncture is usually performed in antecubital vein (Fig. 8-11). Procedure is as follows: • Equipment—a 10 to 20 ml sterile disposable syringe with a 20-gauge needle or Vacutainer. Needle, adaptor and evacuated collection tubes, tourniquet or approximately 20 inch of soft tissue rubber tubing,
Hematological Investigation Normal values are given in Table 8.1.
Collection of Blood Specimen • Capillary blood specimens—these are convenient for office and chair side procedures. The specimen is obtained by pricking the patient’s finger (an earlobe, ankle pad can also be used). Procedure is as follows • Equipment—jar of sponge soaked in 70% alcohol. • Application of alcohol to patient finger—the palmar surface of the patient’s index finger or second finger is gently rubbed with sponge soaked in 70% alcohol. Excess alcohol is wiped off and the alcohol is allowed to evaporate.
Fig. 8-11: Venous blood is taken by venipuncture method.
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less than ½ inch in diameter. Jar of sponges soaked in 70% alcohol and jar of dry sponge. • Preparation of patient—prepare the patient and equipment. Apply the tourniquet and select the vein to be punctured. • Preparation of puncture site—prepare the puncture site with 70% alcohol and air dry. • Collection of blood—insert the needle through the skin and into the vein. Aspirate blood into a syringe or Vacutainer tube and remove the tourniquet. • Maintenance of puncture site—place dry cotton swab over the puncture site and withdraw the needle. Bring the patient’s forearm back against his upper arm while he maintains finger pressure on the cotton at the puncture site with the other hand. • Delivery to laboratory—specimen should be delivered to the laboratory within 1-2 hours in a tube which should be well sealed and protected from breaking. • Arterial blood specimen—arterial blood specimen is obtained by puncturing the radial artery.
Total Erythrocyte Count It gives the number of erythrocytes per cubic millimeter in circulating blood and also gives an indirect estimate of hemoglobin in blood. It is determined by hemocytometer.
Procedure • Office and chair side—the test is performed manually under a microscope by direct counting of the number of cells in diluted sample of blood confined in a calibrated chamber of special glass microscope slide (hemocytometer technique). • Automated procedure—the electronic counting of erythrocyte is usually carried out with equipment such as coulter counter model (Fig. 8-12). The sample of whole
blood is aspirated into the machine and automatically diluted with modified Eagle’s solution before being drawn through three narrow chambers equipped with electrodes. As the cells pass through an aperture, their presence and dimensions are accurately recorded by a drop in voltage across the electrodes. The reading for three aperture tubes is obtained as average and an average RBC count is displayed and printed out by the machine.
Interpretation • Earliest signs and symptoms of hematological disease affecting erythrocytes are anemia and polycythemia. It is reduced in some anemia and increased in polycythemia and dehydration.
Erythrocytes Indices In evaluation of nature of anemia, assistance is obtained by calculating standard indices relating to the size of RBCs. By measuring these indices we can classify anemia as microcytic, macrocytic and normocytic and hypochromic and normochromic (Tables 8.1 and 8.2).
Types • MCH—the hemoglobin content of erythrocyte is referred to as the mean corpuscular hemoglobin (MCH) expressed in picograms of hemoglobin per cell. • MCHC—the concentration of hemoglobin in the erythrocyte is referred to as the mean corpuscular hemoglobin concentration (MCHC) • MCV- average red cell volume referred to as the mean corpuscular volume (MCV) is expressed in cubic microns per cell. Table 8-1: Different erythrocytes indices
Indices
Calculation
MCH
Hemoglobin concentration (g/dl) —————————————— × 10 RBC in million/mm 3
MCHC
Hemoglobin concentration (g/dl) —————————————— × 100 Hematocrit
MCV
Hematocrit ———————— × 10 RBC in million/mm3
Table 8.2: Different types of anemia and erythrocytes indices
Fig. 8-12: Hemocytometer is used to calculate RBC count.
Types of anemia
MCV
MCH
MCHC
Microcytic hypochromic
Decreased
Decreased
Decreased
Macrocytic normochromic
Increased
Increased
Normal
Normocytic normochromic
Normal
Normal
Normal
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Investigation in Dentistry 99 Hematocrit
Technique
It is a measure of volume percent of packed red blood cells in whole blood.
• Photoelectric calorimeter—the hemoglobin concentration is usually measured on anti-coagulated venous blood by reacting the sample with a reagent that converts the hemoglobin to stable colored product. The concentration of this colored compound is measured in photoelectric colorimeter in comparison with the standard. • Drabkin’s method—different methods used are Drabkin’s technique in which hemoglobin is converted into the stable pigment cyanmethemoglobin. Drabkin’s solution contains potassium cyanide and ferricyanide and sodium bicarbonate. • Other method—other techniques used are Sahli’s method (0.1 N hydrogen chloride), oxyhemoglobin method (0.1 sodium carbonate).
Indications • Anemia—the classic signs and symptoms of anemia indicate for the measurement of the hematocrit value. • History of blood loss—history of excessive blood loss, pallor of oral mucous membrane, palate, conjunctiva, nailbeds. • Evaluation of patient for general anesthesia—To evaluate patient’s ability to tolerate general anesthesia or oral surgical procedures. • Others—unexplained syncope, excessive fatigue, glossitis and atrophy of lingual papillae, recurrent and persistent gingivitis and stomatitis.
Technique • Equipment—2 heparinized microhematocrit capillary tubes. A box of matches and microhematocrit centrifuge equipped with reader and magnifier. • Collection of blood—blood is obtained by a finger prick or venipuncture and is allowed to flow by capillary action into two microhematocrit tubes, until each is about ¾th filled. The volume of blood should be free from air bubbles. • Sealing of tube—the end of each tube away from the column of blood is sealed by melting the glass in the flame of a match or small gas jet without heating the blood. • Keeping tube in centrifuge—the tubes are cooled and placed opposite to each other in the slots of the head of the centrifuge, with sealed ends pointing outward. The centrifuge head covers are closed and the centrifuge timer is set for 5 minutes. • Centrifugation—the centrifuge is started and it accelerates to 12,500 rpm and stop automatically at the end of required time. • Results—the centrifuge head covers are removed and with the aid of magnifying lens for greater accuracy, the hematocrit is read by means of scale incorporated in the head of the instrument.
Interpretation • Increased—it is increase in primary and secondary dehydration. • Decrease—hemoglobin concentration decreased in anemia.
WBC Count In the management of dental patients total WBC count is used as one of the index of presence of systemic infection and to rule out possibility of leukemia and malignant neutropenia (Table 8-3). The total WBC count can be calculated manually with a hemocytometer or with an automated cell counter. To count WBCs in the presence of RBCs, RBCs are lysed by diluting the blood sample with dilute acetic acid or equivalent reagent supplied by the manufacture of the automated equipment leaving the WBCs intact. Table 8-3: Interpretation of WBC count
Increased in (leukocytosis)
Decreased in (leukopenia)
• • • • • •
• Aplastic anemia • Influenza, measles and respiratory tract infection • Catarrhal jaundice • Early leukemia • Depression of bone marrow due to certain drugs • Drug and chemical toxicity, shock
Infection –acute and chronic Leukemia Polycythemia Trauma Exercise, fear and pain After general anesthesia
Interpretation • Increase—increase in the value indicates primary and secondary polycythemia and dehydration. • Decrease—value is decreased in anemia.
Measurement of Hemoglobin Concentration It is expressed in gm/dl. It is require to obtain information about circulating RBC’s and the oxygen carrying capacity. It is also used for calculation of MCHC and MCH.
Differential Leukocyte Count As the WBCs in circulating blood are of several types and of varied origin, the total leukocyte count is of limited use without a differential count of the various types of cells present. Five types of WBCs are commonly present in circulating blood. They are neutrophils, lymphocytes, monocytes, basophilis and eosinophils.
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Technique
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Table 8-4: Interpretation of different types of WBCs in disease
• Staining—it is performed on air dried smear of blood stained with Wright’s or other Romanovsky-type stain to differentiate types of WBCs from each other. Nowadays various instruments are used to calculate DLC count (Fig. 8-13) • Relative percentage—the relative percentage of each type of WBC is obtained by counting a minimum of 100 to 200 cells per slide and the fields counted are selected in such a way that the effect of uneven distribution of WBCs in the smear is overcome.
Increased in
Decreased in
Neutrophils • Pregnancy, exercise • Infection, inflammation • Neoplasm, severe hemorrhage • Hemolysis and erythroblastosis fetalis • Intoxication by drugs and poisons like corticosteroids
• • • •
Aplastic anemia Cyclic neutropenia Malignant neutropenia Drug induced myelosuppression • Early leukemia
Lymphocytes • • • • •
Lymphocytic leukemia Mumps—German measles Whooping cough Chronic infection Convalescence from acute infection
• Aplastic anemia • Myelogenous anemia
Monocytes • • • •
Hodgkin disease Monocytic anemia Malaria—kala-azar Sub-acute bacterial endocarditis • Tuberculosis
• Aplastic anemia • Acute leukemia
Eosinophils Fig. 8-13: DLC count is calculated by instrument.
Interpretation It is discussed in Table 8-4.
Platelets
• Parasitic infection • Allergic disease • Drug reaction dermatoses like pemphigus, pemphigoid, atrophic dermatitis • Scarlet fever
• Immune defect • Acute stress • Injection of adrenocorticotropic hormone • Typhoid fever • Aplastic anemia
Basophils
Platelets are small 2 µ to 5 µ particles released from the cytoplasm of large multinucleated cells (megakaryocytes) located in the red bone marrow. Because of the platelet’s small size and tendency to aggregate, (an important phenomenon related to their function in the hemostatic mechanism) platelet counts on peripheral blood smear have a large technical error. Counts are performed manually using a special hemocytometer counting chamber and a phase contrast microscope or by means of an automated cell counter such as the Technicon Autoanalyzer. Interpretation of platelet is discussed in Table 8.5.
Bleeding Time It measures the time required for hemostatic plug to form. Lack of any clotting factor and platelet abnormalities may increase the bleeding time. It is a useful screening test in patients with a history of prolonged bleeding following previous surgery. It should be carried out in patients in whom certain symptoms are with strongly suggestive of bleeding disorders.
• Chronic myelogenous leukemia • Polycythemia • Myelofibrosis Table 8.5: Interpretation of platelets
Increased in (Thrombocytosis) Decreased in (Thrombocytopenia) • • • •
Chronic myelocytic leukemia • Thrombocytopenic purpura Polycythemia vera • Immune reaction Hemolytic anemia • Transfusion Trauma • Aplastic anemia
Technique Equipment • Equipment—sphygmomanometer, cuff, jar of sponges soaked in 70% alcohol and jar of dry sponges, blood lancet, 3 to 4 pieces of filter paper about 1 inch square, stop watch (Fig. 8-14). • Patient position—the patient is seated comfortably with his arm supported on the chair arm or his own thigh. • Application of cuff to patient—the sphygmomanometer cuff is applied to the patient’s upper arm and inflated to 40 mm pressure.
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Investigation in Dentistry 101 • Scrubbing area with alcohol swab—an area on the palmar (inner) surface of the forearm about halfway between elbow and wrist that is free of superficial veins, is located and prepared by scrubbing with an alcohol soaked swab. • Punctured with blood lancet—after the area is air dried, the skin of the prepared area is tensed and punctured with a blood lancet cutting deep enough such that the hit is firmly pressed against the skin of the arm. • Results—the lancet is immediately removed and the time noted on a watch equipped with a seconds hand. Every 30 seconds by the watch, an edge of filter paper is touched against the drop of blood that wells up. The length of time until the bleeding ceases is the bleeding time in minutes. • Cleaning the area—the area is finally cleaned with a swab slightly moistened in 70% alcohol.
done by occluding veins of the upper arm with a blood pressure cuff for five minutes.
Indications • Bleeding abnormalities—it is used to screen for bleeding abnormalities especially where there is suspicion of platelet disorders. • Petechiae in oral cavity—the discovery of petechiae in the oral cavity or on the skin is the most common indication for the capillary fragility test; especially where the petechiae are confined to the oral cavity and could also conceivably have resulted from local trauma or denture irritation. • Scurvy—in dental practice, it is used as a screening test for scurvy, which is an etiological factor in periodontal disease.
Technique
Fig. 8-14: Filter paper, blood lancet are used to calculate bleeding time.
Interpretation • An abnormal bleeding time—it is usually the result of abnormalities in the structure or ability of the capillary blood vessels to contract or abnormalities in the number or functional integrity of the platelets. • Contributing factors—a bleeding time of 5 minutes does not mean that a patient will stop bleeding from any type of wound in 5 minutes. The time for bleeding to stop is related to the way in which the wound is produced, the caliber of the vessels involved in the hemorrhage, the amount to tissue damage adjacent to the wound and systemic factors such as blood pressure and individual response to the type of anesthesia.
Capillary Fragility Test (Tourniquet Test and Rumpel Leede Test) It is the test of the ability of superficial capillaries of the skin of the forearm and hand to withstand an increased intraluminal pressure and a certain degree of hypoxia. It is
• Equipment—sphygmomanometer and cuff, microscope slide. • Patient position—the patient is seated with one arm supported on the chair arm or thigh. • Instruction to patient—the dentist should explain the patient that his blood pressure will be taken and the cuff will be left on a little longer than the patient may be used to. He should be further explained that the procedure may make the patient’s arm a little numb and even painful, but that discomfort will quickly disappear once the cuff is removed. • Examination of hand of patient—during this time, the dentist examines the patient’s forearms and hands for any petechiae and records their location with an ink spot. The blood in a petechial hemorrhage lies extravascularly and should not disappear upon pressure with the surface of a glass microscope slide. • Application of sphygmomanometer—the sphygmomanometer is applied customarily and the patient’s systolic and diastolic arterial blood pressure is recorded. • Inflation of cuff—the pressure in the cuff is reduced to zero and the cuff is reinflated to a point halfway between systolic and diastolic pressure. This pressure is maintained for 5 minutes during which the forearm and hands are examined for development of new petechiae. The patient should not be moved vigorously while the cuff is in place because movement will increase anaerobic muscular glycolysis, lactate accumulation and thus result in pain. • Results—after 5 minutes, the cuff is removed and the patient is allowed to exercise his arm to restore the circulation in the arm. The blood vessels of normal individuals will withstand these conditions and
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petechial hemorrhages will not appear on the forearm and hand from rupture of superficial capillaries. • Positive test—if any unequivocal petechiae develop distal to the cuff (toward the hand) after cuff has been applied, the test is recorded as positive (Fig. 8-15). • Negative test—if only one or two petechiae are seen or if those seen are not convincing in their appearance, a negative test is recorded; retesting is done if required by investigating dentist.
as well as diseases characterized by altered globulins such as the collagen diseases, nephritis, rheumatic fever and dysproteinemias.
Technique • Mechanism—the rate is accelerated when there are changes in the physicochemical properties of plasma or the red cell surface or when the changes in plasma protein cause the RBCs to aggregate. • Westergren method—in the Westergren method, a graduated sedimentation tube is filled with oxalates blood and placed in an absolutely vertical position (Fig. 8-16). • Results—the erythrocyte level is read at 10 minutes intervals and at the end of an hour.
Fig. 8-15: Appearance of petechiae on hand after tourniquet test.
Clotting Time Procedure • Feeling of blood in dry tubes—one millimeter of venous blood is placed in each of the four dry tubes of standard size, maintained in a water bath. • Tilting of tube—the first tube is tilted at 30 seconds interval, until the blood no longer flow. The next tube it tilted until clotting occurs, after which the third and fourth tubes are similarly treated. • Results—the average time between venipuncture and clotting in the last three tubes is expressed in minutes as the clotting time. The normal range is 10 to 25 minutes.
Interpretation • Increases—it is prolonged in diseases affecting stage II and stage IV of coagulation. It is also increased in cirrhosis, hemophilia A and B, factor XI deficiency, hypofibringenemia and heparin and dicumarol anticoagulant therapy.
Erythrocyte Sedimentation Rate (ESR) It is a measure of the rate at which RBCs sediment in a tube of plasma. The test is helpful in following the progress of some chronic infections (tuberculosis and osteomyelitis)
Fig. 8-16: ESR is calculated by Westergren method.
Hematological Investigation not so Frequently Required in Dental Office • Partial thromboplastin time—it is the time, in seconds, that is required for a clot to form in a sample of oxalated plasma, to which a partial thromboplastin reagent and calcium chloride is added. • Prothrombin time—it is the time in seconds that is required for fibrin threads to form in citrated or oxalated plasma, where known amount of tissue thromboplastin and calcium is added. Since last two reagents are present in excess, any delay in clotting in this test is suggestive of an abnormality of the prothrombin complex or a very severe fibrinogen deficiency. • Schilling test—several types of megaloblastic macrocytic anemias of different etiologies are caused by vitamin B12 deficiency. Schilling test is a measurement of patient’s
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ability to absorb orally administrated radioactive vitamin B12 labeled with 60Co. Following oral administration of the radioactive vitamin B12, unlabeled vitamin is given intramuscularly, as a flushing dose to induce urinary excretion of the labeled vitamin, which is measured in a 24 hour urine specimen. Patients with pernicious anemia (who are unable to absorb orally administered vitamin B12) excrete less than 5% of the orally administered dose in comparison with excretion of 8 to 25% by normal individuals. Serum iron and total iron binding capacity—iron deficiency is the most common cause of anemia; however anemia occurs only after depletion of iron stores and iron deficiency may exist for some time before the appearance of anemia. Iron deficiency is usually detected on the basis of the amount of iron bound to transferrin in the plasma (serum iron) and the total amount of iron that can be bound to the plasma transferrin in vitro (total iron binding capacity or TIBC). Bone marrow aspiration—detailed evaluation of patients with anemia, leukemia, multiple myeloma, metastatic malignancy and other space occupying lesions frequently involves study of the immature erythropoietic and leukopoietic cells of the bone marrow. This is accomplished by aspiration of red bone marrow cells through a large bore needle inserted through a trochar into the iliac crest or sternal marrow space. The aspirate is then smeared thinly on a glass slide or coverslip, stained with Wright’s stain and examined in the same ways as a smear of capillary or venous blood. Bone marrow biopsy—bone marrow biopsy is also used where an indication of the spatial relationship and degree of hyperplasia or hypoplasia of the cellular element in the marrow is needed. Platelet survival time—it is measured in thrombocytopenic purpura and other diseases in which rapid destruction of platelet occurs. A sample of autologous or isologous platelets labeled with radioactive 51Cr is added to a sample of patients blood and re-injected intravenously. The amount of radioactivity is then measured in blood samples taken at intervals over the next few days, depending on the design of the experiment. The normal platelet survival time (time required for the circulating radioactivity to drop to 10% of its peak value after injection of 51Cr labeled platelet) is between 8 to 9 days.
Blood Chemistry Detection of Diabetes Mellitus Diabetes mellitus is a disease of insidious onset that is not infrequently complicated by serious tissue changes leading
to permanent cardiovascular, renal, cerebral and optic damage.
Importance of Detection of Diabetes Mellitus in Dentistry • Periodontal therapy—the response of diabetic patients to periodontal therapy may be much less satisfactory than non-diabetic, under similar conditions. • Healing of oral tissue—the healing of oral tissues following surgery in diabetics is slower. Complication like tissue necrosis and secondary infections may occur in diabetic patient. • Oral disease—certain oral diseases are predisposed to occur in association with diabetes mellitus (e.g. thrush, denture sore mouth). • Oral infection—the systemic effects of acute localized oral infections may be much greater in a diabetic than in a non-diabetic.
Indications • Evaluation of patient suspected of diabetes mellitus—for evaluation of a patient suspected of having diabetes mellitus. Its presence should be suspected whenever any of the following are found: history of weight loss in the presence of adequate diet, history of excessive thirst and attendant excessive and frequent urination, history of repeated episodes of boils, skin infections and periodontal abscesses and presence of severe periodontitis with excessive bone loss. • Screening test—as a screening test for diabetes mellitus, where the dentist suspects the occurrence of disease in the absence of characteristic signs and symptoms. • Family history—testing of the patient with a family history of diabetes. • Known diabetes patient—as a measure of degree of control of disease in a patient who is known to be a diabetic but who is not under regular medical care and is unwilling to accept referral to a physician for reevaluation of the disease.
Types • Urine glucose estimation—many diabetics excrete glucose in their urine, testing the urine with commercial available reagent strips (Tes-Tape, Clinistix, Chemstrip) is the most convenient screening method of diabetes (Fig. 8-17). But in patient with mild diabetes urine may not exhibits glycosuria. False positive urine sugar tests also occur in individuals with renal glycosuria. • Blood glucose estimation—this is most accurate method for detection of diabetes mellitus. Three schedules for determination of blood glucose concentration are used:
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• Fasting blood glucose—determination of fasting blood glucose is frequently used as a screening test for hyperglycemia in hospitalized patients. On an outpatient basis, however, maintenance of the fasting state from the evening meal until the next morning is difficult to ensure and may lead to a degree of hypoglycemia that an outpatient cannot tolerate without fainting. • Two hours postprandial blood glucose—determination of the blood glucose two hours after a meal containing 75 gm of carbohydrate (2-hours postprandial blood glucose) is a more sensitive measurement of the hyperglycemia associated with diabetes. Both fasting and 2-hour postprandial blood glucose measurement can be carried out on capillary blood using the Dextrostix, Visidex, or Chemstrip reagent strip. Due to its convenience, simplicity and sensitivity, this test is recommended as the best screening procedure for a dentist to use if he suspects that a patient may be a diabetic and feels that he must explore the problems further by himself prior to medical referral. • Oral glucose tolerance test—glucose tolerance test is one of the procedures used for the definitive diagnosis of diabetes mellitus. It is performed on series of blood samples in a laboratory and is used to confirm the diagnosis of a diabetic patient who does not exhibit constantly elevated fasting blood glucose.
Fig. 8-17: Glucometer used for detection of blood glucose.
Technique Two hour postprandial blood glucose • Diet instructions—patient may take serving of 1 fruit juice plus 1 bowl of cereals with 2 tea spoonful of sugar plus 1 cup of milk plus coffee or tea with sugar plus anything he desires at breakfast at 8 am. If the patient is to be retested in the afternoon, he may eat 1 sandwich plus 1 piece of cake or pie plus coffee or tea with sugar or milk plus anything else he wishes for lunch at 1 pm.
• Equipment—blood lancet, jar of sponges soaked in 70% alcohol and jar of dry sponges. Dextrostix, Visidex, or Chemstrip bG reagent strip, wash bottle, urine jar, reagent strip to test for glycosuria. • Collection of blood sample—blood sample is taken with the help blood lancet. • Application of reagent strip to blood—the first drop that wells up is wiped away and the next few drops are freely applied to the entire reagent area on the printed side of blood glucose reagent strip. The blood is allowed to permeate and react with the reagents contained in the strip for exactly 1 minute. • Removal of blood from strip—the blood is then washed from the strip as completely as possible with a sharp stream of water from the wash bottle or faucet. • Results—the test area of the strip is immediately compared with the color chart on the side of the bottle, matching the strip; if the color obtained is intermediate between two color blocks, the result is inappropriate, otherwise, the value for a matching block is read directly. • Urine glucose—the patient is requested to void a sample of urine in the specimen jar provided. This is tested for the presence of glucose by using the appropriate reagent strip. • Blood glucose—the normal range of blood glucose in the fasting state is approximately 70 to 110 mg/dl. The concentration rises to about 160 mg/dl following a meal in normal persons but returns to the fasting level within 2 hours. In diabetics of moderate severity, fasting levels may reach 200 mg/dl, postprandial levels are greater than this and may persist for longer than 2 hours after meals. The diagnosis of diabetes mellitus should be made only after a complete medical history, physical examination and appropriate laboratory tests carried out by a physician. If the 2 hour postprandial blood glucose is above 140mg/dl, the patient is clearly metabolizing glucose in an abnormal fashion. • Urine glucose—when the blood level of glucose exceeds 160 to 180 mg/dl, the normal renal threshold for glucose is exceeded and so glucose will appear in urine which will give a positive test for glucose. The renal threshold for glucose may become elevated as a result of kidney disease and this phenomenon is an important cause of false negative tests for glucosuria in diabetes mellitus and number of other diseases which are associated with hyperglycemia. Oral glucose tolerance test • Significance—for many years, glucose tolerance test has been accepted procedure for making a definitive diagnosis of diabetes mellitus and for distinguishing diabetes from other causes of hyperglycemia such as hyperthyroidism. Elevated levels for fasting plasma
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glucose, in this context include any concentrations equal to or greater than 140 mg/dl. The OGTT should be administered only to healthy ambulatory patients who are known to be taking no drugs that interfere with the laboratory determination of glucose. Oral glucose challenge—the oral glucose challenge traditionally used in the glucose tolerance test has varied from 50 to 100 gm, administered either as a glucose solution, and commercially prepared carbohydrate load or a meal equivalent to this glucose dose. Subject preparation—the test should be performed in morning, after at least 3 days of unrestricted diet (greater than 150 gm of carbohydrate daily) and physical activity. The subject is made to fast for at least 10 hours but not more than 16 hours before the test (water is permitted during this period). The subject should remain seated and should not smoke throughout the 2 hours of test period. Fasting blood sample—a fasting blood sample should be collected. Sample after oral glucose challenge—subject has to drink the glucose dose in a concentration; no greater than 25 gm/dl of flavored water, in about 5 minutes. Zero time is the beginning of the drink and blood samples are then collected at 30 minutes interval for 2 hours (a total of five blood samples per test). Storage of sample—capillary blood samples are preferred. Blood sample should be collected in a tube containing sodium fluoride to inhibit glycolysis and potassium oxalate to prevent clotting. The sample should be centrifuged and separated within 4 hours and plasma freezes unless glucose levels are to be determined immediately.
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Blood Chemistry Investigation not so Frequently Carried Out in Dental Office • Serum calcium, phosphorus—it is indicated when you suspect Paget’s disease, fibrous dysplasia, primary and secondary hyperparathyroidism, osteoporosis, multiple myeloma, osteogenic sarcoma or metastatic malignancy. It acts as initial screening procedures. The concentration of calcium in serum and body fluids tends to vary inversely with the concentration of inorganic phosphorus (2 mg/dl to 5 mg/dl). The product of serum calcium concentration and serum phosphorus concentration is constant at about 30 to 40 in normal adults, but may be as high as 50 to 60 in growing children. At serum calcium below 7 mg/dl (such as may occur in patients with hypoparathyroidism), signs of tetany (neuromuscular excitability, positive Chvostek’s sign) appear. • Serum alkaline phosphatase—alkaline phosphatase occurs in many tissues of the body, but notably in osteoblasts.
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Increase in serum concentration of this enzyme is seen primarily as a result of increased osteoblastic activity but also in association with obstructive liver diseases and a variety of miscellaneous conditions such as malignancy or abscess of the liver, amyloid disease, leukemia and sarcoidosis. It should be remembered that increased osteoblastic activity is not restricted to sclerosing (radiopaque) bone lesions but may be quite high in lytic (radiolucent) bone lesions also, as a result of remodeling of the surrounding bone that accompanies a lytic lesion. Serum uric acid—concentration usually lies in the range of 4 mg/dl to 8.5 mg/dl for males and 2.8 mg/dl to 7.5 mg/dl for females. Uric acid is a metabolic end product of nucleoprotein metabolism derived from the purine molecule. Increase occurs in acute phases of diseases such as leukemia, lymphomas, anemia or lobar pneumonia; in which there is rapid destruction of large number of DNA rich leukocytes. Measurement of uric acid is important in the evaluation of intrinsic disease of temporomandibular joint, particularly when nodules consistent with gouty tophi are noted about the face or ears. In gout, values of 8 mg/dl to 15 mg/dl for serum uric acid are usually observed. Serum albumin and globulin—the concentrations of serum albumin and globulin, as well as the total serum protein are routinely measured as part of the standard blood chemistry profile. Serum protein electrophoresis—it is useful screening test in patients with suspected oral lesions of multiple myeloma or systemic lupus erythematous. It is usually indicated when radiolucent defect detected in the jaw. In serum protein electrophoresis a small volume of serum is subjected to a low voltage electric current causing the proteins of the serum to migrate at different rates. When the serum proteins are distributed across a piece of filter paper or a block of starch or other gelled supporting medium, they may be separated and stained as relatively distinct bands and the concentration of each serum protein component calculated. Serum bilirubin—jaundice can be recognized by examination of the color of skin, oral mucous membrane and sclera of eyes. It may indicate the presence of hepatitis which can constitute an infectious hazard for a dentist and his patients. Jaundice is usually not evident until total serum bilirubin (derived from red blood cells broken down at the end of their normal 120 days lifespan) rises from a normal range of 0.1 mg/dl to 0.8 mg/ dl to above 2 mg/dl to 3 mg/dl. Thyroid function test—it is currently measured either by uptake of a radioisotope by the thyroid gland or by direct measurement of thyroid hormones, triiodothyronine (T3) and thyroxin (T4) in serum. T4 levels in serum are
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Textbook of Oral Medicine Table 8-7: Normal blood chemistry value
Table 8-6: Chart of normal values
Normal value
Test
Material
Normal value
Hemoglobin
Males—14- 17.4 gm/dl Females—12.3 to 15.3 gm/dl
Amylase
Serum
0.8 to 3.2 U/L
Bilirubin (total)
Serum
0.1 to 1 mg /dl
Red blood cell
Males—4.5 –5.9 million/mm3 Females—4.5 –5.1 million/mm3
Cholesterol (total)
Serum
150-250 mg/dl
WBC
4000-11000 / mm3
Uric acid
Serum
Males—3.5 to 7.5 mg/dl Females—2.5 to 6.6 mg/dl
Platelet count
1,50,000 –4,50,000 /mm3
Calcium
Serum
8.8-10.5 mg/dl
Hematocrit
At birth—54 Adult males—42-50% Adult females—36-45%
Chloride
Serum
98-108 mEq/L
Sodium
Serum
135-148 mEq/L
Potassium
Serum
3.5-5.5 mmol/l
Phosphorus
Serum
2.5-4.5 mg%
SgPT
Serum
5.40 IU/L
SgOT
Serum
5.40 IU/L
Creatinine
Serum
Males—0.7 to 1.4 mg/dl Females—0.6 to 1.3 mg/dl
Folate
Serum Erythrocyte
5-25 mg/ml 166-640 mg/ml
Glucose
Serum (fasting) 70-110 mg/dl Whole blood 60-90 mg/dl Post prandial less than 140 mg/dl
Iron (total) Iron binding capacity Iron saturation
Serum Serum Serum
60-150 µg/dl 250-400 µg/dl 20-55%
Phosphatase acid Alkaline phosphatase
Serum Serum
0.2 to 1.8 U/L 25-100 U/L
Test
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Red cell indices MCV MCH MCHC
80-96 cu micron 27-31 pg 32-36 gm/dl
ESR
Males (under 50) Males (over 50) Females (under 50) Females (over 50)
30% of sites involved). The severity of disease can be characterized on the basis of the amount of clinical attachment loss (CAL) as follows: Slight = 1 or 2 mm CAL; moderate = 3 or 4 mm CAL; and severe ≥ 5 mm CAL and more.
Gingival Diseases Hereditary Gingival Fibromatosis or Fibromatosis Gingiva It is also called as ‘Elephantiasis gingivae’, ‘Congenital macrogingivae’. Hereditary gingival fibromatosis is an uncommon condition characterized by diffuse gingival enlargement (Fig. 24-5), sometimes covering major parts or total tooth surfaces. The enlargement develops irrespective of effective plaque removal. Hereditary gingival fibromatosis may be an isolated entity or part of a syndrome, associated with other clinical manifestations such as hypertrichosis, mental retardation, and epilepsy, hearing loss, growth retardation and abnormalities of extremities. Most cases are related to an autosomal dominant trait. The most common syndrome of hereditary gingival fibromatosis includes hypertrichosis, epilepsy and mental retardation.
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A Fig. 24-5: Fibromatosis gingivae showing diffuse overgrowth (Courtesy Dr Parate).
Clinical Features • Age—it may be present at birth or may become apparent with eruption of deciduous or permanent teeth. • Appearance—it is manifested as dense smooth diffuse or nodular overgrowth of gingival tissue of one or both arches that usually occurs at the time of eruption of teeth (Figs 24-6A and B). It has a characteristic pebbled surface. In some cases, surface has a nodular appearance. • Color—tissue is of normal or pale color. In some cases, it may appear pink. • Consistency—it is often so firm, leathery and dense that it prevents normal eruption of teeth. • Symptoms—it is not painful and shows no tendency for hemorrhage. • Extent—extent may be such that the crown of fully erupted teeth may be hidden. • Significance—the dense firm gingival swelling results in varying spacing between the teeth and change in profile and facial appearance. • Radiological features—in the radiograph, significant bone loss can be present. At the same time, soft tissue is also visible (Fig. 24-7).
B Figs 24-6A and B: Fibromatosis gingivae preventing eruption of teeth in the oral cavity.
Diagnosis • Clinical diagnosis—diffuse fibrous overgrowth is seen clinically and it is readily diagnosed. • Laboratory diagnosis—epithelium is thickened with elongation of rete pegs, although the bulk of the tissue is composed of dense fibrous connective tissue. Bundles of collagen fibers are coarse and show few interspersed fibroblasts or blood vessels.
Fig. 24-7: OPG of patient having gingival fibromatosis.
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Management • Surgical—surgical removal of excessive tissue with exposure of teeth is necessary. However, recurrences are common. • Extraction of teeth—dramatic improvements in gingival enlargements have been observed following extraction of teeth.
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Gingivitis It is the inflammation of the gingiva.
Pathogenesis of Gingivitis (plaque associated) There is increase in numbers of normal flora organisms that (Streptococcus, Capnocytophaga, Actinomyces, etc.) grow in the gingival crevice producing toxins that cause an inflammatory reaction in the gums. Plaque accumulates in the crevice resulting in an inflammatory reaction. Complications include development of periodontitis.
Fig. 24-8: Localized gingivitis involving lower anterior region.
Classification Gingivitis can be classified on the basis of: • Course and duration: • Acute gingivitis—it is of sudden onset and of short duration and can be painful. A less severe form of acute gingivitis has been termed subacute. • Recurrent gingivitis—recurrent gingivitis reappears after having been eliminated by treatment or disappearing spontaneously. • Chronic gingivitis—chronic gingivitis is slow in onset and is of long duration. It is painless unless complicated by acute or subacute exacerbations. • Distribution: • Localized gingivitis—it is confined to the gingiva of a single tooth or a group of teeth (Fig. 24-8). • Generalized gingivitis—generalized gingivitis involves the entire mouth (Fig. 24-9). • Marginal gingivitis—marginal gingivitis involves the gingival margin and may also involve a portion of the contiguous attached gingiva. • Papillary gingivitis—papillary gingivitis involves the interdental papilla and often extends into the adjacent portion of the marginal gingiva (Fig. 24-10). • Diffuse gingivitis—diffuse gingivitis involves the gingival margin, the interdental papilla and the attached gingiva.
Fig. 24-9: Generalized gingivitis showing involvement of entire gingiva.
Stages of Gingivitis • Stage I gingivitis (the initial lesion)—the first manifestation of gingival inflammation is vascular changes, consisting essentially of dilation of capillaries and
Fig. 24-10: Papillary gingivitis involving interdental papilla.
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Gingival and Periodontal Diseases 577 increased blood flow. No clinical signs appear in this stage. It occurs within 2-4 days of plaque accumulation. • Stage II gingivitis (the early lesion)—this stage is usually seen following 4-7 days of plaque accumulation. In this stage, clinical signs of erythema appear, mainly owing to the proliferation of capillaries and increased formation of capillary loops between rete pegs or ridges. Bleeding on probing may also be evident. • Stage III (the established lesion) (Fig. 24-11)—the lesion develops generally after 14-21 days of plaque accumulation. Blood vessels become engorged (Fig. 24-12) and congested, venous return is impaired and blood flow becomes sluggish. The established lesion can be described as moderately to severely inflamed.
Clinical Features of Gingivitis • Symptoms—the earliest symptoms of gingival inflammation are increased gingival fluid production and bleeding from the gingival sulcus on gentle probing. • Color—gingiva becomes redder when there is an increase in vascularization or when the degree of epithelial keratinization is reduced. The color becomes paler when vascularity is reduced and keratinization is increased. The color may be sometimes reddish blue or deep blue, if venous stasis has occurred. The color change starts in the interdental papillae, gingival margins and spreads to the attached gingiva. • Consistency—the consistency of gingiva may be spongy that pits on pressure and there may be marked softness of the gingiva. • Enlargement of gingiva—sometimes in inflammation, there may be gingival enlargement and it may lead to change in the contour of gingiva. Plaque induced gingivitis without local contributing factors Characteristic of plaque-induced gingivitis are discussed in Table 24-2. Table 24-2: Characteristics common to all plaque-induced gingival diseases
Fig. 24-11: Established gingivitis is moderately inflamed.
Fig. 24-12: Stage III gingivitis showing engorgement of blood vessels.
• Stage IV gingivitis (the advanced lesion)—the lesion extends into the alveolar bone and known as the phase of periodontal destruction.
• Signs and symptoms are confined to gingiva. • The presence of dental plaque to initiate or exacerbate the severity of the lesion. • Clinical signs of inflammation (enlarged gingival contours due to edema or fibrosis, color transition to a red or blue-red hue, elevated sulcular temperature, bleeding upon provocation, increased gingival exudates). • Clinical signs and symptoms associated with stable attachment levels on a periodontium with no loss of attachment or on a stable but reduced periodontium. • Reversibility of the disease by removing the etiology(ies). • Possible role as a precursor of attachment loss around teeth.
Plaque-induced gingivitis with local contributing factors • Teeth anomalies—tooth anomalies such as enamel pearls and cemental tears can modify or predispose to plaqueinduced gingival diseases. Enamel pearls are found in 1.1-5.7% of molar teeth and maxillary second molar are most commonly involved. • Dental restoration—subgingival margin of restorations and violation of biologic width can affect the health of adjacent gingival tissue. • Root fracture—root fracture and root perforations during endodontic therapy are associated with inflammation of the gingiva and sometimes, pocket formation due to enhanced plaque accumulation. • Cervical root resorption—cervical root resorption may result in inflammation particularly when a communication is established with the sulcus.
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• Other causes—other cause like deep bite (Fig. 24-13), palatogingival groove (Fig. 24-14) and shallow vestibule (Fig. 24-15) can also lead to gingival inflammation.
3 Fig. 24-13: Deep bite causing gingival disease.
Fig. 24-14: Palatogingival groove causing gingival disease.
Fig. 24-15: Shallow vestibule causing gingival disease.
Gingivitis due to systemic factors • Puberty associated gingivitis—it appears to be exaggerated response of gingival tissues towards high levels of hormones, especially estrogens and testosterone, secondary to plaque accumulation. • Menstrual cycle associated gingivitis—although bright red hemorrhagic lesions have been described prior to the onset of menses, clinically detectable changes do not seem to be associated with the menstrual cycle. However, an increase in gingival fluid by 20% has been described in 75% of women during ovulation. • Pregnancy-associated gingivitis—the exaggerated response of gingiva to local factors can often appear during the second trimester and regress upon parturition. The condition can be reversed with suitably high levels of plaque control. Pyogenic granuloma of pregnancy is a localized mass of highly vascularized tissue arising as an exaggerated response to plaque. It commonly arises from the proximal gingival tissues and has a pedunculated base. It may show ulceration of its thin epithelial lining. Bleeding on mastication or spontaneously may be a presenting complaint. • Diabetes mellitus-associated gingivitis—there is evidence that Type I diabetes in children is associated with gingival changes. However, when this type of diabetes is under good control, the gingival inflammation is less exaggerated. • Leukemia-associated gingivitis—the leukemia has been associated with gingival changes including gingival swelling, redness/blueness, sponginess and a glazed appearance. The leukemia most commonly associated with gingival changes is acute myeloid leukemia. Any other condition affecting the platelet deficiency can affect periodontium. Cyclic neutropenia, a condition characterized by fluctuation in neutrophils count with a periodicity of 14-36 days, is associated with oral ulceration and exaggerated gingival response to dental plaque. • Drug influence gingivitis—the increased use of oral contraceptives by postmenopausal women has been associated with a higher incidence of gingival inflammation and development of gingival enlargement. This phenomenon can be reversed by discontinuation of medications. • Ascorbic acid deficiency gingivitis—severe vitamin C deficiency in humans results in scurvy, a disease characterized by hemorrhagic diathesis and retardation of wound healing. The clinical features include bleeding, swollen gums and loosened teeth. Scurvy results in defective formation and maintenance of collagen, retardation or cessation of osteoid formation and impaired osteoblastic function. It is also characterized by increased capillary permeability, susceptibility to
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Gingival and Periodontal Diseases 579 traumatic hemorrhages, hyporeactivity of the contractile elements of the peripheral blood vessels and sluggishness of blood flow.
Management of Gingivitis • Removal of local irritant—the local irritants should be removed at this stage. • Plaque control—thorough plaque control should be done with scaling and polishing. • Chlorhexidine mouth wash—use of chlorhexidine, on a short-term basis.
Plasma Cell Gingivitis It is also called as ‘Atypical gingivostomatitis’ or ‘Atypical gingivitis’. It is allergic in origin and is caused by some ingredients in chewing gums, dentifrices or various diet components.
Clinical Features • Sex—it is more frequently in women and young adults. • Site—it is located on the oral aspect of the attached gingiva and therefore, differs from plaque induced gingivitis. • Symptoms—patients may complain of a sore and burning mouth, scaling of lips and angular cheilitis. • Appearance—entire free and attached gingiva is edematous, friable, granular, bright red (Fig. 24-16) and bleeds on slightest provocation.
Management • Cessation of exposure—cessation of exposure to allergen resolves the lesion.
Gingival Enlargement Classification • Inflammatory enlargement—it can be acute or chronic . • Drug induced—may occur due to dilantin, nifedipine or cyclosporine. • Combined—it is combination of (inflammatory + fibrotic). • Enlargement due to systemic disease—many systemic diseases like leukemia, Crohn’s disease can cause gingival enlargement. • Neoplastic enlargement—benign and malignant tumor of gingiva can cause enlargement.
Acute Inflammatory Enlargement or Gingival Abscess It results from bacteria carried deep into the tissue, when a foreign substance such as a toothbrush bristle, a piece of apple core or a lobster shell fragment is forcefully embedded into the gingiva.
Clinical Features • Site—it is limited to the marginal gingiva or the interdental papilla (Fig. 24-17). • Onset—it is localized, painful, rapidly expanding lesion that is usually of sudden onset. • Appearance—in early stages, it appears as a red swelling with a smooth, shiny surface. Within 24 to 48 hours, the lesion usually becomes fluctuant and pointed with a surface orifice, from which an exudate may be expressed. • Teeth—the adjacent teeth are sensitive to percussion.
Fig. 24-16: Bright red color inflammation seen in plasma cell gingivitis.
Diagnosis • Clinical diagnosis—bright red color inflammation with history of some allergen. • Laboratory diagnosis—lamina propria is infiltrated by plasma cells.
Fig. 24-17: Acute gingival inflammatory enlargement seen in lower anterior region.
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Diagnosis • Clinical diagnosis—red swelling with shiny surface associated with pain will give clue to the diagnosis. • Laboratory diagnosis—it consists of a purulent focus in the connective tissue, surrounded by a diffuse infiltration of polymorphonuclear leukocytes, edematous tissue and vascular engorgement.
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• Appearance—it originates as a slight ballooning of the interdental papilla or the marginal gingiva. In early stages, it produces a life preserver-like bulge around the involved teeth. It increases in size, until it covers a part of the crown. • Color—lesions may be deep red (Fig. 24-19) or bluish red. They are soft and friable, with a smooth shiny surface and tendency to bleed.
Management • Incision—after topical anesthetic is applied, the fluctuant area of the lesion is incised with a blade and the incision is gently widened to permit drainage. The area is cleansed with warm water and covered with a gauze pad. After the bleeding stops, patient is instructed to rinse every 2 hours with a glassful of water.
Chronic Inflammatory Enlargement Etiology • Local factors • It can be caused by prolonged exposure to dental plaque, which may occur due to poor oral hygiene (Fig. 24-18), abnormal relationship of adjacent and opposing teeth, lack of tooth function, overhanging margins of dental restoration and improperly contoured dental restoration or pontics. • Food impaction, irritation from clasps or saddle areas of removable prosthesis and nasal obstruction. • Habits—such as mouth breathing can cause gingival enlargement, which is more common in the anterior region.
Fig. 24-19: Inflammatory enlargement shows deep red in color.
• Progress—it progresses slowly and painlessly, unless complicated by acute infection or trauma. • Discrete mass—sometimes, enlargement can occur as a discrete, sessile or pedunculated mass, resembling a tumor (Fig. 24-20). They may undergo spontaneous reduction in size, followed by exacerbation and continued enlargement. Painful ulceration, sometimes, occurs between the mass and the adjacent gingiva.
Fig. 24-18: Inflammatory gingival enlargement occur due to calculus and poor oral hygiene.
Clinical Features • Site—the enlargement is generally papillary or marginal and localized or generalized.
Fig. 24-20: Inflammatory gingival enlargement presented as discrete mass.
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Gingival and Periodontal Diseases 581 Diagnosis • Clinical diagnosis—inflammatory enlargement with ballooning of papilla around the teeth will give clue to diagnosis. • Laboratory diagnosis—there is proliferative features of chronic inflammation. Lesions may contain preponderance of inflammatory cells with vascular engorgement.
Management • Removal of local factors—all the factors which are responsible for enlargement should be removed. • Antibiotics—antibiotics should be given. The most commonly used antibiotics is metronidazole. • Flap surgery—periodontal flap surgery is done if necessary.
A
Drug Influence Gingival Enlargements Dilantin Sodium Dilantin sodium is an anticonvulsant drug, which is used to control of epileptic seizures.
Clinical Features • Onset—gingival hyperplasia may begin as early as two weeks after dilantin therapy. • Site—the hyperplasia is generalized throughout the mouth, but it is most severe in maxillary and mandibular anterior region. • Appearance—the first change noted is a painless bead like enlargement of the gingiva, starting with one or two interdental papillae (Figs 24-21A and B). The surface of gingiva shows an increase in stippling and finally, a cauliflower, warty or pebbled surface. As the enlargement increases, the gingival tissue becomes lobulated and clefts are seen between each enlarged gingiva. • Palpation—palpation reveals that the tissue is dense, resilient and insensitive. It shows little tendency to bleed. • Significance—they may develop massively, covering a considerable portion of the crown. They may interfere with occlusion. The presence of an enlargement makes plaque control difficult, resulting in a secondary inflammatory process that complicates the gingival hyperplasia. In hyperplasia associated with Dilantin sodium the presence of dental plaque does not seem to initiate the enlargement. Additional studies have demonstrated that oral hygiene procedures may limit the severity of the lesion but are unable alone to lead to a reversal of the condition.
B Figs 24-21A and B: Dilantin-induced gingival enlargement showing bead-like enlargement.
Cyclosporine It is a potent immunosuppressive agent used to prevent organ transplant rejection and to treat several diseases of autoimmune origin.
Clinical Features • Clinically, it is similar to that induced by Dilantin. • Site—growth starts in the interproximal papillae, more frequently in anterior facial areas, partially covering the crown. • Appearance—the tissue is usually pink, dense and resilient, with stippled or granular surface and little bleeding tendency (Fig. 24-22).
Nifedipine • Action—it is a calcium channel blocker that induces direct dilatation of the coronary arteries and arterioles, improving the oxygen supply to the heart muscles. It is used in the treatment of acute and chronic coronary insufficiency.
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Textbook of Oral Medicine Combined Gingival Enlargement In this type, enlargement of both inflammatory as well as fibrous component are present. It can be localized (Fig. 24-24) or generalized (Fig. 24-25).
3 Fig. 24-22: Drug-induced gingival enlargement showing pink resilient surface due to cyclosporine administration.
• Gingival overgrowth occurs in 20% of the cases. The clinical and histological features are same as seen in Dilantin hyperplasia.
Fig. 24-24: Localized combined gingival enlargement showing inflammatory and fibrous component.
Diagnosis • Clinical diagnosis—enlargement of the gingiva with history of drugs will diagnose the condition (Fig. 24-23). • Laboratory diagnosis—the stratified squamous epithelium covering the tissue is thick and has a thin keratinized layer. The rete pegs are extremely long and thin, sometimes called as ‘test tube’ pegs, with considerable confluence. Mitotic figures are seldom seen.
Fig. 24-25: Generalized combined gingival enlargement.
Pregnancy-induced Gingival Enlargement It can be marginal or generalized and may occur as a single or multiple tumors like masses.
Clinical Features Fig. 24-23: Nifedipine-induced gingival enlargement.
Management • Surgical excision—If hyperplasia interferes with function, surgical excision is recommended. • Discontinue the drug—discontinuing the drug will result in gradual diminution of the bulk of the gingiva.
• Marginal enlargement—it tends to be more prominent interproximally, than on the facial and lingual surfaces. The enlarged gingiva is bright red or magenta, soft and friable and has a smooth shiny surface. Bleeding occurs spontaneously or on slight provocation. • Pregnancy tumor—it is an inflammatory reaction to the local irritants. It usually appears after 3rd month of pregnancy.
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Gingival and Periodontal Diseases 583 • Appearance—the lesions appear as discrete, mushroom like (Fig. 24-26), flattened spherical masses, that protrude from the gingival margins or more frequently from the interproximal space and are attached by sessile or pedunculated base. It tends to expand laterally. The pressure from the tongue and the cheek perpetuates its flattened appearance. • Color—it is generally dusky red or magenta; it has a smooth glistening surface that frequently exhibits numerous deep red, pinpoint markings. • Consistency—the consistency varies from semifirm, but may have a varying degree of softness and friability. • Symptoms—it is usually painless, unless its size and shape foster the accumulation of debris under its margin or interfere with occlusion, in which painful ulceration may occur.
Clinical Features • Age and sex—it occurs in both, males and females in pubertal age group. It also appears in areas of local irritants. • Site—it involves mainly the marginal gingiva and interdental gingiva. • Appearance—it is characterized by prominent bulbous interproximal papillae (Fig. 24-27). Sometimes, only facial gingivae are enlarged, as the mechanical action of the tongue prevents heavy accumulation of local irritants on the lingual surface.
Fig. 24-27: Puberty-induced gingival enlargement showing prominent bulbous papillae.
Fig. 24-26: Mushroom like enlargement seen in pregnant women.
Diagnosis • Clinical diagnosis—mushroom like enlargement in pregnancy will diagnose this condition. • Laboratory diagnosis—the connective tissue consists of numerous, diffusely arranged, newly formed and engorged capillaries, lined by cuboidal endothelial cells. The epithelium exhibits some degree of intracellular or extracellular edema with prominent intercellular bridges and leukocytic infiltration.
Diagnosis • Clinical diagnosis—bulbous enlargement at the onset of puberty will give clue to the diagnosis. • Laboratory diagnosis—microscopic picture is that of chronic inflammatory cells with prominent edema and associated degenerative changes.
Management • Removal of local irritant—after puberty, the enlargement undergoes spontaneous reduction, but does not disappear until local irritants are removed.
Necrotizing Ulcerative Gingivitis
Management • Maintenance of oral hygiene—most gingival enlargement during pregnancy can be prevented by the removal of local irritants and institution of a fastidious oral hygiene.
Puberty-induced Gingival Enlargement It is usually associated with inflammatory type.
It is an endogenous oral infection that is characterized by necrosis of gingiva. It is also called as ‘Trench mouth’ due to its prevalence in combat trenches (Fig. 24-28). Other synonyms for this are ‘Vincent’s infection’, ‘Acute ulceromembranous gingivitis’, ‘Fusospirochetal gingivitis’ and ‘Acute ulcerative gingivitis’. Tissue destruction is caused by endogenous organisms that act either on the tissue or, indirectly by triggering an inflammatory reaction.
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Etiology
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• Role of bacteria—it is caused by fusiform bacilli and spirochetes. In addition to it, bacteroides intermedius is also responsible for ANUG. • Local predisposing factors—poor oral hygiene, pre-existing marginal gingivitis and faulty dental restorations. Deep periodontal pockets offered favorable environment for occurrence of the disease. Area of gingiva is traumatized by opposing maloccluded teeth. As tobacco smoke has a direct toxic effect on the gingiva, smoking and emotional stress can predispose for ANUG. • Systemic predisposing factors • Nutritional deficiency—nutritional deficiency like vitamin C, vitamin B2 accentuate the severity of the pathologic changes induced by the fusospirochetal bacterial complex. • Debilitating disease—chronic diseases like leukemia, aplastic anemia, syphilis, severe gastrointestinal disturbances and AIDS can act as predisposing factors. • Marked malnutrition—it may be predisposing factors to necrotizing ulcerative gingivitis. • Psychosomatic factors—the disease often occurs in association with a stress situation as well as with increase in adrenocortical secretion.
Fig. 24-28: Necrotizing ulcerative gingivitis showing blunting of interdental papilla.
denudation of the roots, accompanied by increase in the severity of complications. • Lymph nodes—regional lymph nodes are enlarged. • Fever—there may be a slight elevation of temperature. • Systemic complications—in severe cases, there may be systemic complications like high fever, increased pulse rate, loss of appetite and generalized lassitude.
Clinical Features • Age—it is most commonly seen in the age group of 16 to 30 years, but can be seen in children from a low socioeconomic group, in underdeveloped countries. • Symptoms—onset is sudden with pain, tenderness, profuse salivation and peculiar metallic taste. Spontaneous bleeding from gingival tissue occurs. There is also a loss of sense of taste and diminished pleasure from smoking. The typical fetid odor ultimately develops, which may be extremely unpleasant. • Signs—teeth seem slightly to be extruded and are sensitive to pressure or have a woody sensation. They are slightly movable and the patient is unable to eat properly. Gingiva may become superficially stained with brown color. There is blunting of interdental papillae (Fig. 24-28). • Appearance—a typical lesion consists of necrotic punched out, crater like ulcerations are developed most commonly on the interdental papillae and marginal gingiva (Fig 24-29). Removal of the lesion leaves raw surface. The surface of gingival crater is covered by a gray, pseudomembranous slough, demarcated from the reminder of the gingival mucosa by pronounced linear erythema. In some cases, ulceration may develop on cheek, lip, tongue, palate and pharyngeal area. If untreated, it may result in progressive destruction of the periodontium and
Fig. 24-29: Necrotizing ulcerative gingivitis showing ulceration of marginal gingiva.
Clinical Classification of NUG • Stage I—only the superior margins of the interdental papillae are affected. There is marked tendency of bleeding on probing. • Stage II—the process spreads to the marginal gingiva with characteristic punched out destruction. • Stage III—the attached gingiva is affected in addition to the interdental papillae and marginal gingiva. • Stage IV—the necrotizing process has resulted in denudation of bone.
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Gingival and Periodontal Diseases 585 Diagnosis
Table 24-3: Herpetic gingivostomatitis
• Clinical diagnosis—punched out ulceration of gingiva with systemic features will give clue to the diagnosis. • Laboratory diagnosis—the surface epithelium is destroyed and is replaced by a pseudomembranous meshwork of fibrin, necrotic epithelial cells, polymorphonuclear neutrophils and various types of microorganisms. The underlying connective tissue is markedly hyperemic with numerous engorged capillaries and a dense infiltration of PMN. Numerous plasma cells may appear in the periphery of infiltrate.
ANUG
Acute herpetic gingivostomatitis
Etiology—interaction Specific viral etiology between host and bacteria, most probably fusospirochetal Necrotizing condition
Diffuse erythema
Punched out gingival margins, Vesicle ruptures and leave a slight pseudomembrane that peels depression or an oval or a spherical off leaving raw areas, marginal ulcer gingiva affected Rare in children
Occurs most frequently in children
No definite duration
Duration of 7 to 10 days
Differential Diagnosis ANUG, presenting as an isolated phenomenon, must be differentiated from severe systemic diseases and in condition where acute inflammation of gingival and periodontal regions are the only associated symptoms. • Agranulocytosis—blood picture shows evidence of a systemic disease and due to diminished immunity lesion is not marked by a severe inflammatory reaction. • Gingival changes due to cytostatic and immunosuppressive therapy—history is relevant. • Benign mucus pemphigoid—erosion, no necrosis and seen in elder adults. • Pemphigus—it follows a chronic course with classical histological picture. It occurs in older patients and skin changes are seen. • Pemphigoid lichen planus—no acute course, no bad breath, whitish changes and skin symptoms. • Gonococcal stomatitis—the oral mucosa is covered with a grayish membrane that sloughs off in areas, to expose an underlying raw bleeding surface. • Syphilitic gingivitis—primary lesion seldom on gingiva, does not spread to neighboring surfaces. • Gingivostomatitis due to Candida—whitish deposits that can be wiped off, no bad breath, less acute picture and demonstration of fungi. • Tubercular ulcer—less acute picture. • Streptococcal gingivostomatitis—it is characterized by a diffuse erythema on the posterior areas of the oral mucosa. But in these cases, necrosis of gingiva is not a feature.
Management • Removal of pseudomembrane—the involved areas are isolated with cotton rolls and dried. A topical anesthetic is applied and after 2 to 3 minutes, the areas are gently swabbed with a cotton pellet to remove the pseudomembrane and nonattached surface. After the area is cleansed with warm water, the superficial calculus is removed.
Table 24-4: Difference between ANUG, diphtheria and secondary stage of syphilis ANUG
Diphtheria
Secondary stage of syphilis
Caused by fusospriochetes
Caused by corynebacterium diphtheriae
Caused by treponema pallidum
Affect marginal gingiva
Rarely affects the marginal gingiva. It affects the throat, fauces and tonsil
Rarely affects marginal gingiva. Any site of the oral cavity can be affected
Membrane removal easy
Membrane removal difficult
Membrane not detachable
Painful condition
Less painful
Minimal pain
Serological findings are normal
Serological findings are normal
Serological findings are abnormal
Doubtful contagiousity
Contagious
Only direct contact can cause this disease
• Rinsing the mouth—the patient is asked to rinse the mouth within every 2 hours, with a glassful of an equal mixture of warm water and 3% hydrogen peroxide. Twice daily rinse with 0.12% chlorhexidine are also effective. • Antibiotics—patients with severe ANUG and lymphadenopathy are treated with antibiotics Penicillin V- 250 or 500 mg, 6 hourly or erythromycin—250 or 500 mg, 6 hourly with metronidazole 400 mg, 8 hourly, for 7 days are the drugs of choice. • Gingival curettage—scaling is performed, if sensitivity permits. After the disease process is diminished, complete gingival curettage and root planning is done. • Supportive treatment—supportive treatment consists of copious fluid consumption and administration of nutritional supplements.
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Non-plaque-induced Gingival Disease Bacterial Origin Gingival Disease
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• Mechanisms—in rare occasions, when non-plaque related microorganisms override the host’s innate immunity, infective gingivitis and stomatitis may occur in immunocompromised or non-immunocompromised individuals. • Organism responsible—such infections may be caused by Neisseria gonorrhoea, Treponema palladium, Streptococci, Mycobacterium chelonae or other microorganisms. • Appearance—the lesions manifest as fiery red, edematous, painful ulcerations, as asymptomatic chancres or mucus patches, or as atypical non-ulcerated, highly inflamed gingivitis. Biopsy supplemented by microbiologic examination reveals the underlying etiology.
Viral-induced Gingival Disease Herpetic Gingivostomatitis • Mechanism—herpes simplex virus has a low infection potential. Hence, after gaining entry into the oral mucosa it penetrates a neural ending and travels to trigeminal ganglion through smooth endoplasmic reticulum and remains latent for years. The virus has also been isolated from normal gingiva, gingivitis, acute necrotizing gingivitis and periodontitis cases. • Appearance—the clinical features of primary herpetic gingivostomatitis include painful, severe gingivitis with redness, ulcerations with serofibrinous exudates and edema accompanied by stomatitis. In its initial stage, it is characterized by the presence of discrete spherical gray vesicles which may occur on the gingiva, labial and buccal mucosa; soft palate, pharynx, sublingual mucosa and tongue. After approximate 24 hours, the vesicles rupture and form painful small ulcers with a red elevated halo-like margin and a depressed yellowish or grayish-white central portion. This occurs in widely separated areas or in clusters where confluence occurs. Fever and lymphadenopathy are common. The incubation period is one week. Healing of ulcers occur spontaneously without scarring in 10-14 days. During the course of the disease, the generalized soreness of oral cavity interferes with eating and drinking. • Management—the treatment includes careful plaque removal to limit bacterial superinfection, which delays the healing. In severe cases, including patients with immunodeficiency, systemic use of antiviral drugs such as acyclovir or valacyclovir is recommended.
Herpes Zoster • Organism—varicella-zoster virus causes varicella (chickenpox) as the primary self-limiting infections which occur mainly in children and later activation of the virus in adults causes herpes zoster (shingles). • Appearance—the intraoral ulcers usually involves gingiva, tongue and palate. The diagnosis is generally obvious due to unilateral occurrence of the lesions associated with severe pain. Healing of lesions take place in 1-2 weeks. • Management—treatment consists of soft or liquid diet, rest, atraumatic removal of plaque and diluted chlorhexidine rinses. This may be supplemented by antiviral drug.
Gingival Disease of Fungal Origin • Candidiasis—the most common intraoral fungal infection is candidiasis which is caused by Candida albicans, the proteinase-positive strain. It usually occurs as a consequence of reduced host defense, reduced salivary secretion, smoking and treatment with corticosteroids and broad-spectrum antibiotics. The most common clinical characteristics of gingival candidial infection is redness of the attached gingiva often associated with a granular surface. A diagnosis of the candidial infection can done on the basis of culture, smear and biopsy. Topical treatment involves application of antifungal, nystatin, amphotericin B or miconazole. • Linear gingival erythema—it is regarded as gingival manifestation of immunosuppression characterized by a distinct linear erythematous band limited to free gingiva. There is no attachment loss or pocket formation and the lesion does not respond to conventional plaque control methods and improved oral hygiene. • Histoplasmosis—it is a granulomatous disease caused by Histoplasma capsulatum. The clinical manifestations include acute or chronic pulmonary histoplasmosis. The oral lesions are initiated as nodular or papillary and later may become ulcerative, painful with the loss of gingival tissue. They are sometimes granulomatous and the clinical appearance may resemble a malignant tumor. The diagnosis is based on clinical appearance, histopathology and/or culture.
Gingival Manifestations of Systemic Condition • Mucocutenous disorders—many mucocutaneous disorders may manifest intraorally in the form of desquamative lesions and ulcerations of gingiva (Fig. 24-31). The most important of these are lichen planus (Fig. 24-30), pemphigoid, pemphigus vulgaris, erythema multiforme and lupus erythematosus. Certain conditions
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Gingival and Periodontal Diseases 587 plaque-induced inflammation. Spontaneous gingival bleeding is also a common symptom of leukemic patients which develops secondary to thrombocytopenia. The primary concern is prevention of infection and bleeding. Careful and strict oral hygiene measures can reduce gingival inflammation. In some cases of iron deficiency anemia, gingival enlargement can occur.
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Fig. 24-30: Desquamative gingivitis present due to lichen planus.
Fig. 24-32: Enlargement of gingiva seen in iron deficiency anemia.
Gingival Recession Types of Gingival Recession (By Miller)
Fig. 24-31: Ulceration of gingiva seen in desquamative type of gingivitis associated with dermatological disorders.
may also present themselves as desquamative gingivitis. These are factitious injuries, graft verses host disease, Wegener’s granulomatosis, foreign body gingivitis, Kindler syndrome and squamous cell carcinoma. • Allergic reaction—allergic reactions in the oral mucosa are uncommon. These reactions are type I (immediate type), which is mediated by IgE, or more often type IV (delayed type) mediated by T cells. The uncommon occurrence of these reactions intraorally may be due to the fact that much higher concentration of allergens is required for an allergic reaction to occur in the oral mucosa than in skin. The allergic reactions can be further classified on the basis of the type of allergen: Reactions due to dental restorative materials and reactions due to oral hygiene products, food and chewing gum. • Hematological disorders—hematological disorders like leukemia may also manifest intraorally. Gingival manifestations in leukemia which includes extensive swelling, ulceration, petechiae and erythema are common in acute than in chronic forms. The pronounced gingival swelling is due to leukemic infiltration and
• Class I—marginal tissue recession not extends to the mucogingival junction. There is no loss of interdental bone or soft tissue. • Class II—marginal tissue recession that extends to or beyond the mucogingival junction, there is no loss of bone or soft tissue in the interdental area (Fig. 24-33).
Fig. 24-33: Class II gingival recession.
• Class III—marginal tissue recession that extend to or beyond the mucogingival junction in addition, there is loss bone and/or soft tissue in the interdental area or there is malpositioning of the teeth (Fig. 24-34).
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Textbook of Oral Medicine scratching of the gingiva with fingernail or pins, oral piercing or overzealous use of tooth pick. • Thermal injury—extensive thermal burns may occur to oral mucosa especially palatal and labial mucosa due to hot beverages, pizza, melted cheese. The lesions may be painful, erythematous or with a slough coated surface. Vesicles may also form and sometimes may present as ulceration, petechiae or erosion.
Foreign Body Reaction
3 Fig. 24-34: Class III gingival recession.
• Class IV—marginal tissue recession that extends to or beyond the mucogingival junction with severe loss of soft tissue or bone interdentally and/or severe malpositioning of the teeth (Fig. 24-35).
Another type of tissue reaction is observed when foreign materials are embedded in the gingival connective tissue due to epithelial ulceration. The common example is amalgam tattoo. Sometimes, chewing on sticks can introduce piece of stick in the gingiva producing an inflammatory reaction.
Carcinoma of the Gingiva It is most commonly seen squamous cell carcinoma and occurs due to habits of tobacco.
Clinical Features
Fig. 24-35: Type IV gingival recession.
Traumatic Lesion of Gingiva • Chemical injury—chemical injury due to various agents have been noticed. Chlorhexidine induced mucosal desquamation, acetylsalicylic acid burn (aspirin burn), cocaine burn, sloughing of mucosa due to dentifrice detergents, necrosis of gingiva due to use of paraformaldehyde are examples of it. • Physical injury—physical injury to gingiva may occur due to heavy brushing forces; high abrasive of dentifrice and horizontal movement of brushing. Overzealous brushing can also produce damage to interdental papilla. • Factitious injury—factitious injuries leading to gingival recession can produce because of picking at or
• Age—it is common in 5th and 6th decades of life. • Site—the carcinoma of mandibular gingiva is more common than the involvement of the maxillary gingiva. The tumor arises most commonly in an edentulous area, although it may develop in a site where teeth are present. The fixed gingiva is involved more than the free gingiva. It usually occurs in premolar-molar area. In maxilla, gingival carcinoma often invades maxillary sinus or it may extend to palate or tonsillar pillars. • Appearance—it is manifested as an area of ulceration, which may be a purely erosive lesion and may exhibit as an exophytic, granular or verrucous type of growth. • Symptoms—in some patients, the first symptom may be loosening of the teeth. • Invasion—quickly spreads from the gingiva to alveolar bone below. The proximity of the underlying periosteum and bone usually invites early invasion of these structures (Fig. 24-36).
Radiographic Features • Types—there are, radiologically, three types of bone destruction, i.e. permeated type, moth eaten type and pressure type. • Permeated type—bone destruction with ill-defined margins. Permeated means permeation of water into sand, with ragged ill-defined borders. It also destroys the mandibular canal. • Moth eaten type—it resembles moth eaten image with remnants of bony fragments.
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Periodontal Disease Periodontitis is defined as an inflammatory disease of the supporting tissues of the teeth caused by specific microorganism resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession or both. The clinical feature that differentiates periodontitis from gingivitis is presence of clinically detectable attachment loss. The clinical classification was simplified to describe the three general clinical manifestations to describe the three general clinical manifestations of periodontitis: chronic periodontitis, aggressive periodontitis and periodontitis as a manifestation of systemic disease.
Etiology of Periodontal Diseases
Fig. 24-36: Carcinoma of gingiva which is extending toward buccal mucosa (Courtesy Dr Suwas Darvekar).
• Pressure type—dish out concavity appearance with relatively smooth margins. • Rarefaction—rarefaction with remnants of small bony fragment. • Cortical bone destruction—cortical bone destruction with pathologic fractures also can occur.
Diagnosis • Clinical diagnosis—ulcerative growth on the gingiva with history of tobacco habit may give clue to the diagnosis. • Radiological diagnosis—comparison between periodontitis and carcinoma of gingiva is described below in Table 24-5. • Laboratory diagnosis—biopsy show features suggestive of squamous cell carcinoma. Table 24-5: Comparison between periodontitis and carcinoma of gingiva Features
Periodontitis
Carcinoma of gingiva
Margin of bone Smooth and well resorption defined
Infiltrative and ill-defined
Sclerotic bony findings
No sclerotic finding
Exist, around the margin of the lesion
Residual small None within the lesion bony fragments
Exist in most of the cases
Size
Localized finding
The condition is usually generalized and if localized, there is a specific cause for it
• Multifactorial—multifactorial, resulting from various hosts and environmental factors. • Open contact—when teeth are not in contact, the patient is said to have open contact. It is dangerous for the periodontium as food debris may trap in it and hence more bone loss occurs, than the areas of closed contact. • Microorganisms—plaque forming bacteria play a role in initiation and progression of destruction of the periodontium, mainly the anaerobic bacteria. When bacteria colonize at the root surface, they spread in the region between the root and gingival margins and stimulate a chronic inflammatory reaction. It results in pocket formation and apical migration of the epithelial attachment and bone loss. • Immune system—Neutrophils, granulocytes and monocytes are very important in causing destruction of the bacteria and thus, preventing periodontitis. It may, sometimes, release lymphocytes and cause microbial destruction. • Secondary local factors—like calculus deposits (Fig. 2437), carious cavities, overhanging margins, perforation by pins or posts, over erupted opposing teeth and gingivally impinging partial dentures.
Management • Surgery—localized lesions, of less than 3 cm in diameter, were cured in 80% of the cases by surgical excision.
Fig. 24-37: Heavy calculus seen in upper posterior region.
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Pathogenesis of Periodontitis It is an inflammation of the supporting structures of the teeth. It starts out as gingivitis that then spreads down to the root surface causing alveolar bone resorption and pocket formation. It can eventually lead to alveolar bone loss and damage to the periodontal ligament then can result in tooth loss. Other complications include periodontal abscess and osteomyelitis of the jaws.
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Periodontal Pockets Classification • Gingival pocket (relative or false)—it is formed by gingival enlargement, without destruction of the underlying periodontal tissues. The sulcus is deepened because of the increased bulk of the gingiva (Fig. 24-38). • Periodontal pocket (absolute or true)—there is destruction of the supporting periodontal tissue; progressive pocket deepening leads to destruction of the supporting periodontal tissues and loosening and exfoliation of the teeth. • Suprabony pocket (supracrestal or supra-alveolar)—in it, bottom of the pocket is coronal to the underlying alveolar bone. • Infrabony (intrabony, subcrestal or intra-alveolar)—in it, bottom of the pocket is apical to the level of the adjacent alveolar bone.
• Degeneration of connective tissue—the cellular and fluid inflammatory exudates cause degeneration of the surrounding connective tissues, including the gingival fibers. • Destruction of collagen fibers—just apical to the junctional epithelium, an area of destroyed collagen fibers develops and becomes occupied by inflammatory cells and edema. Collagen loss may occur due to enzymes, like collagenase and other lysosomal enzymes from polymorphonuclear leukocytes and macrophages, which become extracellular and destroy the collagen. • Proliferation of junctional epithelium—as a consequence of loss of collagen, the apical portion of the junctional epithelium proliferates along the root, extending in finger-like projections. • Detachment of junctional epithelium—as the apical portion migrates, the coronal portion of the junctional epithelium detaches from the root. As a result of inflammation, polymorphonuclear neutrophils invade the coronal end of junctional epithelium. An increase in number of these cells, results in loss of tissue cohesiveness and tissue detachment from the tooth surface. Thus, the bottom of the sulcus shifts apically, resulting in deepening of the periodontal pocket.
Clinical Features • Signs—gingival bleeding or/and suppuration, tooth mobility and Diastema formation may be present. In some cases, pus may be expressed by applying digital pressure. • Symptoms—patient may complain of localized pain or deep pain in the bone. When explored with a probe, the inner aspect of the periodontal pocket is generally painful. • Color—there may be bluish red, thickened marginal gingiva and a bluish red vertical zone from the gingival margin to the alveolar mucosa.
Radiographic Findings
Fig. 24-38: Gingival pocket seen due to enlargement of gingiva.
• Use of gutta percha point—pockets are not detected on radiograph as they are soft tissue changes. Gutta percha points or calibrated silver points can be used, with a radiograph, to assist in determining the level of attachment of the periodontal pocket.
Pathogenesis
Diagnosis
• Microorganism—periodontal pockets are caused by microorganisms and their products, which produce pathologic tissue changes that lead to the deepening of the gingival sulcus. • Inflammatory changes—pocket formation starts as an inflammatory changes in the connective tissue wall of the gingival sulcus.
• Clinical diagnosis—this can be made with the help of periodontal probe (Fig. 24-39). • Radiological diagnosis—it is made with the help of gutta percha point. • Laboratory diagnosis—there may be circulatory stagnation, destruction of the gingival fibers and surrounding tissues, which results in discoloration.
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A Fig. 24-39: Periodontal pocket is examined with the help of periodontal probe.
Management • Pocket irrigation—devices like squeeze bottles and blunt hypodermic needles can be used to irrigate the pocket with chemotherapeutic agents. • Flap surgery—it is done to eliminate pockets.
Periodontal Abscess It is usually culmination of a long period of chronic periodontitis.
Pathogenesis
B
• Pre-existing periodontal pocket—it usually occurs in preexisting periodontal pocket. When such pocket reaches sufficient depth of about 5 to 8 mm, the soft tissues, around the neck of the tooth may approximate the tooth so tightly that orifice of the pocket is occluded. • Multiplication of bacteria—bacteria multiply in the depth of pocket and cause sufficient irritation to form an acute abscess, with exudation of pus into this area. It results in sufficient swelling to destroy the cortical plates of bone.
Figs 24-40A and B: Periodontal abscess showing swelling at the periapical region.
Diagnosis • Clinical diagnosis—severe pain with swelling in the apical region will give clue to the diagnosis. • Laboratory diagnosis—there is central cavity filled with pus walled off on one side by the root and on the other side by connective tissue.
Management Clinical Features • Location—it starts at the gingival crevice and extends down on one or more surface of the root, frequently as far as apical region. • Symptoms—acute episode usually has sudden onset with extreme pain. There is also distension and discomfort. • Signs—they are associated with swelling of the soft tissues overlying the surface of the involved root (Figs 24-40A and B). Tooth is tender and mobile. Pus usually exudes from the gingival crevice.
• Analgesic and antibiotics—suitable analgesics and antibiotics should be given to patient. • Incision and drainage—primary treatment for relief of acute symptoms is incision of the fluctuant abscess, from the depth of the abscess cavity to the gingiva. The incision should extend into the soft tissues of the root surface. • Debridement of root surface—if the surrounding tissue are normal, the tooth may be retained and debridement of the root surface by removal of granulation tissue should be done. Treatment for new attachment and new tissue regeneration should be performed.
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• Extraction of tooth—however, if the roots are denuded beyond the apical thirds of the root, the tooth should be extracted and curettage should be carried out to remove the granulation tissue from the socket.
Chronic Periodontitis
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It is the most common form of periodontitis and is most prevalent in adults but can also be observed in children. It is generally a slowly progressive form of periodontitis which at any stage may undergo acute exacerbation with associated attachment loss. The clinical features are gingival inflammation, bleeding on probing, reduced resistance of the periodontal tissues to probing, loss of clinical attachment and loss of alveolar bone. Variable feature includes gingival enlargement, recession of gingiva, furcation involvement, increased tooth mobility, drifting of teeth and eventually exfoliation of teeth. Chronic periodontitis is subject related with only a few individuals experiencing advanced destruction, affects specific teeth and the progression of inflammatory disease is continuous with brief episodes of localized exacerbation and occasional remission.
Classification It is classified according to extent and severity of diseased sites • According to extent of disease: • Low—1 to 10 sites. • Medium—11 to 20 sites • High—Greater than 20 sites. • According to severity—this can be differentiated to the degree of clinical attachment loss. • Mild—1-2 mm clinical attachment loss. • Moderate—3-4 mm clinical attachment loss. • Severe—more than 5 mm clinical attachment loss (Fig. 24-41).
Fig. 24-41: Generalized severe chronic periodontitis.
Etiology Many risk factors have been associated with initiation of chronic periodontitis or once contracted then the progression of the disease. • Microbial plaque—it is a crucial factor in inflammation of the periodontitis is largely governed by host-based risk factors. • Age—the prevalence of periodontitis increase with age as a result of cumulative effects of disease over a lifetime. • Smoking—smoking has been positively associated with progression of periodontitis. The risk attributed to tobacco for chronic periodontitis is between 2.5 and 7.0. It is not only the risk for developing the disease, but also the response to periodontal therapy is impaired to smokers. • Host-related factors— • PMN—reduction in number and/or function of PMNs. • Drugs—drugs like Phenytoin, nifedipine and cyclosporine predispose to gingival overgrowth and thus may modify preexisting chronic periodontitis. • Hormones—changes in circulating hormones during pregnancy, puberty, and menopause can modify gingival response to plaque. • Immunosuppressant drug therapy—immunosuppressant drug therapy and any disease resulting in suppression of inflammatory and immune processes (such as HIV infection) may predispose the individual to periodontal tissue destruction. • Nutritional deficiency—nutritional deficiencies in animals have shown effects on periodontal tissues but have been proven in human studies. Vitamin C deficiency has been consistently associated with increased gingival bleeding. • Diabetes mellitus—periodontitis severity goes hand in hand with poorly controlled diabetes mellitus. On the other hand, periodontitis may also exacerbate diabetes as it may decrease glycemic control. • Psychogenic disorders—stress and other psychosomatic disorders may have direct anti-inflammatory and/or immunosuppressive effects which are relevant to the etiology of chronic periodontitis and necrotizing ulcerative gingivitis. • Genetic—gingivitis is a general and ubiquitous response to plaque accumulation whereas risk of chronic periodontitis has a high inherited component. The focus of researcher is on the polymorphisms associated with genes involved in cytokine production. An increased risk for chronic periodontitis has been associated with polymorphisms of genes involved in cytokines production but these findings are yet to be confirmed.
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Gingival and Periodontal Diseases 593 Clinical Features • Age and sex—it generally affects both the sexes equally and is seen in older age groups more frequently. • Site—it is usually generalized, although some areas may be involved more deeply than others. • Symptoms—it is usually painless, but sometimes exposed root may be sensitive to heat and cold, in absence of caries. Areas of localized deep pain, sometimes radiating deep into the jaws are established. • Signs—the characteristic finding in it, is gingival inflammation, which results from accumulation of plaque and loss of periodontal attachment. The gingiva is slightly or moderately swollen and exhibits alteration in color from pale to magenta. There is also loss of stippling and gingival bleeding, which may be either spontaneous or easily provoked. • Pocket formation—there is presence of pocket with variable pocket depth. Both, horizontal and angular bone loss can be found (Fig. 24-42).
3 Fig. 24-43: Gingival recession seen in lower anterior region due to periodontal problems.
Fig. 24-42: Chronic periodontitis showing pocket formation.
• Tooth mobility—tooth mobility is found in advanced cases, where bone loss has been considerable. Teeth give off a rather dull sound when tapped with a metal instrument. The embrasures may be opened because the interdental papillae are deficient. • Gingival recession—gingival recession is a common phenomenon in later stages of disease, which may expose the cementum (Fig. 24-43).
Radiological Features • Bone resorption—there is blunting of the alveolar crest due to beginning of bone resorption. Bone loss may occur horizontally, vertically (Fig. 24-44) or sometimes, in furcation area.
Fig. 24-44: Severe horizontal and vertical bone loss seen in chronic periodontitis.
• Loss of interdental bone—loss of corticated interdental crestal margin, the bone edges become irregular or blunted (Fig. 24-45). • PDL space widening—widening of the periodontal ligament space and localized or generalized loss of alveolar supporting bone. • Floating teeth appearance—in case of severe periodontitis, floating teeth appearance is seen (Fig. 24-46).
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Etiology and Pathogenesis
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Fig. 24-45: OPG of chronic periodontitis showing bone loss.
Fig. 24-46: Floating teeth appearance seen in periodontitis.
Diagnosis • Clinical diagnosis—gingival recession, pocket formation with mobility of tooth will diagnose the condition. • Radiological diagnosis—horizontal and vertical bone loss is present. • Laboratory diagnosis—the enlarged free marginal gingiva is densely infiltrated with lymphocytes and plasma cells. The apical borders of the inflamed area approach the crest of the alveolar bone and the crestal fibers of the periodontal ligament.
Management • Oral prophylaxis—scaling and curettage can be done. • Flap surgery—this is the treatment of choice.
Aggressive Periodontitis Aggressive Periodontitis is a group of diseases which was previously defined on the basis of age of onset and was hence named early onset periodontitis. But at the 1999 international classification workshop has clubbed a group
• Virulent microbial infection—the shorter duration of time over which a clinical manifestation of the disease is seen suggests a highly virulent microbial infection or a highly susceptible host, or a combination of both. • Microorganism—many studies have demonstrated that the prevalence of Actinobacillus actinomycetem comitans predominantly in localized aggressive periodontitis (Previously called localized juvenile periodontitis) with other microorganisms such as Capnocytophaga, Eikenella conodens, Prevotella intermedia and motile anaerobes such as campylobacterectus. Gram positive isolates of streptococci, peptostreptococci and Actinomycetes were also obtained. Generalized Aggressive periodontitis, formerly named as early-onset periodontitis and rapidly progressive periodontitis, have been frequently associated with the presence of porphyromonas gingivalis, Bacteroides forsythus and actinobacillus actinomycetem comitans. • Host response—an intense infiltration of polymorphonuclear neutrophils underlines the importance of these cells in the local defense against bacterial aggression and their potential role in host mediated tissue destruction. B-cell and plasma cells form the mononuclear defense cells. Plasma cell dominantly produce IgG and in less amount IgA. The IgG is actively present in GCF which forms a line of defense against initial bacterial invasion. Peripheral blood mononuclear cells of AgP patients may demonstrate reduced autologous mixed lymphocytes reactions, as well as a higher than normal response to B-cell mitogen. A high level of PGE2 and IL1beta is observed in AgP patients. It has been demonstrated that T-helper cells are depressed in numbers compared to T-suppressor cell. Elevated level of antibodies specific to AgP–associated microorganisms have been found in crevicular fluid than in peripheral blood. An important findings in LAP and GAP patients have been decreased migration and function of PMNs. These abnormalities are usually minor in sense that they usually are not associated with infection other than periodontitis . These abnormalities in PMNs have been found to have familial aggregation. Other recent reports contradict suggest hyper-inflammatory state resulting in high levels of serum pro-inflammatory cytokines in AgP patients (Autosomal dominant).
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Gingival and Periodontal Diseases 595 Characteristic of Aggressive Periodontitis • Primary features—aggressive Periodontitis was characterized by following major common features • Medical history—non-contributory medical history. • Rapid loss—rapid attachment loss and bone destruction. • Familial aggregation—familial aggregation of cases. • Secondary features—these are considered to be generals but not universally present are: • Microbial deposit—amount of microbial deposit inconsistent with the severity of periodontal tissue destruction. • Levels of actinobacillus—elevated levels of Actinobacillus Actinomycetem comitans and in some Far East populations, porphyromonas gingivalis. • Phagocytic abnormalities—phagocytic abnormalities are common in this type of periodontitis. • Hyper-responsive macrophage—hyper-responsive macrophage phenotype, including elevated production of PGE2 and IL-1 beta in response to bacterial endotoxins. • Self-arresting attachment loss—progression of attachment loss and bone loss may be self-arresting.
Classification Aggressive Periodontitis was sub-classified at the international workshop into localized and generalized forms. The following were the observed feature: • Localized aggressive periodontitis (LAP): • Circumpubertal onset. • Localized first molar/incisor presentation with interproximal attachment loss on at least two permanent teeth, one of which is first molar and involving no more than two teeth other than first molars and incisors. • Robust serum antibody response to infecting agents. • Generalized aggressive periodontitis (GAP) (Fig. 24-47): • Usually affecting persons under 30 years of age, but patients may be older. • Generalized interproximal attachment loss affecting at least three permanent teeth other than first molar and incisors. • Pronounced episodic nature of the destruction of attachment and alveolar bone. • Poor serum antibody response to infecting agents. It is important to underline that, in the present state of uncertainty regarding both the causative agents and the genetic and environmental susceptibility to Aggressive periodontitis; it is possible that LAP and GAP may simply represent phenotypic variations, of a single disease entity. Conversely, it is possible that different Aggressive periodontitis forms may manifest themselves with a
Fig. 24-47: Generalized type of aggressive periodontitis.
common clinical presentation. This aspect is of great diagnostic and therapeutic importance.
Clinical Features • Age—the age of onset of the disease ranges from the middle to late teens and till 30 years of age • Site—the lesions are more generalized and all or most of the teeth are affected, without any definite pattern of distribution. • Signs—gingiva is acutely inflamed, often proliferated, ulcerated and fiery red (Figs 24-48A and B). Bleeding may occur spontaneously, or on slight provocation. In some cases, gingiva appears pink and free of inflammation; but in spite of this, deep pockets can be revealed on probing. • Systemic features—some patients may have systemic manifestations like weight loss, mental depression and general malaise.
Diagnosis • Clinical diagnosis—rapid loss of periodontal structure with systemic features may suspect this disease.
Management • Antibiotics—if microflora contains gram-positive microorganisms, then it should be treated with 250 mg amoxicillin and 125 mg potassium clavulunate three times daily, for 14 days, along with scaling and root planning. If flora is gram-negative, then clindamycin should be given with dose of 150 mg, four times a day, for 7 days, along with scaling and root planning.
Prepubertal Periodontitis It is a very rare condition which starts during, or immediately after the eruption of primary teeth. There are functional defects of neutrophils and monocytes. It is transmitted as an autosomal recessive trait. It is associated with Papillion-Lefevre syndrome.
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A Fig. 24-49: Prepubertal periodontitis showing involvement of primary teeth.
(Fig. 24-50). There is a presence of deep interdental osseous crater but deep conventional pockets are not found, because the ulcerative and necrotizing character of the gingival lesion destroys the junctional epithelium the removing the mechanism of pocket deepening. Ulceration is frequent finding in this type of periodontitis. As the patients have underlying predisposing factors, it should be treated in consultation with a physician. Medical evaluation and local, topical and systemic antimicrobial should be given, based on the result of laboratory tests. B Figs 24-48A and B: Aggressive periodontitis showing gingival recession and inflammation with loss of attachment.
• Generalized form—in the generalized form, inflammation is extremely acute and destruction of gingiva and alveolar bone is very rapid. Leukocytosis, otitis media, skin and upper respiratory infection may also be present. The disease involves all the primary teeth (Fig. 24-49) and may or may not involve the permanent dentition. It is refractory to antibiotic therapy. • Localized form—in it, only few teeth are affected. Gingiva may appear normal. The progress of disease is slow. Otitis media is an infrequent finding. The disease responds to scaling and antibiotic therapy. Fig. 24-50: Ulcerative periodontitis present in lower anterior region.
Necrotizing Ulcerative Periodontitis It occurs after repeated, long-term episodes of necrotizing ulcerative gingivitis. It can be associated with AIDS. Inflammatory infiltrate in the lesions of ANUG can extend to the underlying bone, resulting in a deep crater like osseous lesion most often located in the interdental area
Tooth Mobility Tooth has a slight degree of physiologic mobility, which varies from different teeth and at different times of the day. Mobility beyond the physiologic range is termed as abnormal or pathologic mobility.
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Gingival and Periodontal Diseases 597 Causes • Trauma from occlusion—it usually results in mobility of the teeth. It occurs initially as result of resorption of the cortical layer of bone leading to a reduced fiber support and later, to adaptation phenomenon, resulting in a widened periodontal space. • Loss of tooth support—it can result in mobility. The amount of mobility depends upon the severity and distribution of bone loss. • Inflammation—extension of inflammation from the gingiva or periapical region, into the periodontal ligament, may increase tooth mobility. • Periodontal surgery—it temporarily increases tooth mobility for a short period. • Systemic disease—some systemic diseases can cause increased tooth mobility, like in pregnancy due to physicochemical changes in the periodontal tissues. • The destruction of surrounding alveolar bone, such as in osteomyelitis or jaw tumor, may also increase tooth mobility.
• Extensive prepubertal destruction of the periodontal bone supporting the dentition (Fig. 24-52B), usually extensive generalized horizontal bone loss. • Calcification of dura.
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Radiographic Features • PDL space widening—there is a widening of periodontal ligament space and a single root may develop an hourglass shape. In multi-rooted teeth widening of periodontal ligament space at apices and in region of furcation is seen. • Angular bone loss—bone loss which surrounds the tooth is also present (Fig. 24-51).
B Figs 24-52A and B: Papillion-Lefevre syndrome showing hyperkeratosis of palms with severe destruction of periodontium.
Clinical and Radiological Features
Fig. 24-51: Angular bone loss present in mobility.
Papillion-Lefevre Syndrome It is an autosomal recessive and inherited disorder. It is a triad of: • Hyperkeratosis of palms of the hand and soles of feet (Fig. 24-52A).
• Hyperkeratosis—there is reddened, scaly, rough palms and soles. • Periodontal finding—It usually begins after eruption of the primary second molars. There is inflamed gingiva and horizontal bone destruction. Loss of entire primary dentition by the age of 5 years and loss of secondary dentition by the age of 20 years. Gingival swelling and severe halitosis. • Radiological features—calcification of dura is seen in radiograph. Periodontal bone destruction is also present.
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Diagnosis
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• Clinical diagnosis—clinical diagnosis is suspected when hyperkeratosis of palm is seen in association with periodontal destruction. • Radiological diagnosis—calcification in dura can be detected radiologically. • Laboratory diagnosis—there is marked chronic inflammation of the lateral walls of the pocket, with predominantly plasma cell infiltrate, considerable osteoclastic activity and apparent lack of osteoblastic activity.
Management • Periodontal management—flap surgery, oral prophylaxis should be done.
Radiological Assessment of Periodontal Diseases Bone loss can be defined as a difference between the present septal bone height and the assumed normal bone height for any particular patient, bearing in mind that the normal bone height varies with age. The main radiographic projections used for periodontal diseases are bitewing, paralleling line angle periapical technique, digital radiography and dental panoramic tomography.
• Less accuracy of bone destruction—radiographic image will tend to show less severe destruction than in the actual in the case. • Soft to hard tissue relationship—soft to hard tissue relationship are not demonstrated on the radiographs. • Technique variation—technique variation and X-ray beam position can considerably affect the appearance of the periodontal tissues. • Burn out—overexposure can cause burn out.
Radiographic Features of Healthy Periodontium • Posterior region—thin, smooth, evenly corticated margins of the interdental crestal bone in the posterior regions. It is just below the Cementoenamel junction. The interdental crestal bone is continuous with the lamina dura of the adjacent teeth. The junction of two forms a sharp angle (Fig. 24-53). • Anterior region—thin, even, pointed margins to the interdental crestal bone in the anterior region. Cortication at the top of the crest is not always evident, mainly due to a small amount of bone between the anterior teeth. Thin and even width of the mesial and distal periodontal ligament space.
Advantages of Radiography in Periodontal Diseases • Identification of causative factors—often valuable in identifying local initiating factors like calculus, poorly contoured or over extended restorations. • Status of periodontium—to know the status of the periodontium such as root length and morphology, crown–root ratio, condition of the alveolar bone around the root and position of the maxillary sinus in relation to periodontal deformities. • Amount of bone present—it offers the clinician to overview of the amount of bone present and serves as a permanent record of the condition of bone throughout the course of the disease. • Treatment outcome—to evaluate treatment measures, particularly following guided tissue regeneration.
Fig. 24-53: Radiograph of normal periodontium.
Radiological Types of Periodontitis
Limitations of Radiography • Overlapping—inability of the viewer to perceive bony defects that are overlapped by existing bony walls. • Mild lesion—earliest mild destructive lesions in the bone do not cause sufficient alteration in the density to be detectable. • Root superimposition—density of the root superimposed with the image of the defect, tends to obscure bone height. Bone loss in furcation areas may be obscured by an overlying root or bony shadow.
Early Periodontitis There are areas of localized erosion of the alveolar bone crest. In the anterior region, there will be blunting of the alveolar bone. In some cases, it presents chisel edge, due to greater destruction of bone at the sides than at the summit. In posterior areas there is loss of the sharp angle between the lamina dura and alveolar crest and it appears rounded off, with irregular and diffuse borders.
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Gingival and Periodontal Diseases 599 Moderate Periodontitis There are two types: Horizontal bone loss • In horizontal bone loss, both, buccal and lingual bone plates and intervening inter-dental bone resorbed (Fig. 24-54). It does not indicate the current activity of disease.
moderate bone loss, but condition may be stable and without continuing bone loss and this may be indicated by a relatively dense apex.
• Appearance—radiographic appearance of loss in height of the interdental alveolar bone with the crest still horizontal and perpendicular to the long axis of the adjacent tooth. • Types—it may be localized (Fig. 24-55) or generalized, depending on the areas involved. It may be mild, severe and moderate depending on the amount of bone loss. • Horizontal bone loss after surgery—some patients, who have undergone periodontal surgery, may show
Osseous defects It is a type of bony lesion that may be seen in moderate periodontitis, other than horizontal bone loss. It is difficult to locate on radiographs. There are various types of osseous defects. • Inter-proximal crater—it is the most common type of bony deformity. It is a trough like depression that occurs in the crest of inter-proximal septal bone between two adjacent teeth. It consists of two side walls vestibular and lingual cortical plates. The image of the side walls that is projected more coronally will be reduced in density, in relation to the image of apical side wall which is superimposed over the other side wall. If two walls are exactly superimposed, the inter-proximal crater may appear as an irregular linear area of reduced density between the adjacent teeth. Craters that are radiographically detected are about 1 mm or more in depth. The apical margin of the defect will not be sharply demarcated and will be such that relatively radiolucent image of the crater will gradually blend with the normal bone is apical to it. • Proximal intrabony defect—it is a vertical defect within the bone. It extends apically, from the alveolar crest and is surrounded by three walls of bone, i.e. hemisepta and two marginal walls (lingual and vestibular) roots of the affected tooth is the fourth wall. • Hemisepta—it is the bone of the interdental septum that remains on the roots of uninvolved adjacent tooth after destruction of either distal or mesial portion of the interproximal bone septum (Fig. 24-56). It occurs as a result of occlusal trauma which is complicated by inflammation. It is more common on distal surfaces of
Fig. 24-55: Horizontal bone loss present in the anterior region.
Fig. 24-56: Hemisepta present in premolar tooth.
Fig. 24-54: Horizontal bone loss present between premolar and first molar.
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teeth. Loss of attachment is increased in tooth mobility and open contact. It is V shaped and sharply outlined. Crestal lamina often appears at the coronal limit of the side wall. Gutta percha point is used to detect such cases. • Inconsistent bony margins—it is the result of uneven resorption of alveolar cortical plates on the lingual or vestibular surface, with the result in that the crests of bony margins are irregular. It occurs when marginal bone is thin and removed by inflammatory process. It forms quite rapidly and remains constant for long periods. Difficult to identify on radiographs because it is obscured by the image of the root. Irregular margins apparent will relatively be opaque and more or less continuous with the lamina dura of interproximal crest, but apical to it. Radiographically it is not possible to determine the side of the tooth affected. • Bony pocket—osseous defects, sometimes, form in the vestibular or lingual bone over the root and they are called as bony pockets (Fig. 24-57). They are surrounded by roots of involved teeth and cortical bone. They are extensions of proximal bony defect. Only detected when there is high degree of contrast between the thinned bone over the root and the surrounding bone.
the major part of the root is often denuded. Bone resorption extends down the side of multi-rooted teeth, eliminating the marginal cortical bone over the root and it reaches the level of furcation and even beyond it. • Site—the most common area for furcation involvement of maxillary 1st permanent molar is from its mesial side. Early maxillary molar furcation involvement between the mesiobuccal or distobuccal roots and the palatal root, produces a characteristic triangular shaped radiolucency at the edge of the tooth (Figs 24-58A and B). The pocket which is situated on the mesial or distal part of a tooth and occupies a small portion of the interdental septum on the lingual or buccal aspect only, may cross the adjacent root and involve the corresponding mesial or distal aspect of the bifurcation, producing only very slight bone changes. • Appearance—mesial and distal furcation involvement is not apparent on radiographs because of presence of one or both cortical plates. If there is sufficient bone loss between lingual and buccal aspect of furcation in
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Fig. 24-57: Bony pocket seen in relation with the mandibular first molar.
Advanced Periodontitis It is defined as the bone loss which is so extensive that the remaining teeth show excessive mobility, drifting and are in jeopardy of being lost due to inadequate support
Osseous Deformities in Furcation of MultiRooted Teeth • Furcation involvement—progressive periodontal disease and its associated bone loss, may invade the bifurcation of multi-rooted teeth. It is found that the level of alveolar crest falls to occupy a position near the apices, so that
B Figs 24-58A and B: Severe bone loss seen in furcation area of molar teeth.
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Gingival and Periodontal Diseases 601 mandibular molar, radiolucent image will be sharply outlined. If it involves only one plate, then the image will be irregular in outline.
Alveolar Dehiscence It results when the marginal bone chips apically and exposes the length of the root surface. The defect is wide and irregular and extends as far as the apex of affected teeth (Fig. 24-59). It occurs on either lingual or vestibular side of the tooth. On radiographs, it will appear as a faint radiopaque line representing its apical extension.
Fig. 24-59: Alveolar dehiscence showing faint line extending at the apex of tooth.
Suggested Reading 1. Armitage GC. Development of classification system for periodontal disease and conditions. Annals Periodontol 1999; 4:1.
2. Bjorn AL, Bjorn H, Girkovic B. Marginal fit of restorations and its relation to periodontal bone levels. I. Metal restorations. Odontology Revy 1969;20:311-21. 3. Cianciola LJ, Park BH, Bruck E, Moscovich L, Genco RJ. Prevalence of periodontal disease in insulin dependant diabetes mellitus (juvenile diabetes). J Am Dent Assoc 1982;104:653-60. 4. Hugoson A. Gingivitis in pregnant women. A longitudinal clinical study. Odontologisk Revy 1971;22:65-84. 5. Lee RE, Lee NZ. The peripheral vascular system and its reactions in scurvy. An experimental study. Am J Physiol 1947;149:465. 6. Loh HS. A local study of enamel pearls. Singapore Dent J 1980; 5:55-9. 7. Mariotti A. Dental plaque induced gingival diseases. Ann Periodontol 1999; 4:7-19. 8. Mariotti A. Sex steroid hormones and cell dynamics in the periodontium. Crit Rev Oral Bio Med 1994;5:27-53. 9. Meister F. Jr, Lommel TJ, Gerstein H. Diagnosis and possible causes of vertical root fractures. Oral Surg, Oral Med, Oral Pathol, 1980;49:243-53. 10. Miranda I, Brunet L, et al. Prevalence and risk of gingival enlargement in patient treated with nifedipine. J Periodontal 2001;72: 605-11. 11. Oliver RC, Brown LJ. Periodontal disease and tooth loss. Periodontal 2000 1993;2:117. 12. Papapanou PN, Lindhe J. Epidemiology of periodontal diseases. In: Lindhe J, Karring T, Lang NP, 4th edn, Blackwell Munksgaard 2003;50-80. 13. Pernu HE, Pajara UH, Lanning M. The importance of regular dental treatment in patients with cyclic neutropenia. Folow-up of two cases. J Periodontol 1996;67:454-9. 14. Scherp HW. Current concepts in periodontal research: Epidemiological contributions. J Am Dent Assoc 1964;68:667-5. 15. Silverstein LH, Koch JP, Shatz PC: Nifedipine-induced gingival hyperplasia. Am Fam Physician 1996;53(4):1069-70. 16. Steinberg SC, Steinberg AD. Phenytoin-induced gingival over-growth control in severely retarded children. J Periodontol 1982; 53:429-33. 17. Wahlstrom E, Zamora JU, Teichman S: Improvement in cyclosporine-associated gingival hyperplasia with azithromycin therapy. N Engl J Med 1995 Mar 16; 332(11):753-4. 18. Wolbach SB, Bessey OA. Tissue changes in vitamin deficiencies. Physiol Rev 1942;22:233.
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TMJ Disorders
Introduction TMJ is a unique joint in which translatory as well as rotational movements are possible and where both the ends of bone articulate, in the same plane, with that of other bone. It is also called as ginglymodiarthrodial type of joint, meaning that it has a relatively sliding type of movement between bony surfaces, in addition to hinge movement, common to diarthrodial joint.
Anatomy of TMJ The TMJ is located between the mandibular fossa (glenoid fossa), the inferior surface of temporal bone and condylar process of the mandible. It is a synovial type of joint and it is distinguished from most of the joints by following points. • Fibrocartilage—articulating surface of the bones is covered by avascular, fibrous connective tissue, which may contain variable number of cartilage cells. Thus called as fibrocartilage. • Point of closure—the two articulating surface complex of bone carry teeth, whose shape and position influence the movement of joint. It is the only joint with rigid end point of closure. • Articulation—it has bilateral articulation with cranium, so both the joints must function together. TMJ is a complex joint as it has an articular disc interposed between the condyle and the temporal bone (Figs 25-1A and B).
Joint Proper Glenoid Fossa The mandibular condyle articulates at the base of the cranium with the squamous portion of the temporal bone. This is called as the glenoid fossa.
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B Figs 25-1A and B: Normal positioning of disc in temporomandibular joint—front and lateral view.
• Surface—this is a continuous surface consisting of three regions: • The posterior slope to the height of convexity of the articular eminence just anterior to the glenoid fossa. • The flattened preglenoid plane continuing anteriorly from the height of eminence. • Entaglenoid process is continuous with the narrow glenoid plane.
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TMJ Disorders • Squamous tympanic fissure—posterior to the glenoid fossa, there is a squamous tympanic fissure, which extends mediolaterally. • Post-glenoid process—the posterior part of the fossa is elevated to form a ridge called the posterior articular ridge. This ridge increases in height laterally to form the thickened cone shaped prominence called the postglenoid process, immediately anterior to the external acoustic meatus. • Entaglenoid process—the lateral border of the fossa is usually raised to form a narrow crest joining the articular tubercle in front, with the post-glenoid process behind. Medially, the articular fossa narrows and is bounded by a bony wall, the entaglenoid process. • Roof—the roof of the glenoid fossa is always thin and even translucent in many skulls. There is clear evidence that the articular fossa is not a stress bearing functional part of TMJ articulation. • Articular eminence—the articular eminence is strongly convex in an anteroposterior direction and somewhat concave in a transverse direction. The degree of convexity varies, with the radius of the curvature varying from 5 to 15 mm.
Mandibular Condyle • Dimension and shape—the condyle is about 15 to 20 mm long and 8-10 mm thick. Its long axis lies at right angle with the plane of the ramus. The condyle is usually quite convex anteroposteriorly and only slightly convex mediolaterally. The mediolateral convexity is often irregular, with medial and lateral slopes divided by a more or less prominent anteroposterior ridge. • Poles—the articular surface of the mandible is seated on its ovoid condylar process. From the anterior view, it has medial and lateral projections called poles. • Lateral pole—the lateral pole of condyle is roughened and often bluntly pointed. • Medial pole—the medial pole is usually rounded and is more prominent than the lateral pole. • Lateral view—in lateral view, the condyle appears tilted forward at the mandibular neck, with its articular surface on its anterosuperior aspect. The articular surface thus faces the posterior slope of the articular eminence, when the jaw is held with teeth in complete occlusion. • Articular surface—the articular surface continues medially down and around the rounded medial pole of the condyle. Medial articular surface faces the entaglenoid process of the temporal bone, when the jaw is held in an occluded position.
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Articular Disc It is composed of dense fibrous connective tissue devoid of any blood vessels or nerve fibers. • Intermediate zone—in the sagittal plane, it can be divided into three regions according to thickness. The central area is the thinnest and is called as intermediate zone. Both anterior and posterior to the intermediate zone, the disc becomes considerably thicker. The posterior border is generally slightly thicker than the anterior border. • Anterior view—from the anterior view, the disc is generally thicker medially than laterally. The precise shape of the disc is determined by the morphology of the condyle and mandibular fossa. During movement, the disc is somewhat flexible and can adapt to the functional demands of the articular surface. • Retrodiscal tissue and lamina—the articular disc is attached posteriorly to an area of loose connective tissue that is highly vascularized and innervated it is called as retrodiscal tissue. Superiorly, it is bordered by the lamina of connective tissue, which contains many elastic fibers, the superior retrodiscal lamina. This gives necessary freedom for anterior movement of the disc. Since this region consists of two areas, it is called as bilaminar zone. • Attachment—the articular disc is attached to the capsular ligament anteriorly, posteriorly as well as medially and laterally. This divides the joint into two distinct cavities; the upper or superior cavity which is bordered by the mandibular fossa and superior surface of the disc and the lower or inferior cavity, which is bordered by the mandibular condyle and inferior surface of the disc. • Synovial fluid—the internal surface of the cavity is surrounded by specialized endothelial cells that form the synovial lining. This lining along with a specialized synovial lining located at the anterior border of the retrodiscal tissue produce the synovial fluid, which fills both the joint cavities. Thus, TMJ is referred to as a synovial joint.
Ligamentous Structures Functional Ligament • Collateral ligaments (Fig. 25-2)—the collateral ligaments attach the medial and lateral borders of the articular disc to the poles of the condyle. It is commonly called as discal ligament and are two in number. The medial one attaches the medial edge of the disc to the medial pole of the condyle and the lateral one, attaches to the lateral edge of the disc to the lateral pole of the condyle. These ligaments are responsible for dividing the joint mediolaterally into the superior and inferior joint cavities. Their function is to restrict the movement of the
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disc away from the condyle, as it glides anteriorly and posteriorly. The reason for it is that they contain collagenous connective tissue fibers which cannot be stretched. They have a vascular supply and are innervated. The innervations provide information regarding the joint position and movement.
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• Temporomandibular ligament (Fig. 25-4)—it is also called as lateral ligament as it is located laterally to the joint. It is composed of two parts, an outer oblique portion and an inner horizontal portion. The outer portion extends from the outer surface of the articular tubercle and zygomatic process, posteroinferiorly to the outer surface of the condylar neck. The inner horizontal portion extends from the outer surface of the articular tubercle and zygomatic process posteriorly and horizontally to the lateral pole of the condyle and posterior part of the articular disc. The oblique portion of the ligament resists excessive dropping of the condyle and therefore acts to limit the extent of mouth opening.
Fig. 25-2: Collateral ligament—A diagrammatic representation.
• Capsular ligament (Fig. 25-3)—the entire TMJ is surrounded and encompassed by the capsular ligament. The fibers of the capsular ligament are attached superiorly to the temporal bone, along the border of the articular surface of the mandibular fossa and articular eminence. Inferiorly, the fibers are attached to the neck of the condyle. It acts to resist any medial, lateral or inferior forces that tend to separate or dislocate the articular surface. Another function is to encompass the joint, thus retaining the synovial fluid. It is well innervated and provides proprioceptive feedback regarding the position and the movement of joint.
Fig. 25-3: Capsular ligament—A diagrammatic representation.
Fig. 25-4: Temporomandibular ligament— A diagrammatic representation.
Accessory Ligaments • Sphenomandibular ligament—it is attached to the spine of the sphenoid bone and extends downwards and laterally to the small bony prominence on the medial surface of the ramus of the mandible, called the lingula. It does not have any significant effect on mandibular movement. • Stylomandibular ligament—it arises from the styloid process and extends downward and forward to the angle and posterior border of the ramus of the mandible. It becomes taut when mandible is protruded but is most relaxed when the mandible is opened. Its function is to limit the excessive protrusive movements of mandible. • Mandibular malleolar ligament—actually, the mandibular malleolar ligament consists of fibroelastic tissue with some ligamentous qualities. It originates from the neck and anterior process of malleus and is inserted on the medioposterior and superior part of the capsule, interarticular disc and sphenomandibular ligament.
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TMJ Disorders Synovial Fluid • Volume—the passive volume of upper and lower joint cavity is 1.2 and 0.8 ml respectively. A small amount of a clear, straw colored viscous fluid is found in the articular spaces, which is known as synovial fluid. • Source—it is secreted by synovial membrane lining the articular disc, the capsule and also by retrodiscal tissue lining. • Properties—synovial fluid is characterized by well defined physical properties of viscosity, elasticity and plasticity. It contains small population of varying cell type such as monocytes, lymphocytes, free synovial cells and occasionally polymorphonuclear leukocytes. The chemical composition of synovial fluid indicates that it is dialysate of plasma, with some added protein and mucin. • Gelation—when the TMJ movements are reduced or restricted due to some reasons, the synovial fluid becomes viscid; its lubricating qualities are seriously impaired, a condition clinically referred to as gelation. • Functions of synovial fluid • Lubricant—it is a lubricant and reduces the mechanical friction between the condyle and the articular disc and the mandibular fossa and articular disc. • Nutritional fluid—it is also a nutritional fluid for the vascular tissues covering the condyle and the articular tubercle and also for the disc. It is elaborated by diffusion from the rich capillary network of the synovial membrane, augmented by mucin secreted by the synovial cells. • Liquid environment—it provides liquid environment for the joint surface. • Cleaning of joint—synovial fluid is also considered to be responsible for the removal of entraneous material shed into the joint cavity. The intimate cells have been demonstrated to possess marked phagocytic properties.
Joint Innervations • Vascular supply—it comes from the branches of the superficial temporal arteries, deep auricular arteries, anterior tympanic arteries and ascending pharyngeal arteries. • Nerve supply—it is innervated by the branches of auriculotemporal nerve, masseteric nerve and the posterior deep temporal nerve, which are branches of the mandibular portion of the trigeminal nerve.
Functional Movement of TMJ • Elevation (jaw closing)—the mandibular elevators include the coordinated functions of masseter, temporal and
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medial pterygoid muscle of both the sides. Temporalis maintains the physiological rest position of the mandible. The posterior fibers of temporalis retract the head of mandible while closing the mouth. Depression—the depression of mandible includes the activity of the lateral pterygoid and the suprahyoid muscles. The inferior head of the lateral pterygoid is the main muscle used for depressing the mandible. The superior head of the lateral pterygoid pulls the articular disc forward, creating the glenoid joint activity. The suprahyoid group of muscles also acts in mandibular movement; by initiating and assisting opening of the jaw. The lateral pterygoid muscle has a major role, particularly when the mouth is opened wide or against resistance by the digastric, geniohyoid and mylohyoid muscle. The infrahyoid group of muscles participates in the activity by fixing the hyoid group to exert a downward pull on the mandible. Protrusion—it is performed by the medial and lateral pterygoid muscle of both the sides. Retrusion—it is performed by the posterior fibers of temporalis and digastric muscle. Lateral excursive movements—in this type of movement, the medial pterygoid and lateral pterygoid of each side, act alternately. If the mandible is moved to the right side the medial pterygoid of right side and the lateral pterygoid of left side act simultaneously.
Diagnostic Studies Radiography It is the most important diagnostic aid in distinguishing among the disorders that may affect the temporomandibular joint. Routine radiographic examination includes conventional radiography like Transcranial, Transorbital and Transpharyngeal view, etc. But main limitation is that it only shows osseous component and hence, the disease is diagnosed much later. • Computed tomography—tomograms are superior to conventional radiography because of their ability to depict a greater portion of the joint. By providing the series of radiograph, tomography can reproduce small changes in the central portion of the TMJ and therefore decreases the false-negative interpretation (Fig. 25-5). • Arthrography—with increasing interest in soft tissue derangement of the TMJ arthrography has assumed an important role in the diagnosis of joint disorders. Defect in the position or structure of the joint disc and its attachment can be determined using arthrography. Arthrography is performed by injecting the contrast media into the joint space and then after radiograph is taken.
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Textbook of Oral Medicine Table 25-2: Second classification
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Fig. 25-5: 3D CT of temporomandibular joint showing condyle and glenoid fossa.
• Electromyography—it provides an objective means of providing monitoring the changes in the muscle activity and therefore can be a valuable aid in diagnosing MPDS and in evaluating the effectiveness of the treatment. • Arthroscopy—steroid induced arthrography, chronic inflammatory changes in the synovium, acute inflammatory disease and gross damage to the condyle and disc could be visualized and diagnosed using arthroscopy in their study. Table 25-1: Weldon Bell classification Masticatory muscle disorders • Protective muscle splitting • Masticatory muscle spasm—MPD • Masticatory muscle inflammation—myositis Derangement of TMJ • Incoordination • Anterior disc displacement with reduction (clicking) • Anterior disc displacement without reduction (mechanical restriction, closed lock) Extrinsic trauma • Traumatic arthritis • Dislocation fracture • Internal disc derangement • Myositis • Myospasm • Tendonitis Degenerative joint disease • Non-inflammatory phase—arthrosis • Inflammatory phase—osteoarthritis Inflammatory joint disorders • Rheumatoid arthritis • Infective arthritis • Metabolic arthritis Chronic mandibular hypomobility • Ankylosis—fibrous and osseous • Fibrosis of articular capsule • Contracture of elevator muscles • Myostatic contracture • Myofibrotic contracture • Internal disc derangement—closed lock Growth disorders of the joint • Developmental disorders • Acquired disorders • Neoplastic disorders
Intracapsular Degenerative joint diseases • Osteoarthritis Inflammatory • Rheumatoid arthritis (and other collagen disorders) • Psoriatic arthritis Infection • Gonorrhea • Spread from contiguous sites • Tuberculosis • Syphilis Developmental • Condylar hyperplasia • Condylar hypoplasia • Agenesis Traumatic • Condylar fracture • Ankylosis • Dislocation • Disc displacement Metabolic • Gout Neoplasia • Benign • Malignant Drug induced • Steroid Extracapsular • Psycho-physiologic (MPD) • Iatrogenic • Traumatic • Those referred from local dental origin • Infection • Otologic • Neoplastic
Classification of TMJ Disorders It is described in Tables 25-1 and 25-2.
Developmental Disorders of the TMJ Hypoplasia of Condyle It is the underdevelopment of mandibular condyle which can be congenital or acquired.
Causes • Prenatal growth disturbances • Hereditary—hereditary anomalies like chromosomal anomalies, achondroplasia, mandibulofacial dysostosis, progeria, Larsen’s syndrome and Goldenhar syndrome can lead to hypoplasia of condyle. • Non-hereditary—non-hereditary disease like Pierre Robin syndrome, radiation to fetus, Mobius syndrome are also causative factors. • Postnatal growth disturbances • Endocrine—hypothyroidism and hypopituitarism causes decrease in secretion of growth hormone resulting in hypoplasia of condyle.
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TMJ Disorders • Trauma—it is the most common cause of hypoplasia. Trauma may occur in infancy or childhood. • Nutritional factors—deficiency of vitamin A and some other nutritional deficiency in the early infancy and childhood can lead to hypoplasia of condyle. • Infection—rheumatoid arthritis can cause inhibition of growth of a component of the joint. • Irradiation—radiation upon the face during the period of growth and extent of the change in the size of the condyle depends to some extent on the amount of radiation that is applied and the age at that time.
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Radiological Features • Condyle—condylar process is short and it tends to assume a more posterior position in the glenoid fossa (Fig. 25-6). The neck of the condyle is slender.
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Clinical Features Unilateral • In this, only one side is involved. Following features can be present in unilateral hypoplasia. • Appearance of face—on the unaffected side, there is elongation of the body of mandible and flat appearance of the face. Body of mandible is short on affected side. • Shifting on affected side—mandible shift towards the affected side on opening. • Malocclusion—malocclusion is present. There may be cross bite on the affected side. • Eruption of teeth—eruption of teeth may be delayed in case of hypoplasia of the condyle. In some cases, it will cause impacted and unerupted teeth. • Ear—there may be deficiency of some parts of the adjacent auditory apparatus. The external ear may be small, deformed, partially or completely absent. Bilateral • In this, both the condyle are affected. Following features are present in this type. • Mandible—when there is bilateral arrest of condylar growth, there is usually symmetrical lack of growth of the mandible. • Micrognathia—due to lack of mandibular growth, micrognathia with the chin retruded to the level of hyoid bone occurs. • Eruption—there is delayed eruption of teeth on the both side. • Class II malocclusion—patient is having Class II malocclusion. It occurs as the mandibular ramus does not increase in height sufficiently to open the space between the upper and lower jaws into which the teeth erupt with concomitant growth of alveolar process. Another reason for this is that posterior growth of the ramus is affected, so the length of the body of the mandible is diminished and the last molars are left within the ramus.
Fig. 25-6: Hypoplasia of condyle occurs on left side (Courtesy Dr Ashok L).
• Ramus and body of mandible—there may be proportionate shortening of the ramus and body on the affected side and the bone tends to be smaller than the opposite side. A shallow sigmoid and antegonial notch is also present. • Coronoid process—coronoid process is relatively large, heavier and posteriorly directed. • Teeth—teeth may be impacted. • Ear—in some cases, there is congenital absence of the auditory canal and middle ear and the tympanic plate is poorly developed, so when the condyle is present, the articular fossa gives an appearance of an increased size. • Bilateral involvement—in cases of bilateral underdevelopment, all the above features plus bilateral antegonial notching is seen.
Diagnosis • Clinical diagnosis—malocclusion, elongation of body of mandible on unaffected side will give clue to the diagnosis. • Radiological diagnosis—size of condyle is easily diagnosed on radiograph.
Management • Surgical—surgical procedures commonly used in unilateral deformities are directed towards contributing bulk and increasing the length by means of bone, cartilage and soft tissue grafts. Most commonly graft is costochondral rib graft. • Orthodontic treatment—it is done to correct malocclusion.
Agenesis of the Condyle It is rare disorder. It is seen in hemifacial macrostomia, Goldenhar syndrome and Hallermann-Streiff syndrome.
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Clinical Features
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• Site—it can occur unilaterally or bilaterally and is a very rare condition. • Symptoms—there are free movement (eccentric movement), anterior open bite, asymmetry of face, altered occlusion. Mastication may be difficult. • Signs—shift of mandible towards the affected side occurs during opening in unilateral type, but it is absent in bilateral type. • Associated anomalies—it is frequently associated with other anomalies like defective and absent external ear, an underdeveloped mandibular ramus or macrostomia.
Radiological Features • Absence of condyle—absence of condyle is easily detected on radiograph.
Diagnosis • Clinical diagnosis—eccentric movement with asymmetry of face. • Radiological features—absence of condyle can be seen radiologically.
Management • Maintenance of dental health—dental intervention can aid by establishment of an acceptable plane of occlusion, maintaining the oral health and offering palliative treatment for discomfort. • Osteoplasty—if the derangements are severe, osteoplasty is advocated.
Hyperplasia of the Condyle It is rare disorder which is characterized by excessive growth of condyles.
Causes • Developmental—it may occur due to trauma during the birth. • Neoplastic—some tumors like chondroma, osteochondroma or osteoma of condyle can lead to hyperplasia of condyle. • Bone disease—fibrous dysplasia, Paget’s disease which affects the bones, may affect the condyle leading to its overgrowth. • Hereditary—this is also suggested the cause for condylar hyperplasia. Condylar hyperplasia can be seen in hereditary syndrome like Klinefelter syndrome. • Endocrine—endocrine disorders like gigantisms as it affects the whole body, it can also affect the condyle causing its overgrowth.
• Hypertrophic arthritis—this is rare condition and it may lead to enlargement of the mandibular condyle. • Local circulatory disturbance—local circulatory disturbance around the condyle may activate bone formation in that area causing its overgrowth.
Clinical Features • Age and sex distribution—it occurs in either sex and there is no predilection for any side. Most common age of occurrence is 15 to 19 years. • Unilateral type—it can affect only one condyle. Following features are present in unilateral type: • Mandibular enlargement—there is progressive enlargement of the mandible on the affected side. • Facial asymmetry—enlargement on the affected side, give rise to facial asymmetry on that side. • Shift in midline—due to facial asymmetry, shifting of the midline of chin to the unaffected side. • Malocclusion—unilateral type will result in cross bite, open bite, and asymmetric protrusion on the affected side. • Bilateral—in this both the condyle are affected. Following features are present in bilateral type: • Anterior cross bite—mandible is larger on both side and is placed more forward than the maxilla. This will result in anterior cross bite (mandibular teeth are anterior to the maxillary teeth). • Signs—obtuse mandibular angle and the sigmoid notch form an arc of a larger circle of mandible. • Relative microdontia—as there is definite disproportion between normal size of crown of teeth and larger size of jaw bones, teeth appear to be smaller as compared to large size of jaw.
Radiological Features • Ramus—the vertical ramus is increased in vertical depth as well as in its anteroposterior diameter. It will result in prevention of occlusion of the posterior teeth. • Body of mandible—body of the affected side of mandible are larger as compared on unaffected side. • Condyle—the condylar enlargement is sometimes symmetrically distributed throughout the whole process. It may retain its normal shape or it may assume a conical, spherical, pear shaped or an uneven and lobulated shape (Figs 25-7 and 25-8). The neck of the condyle may retain its integrity, be enlarged or absorbed into the enlarged head of the condyle. • Articular eminence—the articular eminence is shallower than the opposite normal side, with the distal surface slightly evacuated. • Displacement of condyle—hyperplasia of condyle may result in displacement of condyle from the mandibular fossa.
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Differential Diagnosis • Hemifacial hyperplasia—it is associated with soft tissue and teeth enlargement.
Management • Surgery—unilateral condylectomy should be performed to improve function and esthetics of the patient. • Maxillary osteotomy—some time, there may be occurrence of compensatory maxillary growth. In these cases, maxillary osteotomy should be performed. • Orthodontic therapy—this is done to treat cross bite of the patient.
Double Condyle or Bifid Condyle In this, double headed mandibular condyle is seen. Condyle is divided by an anteroposterior groove.
Cause Fig. 25-7: Large size of condyle seen on the computed tomogram (Courtesy Dr Avinash Kshar and Dr Umarji).
• Trauma—childhood fracture may lead to bifid condyle. • Developmental—persistence of the well vascularized fibrous tissue septa, which is normally present in the condylar cartilage during embryonal and early postnatal life. Possible rupture of some of the blood vessels contained within the septa might impair the ossification of the condyle so as to cause a bifid development of the condylar head. • Abnormal muscle attachment—this will also cause bifid condyle.
Clinical Features
Fig. 25-8: Note large size of condyle on right side (arrow) as compared to on left side (Courtesy Dr Avinash Kshar and Dr Umarji).
• Mandibular angle—the angle of the jaw is right angle in some cases and it may be more obtuse than normal in some cases. • To assess the degree of bone activity—it is done with the help of Scintigraphy using 99mTc.
Diagnosis • Clinical diagnosis—enlargement of mandible with shift in midline will give clue to diagnosis. • Radiological diagnosis—enlargement of condyle can be seen radiologically.
• Age and sex distribution—it is noticed at any age and is more common in females than male with a ratio of 3:2. • Location—it is usually unilateral. But bilateral occurrence can also be seen. • Symptoms—limitation of opening of mouth, a small lateral deviation. In some cases, click of pop is heard while patient open the mouth. • Signs—lateral movement of mandible is limited.
Radiological Features • Bilobed appearance—radiographs will show bilobed appearance of the condyle (Fig. 25-9). • Separate glenoid fossa—there may be two separate glenoid fossa.
Diagnosis • Clinical diagnosis—not so specific. • Radiological diagnosis—bilobed appearance can be seen.
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Textbook of Oral Medicine Radiological Features • Unilateral—In this case irregular nodular growth of the tip of the coronoid process is seen. • Bilateral—there is symmetrical enlargement of coronoid on both sides.
Diagnosis • Clinical diangosis—not so specific. • Radiological diagnosis—coronoid growth can be seen radiologically.
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Management • Coronoidectomy—it is carried out to remove the elongated process of coronoid.
Degenerative Joint Diseases Fig. 25-9: Bilobed appearance seen on radiograph of bifid condyle.
Management • Surgical—as such no treatment is necessary, but if it is causing some problems surgical approach is carried out.
Coronoid Hyperplasia It is rare developmental disorder affecting the coronoid process of mandible.
Causes • Endocrine—as most of the cases are seen in puberty in the males, some sort of endocrine influence is suggested as the cause of coronoid hyperplasia. • Hereditary—some cases are reported in sibling as hereditary factors may also play some role in coronoid hyperplasia. • Tumors—tumors like osteoma and osteochondroma can also cause unilateral enlargement of the coronoid.
Osteoarthritis It is also called as ‘osteoarthrosis’ or ‘degenerative arthritis’. It is primarily a disorder of movable joints characterized by deterioration and abrasion of the articular cartilage with formation of new bone at the joint surface. There is destruction of the soft tissue component of the joint and subsequent erosion with hypertrophic changes in bone. There is breakdown of the connective tissue covering the condyle, articular eminence and the disc. Recently, there are some evidences suggesting that there are some inflammatory components present in osteoarthritis.
Etiopathogenesis (Fig. 25-10) • Overload to joint—the lesion is brought by an increase in the functional demands of the healthy tissue due to repetitive overload on joint. This will result in breakdown of the joint.
Clinical Features • Age and sex distribution—it is seen in 2nd decade of life and most commonly encounter in males in the ratio of 5:1. • Unilateral coronoid hyperplasia—in unilateral type, there is restriction of mandibular movement. It occurs due to enlarged coronoid may impinge on the zygomatic surface causing reduction in the mandibular movement. There is also deviation of mandible on the affected side. • Bilateral coronoid hyperplasia—in this, limitation of movements occur which become more severe as the age progress.
Fig. 25-10: Diagrammatic representation of etiopathogenesis of osteoarthritis of TMJ.
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TMJ Disorders • Deterioration of functional capacity of joint—there may be normal load to the joint but functional capacity is reduced as a part of aging. This occurs due to: • Slower replacement of chondroblasts—as age advances there is slower replacement of chondroblasts and chondrocytes in the joint. • Susceptible fibers—the cartilage matrix turns over less rapidly resulting in available fibers to work for longer period of time. This will make them susceptible to fatigue. • Poor nutrition to joint—as matrix contain less water, the marrow blood flow diminished which results in poor nutrition to the joint. This will make joint desiccated and brittle. • Remodelling theory—by another theory, bone growth does not cease completely after puberty and remodelling of the joint progresses under functional demands. Degenerative joint disease may develop when the remodelling rate of bone exceeds that of the cartilaginous repair. The gross evidence of these changes is the formation of marginal osteophytes with development of new bone in the area adjacent to the cartilage.
Causes of Secondary Osteoarthritis • Developmental—Perthes disease, epiphysiolysis. • Metabolic—alkaptonuria, hemochromatosis. Wilson’s disease and chondrocalcinosis. • Traumatic—intra-articular fracture, menisectomy, hypermobility, long leg arthropathy. • Endocrine—acromegaly, gout. • Others—hemophilia, aseptic necrosis, sickle cell disease, decompression sickness, tabes dorsali etc.
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pain on movements or biting, which may limit mandibular function. Pain usually worse in the evening. Signs—there is deviation of the jaw towards the affected side. Affected joint is swollen and warm to touch. Stiffness of the joint. Crepitations—there is presence of crepitation of the joint, the sound indicates degeneration within the articulating surfaces of the joint or disc. Jaw movement—there is limitation of jaw movements, which becomes increasingly apparent with function. Pain is usually located to the immediate preauricular region. Spasm of muscle—early signs may progress to spasm of the masticatory muscles resulting in stiffness and locking of the jaw. If not treated at this stage, it may lead to irreversible changes in the TMJ. Course—normal course is between 1 to 3 years. Severe symptoms last for about nine months, but gradually burn out leaving little or no disability.
Radiographic Features • Location—degenerative changes located on the lateral and anterolateral wall of the fossa. • Erosion of condyle—first evidence of erosion of condyle on a radiograph occurs on an average, 6 months after the onset of TMJ pain. This will result in enlargement and shallowing of mandibular fossa (Fig. 25-11).
Types • Primary—it is generally described as a condition due to wear and tear and is more common with increasing age. It is commonly seen in patients more than 50 years of age. • Secondary—the joint changes occur in response to recognizable local or systemic factors. It is more commonly seen in young persons.
Clinical Features • Age and sex—it occurs in patients older than 40 years of age and 85% of them are older than 70, with a mean age of 53 years. Females are affected 6 times as frequently as males. • Joints involved—it is common in many joints, but it is not frequently found in TMJ. • Symptoms—there is unilateral pain over the joint, which may be sensitive to palpation. Patient also experience
Fig. 25-11: Erosion of condyle seen in osteoarthritis of TMJ (Courtesy Dr Avinash Kshar).
• Sclerosis—density is increased as a result of sclerosis. Small crescent-like excavation appears at the superior aspect of the condyle just behind the point of articular contact. This is followed by wooly appearance, with spreading of rarefaction in the bone beneath the articular surface.
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Fig. 25-13: Ely’s cyst presented as radiolucent area in the condyle.
Fig. 25-12: Osteophyte formation seen as radiopaque projection on CT scan (Courtesy Dr Avinash Kshar).
• Saucer shaped lesion—fully developed lesions are saucer shaped on PA view. This is also called as the destructive phase. • Flattened articular eminence—eminence is flattened or almost removed and anterior half of the superior convex surface of the condyle is converted into a flat plane. • Eburnation—subchondral sclerosis of the condylar head becomes more dense and more radiopaque, is sometimes referred as eburnation. • Lipping—development of lipping (shell like extension) on the anterior borders. • Osteophyte formation—little shreds of the tissue at the margins of the articular cartilage surface may undergo ossification, so that small bony outgrowths or spurs develop which are called as osteophyte (Fig. 25-12). • Beaking—extensive osteophytic formation is referred as beaking. These usually appear on the anterosuperior aspect of the condyle and lateral aspect of temporal component. In some cases, there is formation of sharp angle, either at the margins or actually on the surface of the articular process. • Joint mice—osteophytes may break off and lie within the joint space, these fragments are called as ‘joint mice’. • Loose body—osteophytes may be separated from its attachment and lie loose in the joint as a type of ‘loose body’. • Ely’s cyst (subchondral cyst) (Figs 25-13 and 25-14)— minute areas of degeneration filled with fibrous tissue are seen just below the bony surface of the condyle. The small radiolucent areas are usually less sharply defined and may have slightly irregular borders. Some are surrounded by an area of increased density, which may
Fig. 25-14: Ely’s cyst seen on CT scan in condylar region (Courtesy Dr Avinash Kshar).
be thin and well defined or relatively wide and not so sharply defined. These areas are regarded as cystic and are given the name ‘Ely’s cyst’. • Joint space—narrowing of the joint space and bony ankylosis may be seen. • Severe cases—in severe cases, glenoid fossa may appear grossly enlarged because of the erosion of the posterior slope of articular eminence. The condyle may be markedly diminished in size and altered in shape due to erosion and destruction of the condylar head.
Diagnosis • Clinical diagnosis—swollen joint in elderly patient with limitation of jaw movement may give clue to the diagnosis. • Radiological diagnosis—Ely’s cyst, osteophytes formation, joint mice, sclerosis, condylar erosion are typical of osteoarthritis • Laboratory diagnosis—biopsy shows cells clumping together and become unevenly distributed throughout the fibrous matrix. It will also show loss of articular surface.
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TMJ Disorders Management • Elimination of the cause—it includes occlusal adjustment or replacement of the missing teeth and ill fitting prosthesis, grinding, treatment of caries and periodontal disease. • Relieving the pressure on joint—occlusal adjustment and occlusal splints may reduce pressure on joint and relieve the symptoms. • Analgesic and anti-inflammatory drugs—for the relief of pain, nonsteroidal anti-inflammatory drugs and analgesics should be given. • Physiotherapy—heat therapy, diathermy and ultrasonic. • Myotherapy—muscle exercises, injection of local anesthetic in TMJ. • Arthroscopic lavage—arthroscopic lavage may give relief in some patients. • Doxycycline—nowadays, low dose doxycycline (collaganase inhibitor, anti matrix metalloproteinase) is giving relief in many patients. • Other therapy—glucosamine, chondroitin sulfate have also shown some success in osteoarthritis of TMJ.
Inflammatory Disorders of the Joint Rheumatoid Arthritis It is a debilitating systemic disease of unknown origin, characterized by progressive involvement of the joint, particularly bilateral involvement of large joints. Bony components of the TMJ are affected secondary to the granulomatous involvement of the synovial membrane that subsequently spreads to the articular surface of the condyle. It is non- suppurative inflammatory destruction of joint.
Etiopathogenesis • Phase one—it result from some systemic infection, which evokes an inflammatory response within the joint. • Phase two—as an autoimmune reaction to the antigen generated by the initial inflammation itself or it may be associated with derangement of the immune response to the exogenous antigen. • Active phase—in the active phase, TMJ may get involved bilaterally. Bony components of the TMJ are affected secondary to the granulomatous involvement of its synovial membrane that subsequently spreads to the articular surface of the condyle. The joint space enlarges with synovial effusion which attacks the fibrocartilage and ultimately produces erosion of the underlying bone. This causes pain, stiffness and limitation of movement. • Chronic phase—chronic phase may follow after active phase. Here, there is proliferation of the synovial membrane due to inflammation this is called as pannus formation. This pannus then encroaches the joint space and causes destruction of the articular cartilage. In this
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lipping of the condyle and marginal proliferation is seen, this result in narrowing of joint space. Here, predominant clinical findings are crepitus, pain on biting and tenderness. The granulomatous tissue replaces the articular surface and small adhesions develop between the articular surface and disc. • Healing phase—the process then enters the healing phase, where the symptoms subside and remodelling of the articular surface occurs. • Psychosomatic—emotional trauma, anxiety and environmental strain can lead to the onset of rheumatoid arthritis. • Immunological—the presence of rheumatoid factor in the serum and synovial fluid of affected patients suggest immunological etiology. Plasma cells and lymphocytes are also present on histological examination.
Clinical Features General • Age and sex distribution—it more commonly occurs in temperate climate and has its highest incidence in women from 20 to 50 years of age. • Sites—in typical cases, small joints of fingers and toes are the first to be affected. Swelling of the proximal but not the distal, interphalangeal joints give the finger as like spindle appearance and swelling of the metatarsophalangeal joints results in broadening of feet. • Symptoms—symptoms include bilateral stiffness, crepitus, tenderness and swelling over the joint. Fever, malaise, fatigue, weight loss, pain and stiffness in the limb are also evident. • Polyarthritis—polyarthritis develops subsequently, large and weight bearing joints are frequently affected. • Subcutaneous or rheumatoid nodules—there is formation of subcutaneous nodules on the pressure points, sites of friction and various vascular lesions, both necrotizing and obliterative types. Severe deformities of extremity can occur as a result of joint collapse, tendon rupture and muscle involvement. • Signs—the joint may become red, swollen and warm to touch. Muscle atrophy around the joint is common. • Hands—in hands, it may produce an ulnar drift. Bursitis can also occur. TMJ involvement • Acute case—in acute cases, there is bilateral stiffness, deep seated pain, tenderness on palpation and swelling over the joint. There is limitation in opening of mouth. • Referred pain—pain on biting is referred to the temporal region, ear and angle of mandible. • Chronic cases—in chronic cases, crepitus is the most frequent finding. Functional disturbances like deviation on opening and inability to perform lateral excursions are common.
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• Anterior open bite—anterior open bite is present due to bilateral destruction and anteroposterior positioning of the condyle. • Ankylosis—fibrous ankylosis of the joint which may be partial or complex occurs in long term. • Complication—subluxation, secondary arthritis, muscular atrophy, and bird-like face can occur.
Radiological Features
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• Joint space—the pannus may destroy the disc and due to this, the joint space may reduce slightly or substantially, depending on the severity of the condition and the length of time. • Condyle—there is flattening of the head of the condyle. Erosion of the condyle can be seen (Fig. 25-15). In condyle, hollowing out appearance of the cartilage is seen. • Articular eminence—bone destruction which occurs in articular eminence may be slight or confined to the posterior surface or to the inferior convexity. Most of the eminence may be destroyed in severe long continued cases.
Fig. 25-16: Sharpened pencil appearance seen in rheumatoid arthritis of TMJ.
• Other features—subchondral sclerosis and flattening of articular surface may occur with subchondral cyst and osteophytic formation. • Radiological staging of rheumatoid arthritis • Stage I—periarticular osteoporosis • Stage II—loss of articular cartilage • Stage III—erosion (Fig. 25-17) • Stage IV—subluxation and ankylosis.
Fig. 25-17: CT scan of erosion of condyle (Courtesy Dr Avinash Kshar) Fig. 25-15: Erosion of condyle seen in rheumatoid arthritis (Courtesy Dr Avinash Kshar).
• Irregular outline of condyle—as the disease continues, the condylar outline becomes increasingly irregular and ragged. In most severe cases, condyle may be completely resorbed, resulting in loss of vertical support and anterior open bite. • Sharpened pencil or mouth piece of flute appearance—in advanced stages, erosion of anterior and posterior condylar surface at the attachment of the synovial lining occurs, which may resemble a ‘sharpened pencil’ or ‘mouth piece of flute’ (Fig. 25-16).
Diagnosis • Clinical diagnosis—subcutaneous nodule, bilateral involvement and pain on biting. Many joints are involved at the same time. • Radiological diagnosis—sharpened pencil appearance, with flattening of articular eminence. • Laboratory diagnosis—biopsy shows proliferation of synovial lining cells with intense infiltration of lymphocytes, plasma cells and polymorphs. Rice bodies are seen histopathologically. Rose Waller test is positive in 70% of the patients with rheumatoid arthritis. There is elevation of RF factor. Antinuclear antibodies are
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TMJ Disorders detected by indirect immunofluorescence. Analysis of synovial fluid is essential for the immediate diagnosis of joint infection, inflammation and degenerative disease.
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Psoriatic Arthritis It is a chronic disease of unknown etiology characterized by skin lesions and sometimes joint involvement.
Etiopathogenesis
Management • Supportive treatment—adequate rest to the joint, soft diet is advocated. • Intra-articular corticosteroid injections—local injection of long acting steroids such as methyl prednisone acetate (20-80 mg for large joint and 4-10 mg for small joint) or triamcinolone hexa-acetomide (10-40 mg for large joint and 2-6 mg for small joint) are given. • Non-steroidal anti-inflammatory drugs—these drugs are inhibitory to prostaglandins. These are used for symptomatic relief. Salicylates (for pain) and antiinflammatory agents like phenyl butazone, indomethacin, ibuprofen, diclofenac and piroxicam can be used. • Immunomodulator—azathioprine is found to be effective in both, high and low doses. • Slow acting anti-rheumatic drugs—these are the antimalarials like hydroxyl chloroquine sulphate, sulphasalazine (500 mg/day) and methotrexate (DPenicillamine and parenteral gold). • Local treatment—it is done with heat, diathermy, jaw exercise or a mouth stretcher. Muscle strengthening exercise and hydrotherapy. • Medical synovectomy—synovial obliteration is achieved with osmic acid or variety of radiocolloids, if pain is present even after injection of steroids. Erbium acetate is used for small joints, while yttrium silicate is used for large joints. • Surgical synovectomy—it accounts for removal of synovial membrane which is responsible for enzymatic destruction of cartilage.
Juvenile Rheumatoid Arthritis It is also called as ‘Still’s disease’ and ‘Juvenile polyarthritis’. It is defined as a chronic synovitis with or without extraarticular manifestations, but it is accompanied by more systemic features than for adults. It occurs in children and has its peak between 1 to 3 years. Initial bilateral polyarthritis of both small and large joints including the cervical spine occurs. There is splenomegaly, lymphadenopathy, leukocytosis, pyrexia and rash. Patient complaint of neck pain, limited range of movement and restricted opening of the mouth. One or both TMJ are involved. It may cause interference with normal condylar growth, leading to micrognathia. This is seen in at least 20% of cases. Persistence leads to deterioration of jaw movement.
• Hereditary—the exact cause is unknown. In some cases, hereditary is the factor, transmitted as a simple dominant trait. • Precipitating factors—in some cases, the precipitating factors include infection by various microorganisms, metabolic disturbances, endocrine dysfunction, neurogenic factors and trauma. • HLA factors—there is evidence that disease is associated with human major histocompatibility (HLA) antigen complex, implying that either the HLA antigen itself or a linked gene is directly involved in the disease process.
Clinical Features General • Location—skin lesions are found on the trunk, arms, face and scalp. • Appearance—skin lesions exhibit broad irregular papules or plaques, which are dull red to brownish in color and are usually covered with a layer of fine silvery scales. • Auspitz’s’ sign—when scraped, they leave behind small bleeding points: this is called as Auspitz’s sign. • Exacerbation—exacerbation occurs after exposure to ultraviolet light. TMJ involvement • Symptoms—preauricular pain, which is usually unilateral. There is difficulty in opening the mouth. • Signs—TMJ is tender. Crepitus, deviation towards the affected side and in small proportion of cases, deformities are seen.
Radiological Features • Articular surface—generalized appearance of irregularity of condylar articular surface. • Osteoporosis—generalized osteoporosis can occur. • Joint spaces—proliferative changes with diminution of joint space.
Diagnosis • Clinical diagnosis—positive Auspitz’s sign with tender TMJ will give clue to the diagnosis. • Radiological diagnosis—generalized irregularity of the bone is present.
Management • Drugs—Systemic drugs like salicylates should be given.
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• Appliance—screw wedge appliance should be made and is given to the patient. • Steroids—for skin lesion local application steroids. • Others—shortwave diathermy, massage exercise, screw wedge appliance.
Infective Arthritis It is also called as ‘septic arthritis’. It may be acute or chronic.
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Etiology • Microorganisms—it is caused by direct spread of organisms like staphylococci, streptococci, pneumococci and gonococci, from an infected mastoid process, tympanic cavity or via blood. • Trauma—it may also be caused by trauma directly to the joint or infection from a maxillary molar and parotid gland. • Osteomyelitis and middle ear infection—it is acute in nature. It can be caused by osteomyelitis and suppurative middle ear infection. • Brucellosis—brucellosis can also cause infective arthritis usually of chronic type but acute infection can occur.
Pathogenesis • Dilatation of blood vessels of synovial membrane—early dilatation of blood vessels of the synovial membrane with serous exudate is accompanied by the usual stages of inflammation. This is followed by suppuration, with formation of pus and ulceration of the synovial membrane. • Erosion of articular disc—the articular disc is eroded and partly destroyed. The cartilage of the head of the condyle and the fossa are similarly affected.
Radiographic Features Acute • Location—erosion usually seen on anterior and superior aspect of the condyle. • Joint space—in early stages, width of joint space may be increased by inflammatory distension in early infective period. This will cause hazy appearance in radiographs. • Articular cortex—articular cortex of the condyle may become slightly radiolucent. Discontinuities and subtle irregularities of anterior cortical surface may be seen (Fig. 25-18). • Osteoporosis—there is considerable osteoporosis of adjacent parts of the condyle and it may extend to whole of the ascending ramus. • Sequestrum—in some cases, there is formation of sequestrum, which if persistent may lead to some added bone destruction. Chronic • Condensing osteitis—in chronic cases, there may be peripheral condensing osteitis and approximation of the joint surface, as the articular cartilage is eroded. • Bone—there may be frank bone destruction. • Condyle—a small cup shaped excavation on the anterior face of the condyle, having a smooth or irregular base is seen. In rare cases, whole of the condyle may be lost with varying amount of eminence.
Clinical Features • Age and sex distribution—it usually occurs in young children with no sex predilection. • Location—it is always unilateral. In some cases of chronic variety bilateral involvement can occur. • Symptoms—there is severe pain on jaw movement, with an inability to place the teeth in occlusion, due to presence of infection in the joint. • Signs—redness and swelling over the joint. In some cases, swelling may be fluctuant and extend beyond the region of the joint. • Lymph nodes—tender cervical lymph nodes on the side of infection. This helps to distinguish septic arthritis from other TMJ disorders. • Chronic cases—it may follow an acute infection, but usually it is chronic. In these cases ankylosis of the joint or facial asymmetry (if the growth centers are involved), may occur.
Fig. 25-18: Infective arthritis showing destruction of condylar surface on right side (Dr Kshar).
Diagnosis • Clinical diagnosis—severe pain in the joint, with sign of inflammation over the joint will give clue to the diagnosis.
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TMJ Disorders • Radiological diagnosis—destructive change in the condyle will give clue to the diagnosis.
Management • Rest to joint—adequate rest to the joint should be given and patient is asked to do limited movements of joint. • Liquid diet—patient should be kept on liquid diet. • Antibiotics and analgesics—appropriate antibiotics and analgesics should be given to patient. • Surgical—if there is suppuration, incision and drainage should be carried out.
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Diagnosis • Clinical diagnosis—joint stiffness associated with forward and stooped posture of the spine joint. • Radiological diagnosis—flattening of joint surface.
Management • Analgesics—NSAID should be given to the patient to relieve pain and inflammation.
Traumatic Disorders of TMJ
Ankylosing Spondylitis
Condylar Fracture
It is also called as ‘Marie-Strumpell disease’ and ‘rheumatoid spondylitis’. It is a chronic inflammatory connective tissue disease that affects the axial skeleton and central joints including the TMJ.
Condyle is displaced medially, inferiorly and anteriorly due to pull from lateral pterygoid muscle. A blow on the point of chin is the usual cause for bilateral fracture of the condyle.
Clinical Features
Classification
• Age and sex distribution—it is more common seen in young adults and is more common in men than in women. • Site—it primarily involve spine joint. This will result in forward and stopped posture. • Signs—joint stiffness results from immobility (during sleep) and is typically relieved by heat and exercise.
Radiographic Features • Flattening—there is flattening of the articular surface of the TMJ (Fig. 25-19). • Osteophytes—osteophytic formation is common. • Erosion—in some cases, erosion of condylar head is seen.
Intracapsular Fracture • Articular surface fracture—fractures involving articular surface. • High condylar fracture—fractures above or through the anatomical neck, which may be termed as high condylar fracture. • Injury to capsule, meniscus and ligament—fractures associated with injury to the capsule, ligament and meniscus. Extracapsular Fracture • High condylar fracture—the fracture runs from the lowest point of the curvature of the sigmoid notch, obliquely downwards and backwards below the surgical neck of the condyle, to the posterior aspect of the upper part of the ramus. • Low or subcondylar fracture—the fracture is influenced in its site and its direction by the insertion of part of masseter muscle and TMJ ligament, the fracture taking the line of least resistance. Such a fracture may be termed as low or subcondylar fracture. • Combined fracture—very nearly the condylar head may be split in the anteroposterior or sagittal plane; the split extending through the neck and producing a combined intra- and extracapsular fracture.
Etiology
Fig. 25-19: Coronal section showing flattening of articular surface (Courtesy Dr Avinash Kshar and Dr Umarji).
• Indirect violence/fight—the ultimate position of the fractured fragment will depend on direction and degree of violence, precise point of application, presence or absence of teeth or denture and the extent of occlusion which exists at the moment of impact.
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• Parade ground fracture—if the blow is sustained centrally on the chin then there is a possibility of bilateral fracture of the condyle. It will protect the vital organs in the middle cranial fossa as the thin neck of the condyle will fracture first. This commonly occurs when a soldier faints on a parade ground and hence named as ‘parade ground fracture.’ • If the teeth are in occlusion—there is no displacement of the condyle. If the teeth are not in occlusion then displacement of the condyle is definite. • Lateral force—if the force of violence is received laterally, then the fracture occurs at opposite condyle.
Clinical Classification • No displacement—crack/fracture is present without tearing of periosteum or of ligament and without significant alteration in the normal relationship of the condylar head to glenoid fossa or neck of the condyle to the ramus. • Deviation—angulations exist between the condylar neck and ramus. • Displacement—overlapping occurs between the condylar processes and the surgical fragment lies lateral to ramus. • Comminuted fracture—may occasionally be encountered. They are usually associated with a fracture of the zygomatic arch and coronoid process, due to severe road accidents and gun shot wounds. • Greenstick fracture—it is seen in cases of children. If the blow is not severe, this type of fracture occurs with medial and anterior angulations, which tend to correct itself spontaneously with the natural growth. • Dislocation—fractured dislocation of the condylar head occurs due to pull of the muscle.
• Rotation of condyle on unaffected side—on the unfractured side, there will be rotation of condyle about a vertical axis. The net result is deviation of the mandible to the injured side. During opening, the external pterygoid of the uninjured side will contract but external pterygoid of the injured side will be ineffective as a result there will be more deviation of the mandible to the injured side.
Clinical Features General • Incidence—condylar fracture accounts for 18% of mandibular jaw fractures. • Location—unilateral fracture of the condyle is more common as compared with bilateral but both occur with or without injury. Fracture is more often associated with dislocation if it is bilateral. • Associated fracture—most of the fractures of condyle are associated with fracture of the opposite side of the mandibular body. • Complication—complication like arthrosis, arthritis, ankylosis and open bite deformity will occur. Unilateral fractures (Fig. 25-20) • Symptoms—pain on the affected side; it is increased when movement is attempted. Patient complains that his teeth do not occlude in the normal fashion. Patient is also not able to bring the jaw forward.
Importance of Muscle Pull • Detachment of disc—the TMJ capsule is strengthened on the lateral aspect by the temporomandibular ligament, whereas medially, it is comparatively weak. Therefore when a fracture with dislocation occurs (particularly if the line of force is parallel to the slope of the articular eminence and condylar head is positioned anterior to the eminence), due to the pull of external pterygoid, detachment of disc may occur. • Dislocation of condyle in upwards direction—in a closed mouth, muscle pull will dislocate the condyle upwards and posteriorly on the fractured site. Due to fracture, the force of external pterygoid muscle will be ineffective whereas masseter and internal pterygoid muscle will exert combined upward lift which results in backward movement of the fractured end of the ramus on the uninjured disc.
Fig. 25-20: Transorbital view of the condylar fracture showing medial displacement.
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TMJ Disorders • Paresthesia of lower lip—paresthesia of lower lip can occur in some cases. It occurs as hemorrhage from the condylar region, tracks across the base of the skull and exerts pressure on the mandibular division of the trigeminal nerves as it emerges from the foramen ovale. • Signs—small localized swelling over the injured TMJ. There is tenderness over the condylar area of the affected TMJ. There is also occasional crepitus and deviation of the mandible to the affected side. • Ear—there is bleeding from the ear on the affected side which results from laceration of the anterior wall of the external auditory meatus, caused by violent movement of condylar head against the skin in this region. • Ecchymosis—hematoma surrounding the fractured condyle may track downwards and backwards below the external auditory canal. It gives rise to ecchymosis below the external auditory meatus. • Limitation of jaw movement—there is painful limitation of lateral excursion towards the normal side. • Gagging—there is gagging of the ipsilateral molar teeth. Bilateral Fractures (Fig. 25-21) • Gagging on molar teeth—all the above signs plus variable degree of gagging of the occlusion on the molar teeth. • Restricted mandibular movement—overall mandibular movements are more restricted, than in unilateral fracture. • Forward displacement of mandible—mandible is displaced forwards in case of bilateral fracture.
Fig. 25-21: Bilateral condylar fracture seen on OPG of the patient.
Fracture Dislocation • Absence of condyle—all the above findings plus a definite absence of condyle in the glenoid fossa (Fig. 25-22). • Unilateral dislocation—if the condylar head is dislocated medially and all edema has subsided due to passage of time, it may be possible to observe a characteristic ‘hollow’ over the region of the condylar head. • Bilateral dislocation—if there is a bilateral dislocation, then there is an anterior open bite present.
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• Central dislocation—it is a rare type of injury which is usually severe and forces the condyle into the cranial cavity through the floor of the articular fossa. It is termed as central dislocation of the TMJ.
3 Fig. 25-22: Fracture dislocation showing absence of condyle in the glenoid fossa (Courtesy Dr Datarkar).
Radiographic Features • View taken—displaced condylar fracture is well demonstrated on AP and lateral projection. Nondisplaced fracture is well seen on AP view (Fig. 25-23). • Increased width of fracture condyle—when fracture occurs, contraction of the lateral pterygoid muscle rotates the transverse axis of the condylar head, so that the medial end moves anteriorly, thus increasing the apparent width of the fractured condyle. • Complete fracture dislocation—in complete fracture dislocation, the condylar head may be inclined medially at an approximate 45° angle to the vertical axis of the ramus. • Anterior displacement of the condyle—if the condylar head has been displaced anteriorly and turned at 90° angle to the vertical axis of the ramus as viewed from the lateral aspect, then only the articular surface of the condylar head will be seen; this will appear as a narrow radiopaque bar situated in the infratemporal fossa. • Condyle split—the condyle may split with little or no displacement of the fragments, or some portion may be separated from head of the bone. Rarely, the whole of the articular portion is crushed and flattened. • CT scan—in difficult cases, CT scan has been demonstrated to show changes in the relationship of the condyle to the mandibular fossa more precisely than the conventional radiographic examination (Fig. 25-24). It is also claimed that it can demonstrate fine bony alterations at the fractured site. • Fracture line—the fracture line is often transverse but usually oblique, starting in the base of the mandibular
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notch and passing slightly or even markedly downwards. In absence of any displacement, it is difficult to visualize such fractures. In the lateral projection, there is often no evidence of any fracture line; but when the posterior margin of the ramus is followed, a sudden step is seen. In some cases there is displacement of the adjacent margins of the fragments, so that the inferior borders of the condylar fragment are superimposed over the adjacent ramus. • Articular surface—the articular surface of the condyle is usually rotated inwards with fracture dislocation.
Management • A simple crack fracture without displacement will not require fixation. Patient should be kept under observation and heavy masticatory forces are to be avoided. • A fracture with slight displacement reduction and immobilization of the mandible for a period of 4 weeks. • Unilateral fractures with dislocation—mandible should be immobilized in normal occlusion for ten days then the fixation is released and movement is encouraged. Patients are kept under observation. • Bilateral fractures with dislocation—arch bar is fitted and reduction is achieved by traction in the incisor area. The mandible is immobilized in normal occlusion for 4 weeks. • Gunning splints—for edentulous patients gunning splints should be used. • Early treatment—to avoid fibrous ankylosis early movement of TMJ are to be achieved. • Other treatment includes relief of acute symptoms, restoration to proper anatomic relation, intermaxillary fixation for restoration of occlusion and early mobilization to minimize scarring.
Ankylosis It is also called as ‘stiff joint’. Ankylosis, a Greek word means fusion of body part. It is an abnormal immobility and consolidation of the joint.
Types
Fig. 25-23: Subcondylar fracture seen on left side—AP view.
• True (intra-articular)—it is any condition that produces fibrous or bony adhesion between the articular surfaces of the TMJ. • False (extra-articular)—it is the one which results from pathologic conditions outside the joint, that result in limited mandibular mobility. • Bony (true)—if bone is present between the articulating surfaces and prevents movements, it is called as bony ankylosis. • Fibrous (false)—if the medium which prevent, the movement is fibrous, it is called as fibrous ankylosis. • Partial—if there is incomplete union between the articulating surfaces, it is called as partial ankylosis. • Complete—if there is complete union between the articulating surfaces, it is called as complete ankylosis.
Etiology
Fig. 25-24: 3D CT scan of patient showing fracture of condyle.
False • Myogenic—the most common problem associated with muscle origin is fibrosis, which may result from chronic infection of the elevator muscles of mastication. Myositis ossificans can also produce limitation of opening.
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• Neurogenic—they include epilepsy, brain tumor, bulbar paralysis and cerebrovascular accidents. • Psychogenic—here, the affected persons exhibit no pain, but patient cannot get the jaws separated also called as hysterical trismus and is apparently produced due to fright. • Bone impingement—the most common is coronoid impingement. Malformation of coronoid such as exostosis or elongation can cause the mandible to impinge on the posterior aspect of the zygoma, when opening is attempted. • Trauma—the formation of fibrous adhesions or cicatrical bands of scar tissues usually occurs after a traumatic accident or burns. • Neoplastic disease like osteochondroma. True • Congenital—abnormal intrauterine development, birth injuries and congenital syphilis. • Trauma—trauma to the chin forcing the condyle against the glenoid fossa, particularly with bleeding in the joint. Malunion of condylar fractures. Injuries are associated with fracture of the malar-zygomatic compound. In the case of injury to the joint, there is hemorrhage within and outside the joint capsule. Injury occurs during the period of active bone formation. There is immobility of the jaw due to pain or any treatment and ankylosis take place. • Inflammatory • Primary inflammation of the joint. • Inflammation of the joint secondary to a local inflammatory process (otitis media, osteomyelitis, etc). • Inflammation of the joint secondary to a bloodstream infection (septicemia, scarlet fever, gonorrhea). • Rheumatoid arthritis is the commonest cause of bilateral ankylosis. Gonococcal arthritis can also cause ankylosis of TMJ. • Inflammation secondary to radiation therapy. • Others—loss of tissue with scarring and metastatic malignancy.
3 Fig. 25-25: Reduced mouth opening seen in patient with ankylosis of temporomandibular joint.
Fig. 25-26: Malocclusion seen in ankylosis patient.
General • Age—it is seen primarily in a young age or between 1 to 10 years. • Symptoms—pain and trismus which is directly related to the duration of ankylosis. Patient also complaint of reduced mouth opening (Fig. 25-25). • Oral problems—depending upon the duration, there may be poor oral hygiene, carious teeth and periodontal problems malocclusion (Fig. 25-26).
• Symptoms—mouth opening is impossible, but the patient may be able to produce several millimeter of interincisal opening. • Appearance—asymmetry of the face with fullness on the affected side (Fig. 25-27) and relative flattening on the unaffected side. • Deviation of face—in unilateral ankylosis, patient’s face is deviated towards the affected side. • Shifting of midline—the chin is retracted on the affected side and slightly bypasses the midline (Fig. 25-28). Slight gliding movement towards the affected side. • Cross bite—cross bite is present due to deviation of mandible and shifting of midline.
Unilateral • Incidence—unilateral ankylosis is more common than bilateral ankylosis.
Bilateral • Bird face appearance—face is symmetrical with micrognathia. There is bird face appearance (Fig. 25-29).
Clinical Features
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Textbook of Oral Medicine • Muscles of mastication—due to long standing ankylosis, atrophy or fibrosis of muscles of mastication may result. • Congenital ankylosis—in case of congenital ankylosis, there is difficulty in introducing the nipple into the mouth of newborn infants. • Signs—class II malocclusion (Fig. 25-30), protrusive incisors and anterior open bite. It is due to the patient’s attempt at forcing food through the anterior teeth for a period of years. Patient also suffer from micrognathia (Fig. 25-31).
3 Fig. 25-27: Fullness of face seen on affected side (left) due to ankylosis of TMJ.
Fig. 25-30: Protrusive incisor seen in bilateral ankylosis.
Fig. 25-28: Shifting of midline on affected side seen in ankylosis patient.
Fig. 25-31: Micrognathia seen in patient with bilateral ankylosis. Fig. 25-29: Bilateral ankylosis showing bird face appearance (Courtesy Dr Lambade).
• Symptoms—no gliding movement. With bilateral ankylosis, neither protrusive nor lateral movements are possible. • An attempt at forced opening—in bony ankylosis, there is no pain but in case of fibrous ankylosis, there is pain.
Radiographic Features Fibrous ankylosis • Appearance—in some cases, there is transverse or oblique dark line, irregular in outline, crossing the mass of dense bone (Fig. 25-32). When a dark line is present, the possibility of fibrous ankylosis is more.
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• Ramus and body of mandible—the ramus is vertical and the angle is reduced in size. The body of the jaw is short • Condyle—the condyle may retain its normal shape, but it can be replaced by shapeless mass of bone, which finds attachment to the base of skull above and to the base of neck of condyle below.
Fig. 25-34: Prominent antegonial notch seen on right side of patient in unilateral ankylosis
Fig. 25-32: Fibrous ankylosis seen in patient showing dark line crossing the bone.
Bony ankylosis • Joint space—joint space is completely or partially obliterated with dense sclerotic bone (Fig. 25-33). Sometimes, large mass of new bone may be seen, radiographically obscuring the condyle and joint space.
• Dark linear shadow—in some cases, there is horizontal, slightly irregular, dark linear shadow in the middle of the new bone, which represents the cartilage and meniscus. • Coronoid process—there may be deepening of the notch which has escaped involvement in the new bone formation and the appearance may be accentuated by the elongation of the coronoid process, which at the same time is narrow and slender. • Computed tomography—this is nowadays valuable aid in determining the extent of ankylosis (Figs 25-35A and B).
A
Fig. 25-33: Complete obliteration of joint spaces. seen in bilateral bony ankylosis.
• Antegonial notch—prominent antegonial notch on the affected side of mandible (Fig. 25-34), along with inferior arching of the mandibular body (secondary to isotonic contraction of the depressor muscles). • Condyle—bone may form around the neck of the condyle and becomes continuous with the base of the skull. Considerable destruction of bone may precede bony ankylosis. The greater part of the condyle may have been destroyed so that the sigmoid or mandibular notch is approximated to the base of the skull. The neck of the condyle, if not completely hidden by the mass of new bone, appears to be shortened; so that the mandibular notch is nearer the zygomatic process than normal. No translation of condyle head during opening.
B Figs 25-35A and B: 3D CT of ankylosis of temporomandibular joint.
Diagnosis • Clinical diagnosis—in bilateral case, bird face appearance or anterior open bite is present. In unilateral cases, deviation of mandible, shifting of midline is present.
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• Radiological diagnosis—absence of joint space with prominent antegonial notch will diagnose this condition. • Laboratory diagnosis—atrophic or destructive changes in the cartilaginous component of the joint with loss of meniscus are a constant finding.
Management
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• Brisement force—forceful opening of the jaws under general anesthesia. • Condylectomy—condyle is excised. • Gap arthroplasty—it is performed in the mandibular neck. Two parallel lines are cut, beginning in depth of the sigmoid notch and carried downwards at an angle of 45 degree at the posterior border of the ascending ramus.
Dislocation It results when condyle is forcefully displaced anteriorly (by failure of muscular co-ordination) out of the articular fossa but remains within the capsule of joint. The direction of condyle is almost always anterior, beyond the articular eminence.
Classification • Anterior—it is more common than other two. • Posterior—it is rare and results from the severe injuries which are sustained at the point of the chin or at the inferior border of the body of the mandible. • Central—same as the posterior dislocation • Medial or lateral—it occurs due to injury to the neck of condyle with its fracture. It is very rare.
Etiology • Extrinsic force—it can occur under G.A. following extraction of teeth or the use of mouth gag, when muscle relaxant is used. • Intrinsic—these are related to attempts of excessive opening of the mouth during eating or yawning and occasionally singing. These types of dislocation are sometimes called as spontaneous dislocations. • Occlusal disharmony—in cases of recurrent dislocation, the etiologic factor is different, like occlusal disharmony producing muscle spasm. • Phenothiazine—occasionally, action of phenothiazine group of drugs produces spontaneous dislocation of the mandible or spasm of the facial musculature. • Other causes like epileptic seizure, yawning, taking too large bite of an apple and rarely, followed sneezing.
Clinical Features Anterior dislocation • Site—anterior dislocation may be unilateral or bilateral. In acute dislocation, there is a history of injury, gagging of molar teeth and anterior open bite. • Symptoms—patient has great difficulty in swallowing and saliva drools over the chin. Pain in the region of temporal fossa and there is a depression where the condylar head is normally situated. • Signs—the mandible is postured forward and movement is extremely limited. The condyle becomes locked anterior to the articular eminence and is prevented from sliding back by muscular spasm. When unilateral dislocation occurs, the teeth will be gagged posteriorly on the side of dislocation and the chin will be deviated towards the normal side. Central dislocation • Cause—the head of the condyle is forced through the floor of the articular fossa, into the floor of middle cranial fossa. In this case, there may be damage to the articular surface of the condyle and fracture of the neck. • Neurological signs—neurological signs like the cerebral contusion, facial nerve paralysis, deafness and bleeding from the ear may also be present. Posterior dislocation • Cause—it results from severe injury, which forces the mandible backwards, so that the condyle penetrates the tympanic plate of the temporal bone. When the upward and backward thrust is applied to the chin, posterior dislocation occurs. • Age—it is more common in elderly people as they have increased gonial angle, which leads to more posterior displacement of the condyle than in the case of an individual having a smaller angle. • Symptoms—there may be tenderness over the affected TMJ, limited mouth opening, anterior open bite and laterognathism.
Radiographic Features • Anterior dislocation—it is difficult to detect radiographically, as there is a wide variation in anterior condylar movements. Condyle is locked in front of the articular disc. Condyle is high on the anterior surface of the eminence and is well up in the infratemporal fossa and stayed there when the patient have closed their mouth. • Central dislocation—radiologically, the anatomy of the articulation is seen to be altered, so that neck of condyle occupies a too high position in relation to the articular fossa.
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TMJ Disorders • Posterior dislocation—radiologically, the anterior portion of the articular fossa is empty and the condyle is seen too far posteriorly. The neck of the condyle may appear short, if the head of condyle maintain its abnormal position. In such a case, the condyle may be seen partly covered by the more radiolucent external auditory canal. In cases when there is posterior dislocation into the tympanic plate, but has been subsequently reduced, it may be possible to identify the damage to the plate in good quality radiograph.
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incomplete dislocation, which generally follows stretching of the capsule and ligaments.
Etiology
• Clinical diagnosis—anterior open bite with gagging of molar teeth will aid in diagnosis. • Radiological diagnosis—empty articular fossa space will diagnose this condition.
• Long continuous opening of mouth in the dental chair or singing, yawning or sleeping on one arm in bed. • Oral surgical procedures excessive movement apparently causes stretching of the joint ligament or rupture of the external pterygoid attachment to the meniscus. • It may follow the chronic degenerative changes of osteoarthritis. • It may be a manifestation of an underlying psychiatric problem, which may be manifested by minor trauma. • Use of phenothiazine derivatives by surgeons may also be responsible (due to hypersensitivity to the drug), it returns to normal after anti-histaminic therapy.
Management
Clinical Features
• Reduction of dislocation—it can be done by the following • Manipulation without anesthesia—some type of sedation should be given to the patient before manipulation. Patient should be sitting on the chair with the operator in front. The thumbs covered with gloves should be pressed down over the buccal shaft area of the mandible, near the lower molar teeth and at the same time elevating the chin with fingers and pushing the entire mandible posteriorly and then upwards. • With local anesthesia—this treatment is based on the principle, that the dislocation is maintained by muscle spasm secondary to painful stimuli, arising from the capsule. The treatment consists of injection of local anesthesia (lignocaine hydrochloride) into the joint. After approximately one minute spontaneous reduction generally occurs without the necessity of manual reduction. Even in bilateral dislocation, unilateral injection is adequate. This is due to the elimination of neural reflex which extends over the muscle bilaterally and patient can close the mouth to normal position. • Under general anesthesia, with the aid of muscle relaxant— if the above mentioned method fails and the patient is unduly apprehensive then this method is used. Postoperatively, the jaws should be immobilized for 10 to 14 days, this help the inflammation and edema to subside.
• Symptoms—cracking noise, temporary locking of the condyle and immobilization of the jaw. Patient describes weakness of the joint while yawning. Pain is associated with last few millimeters of mouth opening. • Signs—the condyle may get locked when the mouth is opened widely and upon closing, it will return with a jumping motion, accompanied by a sound caused by movement of the condyle over the articular eminence. On palpation ‘click’ on opening and sliding of condyle over the articular eminence, are common.
Diagnosis
Radiological Features Excessive excursion of the condyle from rest position to the position when jaw is opened wide (Fig. 25-36).
Fig. 25-36: Subluxation of TMJ observed on panoramic radiograph (Courtesy Dr Tapasya Karamore).
Diagnosis Subluxation (Hypermobility) It is the unilateral or bilateral positioning of the condyle anterior to the articular eminence, with repositioning to normal accomplished physiologic activity. It is self reducing
• Clinical diagnosis—cracking noise will temporary locking of condyle will give clue to diagnosis. • Radiological diagnosis—excessive excursion will be seen radiologically.
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Management
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• Conservative method—here, the objective is to achieve shrinkage of the capsule by a sclerosing agent, which will cause fibrosis of the capsule. It will limit the condylar excursion without deleterious effects on motion and cartilaginous part of the articulating surface of the condyle. The solution used is 5% sodium psylliate or 5% intracaine in oil base. A mixture of equal parts of 0.5% of eucupine in oil and 5% aqueous solution of sodium psylliate has an additional effect. It may be necessary to repeat the injection every 2 to 3 weeks, till fibrosis occurs. • Surgery—insertion of bone graft is done. The joint is exposed; a vertical incision is made in the outer side of the capsule. The edges are overlapped and then sutured so as to tighten the capsule in the anteroposterior plane. After 7 days of intermaxillary fixation, clicking and subluxation will be relieved. Shortening of the temporalis tendon also relieves subluxation.
Internal Derangement or Disc Displacement Here, the disc is abnormally located in relation to other components of the joint. It is usually displaced anteromedially. In some rare casess, disc may be displaced posteriorly. Most of the cases of disc displacement occur due to microtrauma from bruxism or clenching. It can be defined as a malrelationship of the meniscus to the condylar head and articular eminence, where an alteration of its attachment allows the meniscus to assume an abnormal position.
Classification • Anterior displacement with reduction (Fig. 25-37)—In it, as the condyle moves forward, it snaps under the posterior edge of disc producing an audible click and on closing the condyle may again snap under the posterior edge of the disc producing another click. • Anterior displacement without reduction—There is no reduction of condyle in the mandibular fossa in closed position. • Posterior disc displacement—condyle slip over anterior rim of disc during opening. • Disc displacement with intermittent locking. • Disc displacement with perforation.
Etiology • Articular surface remodelling—it occurs due to combination of articular surface remodelling, disc deformation and displacement of either the condyle or the disc from an ideal relationship, which leads to jamming of the disc.
Fig. 25-37: Double contrast CBCT arthrography—it demonstrated anterior displacement of the disc without perforation and dilation of the superior joint space. Also, demonstrates multiple loculi in the anterior region of the joint space (Courtesy Kazuya Honda, Japan).
• Articular eminence—very steep articular eminence increases the risk of disc displacement. • Disc morphology—if the morphology of the disc is altered and if the discal ligaments are elongated, there is increased risk of disc displacement. • Trauma—trauma due to malocclusion results in the spasm of the lateral pterygoid and produces a series of changes.
Pathogenesis • Early changes—Increased muscle tone of the lateral pterygoid →it tends to pull the meniscus anteromedially to the condylar head →the meniscus will move anterior to the condylar head →a click or pop will then occur on early opening as the condylar head reseats into the thin central portion of the meniscus →this type of joint noises occur in early stages of joint disease and can be corrected by relieving the muscle spasm. • Creation of freely moving disc—discal ligaments are not elastic and hence once elongated; they generally remain at that length →the elongated discal ligament and the continuous muscle pull due to spasm results in freely moving disc on the articular cartilage. • Alteration of joint function—if the posterior border of the disc becomes thinned and the retrodiscal laminae and lateral discal ligament becomes elongated →the disc can be translated across the articular surface of the
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•
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condyle →this translatory movement between the disc and the condyle is abnormal →once the disc is displaced anteromedially, normal joint function is altered. Functional displacement—at rest, the resistant force provided by the superior discal lamina will act and hence the condylar head will be positioned on the posterior border of the disc (known as functional displacement). Patient has feeling of tightness at this stage. When the person bites, the muscle pull further stretches the disc, causing arthralgia pain. 1st click—in the closed joint position, the condyle articulates on the posterior border the disc. During opening, the condyle moves forward along with the disc. During this opening movement, the disc suddenly moves posteriorly, so that the condyle establishes a normal relationship with the intermediate zone of the disc. This sudden movement between the condyle and the disc results in clicking sound. Reciprocal click—if the condition persists, then there is elongation of the retrodiscal lamina. At this stage, during closing movements, the condyle moves the intermediate across the posterior border of the disc and just prior to the closed positions a second click is heard. This stage of derangement is called as the reciprocal click. Anterior dislocation with reduction—the patient can open the mouth to a certain extent at which they have a feel of locking. When the patient moves the jaw away from the painful side, opening is suddenly possible as the jaw suddenly becomes free with a pop. The meniscus is present anterior to the condylar head in the closed position. During mouth opening, the meniscus is pushed in front of the condyle until it mechanically blocks any further excursion. In order to reduce the dislocation, the patient needs to move the condylar head in the direction taken by the meniscus under the influence of the muscle. As the normal relationship is established, full opening is possible. When the mouth is opened, in disc dislocation, the condyle moves onto the posterior border of the disc. This creates jamming or catching sensation during opening. In some instances, the patient can move the mandible medially or laterally and abruptly move the condyle over the intermediate zone of the disc. During jaw movements, the disc returns to the normal position with the condyle. Anterior dislocation without reduction—in the next stage, due to continuous stretching caused by dislocation, soft tissue degeneration of the joint takes place and the meniscus becomes distorted and hypertrophied. The remaining elasticity of the bilaminar zone is lost and the meniscus remains anteromedially blocking forward the translation of the condylar head. This results in restricted movements and reduction is no longer possible. Perforation of the disc—due to continuous stretching, the condylar head is positioned on the retrodiscal tissues.
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Due to pressure, tissue breakdown begins with inflammation of the tissue, which is called as retrodiscitis. Due to attenuation perforation occurs in the disc, leading to bone-to-bone contact, which ultimately results in osteoarthritis. • Disc dislocation—if the posterior border of the disc becomes thinner and the retrodiscal lamina and collateral ligament become more elongated, the disc can slip anteriorly through the discal space. This is known as disc dislocation, as there is loss of contact between the articular surfaces of the condyle and the disc.
Clinical Features Anterior disc displacement with reduction • Symptoms—during the disc dislocation, the condyle may articulate on the retrodiscal tissue and may cause pain. • Signs—on physical examination, the joint is tender and reciprocal audible clicking is heard. The jaw is deviated towards the side of the click, till the click occurs and then returns to the midline (Figs 25-38A and B).
A
B Figs 25-38A and B: Deviation of jaw on right side in disc displacement with reduction.
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Anterior disc displacement without reduction • Patient who experiences repeated disc dislocations with reduction may further elongate discal ligament and retrodiscal lamina. Often, elasticity of the retrodiscal lamina is lost. • Closed lock—if the condyle moves forward but the disc is not returned to its normal relationship between the condyle and fossa, a condition known as dislocation without reduction occurs. It is also called as closed lock. • Symptoms—there is joint pain, limited opening, previous clicking with intermittent locking and sensation of something in the joint. The joint locks during opening of the mouth. • Signs—there is joint tenderness with deviation towards the affected side. Terminal stretching produces increased joint pain. • Mouth opening—there is limitation of lateral movement in the joint.
A
Disc displacement with perforation • Symptoms—there is joint pain, clicking with intermittent locking and closed lock. There is also limited opening. • Signs—crepitus and grinding noise. There is also joint tenderness. Posterior disc displacement • Occlusal derangement—sudden inability to bring upper and lower teeth tooth in maximal occlusion. • Pain—there is pain in the affected joint when teeth are tried to bring in occlusion. • Forward displacement—there is forward displacement of mandible on the affected side. • Restricted lateral movement—there is restricted lateral movement to the affected side. • Mouth opening—there is no restriction of mouth opening.
Radiographic Features • Plane radiography—they are not diagnostic; except in cases of perforation of the disc, where there is evidence of degenerative changes in the joint. • Arthrogram—arthrogram is useful in studying the changes. • MRI—in anterior disc displacement, posterior band of the disc located anterior to the superior portion of the condyle is seen in closed mouth sagittal image. In some cases bone marrow edema can be seen (Figs 25-39 and 25-40).
Diagnosis • Clinical diagnosis—clicking sound while opening and closing the mandible with pain in TMJ area. • Radiological diagnosis—MRI is useful in the diagnosis of disc displacement.
B Figs 25-39A and B: (A) Axial section, closed mouth, anteriorly displaced disc. (B) Axial section, open mouth, anteriorly displaced disc, but normal disc condyle relationship (Courtesy Dr Avinash Kshar and Dr Umarji, Government Dental College and Hospital, Mumbai).
Management • Bite plane appliance—it involves one of the bite plane appliances that position the mandible so that the mouth remains slightly open vertically and is placed anteriorly to maintain the disc in a normal relationship to the condyle. Maxillary and mandibular appliances can be used for maintaining the disc reduction during function. The evaluation and adjustment in the appliance should be made monthly, till the condyle return to normal hinge position. TMJ should be stabilized in the position for two months by maintaining the patient on splints. • Occlusal adjustment, restorative and orthodontic treatment— next phase is of occlusal adjustment, restorative treatment and orthodontics or all the three can be done. • Surgical treatment—it is indicated in those patients who have chronic internal derangement, have failed to respond to non-surgical treatment. It includes
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as adhesion. Adhesions can occur in either superior or inferior joint space and can occur with or without disc derangement. Adhesion can begin after prolonged static loading of the joint. The patient wakes up with limited jaw movement. As the patient attempts to move the mandible, a single click is felt (representing freeing of adhesion) and then, the normal range movement is restored. The click only occurs once and cannot be repeated without prolonged period of static loading. Adhesion are best demonstrated on arthroscopy (Fig. 25-41).
A
Fig. 25-41: Arthroscopic observation—band-like fibrous adhesion is observed in the posterior articular cavity (Courtesy Kazuya Honda, Japan).
B Figs 25-40A and B: Coronal section, closed mouth, laterally displaced disc (Courtesy Dr Avinash Kshar and Dr Umarji, Government Dental College and Hospital, Mumbai).
• Disc repositioning procedure—in this, there is removal of tissues from the posterior attachment of the disc with repositioning of disc in its normal position. It is sometimes combined with high intracapsular condylar reduction or an articular eminence re-contouring. • Menisectomy—when it is not possible to repair the disc, interposition material is placed. • Postoperative physiotherapy—postoperative physiotherapy is advocated to establish full range of motion. Bite plane appliance is used for a week followed by occlusal adjustment.
Adhesions The movements between healthy articular surfaces occur without friction. Changes in the articular surfaces and synovial fluid can drastically change this frictionless system. This sticking of articular surfaces has been called
Metabolic Disorders Gout It is a chronic metabolic disorder characterized by acute exacerbations of joint pain and swelling associated with an elevated blood uric acid and deposition of crystals of monosodium urate. Various drugs like thiazide diuretics, operations, trauma, alcohol and rapid weight loss can predispose to this disease.
Clinical Features • Age and sex distribution—seen in middle age with equal sex distribution. It has a hereditary tendency. • Sites—initially, metacarpophalangeal joints are commonly involved. Later foot, ankles, hand, wrist and elbow may be affected. • Symptoms—there is excruciating pain, which may be worsen at night. Sometimes, it is associated with anorexia, fever and general malaise. • Progress—joint returns to normal after few days, with desquamation of the overlying skin.
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• Chronic cases—as the disease becomes chronic, pain and stiffness persist, with irregular swelling. Tophi are found in cartilage of the ear, nose or eyelids. In half the cases, palms of hands may show white streaks along the creases. • TMJ involvement—sudden excruciating pain in the TMJ, followed by rapidly developing swelling. There is also tenderness of the affected area with limitation of movements. Deviation to the affected side while opening the jaws.
Radiological Features • Appearance—there is bony mass protruding from the condyle (Figs 25-42 and 25-43).
Radiographic Features • Punched out lesion—punched out areas in the carpal bone of the hands. In TMJ also, punched out radiolucency can be seen on the condylar cartilage. • Destruction of cartilage—severe destruction of the cartilage can also be seen in some areas. • Calcification in the joint—there is calcification within the joint spaces which may be subtle or massive.
Diagnosis • Clinical diagnosis—multiple joint involvements. Tenderness on the TMJ area can diagnose the disease. • Radiological diagnosis—punched out lesion with calcification in the joint. • Laboratory diagnosis—articular cartilage reveals white chalky deposits. This deposit is also often found in the synovial and adjacent tissues. The cartilage may be fragmented. Crystalline deposits of uric acid are seen. This is followed by small accumulations (microtophi) with surrounding granulomatous foreign body reaction.
Fig. 25-42: Chondroma of condyle showing radiopaque lesion on right condyle.
Management • Diet—diet should be low in uric acid and fat, i.e. sweetbread, meat, extract peas, beans. • Uricosuric agents—increased elimination of uric acid by uricosuric agents like colchicine 0.5 mg every 2 hourly, to a maximum of 6 mg in 24 hours.
Fig. 25-43: Osteoma of condyle on right side (Courtesy Dr Datarkar).
Management
Neoplastic Disorders Benign Tumors
• Surgical—surgical excision of the tumor and orthodontic treatment, to re-establish the occlusion.
Benign tumors reported are osteoma and osteochondroma.
Malignant Tumors
Clinical Features
Types
• Symptoms—there is stiffness of the joint with facial asymmetry. • Signs—deviation of mandible on the affected side. Disordered occlusion, little movement of the condyle on palpation. There are restricted movements of TMJ.
• Intrinsic—it arises from the bone of the condyle, articular fossa and the joint capsule or the articular disc. It includes chondrosarcoma and synovial sac sarcoma. • Extrinsic—the tumors which extend from outside of TMJ, e.g. neoplasm of the parotid gland.
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TMJ Disorders Clinical Features • Age and sex—age of incidence from 17 months to 68 years with male to female ratio being 1:1. • Symptoms—pain on full opening of the mouth and diminished hearing. Swelling of the TMJ is present. Swelling may be huge to cause facial asymmetry. • Signs—the tumor may be fixed to deep structures. Deviation of the mandible to the unaffected side. There is also malocclusion (Fig. 25-44).
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Miscellaneous Disorders Synovial Chondromatosis It is a benign chronic progressive metaplasia that will not resolve spontaneously. Although it is non-neoplastic, it may resemble a malignant condition histologically. It is also called chondrometaplasia. It denotes the condition whereby a cartilaginous focus develops within the synovial membrane of the joint.
Pathogenesis • Predisposing factors—trauma may be a predisposing factor, other factors are malocclusion, occlusal habits, and subluxation or tension sites. • Metaplasia of mesenchymal cell—this is generally believed to occur through metaplasia of mesenchyal cell rests in the underlying connective tissue of the membrane. • Formation of metastatic foci—there is formation of metastatic foci. • Detachment of metastatic foci—foci are detached from the affected membrane and become cartilaginous, and forms mobile bodies within the joint cavity. • Calcification of cartilaginous foci—many of these cartilaginous foci then undergo calcification. These joint bodies acquire a perichondrium, which enables them to grow by proliferation of chondrocytes. Fig. 25-44: Huge swelling seen on right side of patient due to chondrosarcoma of condyle.
Radiological Features • Appearance—irregular destruction of bone in condylar region is present (Fig. 25-45).
Management • It can be treated by surgery, chemotherapy, radiotherapy and combination therapy.
Clinical Features • Age and sex—female to male ratio is 3:1 with greatest incidence at 40-60 years of age. • Site—this affect large joints like knee, elbow, hip and shoulder. This disease is also present in temporomandibular joint. • Symptoms—facial pain, limitation of motion and deviation towards the affected side. • Signs—crepitus, preauricular swelling, enlarged joint with effusion and local tenderness.
Radiographic Features • Loose bodies—this consists of rounded/irregular shaped radiopaque structure in the joint (Fig. 25-46). • Joint space—there is irregularity in the joint space. Joint space is also widened. • Condyle—condylar head is also irregular.
Diagnosis
Fig. 25-45: Irregular destruction seen in the condylar area due to chondrosarcoma.
• Clinical diagnosis—it does not show any diagnostic features • Radiological diagnosis—radiopaque loose bodies seen in the joint space.
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3 Fig. 25-46: Loose bodies seen as rounded shaped in arthroscopic view (Courtesy Dr Honda).
• Laboratory diagnosis—cartilage shows hyperchromatic and binucleated chondrocytes.
Management • Surgical—loose bodies should be removed. • Synovectomy—total synovectomy can be done to prevent recurrence. • Removal of metaplastic foci and synovectomy are the preferred treatment.
Drug Induced Disorders (Steroids) Corticosteroids induce mandibular osteoarthritis. The manifestations depend on the dosage, potency and duration of exposure to excessive steroids. Impaired connective tissue function may lead to calcification of the cartilaginous matrix, resulting in osteoarthritis like changes. Lesions develop initially in the midest of condylar cartilage and then spread to involve the articular cartilage. The effect of steroids on the chondrocyte is inhibitory in nature. The catabolic activity of steroids on the condylar cartilage is due to its inhibitory effect on DNA and RNA synthesis in chondrocytes, with subsequent interference in protein synthesis. In addition, triamcinolone was found to enhance the synthesis and secretion of parahormone in various experimental animals and thereby could elicit the degenerative changes in the joint tissue.
TMJ Dysfunction Syndrome or Myofacial Pain Dysfunction Syndrome When muscle spasm develops, dysfunction as well as pain occurs and the condition usually is designated as MPDS. It is initiated as spasm of one or more masticatory muscle.
• Abnormal occlusion—in case of painful and potentially damaging contact in the occlusion, persons make modifications in the pathway of closure. These corrective movements of the mandible, during closure may elicit muscle strain and spasm, which in turn results in an abnormal pressure on the TMJ. • Tooth muscle theory—occlusal interferences cause an altered proprioceptive feedback, leading to incoordination and spasm of some of the muscles of mastication. • Prosthetics problems—some authors think that interceptive contact, due to faulty complete and partial dentures, over closure, bilateral loss of molar teeth, and increased vertical dimension in partial and complete denture may lead to TMJ dysfunction. There is a change in the myotactic stretch reflex in all above mentioned conditions, which support the view that the TMJ dysfunction can result from over closure. • Orthodontic problems—malocclusion leads to TMJ dysfunction. • Emotional problems—pattern of over behaviors relating to care of teeth, food habits may lead to TMD (temporomandibular dysfunction). Oral habits can cause structural damage or persistent pain. Dysfunction of autonomic nervous system resulting from anxiety and eventually producing structural changes in the end organs. • Psychophysiologic theory—the masticatory muscle spasm is responsible for the signs and symptoms of pain dysfunction syndrome. Persistent myospasm also can cause two other organic changes, namely degenerative arthritis which can arise from continued jaw function with condyle in an abnormal position and contracture degenerative changes in muscle, that accompanies long term spasm. Spasm can be initiated by muscular overextension which is caused by: • Dental restoration—by dental restorations or fixed and removable prosthesis that encroach on the intermaxillary space. • Tooth loss—by muscular over-contraction which is caused by bilateral loss of posterior teeth. • Denture wearer—by settling of partial denture or in patients wearing complete denture. • Oral habits—by muscle fatigue which is caused by oral habits such as clenching or grinding of the teeth. • Dental irritation—it can be initiated by dental irritation like maloccluding restorations or an over hanging margin. • Joint problems—hypermobility caused by lax ligament may give rise to symptoms of TMJ dysfunction. It has been also shown that patient with steep angulations of articular eminence are more predisposed to the TMJ dysfunction syndrome. Degenerative changes secondary
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TMJ Disorders to chronic para-functional habits or over-closure due to bilateral loss of molar teeth result in TMJ dysfunction syndrome.
Pathogenesis • During muscle contraction, the energy is released →there is formation and accumulation of lactic acid →which in turn causes changes in osmolality which results in decrease in the pH →it make the muscle receptor prone to impulse excitation as their critical firing level is impaired →decrease in pH and lactic acid itself causes infusion and effusion of histamine, bradykinin and serotonin and other amines into the area →it causes pathological muscular derangement →these particular areas of muscular derangement are called as ‘trigger zones’ →it is a hypersensitive area from which impulse bombards the CNS and gives rise to referred pain.
Classification • Spasm of lateral pterygoid muscle—it occurs when the teeth are brought into maximum intercuspation and with extended translatory movement. Pain reduces on biting against a separator (as it prevents the intercuspation required to stretch the spastic muscle). It is accompanied by acute malocclusion expressed as anterior displacement of the mandible. • Spasm of elevator muscles- it occurs when biting and chewing efforts are made and while opening the mouth. Pain is not decreased on biting on a separator and is accompanied by trismus with little or no restriction of excursive movements. • Spasm of lateral pterygoid and elevator muscles—in it, pain occurs while biting, chewing, opening, maximum intercuspation and extended translatory movement. Pain is not affected by biting against a separator, except for some decrease of pain with maximum intercuspation and is accompanied by acute malocclusion, trismus but with little or no restriction of excursive movements.
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popping snapping sounds on mandibular movement. • Tinnitus—patient may complaint of tinnitus (ringing in ear) or otalgia (pain in ear) or toothache. The reason behind tinnitus is that bilateral molar loss causes distal condylar movement and direct pressure on the eustachian tube with impingement on the auriculotemporal nerve, which is responsible for the ear symptoms, i.e. tinnitus. • Hearing loss—it may cause irritation of the chorda tympani nerve, resulting in partial or total hearing loss. • Signs—restriction of opening and protrusion may be accompanied by deflection of the mandibular incisal pathway. There is also soreness of muscle, when palpated. Myofacial trigger zones are stimulated by pressure and produce referred pain. • Myospasm—muscle splinting can lead to CNS induce muscular contraction. In some cases, myositis may also occur. • Other features—oral or para-functional habits, such as bruxism, present as indentation on lateral borders of the tongue, ridging of the buccal mucosa and extensive attrition of teeth. • Involvement of various masticatory muscles and their clinical effects. Muscle
Pain refers to
Temporalis
Temple, maxillary teeth Restriction of mandibular TMJ opening, ipsilateral deviation of mandible, deviation of interocclusal space
Clinical effect
Masseter
Mandible, maxillary molar, TMJ, ear
Same as above
External pterygoid
TMJ
Contralateral deviation of the mandible, protrusion of condyle, acute malocclusion
Internal pterygoid
TMJ, retromandibular area, tongue
Restriction of mandibular movements, contralateral deviation of mandible
Laskin’s Diagnostic Criteria for MDPS Clinical Features • Age and sex distribution—it is seen in middle age group with more predilections for women. • Onset—it occurs in episodes of several times a day, at times, with extended symptom free intervals. Usually episodes are seen during increased emotional tension, resulting in increased intra-articular pressure in the joint. • Symptoms—there is masticatory pain which occur due to myalgia, arthralgia or from both. Pain is localized to preauricular area but can be radiated to temporal, frontal, and occipital region. There is difficulty in chewing and restriction of mandibular excursion. Patient also complaint of noise on rubbing, grinding, clicking, and
• Four cardinal signs • Unilateral pain—it is generally a dull ache in nature felt in the ear or the preauricular area or at the angle of the mandible. The pain is more often worse on arising in the morning or relatively mild in the morning, but gradually becomes worse as the day progresses. • Muscle tenderness—the most frequent areas are the neck of mandible and in the region distal and superior to the maxillary tuberosity. • Clicking—clicking or popping noise in the TMJ. • Limitation of jaw function—limitation of jaw function or deviation of the mandible on opening.
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• Negative characteristics • No radiographic evidence—absence of radiographic or biochemical evidence in the TMJ. • No tenderness—lack of tenderness in TMJ area, on palpation via the external auditory meatus.
Management
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Education regarding present illness • Re-educate the patient about the mechanism involved and factors causing or aggravating the disorder. The patient is convinced about the disease status. • Reassurance—the patient is assured of the benign character of the myospasm. The patient should be explained that there will not be any residual deformities after the treatment. • Suggestion—may act as a powerful tool in the treatment. The calm attitude of the clinician and reassurance given suggests the patient that recovery is bound to occur. Let the suggestions act in a natural quiet fashion rather than trying to use it in some spectacular ways. Muscle relaxation techniques and muscle exercise • Tongue exercise—the patient is asked to keep his tongue as posteriorly as possible, in contact with the palate, while keeping the mandible in a retruded position. In this exercise, mainly rotatory movements are performed. • Mouth opening exercise—the patient is asked to open his mouth slowly, rhythmically, within the pain limit, 10 times in succession. Next, the patient is asked to repeat such exercises with the addition of one modification, i.e. voluntary resistance. • Voluntary resistance—this technique is based on the physiologic principle of reciprocal muscle inhibition (reflex inhibition), e.g. on depressing the mandible, the contraction of the depressor muscle group causes an inhibition of the elevator muscles. Thus, if a muscle is subjected to a greater degree of inhibition, its relative relaxation will increase proportionately. This muscular relaxation will increase circulation to the antagonist system. It is during this period of active reflex inhibition, that the noxious stimuli present in and about the trigger zone can be eliminated. Resultantly, the inter-muscular blood vessels get dilated. As more muscle fiber areas relax and fewer remain in spasm, the patient evidences gradual, painless and rhythmic mandibular movements. Pharmacotherapy • Pain control—it is usually achieved by analgesics. Most widely used analgesic is salicylates, the commonest being aspirin. • Tranquilizers—there are major and minor tranquilizers. The tranquilizers used in major psychoses, like
phenothiazine derivatives, having calming effect in anxiety states associated with neurotic personality. It relieves tension, fear and produces a sense of well being. • Antidepressants—they are mood elevators like monoamine oxidase inhibitor, lithium carbonate and caffeine. • Sedative—sedatives are the drugs that reduced excitement. • Hypnotic—hypnotics produce sleep which resembles natural sleep. Biofeedback • EMG biofeedback device—the most commonly used biofeedback device is electromyographic (EMG) biofeedback machine. The device senses cutaneous electrical output. Every time the muscle contracts and electrical current is given off, which diffuses outward and may reach the skin. Current from the muscle nearer to the skin is much earlier to detect than current from deeper muscles. Muscle gives off a specific frequency of electrical output. The biofeedback elaborately gauges the amount of amperage and voltage. This method is noninvasive and painless. • Temperature biofeedback—the temperature biofeedback accounts of placing a delicate thermometer on the skin. The temperature is measured in tenth of degree centigrade. This higher the temperature, the higher the pitch of sound. When there is poor circulation, individual can increase the temperature by this method. Bruxism prosthesis • Soft mouth guard—it is a bruxism guard made up of soft resin. It may be fashioned for either upper or lower teeth and is designed even for centric contact of all the teeth. • Anterior occlusion prosthesis • Lucia jig—it consists of a smooth acrylic rim placed on the lingual aspect of the upper incisors. It should be complete enough to provide complete posterior disocclusion. • Anterior bite plate—this appliance does not produce posterior contact and hence can be used in patients with bruxism. It should not be used for more than one or two weeks as than it may raise the bite. • Mandibular posterior coverage—it covers the posterior teeth of the mandible, when the jaws are closed. It causes bilateral, single point contact on the most distally placed tooth. It is made up of acrylic or metal. • Complete maxillary or mandibular coverage—it covers all occlusal surfaces in either maxillary or mandibular arch. By gripping all the teeth in one arch, it acts as a true splint, preventing the tooth movement and minimizing the number of posterior teeth occluding. In addition, anterior guidance will provide posterior disocclusion in all eccentric movements.
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TMJ Disorders Psychotherapy • Stress impasse stages—the stress impasse stages in the TMJ syndrome are characterized by three distinct steps based on the evolution and progression of the disease. • Stress impasse I—conflict from personality fixation, usually in adolescents, chronic symptoms develop (bruxism, clenching, grinding). • Stress impasse II—onset of acute symptoms (pain, jaw clicking). • Stress impasse III—severe symptoms resulting in TMJ damage. • Treatment plan—the treatment plan includes a three stage programme, which will include basic relaxation exercises, sleep preparation and containment strategies for worry, grief and guilt. Physical medication • Hot packs—the one of moist heat is advantageous. Heat should be applied directly to the trigger zones. Temperature changes can alter the amount of vasodilation substance held within the tissue spaces. The patient should be instructed to place hot fomentation over a particular area for not less than 10 minutes, preceding the therapeutic exercises. Woolen cloth soaked in boiling water is usually used. • Massage—it provides relief from muscle spasm and also improves the local circulation, by reducing the local biogenic amines. • Diathermy and ultrasound—this is a more effective method for the treatment of myospasm of deeper muscles. It produces heat and thus improves the local circulation. • Electrical stimulation (TENS)—tetanizing and sinusoidal current is used in this therapy. It is another effective way to break acute painful muscle spasms. Electrodes are placed over the most painful areas and then tetanizing current is turned on gradually, until good contraction of the affected muscle has been obtained. Current should not exceed the tolerance level. The current is left for 120 minutes. Then with the electrode remaining in the same position, the tetanizing current is switched off and sinusoidal current is gradually applied, till good contraction is obtained. • Oral myofunctional therapy is a program to re-educate the muscles of the mouth and face to work in a balanced relationship. It includes breaking of a habit (Lip biting, tongue thrusting), proper feeding of infant and proper balancing of environmental forces. The appliances used are activator, bionator, Fränkel’s appliance and oral screen. Applied kinesiology • What is it—dental Kinesiology is the study of motion and function of the jaws, oral musculature, the accompanying neurological, vascular and other support system network and the impact these muscle functions
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and neurological dynamics have on dental and systemic health. Its basic application is for reduction and prevention of muscle spasm. • Muscles are tested to identify the weak muscle. The clinician then uses various kinesiologic procedures to increase the stress resistance of the tensed antagonist muscle to a more optimum level. Anesthesia • Muscle and fascia (trigger points)—injection of local anesthetic agent into the painful trigger zones is therapeutically efficient. It permanently terminates the pain-spasm-pain cycle. Local anesthesia breaks the cycle by blocking the nerve impulse conduction and by eliminating pain from that area. Local anesthesia should be used without vasoconstrictor component, i.e. adrenaline. It is important to first isolate the trigger zone. Then, it is gently probed to reach for the most hypersensitive tissue. Once defined, slow infiltration of anesthetic solution is deposited. The patient is then instructed to begin a series of exercises. • TMJ (intracapsular and extracapsular)—many a times, xylocaine is used in conjunction with injection of hydrocortisone for the intra-articular injection into the TMJ. 0.5 ml of 0.5% xylocaine is generally used. • Refrigerated spray—vapocoolant spray, such as ethyl chloride or fluoromethane, is used to reduce muscle spasm by causing counter irritation. Since pain and temperature sensation travel by the same spinal pathways, it is theorized that response to pain impulse originating from the trigger zone, is completely inhibited and thus, inhibition of the vicious cycle is achieved. The spray is applied with a slow sweeping motion over the trigger points. Skin frosting should be avoided. Other therapies • Hypnotherapy—here, the patient’s cooperation is essential and he should follow the suggestions of the hypnotist. It is an individual’s belief that aids him in following the suggestions of the hypnotist. By this method, muscle relaxation is achieved. • Acupuncture—it is a simple, effective and conservative pain control modality. It is accomplished by inserting needles into appropriate joints, at appropriate surfaces called as meridians. These meridian points are generally associated with major nerves, arterial pathways, joints and fascial planes. Rotating a sharp, small needle between the fingers rapidly and pressing it through the skin rapidly, in the acupuncture point provides relief from pain. The patient may feel soreness, distension, heaviness or numbness, if it is placed into so called acupuncture point. However, it should be kept in mind that this therapy is used only to give relief from pain and it will not remove the basic cause.
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• Surgery—various surgical procedures like eminectomy, zygomectomy, menisectomy, high condylectomy with material interposed between the articulating surfaces and orthoplasty plus menisectomy are most frequently advocated. • Restoration—faulty overfilled restorations should be removed to avoid interceptive contact. Sometimes, complete mouth rehabilitation is required to achieve centric occlusion. • Prosthodontic therapy—it has been shown that overclosure due to bilateral loss of posterior teeth can cause TMJ pain. In such cases, bilateral fixed or removable replacement should be done to achieve normal vertical dimension. • Orthodontic therapy—it is indicated in cross bite and traumatic bite. In patient with parafunctional habits, such as bruxism, night guard appliance should be given. • Orthognathic therapy—when there is skeletal discrepancies causing malocclusion, orthognathic surgery is indicated.
Suggested Reading 1. Anil Ghom. Benign tumor of jaw (non-odontogenic), in textbook of oral medicine. Jaypee Brother’s publication 2004; 530-60. 2. Bell WE. Clinical diagnosis of pain dysfunction syndrome. JADA 1969;79:154-60. 3. Berger SS, Stewart RE. Mandibular hypoplasia secondary to perinatal trauma. A report of case. J Oral Surg 1977;35:147-53. 4. Blackwood H. Arthritis of the mandibular joint. Br Dent J 1963; 115:317-24. 5. Blackwood HJJ. Arthritis of the mandibular joint. Br Dent J 1963;115:317-24. 6. Bluick MF, et al. Diagnosis and treatment of internal derangements of the TMJ. Dent Clin North Am 1983; Jul,27(3):561-72. 7. Bruce RA, Hayward JR. Condylar hyperplasia and mandibular asymmetry. J Oral Surg 1968;26:281-90. 8. Bruce RA. Condylar hyperplasia and mandibular asymmetry— A Review. J Oral Surg 1968;26:281-90. 9. Cacioppi J, et al. Condyle destruction concomitant with advance gout and rheumatoid arthritis. Report of case. Oral Surg, Oral Med, Oral Patho 1968;25:919. 10. Cacoppi JT, et al. Condyle destruction concomitant with advanced gout and rheumatoid arthritis: report of a case. Oral Surg, Oral Med, Oral Pathol 1968;25:919-21. 11. Cowan DF, Ferguson MM. Bifid mandibular condyle. Dentomaxillofacial Radiol 1997;26:70-3. 12. Cruin RJ. Incidence of TMJ symptom in male patients with rheumatoid arthritis. JADA 1970;81:129-33. 13. De Bont LG, Dijkgraaf LC, Stegenga B. Epidemiology and natural progression of articular temporomandibular joint. Oral Surg, Oral Med, Oral Patho 1997;83:72. 14. De Leeuw R, Boering G, Stegenga B, Bont LG. TMJ articular disc position and configuration 30 years after intial diagnosis of internal derangement. J Oral Maxillofac Surg 1995;53:234-41. 15. Dijkgraaf LC, Spikervet FK, de Bont LG. Arthroscopic finding in osteoarthritic temporomandibular joint. J Oral Maxillofac Surg 1999;57:1270-80. 16. Dolwick MF. Diagnosis and treatment of Internal derangement of the TMJ. DCNA July 1983;27(3):561-72.
17. Erickson S, Lundberg M. Structural changes in the finger, wrist and TMJ. Acta Odontol Scand 1968;26:111-26. 18. Farmer ED, Lawton FE. Stone’s Oral and Dental Disease (5th edn), 1966;828-30. 19. Freedus MS, William DZ, Doyle PK. Principle of treatment of temporomandibular joint ankylosis. J Oral Surg 1975;33:757-65. 20. Friedman MH, et al. Position paper of the American Academy of the cranio-mandibular Disorders. J Prosthetic Dent 1981;Mar. 45(3):345. 21. Fryman VM. Cranial Osteopathy and its role in disorders of TMJ.DCNA 1983;Jul.27(3):595-611. 22. Gerbino G, Bianchi SD, et al. Hyperplasia of mandibular coronoid process: long term follow up after coronoidotomy. J Craniomaxillofac Surg 1997;25:169-73. 23. Gray RJM, et al. Histopathological and scintgraphic features of condylar hyperplasia. Int J Oral Maxillofac Surg 1990;19:65. 24. Gray RJM, Horner K, Testa HI. Condylar hyperplasia: correlation of histological and scintigraphic features. Dentomaxillofacial Radiol 1994;23:103-7. 25. Greene CS, Laskin DM. Long evaluation of treatment of Myofascial pain dysfunction syndrome: a comparative analysis. JADA. 1983;107:235-8. 26. Gynther GW, et al. Radiographic changes in the temporomandibular in patient with generalized osteoarthritis and rheumatoid arthritis, Oral Surg, Oral Med, Oral Pathol 1996;81: 613. 27. Gynther GW, Tronje G, Holmlund AB. Radiographic changes in the temporomandibular joint in patients with generalized osteoarthritis and rheumatoid arthritis. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1996;81:613-8. 28. Hanson T, et al. Arthrosis and deviation in forms in the TMJ. A macroscopic study in a human autopsy material Acta Odontol Scand 35(3);167-74. 29. Hecker R, et al. Symptomatic Osteoarthritis of TMJ- Report of a case. J Oral Surg 1975;33(10):780-3. 30. Hecker R. Symptomatic osteoarthritis of TMJ, report of case. J Oral Surg 1975;33-167. 31. Isberg A, Isacsson G, Nah KS. Mandibular coronoid process locking. A prospective study of frequency and association with internal derangement of temporomandibular joint. Oral Surg, Oral Med, Oral Pathol 1987;63:275-9. 32. Jagger RG, et al. Multiple myeloma involving the TMJ Report of a case: J Oral Surg 1978; 36(7):557-9. 33. Kai S, et al. Clinical symptoms of open lock position of the condyle relation to anterior dislocation of the temporomandibular joint. Oral Surg, Oral Med, Oral Pathol 1992;74:143. 34. Karlis V, Glickman RS, Zaslow M. Synovial chondromatosis of the temporomandibular joint with intracranial extension: Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1998;86:664-6. 35. Katzberg RW, et al. Anatomic disorders of the temporomandibular joint disc in asymptomatic patient. J Oral Maxillofac Surg 1996;54:147 36. Keen RR, et al. Osteochondroma of the mandibular condyle: case report. J Oral Surg 1977;35:140-3. 37. Kleinman HZ. Gout of the TMJ. Oral Surg, Oral Med, Oral Pathol 1969;27:281-2. 38. Koorbusch GF, Zeitler DL, et al. Psoriatic arthritis of the temporomandibular joints with ankylosis. Oral Surg, Oral Med, Oral Pathol 1991;71:267-74. 39. Kopp S. Subjective symptoms in Osteoarthritis. Acta Odontol Scand 1977;35(4):207-15. 40. Lannetti G, Cascone P, Belli E, et al. Condylar hyperplasia. Cephalometric study, treatment planning and surgical correction (our experience). Oral Surg, Oral Med, Oral Pathol 1989;68:67381. 41. Larheim TA, Bjornland T. Arthrographic finding in the temporomandibular joint in patient with rheumatoid arthritis. J Oral Maxillofac Surg 1989;47:780-4.
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TMJ Disorders 42. Larheim TA, et al. TMJ involvement and dental occlusion in a group of adults with rheumatoid arthritis. Acta Odontol Scand 1983;Oct:41(5):301-9. 43. Larheim TA, Westesson PL. Temporomandibular joint in maxillofacial imaging. Springer 2005;143-77. 44. Leighty SM, et al. Septic arthritis of the TMJ. A review of the literature and report of two cases in children. Int J Oral Maxillofac Surg 1993;22:292. 45. Loh FC, Yeo IF. Bifid mandibular condyle. Oral Surg, Oral Med, Oral Pathol 1990;69:24-7. 46. Loiselle RJ. Symposium on TMJ disorders. JADA 1969;79:145-6. 47. Loury JL. Psoriatic arthritis involving TMJ. J Oral Surg Mar 1975;33 (3):206-8. 48. Lupton DE. Symposium on TMJ disorders; psychological aspect of TMJ disorders. JADA 1969;79:131-6. 49. Lustmann J, Zelster R. Synovial chondromatosis, a review of literature and case report. Int J Oral Maxillofac Surg 1989;18:90. 50. Mayne JG, et al. Arthritis of TMJ. JADA July 1969;79:123-30. 51. Mcloughlin PM, et al. Hyperplasia of the mandibular coronoid process. An analysis of 31 cases and a review of the literature. J Oral Maxillofac Surg 1995;53:250. 52. McNeil C (Chairman AdHoc Committee 1982, Paper presented at the meeting of American Academy of Cranio-mandibular Disorders Chicago). Cranio-mandibular disorders—The state of the art part-2: Accepted diagnostic and Treatment modalities. J Prosthetic Dent 1983;49:393-7. 53. McNeill C, et al. Temporomandibular disorders, diagnosis, management, education and research. JADA 1990;120:253. 54. Merril RG. Habitual Subluxation and recurrent dislocation in a patient with Parkinson’s disease. J Oral Surg July1968;26:473-7. 55. Mikhail M. History and etiology of MPD syndrome. J Prosthetic Dent 1980;44:438-43. 56. Miles DA, Kaugars BS, Dis MV, Lovas GL. Disorders of temporomandibular joint: radiologic/pathologic correlations, WB Saunders, 1991;261-92. 57. Miller GA. TMJ ankylosis-Review of literature and Report of two cases of bilateral involvement. J Oral Surg. Oct 1975;33(10): 792-810. 58. Miyamoto H, Sakashita H, et al. Synovial chondromatosis of the temporomandibular joint. Br J Oral Maxillofac Surg 2000;38: 205-8. 59. Mizukawa JH, et al. Metastatic breast adenocarcinoma of the mandibular condyle-Report of case. J Oral Surg 1978;36(6):44851. 60. Morgan DH, et al. Disease of the temporomandibular apparatusA multidisciplinary approach (2nd edn), CV Mosby and Company, 1982. 61. Musgrove BT. Dislocation of the mandibular condyle into middle cranial fossa. Br J Oral and Maxillofacial Surg 1979;17:17. 62. Musgrove BT. Dislocation of the mandibular condyle into the middle cranial fossa. Brit J Oral and Maxillofacial Surgery 1986; 24(1):7-26. 63. Neville, Damm, Allen, Bouquot. Oral and Maxillofacial Pathology, (2nd edn), Saunders Elsevier, 2004. 64. Ogus H. Regenerative Disease of TMJ in young persons. Br J Oral Surg 1979;17(1):17-26. 65. Palton DW. Recurrent subluxation of TMJ in psychiatric illness. Brit Dent J 1988:153(4):141-4. 66. Perry HT. Symposium on TMJ disorders, Orthodontic viewpoint. JADA 1967;79:137-41. 67. Rasmussen OC. TMJ Arthopathy, clinical, radiologic and therapeutic aspects with emphasis on diagnosis: Int J Oral Surg 1983;12(6):365-97. 68. Richter KJ. Chondrosarcoma of TMJ: report of a case. J Oral Surg 1974;32(10):771-81.
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69. Ronald JB. Synovial chondromatosis of the TMJ. J Oral Surg 1978;36:13-9. 70. Ryon M, et al. Subluxation of TMJ after administration of prochlorperazone report of two cases. J Oral Surg 1968;26: 646-8. 71. Sarhat BG. Developmental facial abnormalities and TMJ. JADA 1969;79:108-17. 72. Sarma UC, Dave PK. Temporomandibular joint ankylosis. An Indian experience. Oral Surg, Oral Med, Oral Pathol 1991;72:660-4. 73. Schwartz HC. Internal derangements of the TMJ, description of clinical syndromes. Oral Surg, Oral Med, Oral Pathol 1984;58: 24-9. 74. Seymour RA. Haemophilus influenza pyarthrosis in a young adult with subsequent TMJ involvement. Br J Oral Surg 1982 20(4):260-3. 75. Seymour RA. Osteoma of the condyle. Oral Surg, Oral Med, Oral Pathol ;52:223. 76. Shaber EP Symposium on TMJ dysfunction, skeletal muscle: Anatomy, physiology and pathophysiology. DCNA July: 1983;27(3):435-43. 77. Shafer. A textbook of oral pathology (4th edn), 1983. 78. Silbermann M et al. Reversibility of systemic corticosteroid induced mandibular osteoarthritis, an experimental study in A/J mice. J Oral Surg 1980;38:660-3. 79. Stadnick G. Congenital double condyle of the mandible causing TMJ, ankylosis-report of a case. J Oral Surg March 1971;29: 208-11. 80. Standnick G. Congenital double condyle of the mandible causing TMJ ankylosis. Report of case. J Oral Surg 1971;28;208. 81. Stellard RE. Symposium on TMJ, Periodontal view point of TMJ disorders JADA 1969;79:142-4. 82. Stewart CL. Osteoarthritis of TMJ in teenaged females. JADA 1983;106(5):638-40. 83. Szentpetery A, Kocsis G, Marcsik A. A problem of bifid mandibular condyle. J Oral Maxillofac Surg 1990;48:1254-7. 84. Toller PA. Osteoarthritis mandibular condyle. Br Dent J 1973; 134:223. 85. Toller PA. Osteoarthritis of the mandibular condyle. Br Dent J. 1973;134:223-31. 86. Tucker MR, Guilford WB, Howard CW. Coronoid process hyperplasia causing restricted opening and facial asymmetry. Oral Surg, Oral Med, Oral Pathol 1984;58:130-2. 87. Whaites E, temporomandibular joint, in essentials of dental radiography and radiology (2nd edn), Churchill Livingstone: 1996;351-70. 88. White SC, Pharoah MJ. Diagnostic imaging of TMJ, in oral radiology, principle and interpretation (5th edn), Mosby, 2004; 516-37. 89. Wiberg B, Wanmam A. Signs of osteoarthritis of the temporomandibular joints in young patients. A clinical and radiographic study. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1998;86:158-64. 90. William N, Alexander. Gonococcal arthritis of the TMJ. J Oral Surg 1973;809. 91. Wooten JW, et al. Oral psorisiform lesion. A possible prosthodontics complication. J Prosthetics Dent 1970;24:145-7. 92. Worth HM. Principles and practice of oral radiologic interpretation. Edn, 1963, Reprint, 1973. 93. Worth HM. The temporomandibular joint; in principle and practice of oral radiologic interpretation; year book medical publisher Chicago, 653-696 94. Yashimura Y, et al. Long term evolution of non-surgical treatment of Osteoarthritis of TMJ. Int J Oral Surg 1982;2(1):7-13. 95. Zide MF, et al. Rheumatoid disease and related arthropathies: Oral Surg, Oral Med, Oral Pathol 1986;61(2):119-25.
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Salivary Gland Disorders
Development of Salivary Gland
Classification of Salivary Glands
The three major sets of salivary gland—the parotid, submandibular and sublingual originate in a uniform manner by oral ectodermal epithelium buds invading the underlying mesenchyme. • Parotid gland—the parotid gland develops in the lateral aspect of stomodeum. Parotid gland buds are the first to appear at the 6th week of intrauterine life, on the inner aspect of cheek, near the angles of mouth and grow back towards the ear. In the parotid and ear region, the epithelial cord of cells branches and canalizes to provide the acini and ducts of the gland. The duct and acinar system are embedded in a mesenchymal stroma, get organized into lobules and become encapsulated. The parotid gland duct, although repositioned, traces the path of embryonic epithelial cord in the adult. • Submandibular gland—it develops in the floor of stomodeum. Submandibular gland buds appear in the 6th week of intrauterine life as a grouped series, forming epithelial ridges on the either sides of the midline, in the floor of the mouth. An epithelial cord proliferates back into the mesenchyme beneath the developing mandible to branch and canalize, forming the acini and ducts of submandibular gland. The mesenchymal stroma is separated off the parenchymal lobules and provides a capsule for the gland. • Sublingual gland—it also develops in floor of stomodeum. It arises in the 8th week of intrauterine life, as a series of about ten epithelial buds, just lateral to the submandibular gland anlogue. These branches and canalize to provide a number of ducts opening independently beneath the tongue. • Minor salivary gland—minor salivary gland begins their development during the third month of life. These glands arise from the oral ectodermal and endodermal epithelium. Labial glands arise during the 9th week of intrauterine life and are morphologically mature by 25th week.
• Exocrine glands—these are the glands whose products are carried away by the ducts leading from the gland. • Mesocrine glands—the secretory products pass through the cell walls losing the cytoplasm. • Serous salivary gland—the salivary glands which produce a thin watery secretion are called as serous. • Mucus salivary gland—these produce a thick, viscous substance called mucus. • Seromucus salivary gland—salivary glands which produce serous and mucus in varying quantities. • Major salivary gland—these are large salivary glands which are located outside the oral cavity and convey their secretions through their ducts. • Minor salivary gland—these are smaller salivary glands confined to the mucus and submucus coat of the oral cavity.
Major Salivary Glands Major salivary glands are parotid, submandibular and sublingual.
Parotid Gland • Location—it comes from the word para—around and otic—ear. It is like an inverted flattened pyramid. It is the largest of the salivary glands weighing about 15 grams each. It lies between the mastoid process and vertical ramus of the mandible. The bulk of the parotid gland is situated in the retromandibular fossa (Fig. 26-1). • Shape—it is wedge shaped, with the broad edge of the wedge lying subcutaneously and the apex lying deep between the parotid fascias. It is divided into superficial and deep lobes by the facial nerve and its branches. It forms an irregular lobulated yellowish mass, lying below the external acoustic meatus, between the mandible and
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the sterno-cleidomastoid. A small part of it, more or less detached lies between the zygomatic arch superiorly and the parotid duct inferiorly is named ‘accessory part’ of the gland. Stensen’s duct—the parotid duct which is called as ‘Stensen’s’ duct is about 5 cm long and has thick walls. It emerges from the substance of the gland to course anteriorly until it reaches the anterior border of the masseter muscle at the point of upper and middle thirds. When it crosses the masseter muscle it receives the duct of the accessory lobe. Around the border of the masseter muscle, the duct turns sharply medially, often embedded in a furrow of the protruding buccal fat pad. In its medial course, the duct reaches the outer surface of the buccinator muscle, where it perforates in an oblique direction anteriorly and medially. It then runs for a short distance obliquely forward, between the buccinator and mucus membrane of the oral cavity and opens on the oral surface of the cheek, opposite the upper second molar. Blood supply—parotid gland is supplied by the external carotid artery and its branches near the gland. Lymphatic drainage—drains first to the parotid nodes and from there to the upper deep cervical nodes. Nerve supply—it is supplied by auriculo-temporal nerve, plexus around the external carotid artery and greater auricular nerve.
Fig. 26-1: Location of parotid and submandibular gland.
• Wharton’s duct—the submandibular duct which is called as ‘Wharton’s duct’, is about 5 cm long and its wall is much thinner than that of parotid duct. It emerges from the middle of the deep surface, of the superficial part, of the gland. It runs forward, beneath the deep part of the gland, between the mylohyoid and hyoglossus muscle. It runs further forward between the medial surface of the sublingual gland and the genioglossus muscle and finally ends by opening into the summit of the sublingual papilla, situated in the floor of the mouth, on the side of the frenulum. The last few millimeters of the duct are often slightly widened. • Arterial supply—the arteries supplying the submandibular gland are derived from the lingual and facial branches of external carotid artery. • Venous drainage—it drains into facial and lingual vein. • Nerve supply—its nerve supply is from the branches of submandibular ganglion through which it receives fibers from chorda tympani. • Lymphatic drainage—passes to the submandibular lymph node.
Sublingual Gland • Location—it lies above the mylohyoid and below the mucosa of the floor of mouth. It is medial to the sublingual fossa of the mandible, on either side of the symphysis menti and lateral to genioglossus muscle. It has about 15 ducts which open directly into the floor of mouth. • Bartholin’s duct—the duct of sublingual gland is called as ‘Bartholin’s duct’. They are eight to twenty in number. Some of the smaller sublingual ducts open into the sublingual fold, in the floor of the mouth, on either side of lingual frenum. Some open into the submandibular duct and others unite to form the “principle sublingual duct” which opens in the floor. • Blood supply—it is supplied by sublingual and submental arteries. • Nerve supply—it is supplied by lingual and chorda tympani nerve. • Lymphatic drainage—it passes to the submandibular lymph nodes.
Submandibular Gland
Minor Salivary Glands
• Shape and size—it is a round biconvex salivary gland situated in the anterior part of the digastric triangle. It is irregular in form and about the size of a walnut. • Location—it is enclosed by two layers of deep cervical fascia. The inner surface of the submandibular gland is in contact with stylohyoid, digastric and styloglossus muscle, posteriorly and with the hyoglossus and posterior border of the mylohyoid muscle, anteriorly.
The minor salivary glands are located beneath the epithelium in almost all parts of the oral cavity. These glands usually consist of several small groups of secretory units, opening via short ducts directly into the mouth. The function of minor salivary glands is not really to produce saliva for mixing with food, but to secrete minor amounts of saliva onto the mucosal surface to keep the mucosa moist.
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• Labial glands—they are found on the submucosa of upper and lower lips and opens onto the inner surface (Fig. 26-2). They are more numerous in the areas close to midline. The labial glands classically have been described as mixed, consisting of mucus tubules with serous demilunes.
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• Gland of von Ebner—lingual glands of von Ebner are posterior lingual serous glands, located between the muscle fibers of tongue, below the vallate papillae. • Posterior lingual glands—posterior lingual glands are located lateral and posterior to the vallate papillae and in association with the lingual tonsils. They are purely mucus in character. • Incisive gland—the incisive glands are a small group of glands found on the floor of the oral cavity close to the insertion of the lingual frenum, behind the lower incisors (Fig. 26-4).
Fig. 26-2: Location of labial gland.
• Buccal glands—they are found in inner cheek region. In the anterior part of the cheek, they are sparse and rather widely and irregularly spaced. They are usually described as continuation of labial glands, as they have similar structure. A group of these glands is situated at the lower posterior corner of the cheek which is called as the ‘molar or retromolar glands’. • Palatine glands—the palatine glands are located in soft palate and posterolateral part of hard palate (Fig. 26-3). They are pure mucus in nature. The excretory ducts may have an irregular contour and opening of the ducts in the palatal mucosa is large.
Fig. 26-4: Location of incisive gland on floor of mouth.
Saliva Composition of Saliva • Source of saliva—saliva is secreted by salivary glands: viz the parotid, submandibular and sublingual glands. These glands produce approximately 1.5 liters of saliva daily: 70% is from the submandibular glands, 25% is from the parotid glands and 5% is from the sublingual glands. Minor salivary glands located on the palate, buccal mucosa and tongue also produce modest amounts of saliva. • Normal stimulated flow of saliva—the normal stimulated flow for different ages can be calculated with following equation:
Fig. 26-3: Location of palatine gland.
• Glossopalatine glands—these are pure mucus glands. They are principally located in the region of the isthmus of the glossopalatine fold but may extend from the posterior extension of the sublingual gland to the glands of soft palate. • Gland of Blandin’s and Nuhn’s—these are the anterior lingual glands. They are located near the apex of the tongue and are chiefly mucus in nature. They are covered by thin mucus membrane of the inferior surface of the tongue. It is compact package of smaller glands that open with several ducts on the inferior surface of the tongue.
0.78 × age + 5.6 = stimulated flow/15 minutes. 5.6 – it is estimated stimulated flow of the infants
• Composition of saliva—saliva is slightly cloudy in appearance due to the presence of cells and mucin. Saliva is slightly acidic and the pH varies from 6.7 to 7.4, specific gravity is 1.002 to 1.012. The resting flow rate of saliva, on an average is about 0.3 to 0.4 ml/min. Saliva contains about 99.5% of water and 0.5% of solid. • Solid • Cellular constituents—consist of yeast cells, bacteria, protozoa, polymorpho-nuclear leukocytes and desquamated epithelial cells.
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Salivary Gland Disorders 641 • Inorganic ions—major (Na+, K+, Cl¯, HCO¯3 ) and minor (Ca++, Mg++, HPO4¯, I, Scn¯ and F¯ ). • Secretory proteins and glycoproteins—various enzymes, large carbohydrate rich protein or mucin, antibacterial substance, group of proteins involved in enamel pellicle formation and calcium phosphate. • Serum constituents—albumin, blood clotting factor, B2 microglobulin and immunoglobulin.
Collection Technique Parotid Collector • Composition—it was developed by Lashley in 1916. It makes possible the collection of parotid fluid uncontaminated by the oral content. It is composed of two concentric circles and is made of either plastic or metal. • Technique—the center circle is designed to fit over the opening of Stensen’s duct and is connected to a graduated collecting tube. The outer concentric circle is attached to a rubber bulb, which exhausts air from the outer circle, when collector is held in place and draws the cheek surrounding the opening of Stensen’s duct into it. • Disadvantage—due to different anatomy, it cannot be used in submandibular and sublingual gland.
Segregator • Composition—it is developed by Schneyer which allows the collection of submandibular and sublingual gland. It is made up of plastic or metal. It must be constructed for each individual on the stone model. In it, preformed basic plastic collector is utilized. • Technique—this plastic is covered with rubber base impression material and placed on the floor of mouth beneath the tongue. In 5 minutes, impression can be removed. A recess is then made in the impression, over the opening of Wharton’s duct and plastic collecting tube is attached. The collector stays in position when the patient places his tongue against the lingual surface of the lower incisors. • Advantage—it may be sorted and reused for the individual patient. It collects saliva from sublingual and submandibular ducts.
Collection of Whole Saliva • Stimulation of saliva—for collection of whole saliva, stimulation of saliva is to be done by asking the patient to suck on sour candy or sour grapes. You can also ask patient to chew on cimer paraffin or rubber bands. A more standardized procedure is to swab a solution of 2% citric acid on the back and side of tongue at 15 seconds
intervals. Secretion can be obtained by draining, spitting and suction. • Draining—in this, the subject is placed with his head inclined forwards, so that saliva will collect in the anterior floor of the mouth. The position of the patient allows the saliva to flow over the lip, where it is collected by funnel. • Spitting—in this, the subject actively spits into the collecting funnel at regular intervals. • Suction—saliva ejector is applied orally in the area of lower incisors and the aspirated fluid is collected after the patient has remained quits for fixed time periods.
Function of Saliva • Digestive function—it participates in digestion by providing fluid environment for solubilization of food and taste substance, through action of enzyme amylase and lipase. It helps in formation of food bolus, which is readily chewed. • Lubricating—it keeps the oral tissues moist and facilitates swallowing and speaking. Mucus glycoproteins provide lubricant for the movement of oral tissues against each other and protection from chemical and thermal insults. • Protection of teeth—it helps to protect the teeth from dental caries by means of, both, cleansing and buffering action of saliva. It also controls the calcium and phosphate concentration in the saliva and around the teeth. • Protection from injury—it dilutes hot or irritant substance and thus prevents injury to mucus membrane. • Maintenance of mucus membrane integrity—the salivary mucin possesses rheological properties which include low solubility, high viscosity, elasticity and adhesiveness which enable them to concentrate on the oral mucosal surface. They provide an effective barrier against desiccation and environmental insult. Salivary mucin binds water effectively and hence serves as natural ‘water proofing’ and helps to maintain these tissues in a hydrated state. The glycosylated mucins of saliva are resistant to proteolysis. This maintains the integrity of mucus membrane by neutralizing the bacterial and PMN proteases. • Antibacterial properties—several salivary substances are capable of inhibiting the growth of microorganisms. They are glycoproteins, antibacterial protein, i.e. lysozome, immunoglobulin IgA, IgG, IgM and lactoferrin. • Debridment and lavage—the physical flow of saliva, augmented by muscular activity of lips and tongue, effectively removes a large number of potentially harmful bacteria from the teeth and mucosal surface. • Anti-carcinogenic activity—mucins limit the penetration of variety of potential irritants and toxins in foods, beverages as well as potentially hazardous agents from tobacco smoke and other sources.
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• Soft tissue repair—presence of nerve growth factor and epidermal growth factor in submandibular saliva accelerates wound healing. • Maintenance of tooth integrity—after the eruption the crown, the tooth is fully formed morphologically, but is crystallo-graphically incomplete. Interaction via diffusion of ions such as calcium, phosphorus, magnesium, fluoride as well as other trace components into the surface of enamel, increases the surface hardness, decreases permeability and increases the resistance to caries. Acquired pellicle, which covers the tooth surface after it begins to function in oral cavity, is made up of salivary proteins and lipids. • Maintenance of pH—it helps in maintenance of neutral pH in oral cavity and in esophagus. The salivary bicarbonates are responsible for maintenance of pH. Saliva also neutralizes the acids produced in bacterial plaque because of bacterial metabolism of carbohydrates. • Excretory functions—many drugs as well as alcohol are excreted into saliva which could theoretically serve as a route of elimination. • Water balance—salivary glands are a part of the control system for maintaining an appropriate level of hydration. Thirst and the need for fluid intake are usually originated by a dry mouth, which activates receptors in the oral cavity. • Hormonal function—polypeptide hormones known as epidermal growth factor, is identical with human urogastrone which is found in high concentration in urine. It is also found in submandibular and parotid saliva.
Examination of Salivary Glands Minor Salivary Glands • Technique—the minor salivary glands can be examined by simply drying the lower lip mucosa with cotton sponge, after eversion using thumb and index finger. Careful observation for the appearance of small globules of fluid emanating from minor gland duct orifice should be done. In situations where atrophy or significant reduction in salivary secretion has occurred, such as in Sjögren’s syndrome, the duct orifices will be marked by small red spot and secretion will not be observed.
• Bimanual palpation—palpation should be performed in the lateral surface of the mandible and on the soft tissues inferior and medial to the angle. Bimanual palpation with the patient’s mouth closed: with the masseter muscle relaxed, this method can be readily performed from the side or behind. Insertion of the index finger along the teeth to the most posterior location in the cheek with application of lateral pressure against the examining thumb on the face, this palpation can be performed. • Examination of Stensen’s duct—Stensen’s duct orifice should be identified adjacent to the upper molar teeth as a small fold or soft tissue flap in the buccal surface. The mucosa in the area should be dried with cotton sponge and the duct orifice observed for secretion while the gland is milked by applying firm pressure. The pressure is applied first in the posterior aspect, beneath the auricle and moving the palpating finger anteriorly and inferiorly, along the course of Stensen’s duct. Clear, colorless secretion that is sufficiently fluid to flow rapidly should be observed emanating from the duct orifice.
Submandibular Glands • Location of swelling—submandibular salivary gland enlargement is characterized by medial and inferior extension, the later resulting in discontinuity if the tissue contours at the inferior border of mandible. • External palpation—external palpation should start with the finger extending towards the midline and the thumb on the body of the mandible. Pressure is exerted, both, superiorly and laterally and the finger is gradually moved beneath the inferior border of the mandible. • Palpation—the patient should be advised to relax the tongue during palpation. Enlarged lymph nodes, except those involved with malignancy, will invariably move laterally with the examining finger, while the submandibular salivary gland will remain stationary. • Bimanual palpation—after this, bimanual palpation should be performed; the examiner placing the 2nd finger of one hand into the floor of the mouth beneath the tongue, the patient resting his teeth on the examiners fingers, while the fingers of the other hand are placed as previously described, that is on the skin beneath and medial to the body of the mandible. While pressure is exerted inferiorly intraorally by the finger, the other hand moves superiorly and laterally so that all organs come between the examiner’s two hands.
Sublingual Salivary Glands Major Salivary Glands Parotid Glands • Location of swelling—swelling of the parotid gland is usually associated with lateral extension of the lobe of the ear and difficulty in opening the jaw widely.
• Location—these are located in the floor of the mouth in the region of the middle third of the tongue, closely applied to its medial musculature attachment. The ductile pattern is extremely variable, frequently communicating with the mouth through a series of small orifice, rather than by means of small collecting ducts.
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Diagnostic Tests of the Salivary Glands
Functional disorders • Sialorrhea • Xerostomia
• Sialography—it is defined as a method of studying the salivary gland and the alveoli of the parotid and submandibular salivary gland radiographically. It is done by injecting radiopaque contrast medium or a retrograde injection of a radiopaque material into the duct system of a salivary gland and the study of its distribution by roentgenogram. • Salivary gland scanning (scintigraphy)—it is used for studying the glandular parenchyma. The salivary gland tissues take up compounds of periodic group VII elements such as iodine, bromine and technetium. It provides indication of salivary gland functions and allows bilateral comparisons and images of all four major salivary glands at the same time. • Ultrasonography—it involves the transmission of energy into the salivary tissues, receiving of the energy after it has been reflected by the tissues and recording it so that it can be presented for interpretation. It is also useful in identification of radiolucent stone. Different echo signals are obtained from different tumors. • Computerized tomography—it demonstrates small differences in soft tissues X-ray examination and distinction between gland and the adjacent soft tissues is greatly improved. It is usually done in cases of discrete swelling, both intrinsic and extrinsic to the salivary gland. • Arteriography—it will define the vasculature of the tumor but also delineates the origin of vascular supply. • Biopsy—it has been the most significant advancement in diagnosis and appropriate treatment of major salivary gland tumors. • Flow rate studies—comparative study of flow rate from major salivary glands is done over a time period. It provides information about salivary gland functions. • Magnetic resonance imaging—it is useful in discrete swelling of salivary glands and provides excellent soft tissue details. It readily enables differentiation between the normal and abnormal.
Obstructive disorders • Sialolithiasis • Mucus plug • Stricture and stenosis • Foreign bodies • Extra-ductal causes
Classification Developmental disorders • Aberrancy • Aplasia and hypoplasia • Hyperplasia • Atresia • Accessory ducts • Diverticuli • Congenital fistula
Cyst • Mucocele • Ranula Asymptomatic enlargement • Sialosis • Allergic • Associated with malnutrition and alcoholism Infection • Viral infection • Bacterial infection • Mycotic infection Autoimmune disorders • Sjögren’s syndrome • Mikulicz’s disease • Uveoparotid fever • Recurrent non-specific parotitis
Developmental Disorders of Salivary Gland Aberrancy It is defined as the situation in which the salivary gland tissue develops at a site where it is not normally found. It is also called as ectopic salivary gland. Ectopic salivary tissue can develop anywhere within the territory of the first and second branchial arches, in the lateral neck, pharynx or middle ear.
Clinical Features • Site—true aberrant salivary glands are most frequently reported in the cervical region, near the parotid gland or body of the mandible. The salivary gland tissue in the mandible is found posterior to the first molar and often has a small communication with a major salivary gland. • Developmental lingual salivary gland depression—the aberrancy of the salivary gland tissue represents only an extreme example of the condition known as the ‘developmental lingual mandibular salivary gland depression’. It is the developmental inclusion of the
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glandular tissue within or more commonly, adjacent to the lingual surface of the body of the mandible, in a deep well circumscribed depression. It was first described by Stafne in 1942 and hence referred to as ‘Stafne’s cyst’. • Salivary tissue in neck—salivary tissue is regularly found in lymph nodes within the neck and can be mistaken for metastatic disease, if found in a neck dissection specimen. • Gingival salivary gland choristoma—ectopic salivary gland tissue has been reported to occur in the gingiva, where it may be described as ‘gingival salivary gland choristoma’. • Clinical significance—they may become site for development of a retention cyst or neoplasm.
Aplasia and Hypoplasia Aplasia or agenesis is the congenital absence of the salivary gland. It was first described by Gruber in 1885. Aplasia may occur in association with other developmental abnormalities such as atresia of lacrimal puncta and congenital malformation of temporomandibular component.
Fig. 26-5: Hypoplasia of the unilateral parotid gland (Plain CT). Size of the left parotid gland (yellow arrow) is remarkably smaller compared with normal size of the right parotid gland (red arrow) (Courtesy M Shimizu).
Diagnosis
• Ectodermal origin—Macdonald suggested ectodermal origin for this anomaly.
• Clinical diagnosis—decreased production of saliva without any other visible clinical anomalies this disease should be suspected. • Radiological diagnosis—Computed tomography will be able to diagnose this lesion.
Clinical Features
Management
• Sites—any one of the glands or group of glands is missing, either unilaterally or bilaterally. Hypoplasia of salivary gland is rare but hypoplasia of parotid gland has been reported to be present with Melkersson-Rosenthal syndrome. • Symptoms—patient complains of xerostomia, which may be so severe as to necessitate the constant sipping of water throughout the day and particularly, during meal times. • Significance—the lack of saliva results in rampant dental caries and early loss of deciduous and permanent teeth. • Appearance of oral mucosa—the oral mucosa appears dry, smooth, or sometimes pebbly and shows a tendency for accumulation of debris. • Signs—patients exhibit characteristic cracking of lips and fissuring of the corners of mouth.
• Maintenance of oral hygiene—institution of scrupulous oral hygiene in an attempt to decrease dental caries and preserve the teeth as long as possible.
Causes
Radiological Features • CT features—it is sometimes observed that unilateral gland is missing (Fig. 26-5) or is very small compared to the contralateral side with congenital or posterior reasons. As they are mostly asymptomatic, the condition is mostly diagnosed by chance.
Hyperplasia of Salivary Gland Hyperplasia is the increase in the size of salivary gland.
Causes • Hormonal disorders—endocrine disorders and menopause. • Metabolic disorders—gout, diabetes mellitus. • Autoimmune—Sjögren’s syndrome, Waldenstrom macroglobulinemia. • Syndrome—aglossia-adactylia syndrome, Heerfordt’s syndrome and Felty’s syndrome. • Miscellaneous—hepatic disease, starvation, alcoholism, inflammation, benign lympho-epithelial lesion, adiposity, hyperthermia, oligomenorrhea and certain drugs.
Clinical Features • Prevalence—it is more common in minor salivary glands of the palate.
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Salivary Gland Disorders 645 • Size and site—palatal gland hyperplasia appears as small localized swelling of varying size, measuring from several millimeters to 1 cm, usually on the hard palate or at junction of hard and soft palate. • Surface—the lesion has an intact surface and is firm, sessile and normal in color. • Symptoms—it is usually asymptomatic.
Radiological Features • CT features—Computed tomography will diagnose this condition.
Congenital Fistula Patients with branchial cleft anomalies usually present with unilateral, painless swelling in the region of parotid. Rarely, they are bilateral. They form sinus tracts either in the crease behind the pinna or in front of tragus. They discharge saliva intermittently. Abscess formation, due to secondary infection, may occur. Complete surgical excision of the sinus tract is essential. The dissection is often very extensive and full dissection of facial nerve may be required.
Developmental Salivary Gland Defect
Diagnosis • Clinical diagnosis—it is not specific. • Radiological features—computed tomography will diagnose this condition.
Management • Excision for microscopic examination—as it cannot be differentiated from minor salivary gland tumors, it becomes essential to excise it for microscopic examination.
Atresia It is the congenital occlusion or absence of one or two major salivary gland ducts. Usually the submandibular duct in the floor of the mouth fails to cannulate during embryological development. The newborn infant presents, within 2 or 3 days of life, with submandibular swelling on the affected side due to the presence of a retention cyst. It may produce a relatively severe xerostomia.
Accessory Duct An accessory parotid lobe is the most common developmental anomaly. It occurs in as many as 20% of subjects. Its position is constant, arising from the horizontal component of the parotid duct as it crosses the masseter muscle. Its importance lies in the fact that any of the diseases that can affect the salivary glands, may involve the accessory lobe and lead to diagnostic confusion, as the possibility is not considered. This is because the symptoms and signs are not within the normal anatomical territory of the parotid. Presence of additional duct in some salivary glands has been reported.
Diverticuli They are small pouches or out pocketing of the ductal system of one of the major salivary glands. Their presence leads to recurrent episodes of acute parotitis.
It is also called as ‘static bone cavity or cyst’, ‘Stafne’s cyst or defect’, ‘lingual mandibular bone cavity’, ‘lingual cortical mandibular defect’, and ‘latent bone cyst’. It is the developmental inclusion of glandular tissue within or more commonly, adjacent to the lingual surface of the body of mandible. It was recognized by Stafne in 1942. Mandible develops around the lobe during development. As it remains stable in size, it is called as ‘static bone cyst’.
Clinical Features • Incidence and sex—it is rare. Males are affected more commonly than females. • Site—it is located in the posterior body of the mandible. • Sublingual gland bony defect—in some cases cortical defect can also occur in anterior region. These defects are related to sublingual gland. • Symptoms—it is asymptomatic and only diagnosed on radiographical examination. • Sign—sometime a notch or depression can be palpable on clinical examination in the posterior area.
Radiographic Features • Site—it is found below the mandibular canal and above the inferior border of mandible, just anterior to the angle of jaw and below and just posterior to third or second molar (Fig. 26-6). • Size and shape—round or ovoid radiolucency that will vary in size from 1 to 3 cm in diameter. It is occasionally bilateral. • Borders—it is well defined by dense radiopaque border that is the result of the rays passing tangentially through the relatively thick wall of depression. • Sublingual bony defect—in some instances, round or ovoid radiolucency may occur in the anterior segment of the mandible, generally appearing as a rather poorly circumscribed lesion, somewhere between the first premolar and central incisor area. This may be caused by impingement of sublingual gland.
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3 Fig. 26-6: Stafne’s bone cyst presented as radiolucency below the mandibular canal and surrounded by well corticated border (Courtesy Dr Tapasya Karamore).
Diagnosis • Clinical diagnosis—it is not possible or suspect this disease clinically. • Radiological diagnosis—round radiolucency located below the mandibular canal in molar area will diagnose this condition.
Differential Diagnosis • Radicular—it is associated with carious tooth and radiolucency is attached to the root of teeth. • Residual—pre-extraction radiograph shows tooth with evidence of deep caries.
Management No treatment is necessary as the patient is asymptomatic.
Functional Disorders of Salivary Gland
• Drugs—certain drugs have the ability to stimulate salivary flow. Such drugs are known as ‘sialogogues’. Increased salivation due to drugs can result from a variety of its pharmacologic effects. Besides acting on the parasympathetic and sympathetic receptors, drug action can lead to sialorrhea by direct CNS stimulation or as a result of nasal and oropharyngeal irritation, which leads to afferent stimulation of salivary nuclei. Drug which can cause sialorrhea are lithium and cholinergic agonists. • Local factors—it can be the result of, different types of stomatitis, ANUG, erythema multiforme. • Systemic disease—paralysis, alcoholic neuritis, Parkinson’s disease, epilepsy, Down’s syndrome, undetermined neuromuscular disorders or following a head injury or stroke. • Protective buffering system—episodic hypersecretion of saliva or ‘water brash’ may occur as protective buffering system to neutralize stomach acid in individual with gastroesophageal reflux disease. • Miscellaneous—psychic factor, metal poisoning and facial paralysis.
Clinical Features • Drooling—the salivary flow is more in infancy and childhood, but the drooling observed in infants is related to inadequate swallowing rather than excessive production. Drooling or sialorrhea can be a devastating problem for the affected child or adult. • Symptoms—the problem may range from mild embarrassment and discomfort to emotional and physical impairment. The involved person may require numerous clothings and/or bib changes per day. • Signs—he or she may develop cheek scarring, lip chapping or infection from constant exposure to saliva. The soiling of clothes, carpets, furniture, books and people, often results in social rejection, employment difficulties and stigmatization.
Management
Sialorrhea (Ptyalism) An increased salivary secretion is termed as ‘sialorrhea’ or ‘ptyalism’.
Mechanisms The secretory innervations of the salivary glands are primarily under the control of the parasympathetic nervous system. Stimulation of the parasympathetic system causes profuse secretion of watery saliva. Some persons are unable to swallow their saliva fast enough to prevent drooling.
• Treatment in children—no treatment is recommended in children less than four years of age with only mild or moderate amount of drooling, which may improve spontaneously. • Oral motor training—oral motor training, intended to improve motor skills, is the key non-surgical management modality and all patients (if appropriate) should have a minimum of six months of this type of therapy format, before any surgical management is considered.
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Salivary Gland Disorders 647 • Biofeedback—biofeedback utilizes conditioning techniques to train the patients to swallow more frequently. It has been utilized in aware patients with only a modest drooling problem and who have very motivated parents. • Removal of local factors—situational factors that may contribute to drooling should be eliminated if possible, i.e. dental disease, nasal airway obstruction, poor seating and inappropriate medications. • Atropine—the anti-cholinergic drug, atropine sulfate, has been shown to reduce the amount of resting secretion, intraoral accumulation and pharyngeal-laryngeal pooling of saliva in more than 50% of patients. • Mechanism of action—the drug is a competitive antagonist of muscarinic actions of acetylcholine. It does not prevent the release of acetylcholine, but antagonizes the effect of this neurotransmitter on the effector cells. This action results in drying of the mouth through reduction of salivary gland secretions. Atropine-induced inhibition of salivation occurs within 30 minutes to one hour. Inhibition peaks within two hours after oral administration, but can persist for up to four hours. • Dose—the usual oral dose for adults is 0.4 mg, every 4 to 6 hours. In children, the suggested dose is 0.01 mg/kg, but generally not exceeding 0.4 mg, every 4 to 6 hours. • Contraindication—due to potential side effects, atropine sulfate is contraindicated in patients with asthma, glaucoma or synechia (adhesions) between the iris and lens of the eye. • Other drugs—other drugs which are used as antisialogogue are scopolamine (0.4-0.6 mg), methantheline (50-100 mg) and propantheline (15-30 mg). • Surgery—surgery is a primary recommendation in individuals with a cognitive delay and profuse drooling and secondarily in those that have failed to non-surgical therapy for a minimum of six months. • Relocation of duct—relocation of submandibular and parotid duct posteriorly to the tonsillar fossa. This will reduce salivary flow and drooling. • Bilateral tympanic neurectomy—sectioning of chorda tympani destroys parasympathetic innervations to the glands.
Xerostomia It is the subjective clinical condition of less than normal amount of saliva. It is dryness of mouth, which is a clinical manifestation of salivary gland dysfunction.
Etiology • Radiation induced—ionizing radiation to head and neck region for the treatment of cancer results in pronounced
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changes in the salivary glands located within the primary beam. The degree of damage caused by the radiotherapy is related to dose-time-volume factor. Damage to the acinar cells has been noted with a single 100 rads dose of X-rays. Radiation sensitivity decreases in following order: the parotid gland, submandibular, sublingual to minor glands. Serous aciner cells appear to be more sensitive to radiation, than the mucus cells. As the dose is increased, disorganization and destruction of the acinar cells occur, resulting in their replacement by fibrous or faulty tissues. Both, the stimulated and unstimulated salivary flow rate decreases dramatically with increasing radiotherapy. Pharmacologically induced xerostomia—there are about 500 drugs which can cause xerostomia. The classes of drugs which cause xerostomia include anticonvulsants, antiemetics, antihistaminics, anti-hypertensives and antispasmodics. The mode of action for decreased salivary flow is generally related to the para-sympathetic activity, usually an antimuscarine effect. Other actions that can decrease salivation are generally more miscellaneous and include vasoconstriction of salivary glands, changes in fluid and electrolyte balance and changes in acinar or ductal function. Local factors—local factors like decreased mastication, smoking and mouth breathing can also lead to xerostomia. Developmental—developmental abnormalities of salivary glands, tumors, autoimmune states and certain diseases which affect afferent or efferent portions of neural transmission reflex are some of the other causes of xerostomia. Systemic alternations resulting in xerostomia • Nutritional—certain deficiency states like pernicious anemia, iron deficiency anemia and deficiency of vitamin A and hormones can cause xerostomia. • Fluid loss—fluid loss associated with hemorrhage, sweating, diarrhea, vomiting. • Diabetes mellitus—it is associated with xerostomia. • Sjögren syndrome—xerostomia is also common in Sjögren syndrome. • Other disease—systemic diseases, which are accompanied by high temperature and dehydration, usually result in diminished salivation. Xerostomia may also be found in HIV infection, sarcoidosis, and graft versus host resistance.
Clinical Features • Effect of xerostomia on oral functions—patient may notice increased thirst, increased uptake of fluid especially while eating. There is also frequent use of means like chewing gums and consumption of sour candy. Patient
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also gets difficulty in swallowing, speech and eating dry food. There is also burning and tingling sensations in the mouth. There is also complaint of frequent oral infections, intolerance to dental appliances and abnormal taste in the mouth. Salivary gland enlargement—painful salivary gland enlargement is also present. Effect of xerostomia on normal functions—many times, xerostomia is accompanied by hypofunction of other secretory glands. Blurred vision and ocular dryness. Itching, burning and sandy sensation in eye. There is also dryness of pharynx and skin. Itching and burning sensation of vagina. Clinical signs of xerostomia—dryness of lining oral mucosa. Oral mucosa appears thin, pale and feels dry. Tongue blade may adhere to soft tissues. Tongue may manifest deficiency by atrophy of the papillae, inflammation, fissuring, cracking and denudation. There is also increased incidence of dental caries. Candidiasis—pseudo membranous and hyperplastic form of candidiasis occurs. The reason for occurrence candidiasis is absence of normal cleansing and antimicrobial activity of the saliva. Residual saliva—residual saliva which remains is foamy, thick and ropey.
Management Stimulation of salivary production • Local stimulation—chewing of gums, mints, paraffin and citric acid containing lozenges and rinses. Disadvantages of it are: • Effects are short lived. • Frequent application can be inconvenient. • Citric acid may irritate oral mucosa. • Continuous use may contribute to demineralization. • Systemic stimulation • Bromhexine—it is a mucolytic and mucokinetic agent, capable of inducing thin copious bronchial secretions. Dose—adults (8 mg TDS), children 1-5 years (4 mg BD) and children 5-10 years (4 mg TDS). • Anethole trithione (ANTT)—it is a directly acting cholinergic agonist which acts by neurostimulation. Dose 1 to 2 tabs (25 mg) TDS. • Pilocarpine—pilocarpine is a cholinergic parasympathomimetic agent with a broad range of pharmacologic effects. It increases the secretion by exocrine glands and can affect the sweat, salivary, lacrimal, gastric, pancreatic, intestinal glands and mucosal cells of the respiratory tract. The usual dose is 5 mg, TDS. It produces short duration of (3 hours) increased salivary flow, without the accompanying side effects. It should not be used in patients suffering from asthma.
Symptomatic treatment • Salivary substitute—there are number of salivary substitute available for the treatment of xerostomia. Most commonly contain carboxymethylcellulose or hydroxyethylcellulose as lubricants and variety of artificial sweeteners, preservative and chloride or fluoride salts. Disadvantages are: • Their regular use is inconvenient to the patient. • Most of them are more viscous than the natural saliva. • They are expensive. • They fail to provide antimicrobial and other protective functions of natural saliva. • Composition of artificial saliva • Carboxymethylcellulose—10 gm/l. • Sorbitol—30 gm/l. • Potassium chloride—1.2 gm/l. • Sodium chloride—0.843 gm/l. • Magnesium chloride—0.051 gm/l. • Calcium chloride—0.146 gm/l. • Dipotassium hydrogen phosphate—0.342 gm/l. • Oral hygiene product—patient should use oral hygiene product which include lactoperoxidase, lysozyme, and lactoferrin. • Discontinuous of drug—drug which is causing xerostomia should be discontinued. Suggestions to the patient having xerostomia • Sweet and tart food—try very sweet or tart foods and beverages such as lemonade; these foods may help to produce more saliva. (Do not try this in sensitive teeth or sore throat.) • Sucking of sugar free candy—suck on sugar-free hard candy (avoiding those with citric acid), popsicles or chew sugar-free gum. These can help produce more saliva. • Sucking ice cubes—try sucking ice cubes or ice lollies. Home-made lollies can be easily made by freezing fresh juice in ice-cube trays or in special lolly containers with sticks, which can be bought from many kitchenware shops. • Don’t take following thing—avoid chewable vitamin C and acidic, sugared lozenges. Avoid dry foods such as cookies, toast and crackers, or soften them with liquids before eating. Avoid chocolates, peanut butter and pastry: they stick to the roof of mouth. Avoid over salty foods. • Soft and liquid food—use soft and liquid foods, which may be easier to swallow. • Drink frequently—have a sip of water every few minutes to help in swallowing and talking more easily. Carry a small water bottle for frequent sips during the day.
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Salivary Gland Disorders 649
Obstructive Disorders
Clinical Features
Sialolithiasis It is the formation of calcific concretions within the parenchyma or ductal system of the major or minor salivary glands. It is also called as ‘salivary gland stone’ or ‘salivary gland calculus’. These are stones within major and minor salivary glands. These are the most common calcifications found in soft tissues of oro-orbital region.
Composition • Calculus—the calculus consists of laminated layers of organic material, covered with concentric shells of calcified material. • Crystalline structure—the crystalline structure is chiefly hydroxyapatite and contains octacalcium phosphate. • Chemical composition—the chemical composition is principally calcium phosphate and carbon with traces of magnesium, potassium, chloride and ammonium.
Etiopathogenesis • Neurohumoral mechanism—a neurohumoral condition, leading to salivary stagnation, results in a nidus and matrix formation. • Metabolic mechanism—in the presence of coexisting inflammation, a metabolic mechanism favors precipitation of salivary salts into the matrix.
Prevalence Submandibular (83%) calculi are more commonly seen than the parotid (10%) or sublingual (7%) calculi, due to following factors. • Anatomic factors • The length and irregular course of Wharton’s duct. • The submandibular gland and ductal system lies in a dependent position. • The greater size and position of the orifice. • The orifice is much smaller than duct lumen. • Physiochemical factors • High mucin content of saliva. • Great degree of alkalinity with high percentage of organic matter. • Greater concentration of calcium and phosphate salts. • Low content of carbon dioxide. • Richness in phosphatase enzyme.
Types • Ductal sialoliths—it is located in the duct of gland. • Glandular sialoliths.
• Age and sex—they are usually encountered in middle aged patients with slight predilection for occurrence in men. • Symptoms—the symptoms of sialolithiasis vary but intraglandular stones seem to cause less severe symptoms than the extraglandular or intraductal types. On occasions, there may be complete absence of subjective symptoms. • Pain—many patients complain of moderately severe pain. The occlusion of the duct prevents the free flow of saliva and this stagnation or accumulation of saliva, when under pressure, produces pain. • Swelling—patient also complains of intermittent transient swelling during meals, which resolves after meals. As the calculus itself rarely blocks a duct completely, the swelling subsides as salivary demand diminishes and as saliva seeps past the partial obstruction. • Systemic symptoms—if no treatment is instituted, it appears as a pronounced exacerbation characterized by an acute suppurative process with attendant systemic manifestations such as fever and malaise. • Signs • Pus—pus may exude from the duct orifice. • Surrounding tissue—the soft tissues surrounding the duct show a severe inflammatory reaction. It appears as swelling, redness and tenderness. • Palpation—stones in the more peripheral portion of the duct may often be palpated, if they are of sufficient size. • Ulceration—sometimes, the overlying mucosa may ulcerate over the stone allowing the calculus extend into the oral floor. • Absence of saliva—no saliva is seen to be coming out through the duct orifice. • Swab test—if stone is present in one duct only then saliva will not come out from that duct. It can be tested by placing two dry swabs one on each orifice and some lemon juice is dropped on the dorsum of the tongue. A minute later patient is asked to move the tongue up. The swab on the orifice of the duct where the stone is impacted will remain dry, whereas the other swab will be wet. • Size—it usually occurs as a solitary concretion varying in size from a few millimeters up to several centimeters. • Stones in minor salivary glands—sialolithiasis of minor salivary gland is a rare occurrence. The most common site is buccal mucosa either near the commissure or in proximity to the mandibular mucobuccal fold. It is more common after the age of 39 years. The lesions appear as firm, freely movable masses, deeply situated into the mucosal surface.
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Radiographic Features
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• View taken—projection for submandibular duct stone is standard mandibular occlusal view and for parotid gland, periapical view in the buccal vestibule. Reduce the exposure to avoid burnout of sialoliths. • Silography—sialography is indicated when sialoliths are radiolucent. There is ductal dilatation caused by associated sialodochitis. The film usually shows contrast medium present behind the stone. • Site—there is white or gray opacity situated somewhere in the region of the glandular apparatus. It may be solitary or multiple. • Radiodensity—they are almost radiopaque, so that even very small ones are visible in well prepared radiograph (Fig. 26-7).
Fig. 26-8: Small size salivary stone present as radiopacity in ramus of mandible (Courtesy Enzio Rovigutti).
Fig. 26-7: Well defined radiopacity seen at the angle of mandible due to salivary stone (Courtesy Enzio Rovigutti)
• Shape—it is usually oval shaped and is cylindrical with multiple layers of calcification. • Borders—smooth borders with even radiodensity. • Size—the size varies from little more than a pinhead up to a length of an inch (Fig. 26-8) or more, with a girth of about 5 mm. • CT—it will show dense radiopaque area in contrast study (Fig. 26-9).
Diagnosis • Palpation—palpation is an indispensable tool in the diagnosis of sialoliths. Palpation of the suspected gland frequently reveals it to be larger or firmer than the normal gland of the opposite side. Digital manipulation will produce a flow of saliva through the duct orifice and will allow visual inspection of the salivary fluid. During examination, the soft tissues overlying the duct should be manually stretched. Often, the physical distortion caused by the presence of calculus will become apparent. In addition yellowish color of the calcific deposits may
Fig. 26-9: Well defined radiopaque area seen in submandibular gland (Courtesy Dr Iswar).
be seen through the distended and thinned mucus membrane. • Metallic duct probe—a metallic duct probe can also valuable. Careful probing of the duct with a metallic probe will indicate the existence as well as the location of calculus. • Radiographic examination—radiographic examination usually reveals the presence of calcific deposits. • Sialography—sialography is an invaluable aid in isolating the sialoliths which had not been identified on the standard intraoral and extraoral radiography.
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Salivary Gland Disorders 651 Differential Diagnosis • Gas bubble—it should not be confused with gas bubbles introduced during sialography. Gas bubbles are more easily removed and are more circular than sialoliths. • Hyoid bone—bilateral on panoramic radiography. • Myositis ossificans—restriction of mandibular movements. • Phleboliths—no sialadenitis present. They are more or less rounded and contain laminations or central dark area. • Calcific submandibular lymph nodes—if painful swelling accompanies the calcified mass, it is usually sialolith. • Chondrodystrophia calcificans congenita—it is sometimes associated with calcification in the neck, which can resemble the submaxillary calculi in the radiographs.
Management • Manual manipulation—in case of small stone, gentle massage of the gland should be done. It will help to move the stone toward the duct orifice. Sialogogues, moist heat and increased fluid intake will also promote the passage of stone. • Stone in the submandibular duct—if the stone is palpated near the orifice of the duct it can be removed by an incision made directly over it through the mucus membrane of the mouth. • Stone in the submandibular gland—in this case, excision of gland is advised. • Antibiotics—if acute infection is present, then antibiotics should be given. • Salivary gland endoscopy—this is newer method which is useful in removal of sialoliths. • Lithotripsy—this is fragmentation of stone in the gland. Nowadays, extracorporeal shock wave lithotripsy has been successful in many patients.
Mucus Plugs These are incompletely mineralized sialoliths. Clinical symptoms and signs are same as that of stones. The diagnosis of mucus plug is based upon clinical history, radiography and sialograms. If sialograms confirm the intraductal obstructive disease secondary to non-mineralized intraductal object, the diagnosis of mucus plug can be made.
• Acute trauma—acute trauma with resultant edema and/ or scarring. • Tumor—intraductal tumor formation.
Types • Papillary obstruction—it may be either acute ulcerative obstruction or chronic fibrotic stenosis. Acute ulcerative obstruction is usually caused by acute trauma to the papilla and is treated conservatively with saline rinses and salivary gland massage. The ulcer generally heals without scarring and the symptoms will subside in such cases. In chronic fibrotic papillary obstruction irritations to papilla has been recurrent and scarring exists. • Duct obstruction—it may be due to a variety of factors. In cases of ductal obstruction secondary to acute trauma treatment is directed towards providing the duct patency until the edema is resolved. When the ductal obstruction occurs secondary to irritation or scar contracture, sialograms are helpful in localizing the status of gland. If the gland is healthy, progressive and frequent dilatation of involved duct with lacrimal probes is generally successful in relieving the symptoms and signs. If this does not prove beneficial, ductoplasty is indicated.
Foreign Bodies Rarely, foreign bodies become lodged within Wharton’s duct and less commonly in Stensen’s duct. Toothbrush bristles, toothpicks, spikes of wheat, fish bone, portions of fingernail have been reported within the salivary gland duct and act as causes of obstructive and/or inflammatory disease of the salivary gland.
Extraductal Causes Muscle pressure, tumors, enlarged lymph nodes and denture flanges associated with the primary salivary duct can cause obstructive signs and symptoms.
Parotid Fistula It may arise from parotid gland or duct. It may be internal, when it opens inside the mouth and external, when it opens to the exterior.
Strictures and Stenosis
Causes
These are the rare conditions occurring in the salivary gland area.
• Traumatic—penetrating injury particularly by glass splinters. • Parotid abscess—rupture of parotid abscess. • Inadvertent incision—inadvertent incision while draining of parotid abscess. • Complication—complication of superficial parotidectomy.
Etiology • Irritation—irritation from prosthetic appliances, maloccluded or malpositioned teeth.
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Clinical Features • Symptoms—the main complaint is opening in the cheek with discharge. • Signs—discharge come out only during meals. • Adjacent skin—there may be excoriation of the neighborhood skin.
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• It will give an indication whether the fistula is in relation to the main duct, ductile or to the gland.
Diagnosis • Clinical diagnosis—discharged from Stensen’s duct after trauma or surgery. • Radiological diagnosis—it will exactly diagnose the parotid fistula.
Management • Reconstruction of the duct—it is done by surgical approach.
Cysts of Salivary Gland Mucocele It is a term used to describe the swelling caused by pooling of saliva at the site of injured minor salivary gland. It is also called as ‘mucus extravasation phenomenon, mucus escape reaction’. It is not true cyst it lacks an epithelial lining.
Fig. 26-10: Mucus extravasation cyst seen on lower lip (Courtesy Dr Parate).
• Size—the mucocele may be only 1-2 mm in diameter, but is usually larger; majority of them being between 5 and 10 mm in diameter. • Appearance—superficial cyst appears as bluish mass, as the thin overlying mucosa permits the pool of mucus fluid to absorb most of the visible wavelength of light (Fig. 26-11). If inflamed, it is fluctuant, soft, nodular and dome shaped elevation. Deeper lesions have the color of normal mucosa and are firmer. ]
Etiopathogenesis • Trauma—it is caused by laceration of a minor salivary gland duct by trauma resulting in extravasation of mucus into the connective tissue. There is accumulation of mucus in the connective tissue and with the continuous pooling of saliva a clearly demarcated cavity develops which has no epithelial lining.
Clinical Features • Age and sex—mucus extravasation cysts occur in younger patients. The reason for occurrence in young people as they are more prone to trauma that induce mucin spillage. It is equal in both sexes. • Site—they are very common and occur most frequently on the inner aspect of lower lip (Fig. 26-10); but may also occur on the palate, cheek, tongue and floor of mouth. The lesion may lie fairly deep in the tissues or may be exceptionally superficial. • Symptoms—patient may complain of painless swelling which is frequently recurrent. The swelling may suddenly develop at meal time and may drain simultaneously at intervals.
Fig. 26-11: Bluish color of mucocele seen on lower lip.
• Shape—the swelling is round or oval or dome shaped (Fig. 26-12). • Consistency—it is either soft or hard depending upon the tension in the fluid. It cannot be emptied by digital pressure. • Aspiration—on aspiration, it yields sticky viscous clear fluid. • Superficial mucocele—it is present as single or multiple tense vesicles that measures 1 to 4 mm in diameter. The lesion burst leaving shallow painful ulcer that heals
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Salivary Gland Disorders 653 Types • Superficial—the superficial variety may develop as a retention or extravasation phenomenon associated with trauma to one or more of the numerous excretory ducts of the sublingual salivary gland. • Plunging or cervical—it ramifies deeply into the neck.
Clinical Features • Age and sex—it is usually fun in children and young adults with no sex predilection. • Site—the typical position is on the floor of the mouth (Fig. 26-13), below the tongue and on the side of frenum. They are usually unilateral. Fig. 26-12: Dome-shaped swelling of mucocele (Courtesy Dr Parate).
within a few days. It is seen on soft palate and posterior buccal mucosa. • Recurrence—patient may give history of recurrent swelling which ruptures and reappears again after some time.
Diagnosis • Clinical diagnosis—dome shaped soft swelling on lower lip which is lateral to midline is typical features of mucocele. • Laboratory diagnosis—in biopsy, it shows vacuolated macrophages which are sometimes called as ‘muciphage’.
Differential Diagnosis • Vascular lesion and superficial non-keratin cyst—aspiration should be done. • Early Mucoepidermoid tumor and adenocarcinoma— induration is present.
Management • Surgical excision—complete excision of the mucocele should be done under local anesthesia. To avoid recurrence, adjacent minor salivary gland should also be removed which are feeding the lesion. • Cryosurgery—surgery with cryoprobe is also helpful in managing the mucocele.
Ranula It is derived from Latin word ‘Rana tigerina’, i.e. frog belly. The term ranula is used for the mucoceles occurring in the floor of the mouth, in association with ducts of submandibular or sublingual glands.
Fig. 26-13: Unilateral swelling seen on left side in floor of mouth (Courtesy Dr Datarkar)
• Symptoms—it develops as slowly enlarging painless mass on one side of the floor of mouth. When the swelling suddenly grows, it may be painful. Big ranula may cause difficulty in speech or eating. • Appearance—they produce blue shaped swelling (Fig. 26-14) like a frog’s belly, hence it was given the term ‘ranula’ (‘ranula’ in Greek mean frog’s belly). The overlying mucosa of the swelling is normal in appearance. • Shape—it is spherical or dome shaped with only superficial half is visible. • Size—it is smaller in early morning and largest just before meals, due to increased secretory activity in periods of gustatory stimulation and water absorption from the pooled mucus during inactive period. • Consistency—it is soft and tends to fluctuant. It cannot empty by pressure and is non-pulsatile. • Fluctuation and transillumination—both tests are positive. The ranula is typically known as brilliant translucent swelling. • Aspiration—aspiration yields sticky clear fluid. • Plunging ranula—when intrabuccal ranula has a cervical prolongation, it is called as deep or plunging ranula.
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Fig. 26-14: Blue shaped swelling seen of ranula.
• Origin—it is derived from cervical sinus. • Location—it lies along the posterior border of the mylohyoid muscle and appears in the submandibular region. • Appearance—sometimes, plunging ranula herniates through the mylohyoid muscle and cause a swelling in suprahyoid or infrahyoid region. • Bidigital palpation—to palpate plunging ranula, bidigital palpation should be performed. One finger is placed inside the mouth on the ranula and the other finger is placed on the swelling in the submandibular region. If pressure on the first finger causes sense of fluctuation on 2nd finger or vice versa, then it is plunging ranula.
Radiological Features • CT features—On CT, the lesion is observed as a homogeneous, water density mass with clear boundary (Fig. 26-15A) • MRI features—on MR images, the lesion shows low signal intensity on T1 weighted images; very high signal intensity on T2 weighted images. On sonograms, the plunging ranulas are observed as a well-delineated, but not round, anechoic mass (Fig. 26-15B).
Diagnosis • Clinical diagnosis—blue shaped swelling in floor of mouth in lateral position will go in favor of ranula. • Radiological diagnosis—MRI and CT scan will demonstrate lesion.
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B Figs 26-15A and B: Simple ranula. (A) T1 weighted MR image shows lower signal intensity than that of muscles in the left sublingual region; (B) T2 weighted MR image of the same case. Note the remarkably high signal intensity of the lesion (Courtesy M Shimzu).
Management • Surgical excision—they are best treated by surgical excision including a portion of the surrounding tissues. • Partial excision with marsupialization—the major part of the cyst wall together with its overlying mucus membrane is excised.
Salivary Duct Cyst It is also called as ‘mucus retention cyst, mucus duct cyst, and sialocyst. It is true cyst as it is lined by epithelium.
Differential Diagnosis
Etiopathogenesis
• Sublingual dermoid—it is more often in midline and it is not translucent, while ranula is translucent. • Submandibular lymph nodes swelling—it is hard or firm in consistency.
• Obstruction—it is caused by obstruction of minor salivary gland duct which causes the backup of saliva. This continuous pressure dilates the duct and forms a cyst like lesion.
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Salivary Gland Disorders 655 Clinical Features • Age and sex distribution—retention cysts occur most often in older patients with no predilection for any sex. • Site—this is most common in parotid gland. Intraorally, it is common on floor of mouth, buccal mucosa and lips. • Appearance—it is slow growing and looks like mucoceles. It is soft, fluctuant swelling which appear bluish. • Multiple retention cyst—in some cases, patient may develop multiple painful nodules which demonstrated as dilated ductal orifices on the mucosal surface.
Diagnosis
• Site—the enlargement is usually bilateral and may present a course of recurrent painless enlargement of gland. The parotid gland is more frequently affected. • Appearance—swelling of the preauricular portion of the parotid gland is the most common symptom, but retromandibular portion of the gland may also be affected.
Radiological Features • Sialography—on sialography, leafless tree appearance is seen (Fig. 26-16). This appearance is caused by compression of finer duct by hypertrophic aciner cells.
• Clinical diagnosis—it is very difficult to differentiate between mucocele and retention cyst. • Laboratory diagnosis—biopsy shows lining of epithelium which consists of cuboidal, columnar or atrophic squamous epithelium surrounding thin or mucoid secretion in the lumen.
Management • Surgical excision—it is treated by conservative surgical excision. • Antibiotics—in some cases of multiple retention cyst, antibiotics like erythromycin and chlorhexidine mouth is helpful in relieving the pain of the patient. • Sialogogues—this is helpful in stimulating salivary flow and thereby preventing an accumulation of mucin.
Asymptomatic Enlargement of the Salivary Gland Sialosis (Sialadenosis) It is characterized by non-neoplastic non-inflammatory enlargement of the salivary gland.
Etiopathogenesis • Systemic disease—the condition is found in association with systemic diseases especially cirrhosis, diabetes, ovarian and thyroid insufficiency, alcoholism, general malnutrition, anorexia nervosa, and malnutrition. • Neurogenic medication—neurogenic medication like antihypertensive drugs, psychotropic drugs and sympathomimetic drugs can cause sialosis. • Mechanism—above disease may result in dysregulation of the autonomic innervations of the salivary acini causing an aberrant intercellular secretory cycle.
Clinical Features • Age and sex distribution—it more commonly affects the females. As such there is no age predilection.
Fig. 26-16: Leafless tree appearance seen in sialosis (Courtesy M Shimzu)
Diagnosis • Clinical diagnosis—bilateral non-inflammatory enlargement of parotid gland gives one clue to the diagnosis. • Radiological diagnosis—leafless tree appearance seen in this disease. • Laboratory diagnosis—a characteristic alteration in the chemical constituents of saliva is a distinguishing feature of sialosis. Significant elevation of salivary potassium and concomitant decrease in salivary sodium is observed.
Management • Control of underlying cause—this is most important management for sialosis. • Partial parotidectomy—it can be performed if swelling becomes cosmetic concern.
Allergic Sialadenitis In some cases, it may not appear as a true hypersensitivity reaction but rather as a toxic or idiosyncratic reaction to drugs that cause decreased salivary flow, resulting in secondary infection.
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Etiopathogenesis
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• Drugs—various drugs which have been reported to cause allergic sialadenitis include sulfisoxazole, phenothiazines, iodine containing compounds, mercury, thiouracil and phenylbutazone. • Mechanism—the exact mechanism of salivary gland enlargement and loss of function following administration of these drugs is not known. Most of the drugs cause decrease in capillary permeability, whereas others cause sodium and chloride retention, which subsequently leads to edema.
bilateral swelling of the salivary glands. It mainly affects major salivary glands, but also affects the testis, meninges, pancreas, heart and mammary glands. It is caused by paramyxovirus. Incidence of mumps decreases after vaccine is available since 1967.
Transmission • Saliva and urine—it usually spreads from human reservoir, by airborne infection of infected saliva and possibly urine.
Clinical Features
Clinical Features • Appearance—the clinical appearance of allergic sialadenitis varies, but in most of the cases, there is bilateral parotid gland enlargement following the administration of the drug. • Symptoms—the enlargement may be painful and is usually associated with conjunctivitis and skin rashes.
Diagnosis • Clinical diagnosis—enlargement of gland with skin rashes and conjunctivitis.
Management • It is a self-limiting disease and needs no treatment. But in some cases, secondary bacterial infection may develop and need treatment.
Associated with Malnutrition or Alcoholism Asymptomatic enlargement of the parotid gland may occur in patients with nutritional deficiency, especially vitamin A and alcoholism. The patient usually gives history of longterm gradually increasing swelling of the parotid gland. Clinically, the swelling is asymptomatic and can occur bilaterally. Palpation of enlarged gland reveals a normal tone and non-tender swelling. Simultaneous swelling of the submandibular salivary gland is a rare finding. The flow has been reported to be increased, but composition of the saliva remains unchanged, except for the elevated amylase level.
Viral Infection
• Age and sex—it is more common in boys than in girls and most often seen between the age of 5 and 15 years. • Incubation period—it is of 2 to 3 weeks and patient is contagious from one day before clinical appearance of the lesion. • Site—the parotid gland is most commonly involved and it is usually bilateral. Submandibular gland may also be involved, although this is less noticeable and cause less pain. Both the parotid glands may involve simultaneously, but more commonly one parotid gland swells 24 to 48 hours after the other. • Prodromal symptoms—it is preceded by onset of headache, chills, moderate fever, vomiting and pain below the ear which lasts for about one week. • Onset—it is then followed by sudden onset of salivary gland swelling which is firm somewhat rubbery or elastic and without purulent discharge from the salivary gland duct. • Symptoms—it produces pain upon mastication especially while eating sour food. • Signs—the enlargement of parotid gland causes elevation of ear lobule. Swelling may extend upto posterior border of mandible. • Sublingual gland involvement—its involvement of sublingual gland occur bilaterally. It may produce swelling in the floor of mouth. • Ductal papilla—papilla on the opening of parotid duct is often puffy and reddened. • Course—most of the cases are self-limiting, with salivary gland enlargement subsiding within a week.
Complications
Various viruses like paramyxovirus, cytomegalovirus, parainfluenza type-3 and coxsackie virus may infect salivary glands and cause its enlargement.
Mumps It is also called as ‘epidemic parotitis’. It is an acute contagious viral infection, characterized chiefly by unilateral or
• Orchitis—When mumps occur in adult males, orchitis (inflammation of the testis) is of great danger and ensues in 20% of the cases. It may result in sterility. • Pancreatitis—involvement of pancreas producing acute pancreatitis often causes an elevation in serum lipase. • Meningitis—meningitis and encephalitis can occur as complication of the disease.
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Salivary Gland Disorders 657 • Others—deafness, mastoiditis, meningoencephalitis, epididymitis and myocarditis, have also been reported.
Diagnosis • Clinical diagnosis—the presence of parotitis and accompanying systemic signs of viral infections. • Laboratory diagnosis—salivary amylase level is increased. A paramyxovirus may be isolated from saliva for as long as 6 days before and up to 99 days after the appearance of salivary gland swelling.
Management • Vaccination—prevention with live attenuated vaccine is the best method of controlling the disease. Vaccine should be given in 12 to 15 months of life. It should be repeated at the age of 4 to 5 years. • Symptomatic treatment—symptomatic treatment is given to control pain and swelling. Mainly non-aspirin analgesic and antipyretic should be given. • Rest—bedrest is recommended to minimize the chances of orchitis. • Diet restriction—patient should avoid sour foods and drinks to decrease salivary gland discomfort.
Cytomegalovirus Inclusion Disease It is also called as ‘salivary gland virus disease’. It is caused by cytomegalovirus, a herpes virus. It is common in immunosuppressed adult. Although it is congenital in nature, it is usually secondary to concurrent disease which has caused debilitation. It affects primarily in newborn infants and children, but adults are also affected. In newborns, infection is generalized and is usually fatal with involvement of liver, lungs and central nervous system. Infants who survive the infection may have permanent central nervous system involvement, including metal retardation and seizures. There may be hepatosplenomegaly, hemolytic anemia and hemorrhagic tendency. It may cause clinical disease of salivary gland, causing enlargement of the gland.
Etiology • Microorganisms—it is most commonly caused by penicillin resistant Staphylococcus aureus or streptococci viridians. • Host factor—it may be caused due to decreased host resistance, decreased salivary secretion and decreased bactericidal effect of saliva. • Predisposing factors—it can occur in conditions such as dehydration, malnutrition, cancer and surgical infections. • Surgical procedure—it is common when major surgical procedure is carried out in patient with poor oral hygiene. • Oral hygiene—poor oral hygiene is an important contributory factor. • Drugs—drugs like anti-Parkinson’s, diuretics and antihistaminic have been reported to be a contributory factor for acute bacterial sialadenitis.
Clinical Features • Age—most of the cases occur in adults but neonates and childhood form of the disease may occur. • Site—unilateral involvement of parotid gland is common. • Prodromal symptoms—it begins with the elevation of body temperature and sudden onset of pain at the angle of the jaw which is intense when the extensive infection is contained within the confines of the parotid capsule. • Symptoms—the localized symptoms are accompanied by fever, leukocytosis and other generalized signs and symptoms of acute bacterial infection. • Signs—parotid gland is tender, enlarged and the overlying skin is warm and red. The swelling usually causes elevation of the ear lobule (Fig. 26-17) and the overlying skin is characteristically warm and red.
Bacterial Infection Bacterial infection of salivary gland may be recurrent and generally develops owing to spread of microorganisms from the oral flora along the excretory duct.
Acute Bacterial Sialadenitis It is also called as ‘acute suppurative parotitis. Most of the bacterial infection occurs as results of ductal obstruction of decreased salivary flow.
Fig. 26-17: Enlargement of parotid gland with elevation of ear lobules in acute bacterial sialadenitis.
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• Salivary duct—early in the disease, flecks of purulent material can be expressed from the salivary duct orifice. Intraorally, the parotid papilla may be inflamed and pus may exude or be milked from the duct of the affected gland. • Lymph nodes—cervical lymphadenopathy usually develops. • Spread of infection—if infection is not eradicated, pus may penetrate the gland and spread into the surrounding tissues by following routes: • Downwards into the deep facial plane of neck. • Backwards into the external auditory canal. • Outwards into the skin of face. • Postoperative parotitis—it develops 5 to 7 days after the operation. • Symptoms—the clinical symptoms are sudden in onset with developmental of warm, firm or indurated swelling at the angle of jaw and over the cheek. It may be associated with local pain and tenderness. The swelling may cause trismus. • Signs—the swelling is usually brawny edematous and often causes elevation of ear lobule. The pus can be observed flowing from the opening of duct or it can be produced by a gentle milking action of cheeks. • Prevention—certain preventive measures should be taken to prevent such complication. The fluid and electrolyte balance of the body should be maintained during postoperative period. Good oral hygiene should be established prior to and after the surgery. • Subacute necrotizing sialadenitis—it is salivary inflammation occurs in teenager and young adults. It involves minor salivary gland. It presents as painful nodules which is covered by intact erythematous mucosa.
Radiological Features • Sonography—the affected gland shows swelling, increased vascularity, however, echo level is not decreased. • CT features—when the glands are involved in cellulitis, swelling of the glands and obscuration of the glands’ contour can be observed. On enhanced CT, the affected glands are seen with a higher CT values compared with the normal side because of the increased vascularity (Figs 26-18A and B).
Diagnosis • Clinical diagnosis—tender parotid gland with elevation of ear lobule with purulent material seen from Stensen’s duct. • Radiological diagnosis—sonography and computed tomography will diagnose this condition.
A
B Figs 26-18A and B: Sonograms of acute sialadenitis of the submandibular gland scanned perpendicular to the mandibular plane (left side: cranial, right side: caudal). (A) The left submandibular gland shows swelling, however, normal echo level. The black lines inside the gland are not dilated ducts, they are blood vessels; (B) The gland shows increased vascularity (Courtesy Dr M Shimizu).
Management • Oral hygiene—meticulous oral hygiene should be practiced. Oral hygiene should be maintained by debridement and irrigation. • Diet—soft diet should be given as chewing is painful. • Antibiotics—it is treated aggressively with antibiotics. Even death can result in debilitated patients. Specimen of purulent material should be immediately sent to laboratory for sensitivity and culture. Treatment usually starts with high dose of parenteral antibiotics active against penicillin resistant Staphylococcus. • Electrolyte balance—the patient must be adequately hydrated and the electrolyte balance should be properly maintained with intravenous fluids. • Stimulation of saliva—salivation should be stimulated to facilitate drainage by sucking the sour hard candy.
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Salivary Gland Disorders 659 • Surgical drainage—if improvement does not occur, surgical drainage of the affected gland should be performed.
Chronic Bacterial Sialadenitis It is usually caused by Streptococcus viridans, E coli or proteus. As compared to acute parotitis, it can be seen in normal children or in adults.
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Etiology • Ductal obstruction—it results due to recurrent or persistent ductal obstruction. • Other causes—congenital stenosis, Sjögren’s syndrome, or previous viral infection or allergy.
Fig. 26-20: Chronic sialadenitis showing dilatation of excretory duct and multiple ectasia (Courtesy M Shimizu).
Clinical Features • Age—the childhood form commonly begins between the ages of 3 and 5 years and is usually unilateral. • Symptoms—the pain is usually minimal and antibiotic therapy resolves the infection within a week. • Appearance—it appears as a unilateral swelling at the angle of the jaw in a patient with the history of similar occurrence (Fig. 26-19). • Signs—salivary flow is accompanied by flecks of purulent material. After several recurrences, fibrosis of the glandular parenchyma occurs, which leads to decreased salivary flow.
Diagnosis • Clinical diagnosis—minimum pain in parotid gland area with purulent material seen from duct of gland. • Radiological diagnosis—dilation and multiple ectasia seen on the radiograph.
Management • Radiation therapy—it is used extensively to cause fibrosis of salivary gland, but there are then increase incidences of head and neck tumors. • Surgical removal—total removal of parotid gland in cases of intractable cases. But is risk of facial nerve palsy. • Antibiotics injection—intraductal injection of erythromycin or tetracycline. In it, cannulate the duct and anesthetize the area with an infusion of lidocaine directly in the duct system, which is followed by infusion of antibiotics into the duct at a concentration of 15 mg/ml. • Ligation of Stensen’s duct—ligation of Stensen’s duct is a relatively simple procedure and can lead to fibrosis.
Chronic Sclerosing Sialadenitis It is chronic inflammatory disease. It is also called as ‘Kuttner’s disease’ and is common in submandibular gland.
Pathogenesis
Fig. 26-19: Chronic bacterial sialadenitis presenting as swelling at angle of jaw (Courtesy Dr Chole).
• It is caused by salivary ductal calculi causing subsequent pyogenic bacterial infections. It can lead to chronic inflammation, ensuring in the atrophy of mucus and serous cells and hyperplasia of the involved connective tissue leading to formation the tumor like swollen masses.
Radiological Finding
Clinical Features
• Sialograms show multiple ectasias and dilatation of the main excretory duct (Fig. 26-20).
• Appearance—there is enlargement of the glands, resulting in fibrous tumor like masses.
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Radiographic Features
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• Sialectasis—dots or blobs of contrast medium within the gland: appearance known as sialectasis caused by inflammation of the glandular tissue, producing saccular dilatation of the acini. • Sausage link appearance—dilated ductal lumen and constricted ductal system (sausage-link appearance). • Absence of terminal branches—in cases of chronic sclerosing sialadenitis there is absence of terminal ductal branches and presence of constricted ductal lumen within the gland.
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Diagnosis • Clinical diagnosis—not so specific. • Radiological diagnosis—sialectasis with sausage link appearance with absence with terminal branches will diagnose this condition.
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Management There is no specific treatment for this disease. In some cases removal of gland is recommended.
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Autoimmune Disorders
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Sjögren’s Syndrome It is a chronic inflammatory disease that predominately affects salivary, lacrimal and other exocrine glands. It was first described by Henrik Sjögren in 1933. It predominately affects middle aged and elderly women. •
Types • Primary Sjögren’s syndrome—it is also called as sicca syndrome and it consists of dry eyes (xerophthalmia) and dry mouth (xerostomia). • Secondary Sjögren’s syndrome—it consists of dry eyes, dry mouth and collagen disorders usually rheumatoid arthritis or systemic lupus erythematous.
Etiology and Pathogenesis • Immunological findings—the lesion in this syndrome is immunologically mediated inflammatory exocrinopathy. It begins with periductal infiltration of the tissue by mononuclear cells. • Autoantibodies—the B cell hyperactivity may result from deficiency of suppressor T lymphocytes or B lymphocytes by producing autoantibodies against them. Antinuclear antibodies found in patients with Sjögren’s syndrome are directed against many nuclear antigens, most commonly to DNA histone. Patients with secondary Sjögren’s syndrome tend to develop antibodies against
the EBV-associated nuclear antigen antibodies RANA (rheumatoid arthritis nuclear antigen). Polyclonal hyperglobulinemia—serum immunoglobulin levels of IgG and IgM are also raised. B2 microglobulin—serum salivary level of B2 microglobulin is raised in minority of patients and correlates with salivary lymphocyte infiltrate. Immune complex—circulating immune complexes are found in patients with primary and secondary Sjögren’s syndrome. Cell mediated immune response—delayed hypersensitivity response to skin testing is more depressed in patients with secondary Sjögren’s syndrome than in patients with primary Sjögren’s syndrome. Lymphokine production in response to antigen present in normal salivary tissue, is increased in patients with Sjögren’s syndrome. Natural killer cell activity—augmented natural killer cell activity is impaired in some patients with Sjögren’s syndrome. Although natural killer cells provide a defense against viral infection and tumor cell, their role in Sjögren’s syndrome is unclear. Virologic aspect—culture of saliva does not show any specific microorganisms and serologic studies have failed to show increased titers of antibodies, except to cytomegalovirus (CMV). Genetic aspect—genetic effects of Sjögren’s syndrome depend on HLA-linked and non HLA-linked genes. Relatives of a patient with Sjögren’s syndrome often show a high incidence of connective tissue diseases. Primary Sjögren’s syndrome is associated with HGLAB8 and DR 3 and secondary Sjögren’s syndrome is associated with HLA-B8 DR4 and BW44. Lympho-proliferative malignancy—enlargement of salivary glands in patients with Sjögren’s syndrome is occasionally massive and associated with enlargement of regional lymph nodes, a condition known as ‘pseudo lymphoma’. Malignant B cell lympho-proliferation has been shown to affect patients with Sjögren’s syndrome
Clinical Features • Age and sex distribution—it is more commonly seen in middle age adults. It is most commonly found in females with 90% of cases are reported in them. • Eyes—the effect on eye is called as keratoconjunctivitis sicca (dry). The patient usually complains of dry eyes or continuous irritation in the eyes. Severe lacrimal gland involvement may lead to corneal ulceration as well as conjunctivitis. • Connective tissue disorders—in patients with secondary Sjögren’s syndrome, rheumatoid arthritis is typically long standing and clinically obvious feature. Patients may have small joint and ulnar deviation of fingers and rheumatoid nodules.
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Salivary Gland Disorders 661 • Dryness of other organ—dryness of pharynx, larynx and nose are noted by some patients. This is accompanied by lack of secretion in the upper respiratory tract, may lead to pneumonia. Vaginal dryness may be also complained by some females.
Oral Manifestation • Symptoms—xerostomia is a major complaint in most of the patients. But many patients do not complain of dry mouth, but rather of an unpleasant taste, difficulty in eating dry food, soreness or difficulty in controlling dentures. • Signs—Pus may be emitted from the duct. Angular stomatitis and denture stomatitis also occur. • Enlargement—dry mouth may be accompanied by unilateral or bilateral enlargement of parotid gland, which occurs in about one-third of the patients and may be intermittent. Enlargement of submandibular gland may also occur. • Saliva—clinically, the mouth may appear moist in early stages of Sjögren’s syndrome but later, there may be lack of the usual pooling of saliva in the floor of the mouth and frothy saliva may form along the lines of contact with oral soft tissue. • Mucosa—in advanced cases, the mucosa is glazed, dry and tends to form fine wrinkles. Soreness and redness of mucosa is usually the result of candidial infection. • Speech—in some patients, there may be ‘clicking’ quality of their speech, caused by sticking of the tongue to the palate. • Tongue—the tongue typically develops a characteristic lobulated, usually red surface with partial or complete depapillation. There is also decrease in number of taste buds, which leads to an abnormal and impaired sense of taste. • Dental caries—dental caries is severe and gross accumulation of plaque may be obvious. • Periodontal disease—periodontal disease can also occur. • Acute bacterial sialadenitis—Sjögren’s syndrome is the most common underlying cause of acute bacterial sialadenitis in ambulated patients. Such infections are usually either staphylococcal or pneumoccocal and usually cause swelling of the salivary gland. The overlying skin is red, tender and shiny. • Lymph nodes—the regional lymph nodes may be enlarged and tender.
Radiological Features • Sialography—if the salivary flow rate is equivocal, sialography can be used to detect the damage. The most typical finding in Sjögren’s syndrome is that of
‘sialectasia’, which typically produces a ‘snowstorm appearance (Fig. 26-21) as a result of leakage of contrast medium. Atrophy of ductal tree may also be seen; emptying of the duct is also typically delayed. In some cases it will show ‘cheery blossom’ or fruit laden branchless tree (Fig. 26-22) appearance of the obstructed ductal system.
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Fig. 26-21: Snowstorm appearance seen in Sjögren’s syndrome on sialography (Courtesy M Shimizu).
Fig. 26-22: Branchless fruit laden tree appearance seen in Sjögren’s syndrome (Courtesy M Shimizu).
• Salivary scintiscanning—salivary scintiscanning with technetium pertechnetate may be useful in demonstrating impaired salivary function in patients with Sjögren’s syndrome. The changes correlate with both salivary flow rate and labial gland abnormalities.
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Diagnosis • Clinical diagnosis—xerostomia, keratoconjunctivitis sicca with parotid enlargement may aid in diagnosis of Sjögren’s syndrome • Sialography—snowstorm and branchless fruit laden tree appearance. • San Diego criteria for diagnosis of Sjögren’s syndrome.
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Primary Sjögren’s syndrome
Secondary Sjögren’s syndrome
• Ocular dryness—Schirmer’s test less than 8 mm wetting per 5 minute, positive rose Bengal staining of cornea • Dry mouth—decreases parotid flow Lashley cups method • Systemic autoimmunity— elevated Rh factors, elevated antinuclear antibody and presence of anti-SS and anti-SS-B antibodies
• Signs and symptoms of primary Sjögren syndrome • Rheumatoid arthritis, SLE, Polymyositis, scleroderma or biliary cirrhosis • Exclusion of sarcoidosis, preexisting lymphoma, HIV, Hepatitis B or C, primary fibromylgia and known cause of keratitis sicca and salivary gland enlargement.
Laboratory Investigations • Rose Bengal staining test—keratoconjunctivitis sicca is characterized by corneal keratotic lesion, which stains pink when ‘rose Bengal’ dye is used. • Schirmer test—the reduced lacrimal flow rate is measured by this test. A strip of filter paper is placed in between the eye and the eyelid to determine the degree of tears which should be measured in millimeter. When the flow is reduced to less than 5 mm in a 5 minute sample, patient should be considered positive for Sjögren’s syndrome. • Sialometry—salivary flow rate estimation is a sensitive indicator of salivary gland function. Parotid glands make the major contribution to total salivary flow and are the most consistently affected glands in patients with Sjögren’s syndrome. Stimulated flow rate in symptomatic primary and secondary Sjögren’s syndrome is usually below 0.5 to 1.0 ml/minute (normal 1 to 1.5 ml/ minute). • Sialochemistry—parotid saliva in Sjögren’s syndrome contains twice as much total lipid and has elevated content of phospholipids and glycolipids than the normal saliva. The sodium chloride and phospholipids levels are higher in saliva of Sjögren’s syndrome patient. • Immunologic—a routine autoantibody profile can usually be carried out with the particular aim of detecting rheumatoid and antinuclear factors. • Hematological investigations—it is necessary, particularly to exclude anemia. ESR or plasma viscosity, leucopenia occasionally may also be found. • Microbiological investigations—a swab from oral mucosa should be taken to confirm candidiasis, if there is soreness and erythema. Examination of pus is also
of course essential as a guide to antimicrobial treatment, if acute sialadenitis develops. • Salivary gland biopsy—the changes in minor glands of lower lip show close correlation with those in the major salivary glands and provide a safe and convenient source of material.
Management • Ocular lubricant—keratoconjunctivitis is treated by instillation of ocular lubricants, such as artificial tears coating methylcellulose and xerostomia is treated by saliva substitutes. • Oral hygiene maintenance—scrupulous oral hygiene and frequent fluoride application is indicated to reduce these problems. • Salivary stimulant—bromhexine, pilocarpine and cevimeline can be used to stimulate salivary flow. • Surgery—surgery for enlargement of salivary gland is only recommended when the enlargement is casing discomfort to the patient.
Mikulicz’s Disease or Benign Lympho-epithelial Lesion It was first described by Mikulicz in 1888 as symmetric or bilateral, chronic, painless enlargement of lacrimal and salivary glands. It exhibits both inflammatory and neoplastic characteristics. Initially, Mikulicz’s disease was confused with disease processes such as leukemia and tuberculosis and in these cases, it is called as Mikulicz syndrome. Mikulicz’s disease is term used only for benign lymphoepithelial lesion involving parotid and lacrimal gland.
Clinical Features • Age and sex—it occurs more commonly in women in middle and later life. • Site—it is manifested as a unilateral or bilateral enlargement of parotid and/or submandibular gland. • Prodromal symptoms—the onset of the lesion is some times associated with fever, upper respiratory tract infection, oral infection, tooth extraction or some local inflammatory disorders. • Symptoms—in some cases, there is mild local discomfort, occasional pain and xerostomia. • Signs—there is often diffuse, poorly outlined enlargement of salivary gland rather than formation of a discrete tumor nodule. The enlargement varies in size but generally few centimeters in diameter. There is history of alternating increases and decreases in the size of mass, from time to time. • Duration—the duration of the tumor mass may be only a few months or many years.
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Salivary Gland Disorders 663 Diagnosis • Clinical diagnosis—unilateral or bilateral enlargement of parotid and lacrimal gland may aid to diagnosis. • Laboratory diagnosis—biopsy shows solid nest or clumps of poorly defined epithelial which termed as ‘epimyoepithelial islands’.
Management • Surgical excision—surgical removal of involved gland should be carried out. Prognosis is good.
Uveoparotid Fever It is a form of sarcoidosis and it is also called as ‘Heerfordt’s syndrome’. It consists of a triad of— • Uveitis—inflammation of uveal tract of the eye. • Parotid swelling—firm, painless and bilateral enlargement of parotid gland. • Facial palsy
Etiology • Infection—tuberculosis was earlier thought to be the causative agent. • Hereditary—hereditary factors also play an important role in this syndrome. • Autoimmune—autoimmune mechanism of the body can also be responsible.
Clinical Features • Age—it usually occurs in 3rd and 4th decades of life. • Prodromal symptoms—prodromal symptoms lasting from a few days to several weeks are the usual initial signs of the disease and patient complains of fever, malaise, weakness, nausea and night sweat. • Appearance—it appears as a bilateral, firm, painless parotid swelling. The parotid swelling lasts from several months to several years. • Involvement of other gland—submandibular, sublingual and lacrimal gland swelling may develop independently or during the course of the parotid swelling. • Sarcodial lesion—sarcodial lesion may also be found in the oral cavity. • Uveitis—it is an inflammation of the uveal tract, is a feature of this disease. Although ocular symptoms are usually bilateral, they become more apparent before the appearances of parotid swelling. • Nerve involvement—the most common nerve involved is facial nerve. there is unilateral or bilateral seventh nerve paralysis. The neurological signs may precede, follow or appear simultaneously with parotid swelling. There
is trigeminal paresthesia, eyelid ptosis, polyneuritis, intercostal neuralgia and spinal nerve impairment accompanied by weakness and muscle atrophy have been reported.
Radiographic Features • The sialographic picture merely shows the severity and duration of the disease process within the particular gland.
Diagnosis • Clinical diagnosis—parotid swelling with facial palsy and uveitis will diagnose this syndrome. • Laboratory diagnosis—it will reveal a characteristic sarcoid nodule.
Management • Corticosteroids—it is largely asymptomatic as it may undergo spontaneous remission. Corticosteroid can be used in cases of acute exacerbation.
Recurrent Non-specific Parotitis It occurs in children as well as in adults, with the average age of onset being between 3 and 4 years. The disease may disappear with puberty, but often progresses into adult life. Males are more commonly affected than females. A congenital defect and allergy have been suggested as the possible causes. The disease is characterized by a sudden onset of parotid swelling. Both unilateral and bilateral parotid involvement has been reported. Swelling develops rapidly and may persist for a few days to a year. Diminished salivary flow has also been noted during the period of both exacerbation and remission. Moderate rise in total serum protein. Serum gammaglobulin levels may also be increased.
Tumors of Salivary Glands It is important to note that neoplasms arise not only in major salivary glands, but also in minor salivary glands.
Classification See Tables 26-1 and 26-2.
Firmness of the Tumor Firmness results from dense aggregates of nests and cords of closely packed tumor. Fibrous tissue and hyaline area as well as cartilage like and bone like tissue. Softness results from fluid production and its retention phenomenon.
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Table 26-1: WHO 1991
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Adenoma • Pleomorphic adenoma • Myoepithelioma • Basal cell adenoma • Warthin’s tumor • Oncocytoma • Canalicular adenoma • Sebaceous adenoma • Ductal papilloma • Inverted ductal papilloma • Intraductal papilloma • Sialadenoma papilliferum • Cystadenoma • Papillary cystadenoma • Mucinous cystadenoma • Monomorphic adenoma • Adenolymphoma (Warthin’s tumor) • Oxyphilic adenoma (oncocytoma) • Other types • Basal cell adenoma • Canalicular adenoma • Mucoepidermoid tumor • Acinic cell tumor
Benign seldom recurrent • Warthin’s tumor • Oncocytoma • Monomorphic salivary adenomas Benign, often recurrent • Pleomorphic adenoma • Mucoepidermoid tumor (low grade) • Acinic cell tumor Malignant • Carcinoma in pleomorphic adenoma • Adenoid cystic carcinoma • Acinic cell tumor • Mucoepidermoid tumor (high grade) • Squamous carcinoma • Adenocarcinoma • Undifferentiated carcinoma
Carcinoma • Acinic cell carcinoma • Mucoepidermoid carcinoma • Adenoid cystic carcinoma • Polymorphous low grade adenocarcinoma • Epithelial myoepithelial carcinoma • Basal cell adenocarcinoma • Sebaceous carcinoma • Papillary cystadenocarcinoma • Mucinous adenocarcinoma • Oncocytic carcinoma • Salivary duct carcinoma • Adenocarcinoma • Malignant myoepithelioma • Carcinoma in pleomorphic adenoma (Malignant pleomorphic adenoma) • Squamous cell carcinoma • Small cell carcinoma • Undifferentiated carcinoma • Other carcinomas Non-epithelial tumors Malignant lymphoma Secondary tumors Unclassified tumors Tumor like lesions • Sialadenosis • Oncocytosis • Necrotizing sialometaplasia • Benign lymphoepithelial lesions • Salivary gland cyst • Chronic sclerosing sialadenitis of submandibular gland • Cystic lymphoid hyperplasia in AIDS
Firm tumor
Soft tumor
• Pleomorphic adenoma • Adenoid cystic carcinoma • Mucoepidermoid tumor of high grade • Carcinoma in pleomorphic adenoma • Acinic cell carcinoma • Oncocytoma
• Well differentiated Mucoepidermoid tumor • Papillary cyst adenoma • Mucus producing adenocarcinoma • Warthin’s tumor
Clinical Staging of Salivary Gland Tumors By Spiro Staging of salivary gland neoplasms appear to be initiated by Spiro. It is as follows: • T1—0 to 3 cm and solitary and freely mobile and CRVII intact. • T2—3.1 to 6 cm and solitary and freely mobile or skin fixation and CRVII intact. • T3—6 cm or multiple nodules or ulceration or deep fixation or CRVII dysfunction. • Patient with T1 and T2 lesion are placed into stage I and II respectively. • Any patient with clinical evidence of metastasis of lymph nodes or with T3 lesion is considered to be in stage III.
By American Joint Committee • Primary tumor • Tx—tumor that cannot be assessed by the rules. • T0—no evidence of primary tumor. • T 1 —tumor 2 cm or less in diameter, without significant local extension. • T2—tumor 2-4 cm in diameter without significant local extension. • T3—tumor more than 4 cm but not more than 6 cm in diameter without significant local extension.
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Salivary Gland Disorders 665 • T4a—tumor over 6 cm in diameter without significant local extension. • T 4b —tumor of any size with significant local extension. • Nodal involvement (N) • Nx—regional lymph node cannot be assessed. • N0—no regional lymph node metastasis • N1—clinical or histologically positive regional lymph nodes. • Distant metastasis (M) • Mx—distant metastasis cannot be assessed. • M0—no distant metastasis. • M1—distant metastasis. • Stage grouping is performed as follows. • Stage I—T1N0M0 or T2N0M0 • Stage II—T3 N0M0 • Stage III—T1 or T2, N1 M0, or T4a or T4b N0 M0 • Stage IV—T3 N1 M0, T4a or T4b N1 M0, any T any N M1
Benign Tumors Pleomorphic Adenoma
Fig. 26-23: Swelling of parotid gland seen in cases of pleomorphic adenoma.
• Symptoms—small, painless, quiescent nodule which slowly begins to increase in size, sometimes intermittently. • Shape—the tumor tends to be round or oval when it is small, as it grows bigger it becomes lobulated. In some cases, intraorally swelling may be observed (Fig. 26-24).
The term pleomorphic adenoma was suggested by Willis characterizing the unusual histological pattern of the lesion (pleomorphic or mixed appearance). It is a benign mixed tumor of the salivary gland. It is also called as ‘iceberg tumor’, ‘endothelioma’, ‘branchioma’, or ‘enchondroma’. It is most common salivary gland tumor.
Pathogenesis • Myoepithelial cells—myoepithelial cells are responsible for morphologic diversity of tumor including production of fibrous, mucinous, chondroid and osseous structures. • Differentiation of ductal reserve cells—intercalated duct reserve cells can differentiate into ductal and myoepithelial cells and the later can then undergo mesenchymal metaplasia since they inherently have smooth muscle like properties. • Neoplastic altered epithelial cells—a neoplastically altered epithelial cell with potential for multidirectional differentiation may be responsible for pleomorphic adenoma.
Clinical Features • Sex and age—women to men ratio is 6:4. It is common in 4th to 6th decades but also seen in young adults and children • Site—parotid 90% and intraoral palatal gland on lip. In parotid involvement, superficial portion is most commonly affected (Fig. 26-23).
Fig. 26-24: Intraoral view pleomorphic adenoma showing swelling in the palate (Courtesy Dr Parate).
• Size—it may increase to cricket ball size or even more, weighing in pounds and in intraoral cases, not more than 1 to 2 cm in diameter. If neglected lesion can grow bizarre proportions. • Dumbbells shaped appearance—in some cases, lesion grows in medial direction between ascending ramus and stylomandibular ligament resulting in dumble shaped appearance. • Surface—its surface is smooth. Sometime, it is bosselated and is occasionally crossed by deep furrows.
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• Fixation—no fixation, either to deeper tissues or overlying skin. • Consistency—it is firm and rubbery to feel. Sometimes cystic degeneration may be seen. • Palatal tumor—it is seen on lateral aspect of the palate. They are smooth surface and dome shaped (Fig. 26-25). • Signs of malignant transformation—accelerated growth rate, tumor irregularity on palpations, necrosis and painful ulceration and facial nerve involvement.
3 Fig. 26-26: Ball in hand appearance seen on sialography in pleomorphic adenoma (Courtesy M Shimizu).
Fig. 26-25: Dome-shaped swelling on lateral aspect of palate due to pleomorphic adenoma of the minor salivary gland (Courtesy Dr Chole).
Diagnosis • Clinical diagnosis—smooth surface enlargement in the parotid region will suspect pleomorphic adenoma. • Sialography—ball in hand appearance seen (Fig. 26-26). • CT diagnosis—this will also help to know exact extension of location (Fig. 26-27). • Laboratory diagnosis—biopsy shows cuboidal cells arranged in tubes or duct-like structures, which begin to resemble the normal ductal epithelium. Duct-like spaces contains eosinophilic coagulum.
Management • Surgical excision. • Parotid gland—tumor and the involved lobe of gland is removed. • Submaxillary gland—removal of the gland and tumor in continuity. • Intraoral lesion—extracapsular incision. • Hard palate—excised with overlying mucosa. • Lip, soft palate—enucleation or extracapsular excision. • Recurrence rate—recurrence rate is 5 to 30% due to hypocellularity, incomplete resection and encapsulation.
Fig. 26-27: CT scan showing extension of pleomorphic adenoma involving parotid gland
Monomorphic Adenoma Monomorphic adenoma is divided into three groups by WHO, i.e. adenolymphoma (Warthin’s tumor), Oxyphilic adenoma (oncocytoma) and other histologic patterns like basal cell adenoma and canalicular adenoma. But
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Salivary Gland Disorders 667 Warthin’s tumor and Oxyphilic adenoma are recognized separate entity nowadays; so only included in monomorphic adenoma are basal cell adenoma and canalicular adenoma.
• Laboratory diagnosis—biopsy shows long strands or cords of epithelial cells, arranged in a double row. It shows ‘party wall’.
Basal Cell Adenoma
• Surgical excision—it can be treated by simple enucleation and surgical excision. Recurrence rate is rare.
It derived its name by baseloid appearance of the tumor cells.
Clinical Features • Age and sex—it is more common in females. Older age group, usually over 60 years of age are affected. • Site—it occurs primarily in major salivary glands particularly in the parotid gland and intraorally, upper lip. • Symptoms—the tumor is usually painless and is characterized by slow growth. • Membranous basal cell adenoma—this type of variant of basal cell adenoma occurs in association with appendage tumors like dermal cylindroma and trichoepitheliomas.
Diagnosis • Clinical diagnosis—it is difficult to make clinical diagnosis. • Laboratory diagnosis—biopsy shows fairly well defined connective tissue capsule. The cells are isomorphic and baseloid with round to oval nuclei.
Management
Warthin’s Tumor It is also called as ‘adenolymphoma’ and ‘primary cystadenoma lymphomatosum’. This tumor was first described by Albrecht and Arzt but it usually bears the name of Warthin in the recognition of the pathologist who first described it in USA in 1929.
Development • Heterotrophic salivary gland tissue—tumor arises from salivary gland tissue entrapped with para-parotid or intra-parotid lymph nodes during embryogenesis. • Delayed hypersensitivity disease—it is most likely a delayed hypersensitivity disease, the lymphocytes being an immune reaction to the salivary ducts which undergo oncocytic change. • Secretory immune response—Hsu has suggested that it is an exaggerated secretory immune response. • Other factors—other factors like smoking and EpsteinBarr virus have also been responsible for Warthin tumor.
Clinical Features
Management • Surgical excision—it is treated by surgical excision and recurrence is seldom seen.
Canalicular Adenoma It occurs exclusively in minor salivary gland.
Clinical Features • Age and sex—it is common in patient over the age of 60 years with no sex predilection. • Site—it originates primarily in the intraoral accessory glands. It occurs in upper lips followed by palate, buccal mucosa and lower lip. • Symptoms—it presents as a slowly growing, well circumscribed, firm nodule. • Signs—it is firm and fluctuant to palpation.
• Age and sex—it is common in men (male to female ratio is 5:1). It is common in 6th decade. • Site—the tumor occurs almost exclusively in the parotid gland. It always occurs in the lower portion of the parotid gland. The tumor is generally superficial, lying just beneath the parotid capsule or protruding through it. • Symptoms—the usual complaint is painless slow growing tumor over the angle of jaw. Involvement may be bilateral or may be multifocal. • Size and shape—the tumor does not attain a large size and the usual size is 1-3 cm in diameter. It is spherical in shape. • Surface—it is smooth (Fig. 26-28) and it is well circumscribed, movable. • Consistency—it classically feels doughy and compressible on palpation. It is firm on palpation and is clinically indistinguishable from other benign lesions of parotid gland.
Diagnosis
Radiological Features
• Clinical diagnosis—firm fluctuant swelling on upper lip may suspect the diagnosis of canalicular adenoma.
• CT/ MRI features—Warthin tumor is observed as a round or oval shaped mass with smooth, well-delineated
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Textbook of Oral Medicine Diagnosis • Clinical diagnosis—difficult to diagnose. • Laboratory diagnosis—it is an adenoma exhibiting cyst formation, with papillary projections into the cystic spaces and lymphoid matrix showing germinal centers.
Management • Superficial parotidectomy—it is done as tumor is usually located in superficial part of the parotid gland.
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Oncocytoma
Fig. 26-28: Smooth swelling occurs due to mass in tail of parotid gland in Warthin tumor (Courtesy Dr Chole).
It is also called as ‘oxyphilic adenoma’, ‘acidophilic adenoma’. It is an uncommon tumor composing less than 1% of salivary neoplasms. The term oncocytoma is derived from the resemblance of these tumor cells to apparently normal cells, which have been termed as ‘oncocytes’. These cells are predominately seen in duct lining of glands in elderly persons.
Clinical Features contour. It contains cystic parts, which are seen on CT, MR images (Fig. 26-29) and sonograms. • Sonography—on sonograms, this tumor is observed as a very clearly delineated mass with multiple cystic areas. On Doppler mode, relatively abundant vascularization is observed.
Fig. 26-29: Warthin tumor: T1 weighted MR image shows round shaped mass with smooth, well-delineated contour in the lower pole of the left parotid gland. Signal intensity is higher than that of muscle (Courtesy Dr Shimizu).
• Age and sex—it is more common in women than in men and occurs almost exclusively in older persons. • Site—it usually occurs in the parotid gland. • Size—the tumor usually measures 3 to 5 cm in diameter and appears as a discrete encapsulated painless mass (Fig. 26-30) which is sometimes nodular. Pain is generally absent. • Oncocytosis—an interesting condition called ‘oncocytosis’ of parotid gland has been described. It is characterized by nodules of oncocytes involving the entire gland or a large portion. It is usually bilateral.
Fig. 26-30: Discrete encapsulated painless mass seen in oncocytoma (Courtesy Dr Parate).
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Salivary Gland Disorders 669 Diagnosis
Clinical Features
• Clinical diagnosis—it is difficult to differentiate with other benign condition. • Laboratory diagnosis—biopsy shows large cells with eosinophilic cytoplasm, distinct cell membrane. It is arranged in rows and cords.
• Simple or intraductal papilloma—it is present as an exophytic lesion with a papillary surface and is pedunculated. It is usually reddish in color and present on the buccal mucosa or palate. It is ill-defined. • Inverted ductal papilloma—it is present asymptomatic nodules of the oral mucosa of adults. It is more commonly seen on lip. It may show pit or indentation in the overlying surface mucosa.
Management • Surgical excision—surgical excision of tumor should be carried out. Facial nerve should be preserved.
Myoepithelioma It is an uncommon salivary gland tumor. It occurs in adults and has equal sex distribution. Parotid gland is most commonly involved and the palate is the most frequent intraoral site of occurrence. The clinical features are same as pleomorphic adenoma. The tumor is composed of spindle shaped or plasmacytoid cells or combination of the two cell types. These cells may be set in myxomatous background, which may vary from scanty to copious. It is managed by surgical excision.
Ductus Papillomas These are the group of tumor characterized microscopically by papillomatous pattern.
• Sialadenoma paipilliferum—the lesion occurs in adults as an exophytic papillary lesion of the hard palate.
Diagnosis • Clinical diagnosis—it is difficult to make. But small swelling in relation with minor salivary gland, one should suspect ductal papilloma. • Laboratory diagnosis—on biopsy, it shows multiple exophytic papillary projection which is covered by stratified squamous epithelium.
Management • Surgical excision—it is best treated by conservative surgical excision.
Malignant Tumors Peripheral Mucoepidermoid Carcinoma
Types • Simple or intraductal papilloma—appears as submucosal swelling. • Inverted ductal papilloma—is present most commonly on lip. • Sialadenoma papilliferum—is seen most commonly on palate (Fig. 26-31).
The term mucoepidermoid tumor was introduced in 1945 by Stewart, Foote and Becker. It accounts for 6 to 9 % of the salivary gland tumors and for about 1/3rd of all malignant tumors of the salivary glands. It consists, of both, mucus secreting as well as epidermoid type of cells as its name suggests. It is of mainly two types, i.e. benign and malignant based upon clinical nature and histologic feature of the lesion.
Clinical Features
Fig. 26-31: Ductus papilloma presenting as swelling on hard palate.
• Age and sex—it occurs in equal distribution in men and women and occurs in the 3rd and 5th decade. • Site—about 60% occur in parotid gland (Fig. 26-30) and 30% in the minor salivary glands, especially those of the palate. It can be seen on buccal mucosa, tongue and retromolar area. • Onset—it appears as a slowly enlarging painless mass, which simulates pleomorphic adenoma (Figs 26-32A and B). • Symptoms—pain and facial nerve palsy can be seen in some patients. Other findings such as lacrimation, trismus, nasal discharge, and blood tinged saliva can also be seen.
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3 Fig. 26-33: Mucoepidermoid tumor occurring on buccal mucosa (Courtesy Dr Soni).
A
B Figs 26-32A and B: Mucoepidermoid carcinoma of parotid gland. (A) Extraoral view, (B) Intraoral view (Courtesy Dr Parate).
• Low grade tumor—the tumor of low grade malignancy usually appears as a slowly enlarging, painless mass, which stimulates pleomorphic adenoma. It seldom exceeds 5 cm in diameter (Fig. 26-33). • High grade malignancy—the tumor of high grade malignancy grows rapidly and does produce pain as an early symptom. It tends to infiltrate the surrounding tissues and in high percentage of cases it metastasizes to the regional lymph nodes. Distant metastases to lungs, bones, brain and subcutaneous tissue are common. In some cases, extraoral ulceration can also be seen (Fig. 26-34). • Minor gland tumors—it appears as asymptomatic tumors which is blue or red in color.
Diagnosis • Clinical diagnosis—it is difficult to make clinical diagnosis of mucoepidermoid carcinoma.
Fig. 26-34: Mucoepidermoid carcinoma showing extraoral ulceration
• Radiological diagnosis—computed tomography will diagnose this condition (Fig. 26-35). • Laboratory diagnosis—biopsy shows mucus-secreting cells, epidermoid type cells and intermediate cells. Biopsy also shows sheets or nests of epidermoid cells and similar nests of mucus cells, usually arranged in a glandular pattern and showing microcyst formation.
Management • Subtotal parotidectomy—early stage tumor is managed by subtotal parotidectomy and facial nerve preservation. • Total removal—advanced cases need total removal of the parotid gland.
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Salivary Gland Disorders 671 Radiological Features • Site—it occurs in premolar-molar area of mandible, above mandibular canal. • Appearance—it presents as a unilocular or multilocular expansile mass (Fig. 26-36). • Margin—it is most often well defined, well corticated and often crenated or undulating in nature. • Soap bubble or honeycomb appearance—lesion may have soap bubble or honeycomb internal structure.
Fig. 26-35: Computed tomography showing growth on right side in parotid gland (arrow).
• Radical neck dissection—it is indicated for the person who has clinical evidence of metastasis. • Radiotherapy—it can be given in some cases of intermediated type of mucoepidermoid carcinoma.
Central or Intraosseous Mucoepidermoid Carcinoma It is an epithelial tumors originating in the bone and is believed to be derived from salivary gland.
Origin • Entrapment of retromolar mucus gland—it may originate from entrapment of retromolar mucus glands within the mandible, which subsequently undergo neoplastic transformation. • Embryonic remnants of submaxillary gland—it may also form from developmentally retained embryonic remnants of the submaxillary gland within the mandible and neoplastic transformation of the mucus secreting cells commonly found in the epithelial lining of dentigerous cyst.
Clinical Features • Age and sex distribution—it is most commonly seen in middle age individual. It is more common in females than males. • Site—it occurs in mandible in premolar-molar area. It does not extend anteriorly beyond the premolar region. • Symptoms—patient complains of painless swelling. There may be paresthesia of inferior alveolar nerve. • Sign—swelling may cause facial asymmetry. Tenderness is present. Regional lymph nodes are enlarged.
Fig. 26-36: Multilocular lesion seen in premolar molar area (Courtesy Dr Parate).
• Effect on surrounding structure—the buccal and lingual cortical plate, inferior border of the mandible, alveolar crest may be thinned and grossly displaced. The mandibular canal is depressed or pushed laterally or medially. Lamina dura of the teeth may be lost.
Diagnosis • Clinical diagnosis—not so specific. • Radiological diagnosis—soap bubble and honeycomb appearance may be seen.
Differential Diagnosis • Ameloblastoma—radiologically, it is difficult to differentiate. Diagnosis should be confirmed by histopathological investigation. • Odontogenic myxoma—there is history of missing tooth. • Central giant cell granuloma—it frequently crosses the midline.
Management • Surgical excision—it is treated by surgical excision of tumor. • Neck dissection—neck dissection should be carried out in case of metastatic.
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• Adjunctive radiotherapy—postoperative radiation therapy may be required for control of metastasizing disease.
Acinic Cell Tumor It is also called as ‘acinic cell or serous cell adenoma’. It accounts for approximately 1% of all salivary gland tumors. It shows serous acinar differentiation.
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Clinical Features
sinusitis, ear infection, epistaxis, signs of cranial nerve involvement and visual disturbances. • Metastasis—the incidence of metastases is more and the organs involved include cervical lymph nodes, lungs, brain, liver and kidneys.
Radiological Features • Appearance—CT scan will demonstrate destructive lesion (Fig. 26-37).
• Age and sex—it occurs in middle age and twice common in women. • Site—it arises exclusively in the superficial lobe and tail of the parotid gland. The most common intraoral sites are the buccal mucosa and lip. • Symptoms—it is painless and grows slowly. • Signs—exact delineation of the lesion is difficult and attachment to the overlying skin and muscle may occur. • Progress—some of these lesions run a rapid course with hematogenous and lymphatic metastases, while others are more slowly progressive. Locally invasive growth may be encountered in some lesions.
Diagnosis • Clinical diagnosis—not possible. • Laboratory diagnosis—biopsy shows thin capsule, which composed of cells of varying degrees of differentiation. Well differentiated cells bear remarkable resemblance to normal acinar cells, whereas less differentiated cells resemble embryonic ducts and immature acinar cells.
Management • Lobectomy—superficial lobe of the parotid gland should be excised, is the treatment of choice. Recurrence rate varies from 8 to 59%.
Adenoid Cystic Carcinoma It is also called as ‘cylindroma’, ‘adenocystic carcinoma’ and ‘baseloid mixed tumor’. It is best recognized salivary gland malignancy.
Clinical Features • Age—it occurs in the 5th and 6th decade of life. • Site—most common glands involved are the parotid, submaxillary and the accessory glands in palate and tongue. • Symptoms—the most common initial symptom is presence of mass followed by local pain, facial nerve paralysis in case of parotid tumor and tenderness. • Signs—some of the lesions exhibit surface ulceration. Other findings include nasal obstruction, proptosis,
Fig. 26-37: This tumor shows bone destruction and absorption of the dental root. Some fine calcification can also be seen in the tumor(Courtesy Dr Shimizu).
Diagnosis • Clinical diagnosis—not possible. • Laboratory diagnosis—biopsy shows basal cells arranged in anastomosing cords or may contain a mucoid material producing the typical cribriform ‘honeycomb’ or ‘Swiss cheese’ pattern. The stromal connective tissue becomes hyalinized and surrounds the tumor cells, forming a structural pattern of cylinder from which the lesion originally derived the name ‘cylindroma’.
Management • Surgical excision—surgical excision is the treatment of choice. Recurrence rate is about 60 to 92%. Long-term follow up is hence essential. • Adjunct radiotherapy—surgery should be accompanied by radiation therapy.
Adenocarcinoma It is a malignant epithelial tumor showing tubules or papillary glandular formation. All adenocarcinoma are
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Salivary Gland Disorders 673 highly malignant and metastasize to regional lymph nodes and general viscera. Computed tomography will diagnose this malignant tumor (Fig. 26-38).
3 Fig. 26-38: Enhanced CT shows round, slightly enhanced mass with bone invasion in the lingual side of the left retro-molar region. Bone invasion suggests malignant nature of this tumor
Fig. 26-39: T1 weighted MR image shows several masses in the left parotid gland. The relatively well-delineated mass in the middle shows low signal intensity (Courtesy Dr Shimizu).
Management
Malignant Pleomorphic Adenoma It is also called as ‘malignant mixed tumor’. It is uncertain that these tumors represent the previously benign lesions which have undergone transformation into malignant form or are malignant lesion right from the onset. It accounts for 1% of all parotid tumors and 7% of all malignant tumors.
Clinical Features • Age—the tumor occurs from 2nd to 9th decades, but most frequently in 5th and 6th decade. The average age of patients with malignant pleomorphic adenoma is about ten years older than the patients with benign form of the disease. • Symptoms—pain is more frequently a feature of malignant, than the benign pleomorphic adenoma • Size—the tumors are usually larger than benign ones. • Signs—there is often fixation of the tumor to underlying structures as well as to overlying skin or mucosa.
• Surgical—surgical excision with local node dissection should be carried out. These neoplasms exhibit a high recurrence rate after surgical removal as well as a high incidence of regional lymph node involvement.
Epidermoid Carcinoma It is also called as ‘squamous cell carcinoma of salivary glands’. It is thought to be ductal in origin, since duct may undergo squamous metaplasia with ease. It exhibits infiltrative properties and early metastasis. It recurs readily. It is not a common lesion and arises more frequently in the major salivary gland. The combined use of surgery and radiotherapy is more beneficial.
Undifferentiated Carcinoma
Radiological Features
The tumor is composed of round or spindle cells that are poorly differentiated. Undifferentiated carcinomas infiltrate the surrounding structures and readily metastasize to cervical lymph nodes.
• CT features—CT/MRI features will show malignant changes in the tumors (Fig. 26-39).
Metastatic Carcinoma
Diagnosis • Clinical diagnosis—not possible. • Laboratory diagnosis—biopsy shows malignant component. There is presence of nuclear hyperchromatism and pleomorphism, increased or abnormal mitosis and destruction of normal tissues.
Salivary glands may be a site for tumor metastases, since the parotid gland contains as many as 20 to 30 lymph follicles. Parotid and paraparotid lymph nodes are favored sites for metastases from malignancy of the temple, scalp and ear and occasionally from the face, neck and palate. The most common metastasizing tumors are melanoma and squamous cell carcinoma.
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It is a non-neoplastic inflammatory self-healing reaction of salivary gland tissues, which both clinically and histologically mimics a salivary gland malignancy. It usually affects the minor salivary glands. It was predicted that trauma causes ischemia of the minor salivary glands. This benign self-limiting lesion has been often confused with malignancy thereby causing unnecessary surgery.
• Symptoms—it is usually painless or may cause only slight pain. The patient may have numbness in the palate, or area of ‘looseness’ in palate. Pieces of tissue may fall out from the palate. There may be referred pain to ear or pharynx. • Signs—the lesion begins as a larger ulcer or ulcerated nodule, which may be unilateral or bilateral. The ulcer is well demarcated from surrounding normal tissue and often has an inflammatory reaction around the edge of the lesion. Margins of ulcer in some cases, may be indurated and inflamed. The lesion is covered by an inflammatory exudate and necrotic debris, however, the margins of ulcer are usually clean, sharp and the granulation tissue often can be seen at the superficial aspect. • Size—the lesion itself is most often a deep, craterlike, non-draining ulcer 1 to 3 cm in diameter.
Etiology and Pathogenesis
Diagnosis
• Local ischemia—it may be due to physical, chemical, infective or local vasculitis. • Trauma—trauma from various factors such as denture wearing and recent surgery may be a causative factor. • Other factors—in some cases, smoking and alcohol intake can lead to this condition. It can also occur in upper respiratory tract infection.
• Clinical diagnosis—ulcerative swelling in the palate will aid in the diagnosis. • Laboratory diagnosis—in biopsy, it shows acinar necrosis and squamous metaplasia of salivary ducts.
Connective Tissue Tumors Hemangioma is the only common tumor of this group and the most frequently seen in young infants. The involved glands appear hypertrophied. There is blue discoloration of the overlying skin. Lipoma may occur in the parotid gland. The facial nerve, occasionally gives rise to a neural tumor. True sarcoma is extremely rare.
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Necrotizing Sialometaplasia
Clinical Features • Age and sex—it is more common in males than females. Occurs in 4th and 5th decade. • Site—most of the cases occur in palate, although cases of lip or retromolar pad also have been reported. • Onset—there may be early mild swelling which appears as non-ulcerated swelling (Fig. 26-40).
Differential Diagnosis • Traumatic—short duration and history. • Aphthous ulcer—short duration, painful and heals in 2 to 3 weeks. • Squamous cell carcinoma—rare on palate, older age and biopsy. • Syphilis—painless indurated edema, painless lymph node swelling and serology. • Non-Hodgkin’s lymphoma—biopsy.
Management • Self limiting—it is a self-limiting condition. It does not require any treatment. The healing occurs in six to twelve weeks via secondary intention. • Debridement—debridement and saline rinses may aid in the healing process.
Minor Salivary Gland Tumor
Fig. 26-40: Bilateral swelling seen in palatal region due to necrotizing sialometaplasia. Slight ulceration seen on the swelling.
Early minor salivary gland tumor is usually nodular or dome, shaped elevation, with smooth contour. Overlying mucosa is normal or appears smooth and glossy, due to tension. After trauma, ulcer appears which is persistent and becomes necrotic. Its occurrence in an posterior aspect of hard palate; next commonly on upper lip, buccal mucosa, retromolar region, tongue and floor of mouth. There is higher frequency in women with age 30 to 39 for benign and 40 to 49 for malignant tumors.
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Salivary Gland Disorders 675 Mucoepidermoid and adenocarcinoma are common variety. Lung is the common site of distinct metastasis. Radiologically, it may present well defined saucer like depression of underlying bone in contrast to malignant tumor which invades the bone and produce ragged radiolucent defect. On sialography, an area of under filling within the gland, due to ductal compression by the tumor is seen. The ducts adjacent to the tumor are usually stretched around this is known as ‘ball in hand’ appearance. Retention of contrast media in the displaced ducts during the emptying phase is seen.
Suggested Reading 1. Abbey LM. Solitary intraductal papilloma of the minor salivary glands. Oral Surg, Oral Med, Oral Pathol 1975;40:135-40. 2. Aguirre JM, Echebarria MA, et al. Warthin tumor: a new hypothesis concerning its development. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1998;85:60-3. 3. Apruzzese D, Longoni S. Stafne’s cyst in an anterior location. J Oral Maxillofac Surg 1999;57:333-8. 4. Ariji E, Fujiwara N, Tabata O, et al. Stafne’s bone cavity: a classification based on outline and content determined by computed tomography. Oral Surg, Oral Med, Oral Pathol, 1993; 76:375-80. 5. Atkinson JC, Fox PC. Sjögren’s syndrome: Oral and dental considerations. JADA 1993;124:74-86. 6. Atkinson JC, Travis WD, Pilemer SR, et al. Major salivary gland function in primary Sjögren’s syndrome and its relationship to clinical features. J Rheumatol l990;17:319-22. 7. Auclair PL, Goode RK, Ellis GL. Mucoepidermoid carcinoma of intraoral salivary gland. Cancer 1992;69:2021-30. 8. Avery J K. Oral development and histology, 1st edition, BC Decker Inc, Philadelphia, 1988. 9. Brannon RB, Fowler CB, Hartman KS. Necrotizing sialometaplasia: clinicopathologic study of sixty nine cases and review of literature. Oral Surg, Oral Med, Oral Pathol 1991;72:317-25. 10. Brookstone MS, Huvos AG. Central salivary gland tumor of the maxilla and mandible: a clinicopathological study of 11 cases with an analysis of literature. J Oral Maxillofac Surg 1992;50:22936. 11. Chau MNY, Radden BG. A clinicopathological study of 53 intraoral pleomorphic adenoma. Int J Oral Maxillofac Surg 1989; 18:158-62. 12. Correl RW, Jensen JL, Rhyne RR. Lingual cortical mandibular defect: a radiographic incidence study. Oral Surg, Oral Med, Oral Pathol 1980;50:287-91. 13. Daley TD, Gardner DG, Smout MS. Canalicular adenoma. Oral Surg, Oral Med, Oral Pathol 1984;57:181-8. 14. Damm DD, White DK, et al. Benign solid oncocytoma of intraoral minor salivary glands. Oral Surg, Oral Med, Oral Pathol 1989; 67:84-6. 15. Daniels TE. Sjögren’s syndrome: Clinical spectrum and current diagnostic controversies. Adv Dent Res l996;10:3-8. 16. de Visscher JGAM, van der Wal KGH, de Vogel PL. The plunging ranula: pathogenesis, diagnosis and management. J Craniomaxillofac Surg 1989;17:182-5. 17. Ellis GL, Auclair PL, Gnepp DR. Surgical Pathology of the Salivary Glands. Major Problems in Pathology Vol 25. Philadelphia, USA: WB Saunders, 1991. 18. Epstein JB, Scully C. The role of saliva in oral health and the cases and effect of xerostomia. J Can Dent Assoc 1992;58:217-21.
19. Escudier MP, Drage NA. The management t of Sialolithiasis in 2 children through use of extracorporeal show wave lithotripsy. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1999l;88:449. 20. Eversole LR. Oral sialocyst. Arch Otolaryngol 1987;113:51-6. 21. Eveson JW, Cawson RA. Tumors of minor (oropharyngeal) salivary gland: a demographic study of 336 cases. J Oral Pathol 1985; 14:500-509. 22. Eveson JW. Superficial mucocele: pitfall in clinical and microscopic diagnosis. Oral Surg, Oral Med, Oral Pathol 1988; 66:31822. 23. Fantasia JE, Miller AS. Papillary cystadenoma lymphomatosum arising in minor salivary gland. Oral Surg, Oral Med, Oral Pathol 1981;52:411-6. 24. Fowler CB, Brannon RB. Subacute necrotizing sialadenitis: a report of 7 cases and review of literature. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 2000;89:600-609. 25. Galloway RH, Gross PD, et al. Pathogenesis and treatment of ranula: report of three cases. J Oral Maxiilofac Surg 1989;47:299302. 26. Gardner DG, Daley TD. The use of terms monomorphic adenoma, basal cell adenoma and canalicular adenoma as applied to salivary gland tumors. Oral Surg, Oral Med, Oral Pathol, 1983; 56:608-15. 27. Ghom Anil. Textbook Oral Radiology: Elsevier publication: New Delhi: 2008. 28. Guggenheimer J, Moore PA. Xerostomia: etiology, recognition, and treatment. JADA 2003;134:61-9. 29. Hamper K, Mausch HE, et al. Acinic cell carcinoma of salivary gland: the prognostic relevance of DNA cytophotometry in retrospective study of long duration. Oral Surg, Oral Med, Oral Pathol 1990;69;68-75. 30. Hasler JF. Parotid enlargement: a presenting sign in anorexia nervosa. Oral Surg, Oral Med, Oral Pathol 1982;53:567-73. 31. Imbery TA, Edwards PA. Necrotizing sialometaplasia: literature review and cases report. JADA 1996;127:1087-92. 32. Inagaki M, Yuasa K, et al. Mucoepidermoid carcinoma in the mandible: finding of panoramic radiography and computed tomography. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1998; 85:613-8. 33. Jensen JL, Howel FV, et al. Minor salivary gland calculi: a clinicopathologic of forty seven new cases. Oral Surg, Oral Med, Oral Pathol 1979;47:44-50. 34. Johnson A. Inflammatory conditions of the major salivary glands: Ear Nose Throat 1989;68:94-102. 35. Kirstila V, Lenander-Lumikari M, et al. Effects of oral hygiene product containing lactoperoxidase, lysozyme and lactoferrin of the composition of whole saliva and on subjective oral symptoms in patient with xerostomia. Acta Odontol Scand 1996;54:391-7. 36. Lieblich S. Episodic supersalivation (idiopathic paroxysmal sialorrhea): a description of new clinical syndrome. Oral Surg, Oral Med, Oral Pathol 1989;68:159-61. 37. Lily JP, Fotos PG. Sjögren’s syndrome: Diagnosis and management of oral complications. Gen Dent l996;44:404-8. 38. Linder TE, Brestel R, Schlegel C. Mumps virus infection: case report or unusual head and neck manifestation. AM J Otolaryngol 1996;17:420-3. 39. Lindvell AM, Jonsson R. The salivary gland component of the Sjögren syndrome. Oral Med, Oral Surg, Oral Pathol 1986;62:3242. 40. Madel L, Tamari K. Sialorrhea and gastrointestinal reflux. JADA 1995;126:1537-41. 41. Maiorano E, Favia G, Ricco R. Sialadenoma papilliferum: an Immunohistochemical study of five cases. J Oral Pathol Med 1996; 25:336-42. 42. Maynard JD. Management of pleomorphic adenoma of the parotid gland. Br J Surg 1988;75:305-08. 43. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology (2nd edn), Saunders Elsevier, 2004.
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44. Pedersen AM, Reibal J, Neutofte. Primary Sjögren syndrome: subjective symptoms and salivary findings. J Oral Pathol Med 1999;28:303-11. 45. Penfold CN. Mikulicz syndrome. J Oral Maxillofac Surg 1985; 43:900-905. 46. Perzin KH, Gullane P, Clairmont AC. Adenoid cystic carcinoma arising in salivary gland: a correlation of histological pattern and clinical course. Cancer 1978;42:265-82. 47. Pogrel MA. The intraoral basal cell adenoma. J Craniomaxillofac Surg 1987;15:372-5. 48. Rubin P, Holt FJ. Secretory sialography in disease of the major salivary gland. AJR Am J Roentgenol 1957; 77:575-98. 49. Russotto SB. Asymptomatic parotid gland enlargement in diabetes mellitus. Oral Surg, Oral Med, Oral Pathol 1981;52:594-8.
50. Soto-Rojas AE, Villa AR, Sifuentes-Osornio J, et al. Oral candidiasis and Sjögren’s syndrome. J Rheumatol 1998; 25(5): 911-5. 51. Stafne’s EC. Bone cavity situated near the angle of the mandible. J Am Dent Asso 1942;29:1969-72. 52. Standish SM, Shafer WG. The mucus retention phenomenon. J Oral Surg 1959;17:15-22. 53. Tal H, Altini M, Lemmer J. Multiple mucus retention cyst of the oral mucosa. Oral Surg, Oral Med, Oral Pathol 1984;58:692-5. 54. Tkeda Y. Diffuse hyperplastic oncocytosis of the parotid gland. Int J Oral Maxillofac Surg 1986;15:765-8. 55. Williams HK, Connor R, Edmondson H. Chronic sclerosing sialadenitis and review of literature. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 2000;89:720-3.
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Disorders of Maxillary Sinus
Introduction Paranasal sinuses are the air filled spaces present with some bone around the nasal cavities. The sinuses are frontal, maxillary, sphenoidal and ethmoidal. Because of the close proximity of the maxillary teeth with the maxillary sinuses, these are the most important paranasal sinuses in dental point of view. They are the largest air filled sinuses surrounding the nose.
Development of Maxillary Sinus • Formation of maxillary process—during 4th week of embryonic life, the dorsal portion of the 1st pharyngeal arch forms maxillary process. It extends forwards beneath the developing eye and gives rise to the maxilla, the zygomatic bone and part of the temporal bone.
• Evagination from primitive ethmoid infundibulum—the maxillary sinus starts to develop at about 12 weeks as an evagination from the primitive ethmoid infundibulum in the lateral wall of the middle meatus of the corresponding nasal cavity when the nasal epithelium invades the maxillary mesenchyme. • Sinus at birth—at birth, maxilla is filled with deciduous tooth germs which are very close to the orbital floor so the superior dental nerves and vessels have very short distance to travel to reach the teeth. • Separation of alveolar and orbital aspect—the alveolar and orbital aspects of the maxilla gradually become separated by the cancellous bone which is then resorbed as the sinus enlarges. • Pneumatization of maxilla—pneumatization of the maxilla commences just below the orbital floor. • Expansion of maxillary sinus—down growth of the maxillary sinus leaves the ostium in a position
Fig. 27-1: Position of maxillary sinus.
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unfavorable for gravitational drainage. The maxillary sinus expands not only downward but also forward and backward from its initial evagination, the site which persists as the antronasal duct. It undergoes concurrent lateral expansion and by the end of the first year, extends beneath the orbit as far as the infraorbital canal (Fig. 27-1). • Sinus at the end of 2nd year—by the end of 2nd year, the sinus has reached about half to its adult size. • Facial growth—as the facial growth is continued by surface deposition on the face, alveolar processes and palate, it is accompanied by the resorption of the internal structure of the maxillary sinus.
Anatomy of Maxillary Sinus It is also called as the ‘antrum of Highmore’. They are the paired structures located largely in the body of maxilla and are mirror image of each other. Maxillary antrum contains air and is lined by mucoperiosteum with a pseudostratified ciliated columnar epithelium. • Shape—it is pyramidal in shape with its base directed medially towards the lateral wall of the nose and the apex directed laterally in the zygomatic process of the maxilla. • Size—size is variable, varying up to 3.5 cm in height and 2.5 cm in width and 3.2 cm anteroposteriorly. • Hiatus semilunaris—it opens into the middle meatus of the nose in the lower part of the hiatus semilunaris. • Roof—it is formed by the floor of the orbit and is transversed by the infraorbital nerve. The roof is flat and slopes slightly anteriorly and laterally. The most medial part of the roof forms the sloping wall of the maxilloethmoidal sinuses, from which disease may spread to the maxillary sinus. Antral infection may involve infraorbital vessels and nerve and malignant tumors growing in the sinus may involve the orbit. • Floor—it is curved rather than flat and is formed by the alveolar processes of maxilla and lies about 1 cm below the level of the floor of the nose. Roots of upper molars and premolar may ridge the floor or project into it. Floor may be subdivided by incomplete bony septa lying between the roots of the teeth, especially in the posterior part of the sinus. The 1st and 2nd molar’s roots are the most commonly present in close proximity with the maxillary sinus followed by the premolars and 3rd molar. • Medial wall—it is bounded by the nasal cavity. Medial wall is generally slightly convex toward the sinus. • Posterior wall—it is related to the pterygopalatine fossa. The posterior wall bulges posteriorly towards the infratemporal fossa. • Lateral wall—it is related to zygoma and cheek.
• Anterior wall—it is related to the cheek. It is depressed by canine fossa on the anterior surface of the maxilla and is convex toward the interior of the sinus. • Radiological anatomy—an antrum appears radiographically as a radiolucent cavity in the maxilla, with well defined, dense, corticated radiopaque margins or walls. The internal bony septa and blood vessel canals in the walls all produce their own shadow. • Arterial supply—facial, infraorbital and greater palatine arteries. • Venous drainage—into the facial and pterygoid plexus of veins. • Lymphatic drainage—drains into the submandibular nodes. • Nerve supply—it is supplied by infraorbital and anterior, middle and posterior superior alveolar nerves.
Function of Maxillary Sinus • Reduction of weight of the facial skeleton—as the maxillary sinus is filled with air rather than cancellous bone, lightens the face by approximately the weight of a pair of spectacles. • Phonetic resonance and auditory feedback—the sinuses may act as a resonating box for the singing voice. The sinuses also affect the conductance of the voice to one’s ear. • Insulation—the sinuses may insulate the orbits from intranasal temperature variations. • Air conditioning—the maxillary sinus contain some serous gland whose watery secretion evaporates to humidify the contained air. • Water conservation—the sinuses may act as accessory heat exchanges, warming inspired air to increase its moisture content. • Olfaction—pneumatization may have evolved to increase the area of olfactory mucosa thereby improving the sense of smell.
Examination and Investigation of Maxillary Sinus • Clinical examination • Examination of middle third of face—the middle third of the face should be inspected for the presence of asymmetry, deformity, swelling, erythema, ecchymosis or hematoma. Epiphora, nasal obstruction, epistaxis or other discharge or odor from the nostril should be noted. • Extraoral palpation—examination should include palpation of the facial wall of the sinus above the premolar, where the bone is thinnest, either through the soft tissue of the cheek or more directly intraorally.
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• Intraoral examination—intraoral examination should be performed for alveolar ulceration, expansion, tenderness or paresthesia of the upper molar and premolar region. Palatal ulceration should be biopsied if there is no obvious cause and it does not heal within 1 week. Rhinoscopy—a nasal speculum and headlight or mirrors are necessary for proper examination of the nasal passage. A topical vasoconstrictor may decrease the size of a large inferior turbinate which obstruct the view of the middle turbinate and middle meatus. When the middle meatus is exposed, the hiatus semilunaris and bulla ethmoidalis are seen anteriorly and it is possible to cannulate or probe the ostium more posteriorly. Pus may be seen in middle meatus. Nasendoscopy—under local anesthesia, the nasal opening of the maxillary sinus in the middle meatus may be examined thoroughly using a narrow fiberoptic endoscope. It is important as sinus diseases usually start in the middle meatus. Transillumination—it is performed in the darkened room by insertion of an electrically safe bright light into the mouth (with the lip closed) after removal of maxillary prosthesis. A difference in luminosity between two sinuses which are seen best at the medial third of the infraorbital rim indicates the presence of unilateral disease. A large cyst filled with clear fluid will be opaque on radiograph but brilliantly clear on transillumination. Good transillumination indicates presence of air in the sinus while failure of transillumination indicates presence of pus, solid lesion or mucosal thickening. Bacteriology and cytology—proof puncture of the antrum is usually performed through the inferior meatus to confirm radiological appearances. After topical application of vasoconstrictor and analgesic spray, a ‘trocar and cannula’ is passed under the attachment of the inferior turbinate up to the genu where it will naturally rest. The body of trocar is held in the palm of the hand with the index finger running along its haft to provide control and a stop. It is directed towards the tragus of the ipsilateral ear while the patient’s head is held still. Moderate pressure with a rotary movement will lead to perforation of the thinnest part of the lateral inferior meatal wall, which is just behind the lacrimal duct orifice. Trocar and cannula is advanced to the lateral sinus wall and then withdrawn several millimeters before the trocar is removed. An aspirate is withdrawn into an empty syringe and sent for bacteriological and cytological examination. Fiberoptic antroscopy—in this, sinuses unresponsive to treatment or any suspicious areas which is seen radiographically, can be examined by direct vision through an endoscope. It can be performed under local
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anesthesia as an outpatient procedure. The antrum is entered using a sharp trocar and cannula which can be pushed directly through the anesthetized oral or nasal mucosa, bone and sinus mucosa into the antrum. The trocar is then removed and the endoscope is inserted along the cannula and attached to a light source. It is mainly used in orbital blowout fracture where clinical and radiological examination is inconclusive. • Radiography: • Periapical—it will show the floor, the base of antral cavity and relationship with upper posterior teeth. • Caldwell posteroanterior—good visualization of frontal sinus and ethmoidal air cells, nasal cavity and superior portion of the maxillary antrum. • Water’s view—visualization of maxillary sinus, when the mouth is open; sphenoid sinus can also be seen. It usually shows the roof or upper borders, medial wall and allows comparison of both maxillary sinuses. • Lateral skull view—examination of sphenoid and maxillary sinuses especially anterior and posterior walls. • Submentovertex—to define extent of the sphenoid sinus. • Computed tomography—delineation of soft tissues in the sinus. It allows comparisons of the two sides (Fig. 27-2) of maxillary sinus.
Fig. 27-2: CT scan showing maxillary sinus.
• Scintigraphy—radioactive isotopes are used diagnostically to demonstrate physiological changes in tissue that often precede anatomical changes or therapeutically to destroy tumor cells. Extension of antral carcinoma to involve bone produces an osteoblastic
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response ahead of the advancing malignant bone destruction. This is evident in the delayed phase of a radionuclide bone scan as bone destruction becomes visible on the radiograph. • Ultrasound—bony wall of the sinus is so thin that high power, short duration sound waves from a transmitter are able to pass through it. They are reflected back to the receiver when they hit an impenetrable object. It is effective in distinguishing normal sinuses, chronically inflamed sinus lining and if sinus is filled with fluid, tumor or scar. • Magnetic resonance imaging—MRI is extremely sensitive in demonstrating maxillary antrum pathology due to the high signal intensity on T2-weighted image of almost soft tissue abnormalities, contrasted with the absence of signal from both air within the sinus and the surrounding cortical bone.
Classification of Maxillary Sinus Disorders It is described in Tables 27-1 to 27-3. Table 27-1: First classification A. Traumatic • Fracture of maxilla, nasal bone, zygoma and orbital floor • Hematoma • Foreign bodies—root piece, bullet injury, antroliths • Oroantral fistula B. Inflammatory • Acute and chronic sinusitis • Local hyperplasia from odontogenic infection • Antral polyp • Osteomyelitis C. Cysts Intrinsic Extrinsic • Mucus retention cyst • Odontogenic • Serous cyst • Radicular • Pseudocyst • Dentigerous • Primordial • Keratocyst • Non-odontogenic • Globulomaxillary • Traumatic • Aneurysmal bone cyst (ABC) D. Neoplasms Odontogenic • Ameloblastoma • Adenoameloblastoma • Calcifying Epithelial Odontogenic Tumor (CEOT) Non-odontogenic • Exostosis • Enostosis Malignant • Squamous cell carcinoma • Midline lethal granuloma E. Metabolic • Fibrous dysplasia • Leontiasis ossea
Table 27-2: Second classification A. Infection/Inflammation • Acute sinusitis • Chronic sinusitis B. Trauma • Oro-antral communication • Fracture of the maxillofacial skeleton • Foreign bodies within the antrum C. Cysts • Intrinsic • Extrinsic D. Tumors • Intrinsic • Extrinsic E. Others bone abnormalities • Fibrous dysplasia • Paget’s disease • Osteopetrosis
Table 27-3: Third classification Developmental • Crouzon syndrome • Treacher Collins syndrome • Binder syndrome Inflammatory • Mucositis • Maxillary sinusitis • Empyema Cyst Non-dental • Benign mucosal cyst of maxillary antrum • Mucocele • Surgical ciliated cyst Dental • Radicular cyst • Dentigerous cyst • Globulomaxillary cyst • Odontogenic keratocyst Benign tumor • Antral polyp • Antral papilloma • Osteoma • Ameloblastoma Malignant tumor • Squamous cell carcinoma • Invasion of the maxillary sinus by local malignant disease • Metastatic carcinoma of the maxillary sinus Traumatic • Fractured root • Sinus contusion • Blowout fracture • Isolated injury • Complex fracture • Oroantral fistula • Foreign bodies Calcification • Antroliths Miscellaneous • Fibrous dysplasia • Pseudotumor
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Developmental Disorders • Crouzon syndrome—early synostosis of the sutures produce hypoplasia of the maxillae and therefore the maxillary sinus, together with the high arched palate. • Treacher Collins syndrome—Mandibulofacial dysostosis is associated with grossly and symmetrically underdeveloped maxillary sinuses and malar bones. • Binder syndrome—maxillonasal dysplasia (Binder syndrome) involves hypoplasia of the middle third of the face. There is maxillary retrognathism, smaller maxillary length and frontal and maxillary sinus hypoplasia.
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Inflammatory Disorders They are caused by chemical irritation, introduction of foreign body, facial trauma, etc.
Mucositis It is the name given when there is thickened mucous membrane of maxillary sinus. Normally, mucous membrane of maxillary sinus is about 1 mm in thickness. When the lining mucosa becomes inflamed from either infection or an allergic process, it may increase in thickness by about 10 to 15 times. This inflammation is called as mucositis.
Fig. 27-3: CT coronal section showing fine mucosal thickening, involving medial and lateral wall along with the floor of the maxillary sinus bilaterally (Courtesy Dr Ashok L).
Maxillary Sinusitis
Causes • Inflammatory disease—dental inflammatory lesion such as periodontal disease or periapical disease may cause localized mucositis.
Clinical Features It is usually asymptomatic and it is discovered on routine radiograph.
Radiological Features • Appearance—image is detected on a radiograph as a band, noticeable more radiopaque than the air filled sinus and paralleling the bony wall of the sinus. • Size—mucosal thickening can vary from a few millimeters to a thick, hypertrophic, redundant mucosa (Fig. 27-3).
Diagnosis • Clinical diagnosis—not possible to make clinical diagnosis. • Radiological diagnosis—parallel radiopaque band seen in the wall of sinus will diagnose this lesion.
Management • Removal of cause—it will disappear after removing the cause.
Inflammation of the mucosa of the paranasal sinuses is referred to as sinusitis. When maxillary sinus is involved, it is called as maxillary sinusitis. When all the sinuses are involved, it is called as pansinusitis.
Types (depending upon duration) • Acute—This type is associated with severe pain in sinus area. • Subacute—it is an interim stage between acute and chronic sinusitis. • Chronic—it develops as a result of neglected and overlooked dental focus of infection. The lining becomes thicker and irregular.
Etiology Dental causes • Periapical infection from the teeth—it may follow dental infection particularly from upper molar and premolar teeth. The anatomic proximity of the roots of the maxillary bicuspids and molar teeth to the floor of the sinus leads to potential infection of the sinus by direct extension of an apical abscess. • Oroantral fistula—the accidental opening in the floor of the maxillary sinus during dental extraction is called as oroantral opening.
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• Periodontitis—it may spread from a deep pocket of marginal periodontitis. • Traumatic—injury of facial bones especially nasal bones and malar bones. • Dental material in the antrum—perforation of endodontic filling substance. If root canal is overfilled then there are more chances of gutta purcha point to be inserted into the maxillary sinus. • Implant—implants are used in the upper edentulous jaw to aid the retention of dentures or bridges or replace missing teeth. Implants are also used when there is insufficiency of bone to support the denture. In these cases as bone is thin, implant can penetrate the nose or sinus. • Infected dental cyst—cysts which have become infected and involve the maxillary sinus can also cause sinusitis. Non-dental causes • Mechanical obstruction of ostium • Common cold—it is the most common cause of mechanical obstruction of ostium. It will produce inflammatory edema of the nasal mucosa which obstruct the antronasal duct and cause mucus to accumulate in the sinus. Trapped mucus becomes secondarily infected by local commensal bacteria. • Allergic rhinitis—it may cause maxillary discomfort due to edema round the ostium and retention of secretion. • Other conditions—deviated nasal septum, presence of nasal polyp and prolonged nasotracheal intubation can cause stagnation and relative anaerobiasis. • Direct bacterial contamination—infected material may also be introduced directly by jumping or hydrosliding feet first into contaminated water without holding the nose or during diving, when pressure changes in the nose force nasal secretion into the sinus. • Immune deficiency—sinusitis can occur in immune deficiency state, like leukemia, lymphoma and AIDS. • Influenza—it can also occur in influenza when bacteria invade as secondary microorganisms. • Blood borne infection—it can also occur in some cases of blood borne infection. • Disease of maxillary sinus—benign mucosal cyst or tumors of the maxillary sinus can also lead to maxillary sinusitis.
Clinical Features Acute maxillary sinusitis • Symptoms—the main symptom is severe pain which is constant and localized. Pain may be felt in the area of eyeball, cheek and frontal region. Pain may be exacerbated by stooping or lowering the head. Pain is
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increased by biting on the affected side but unaffected by drinking hot, cold or sweet fluids. Pain may be referred to various areas including the teeth, orbit, head and ear. Pain in the teeth may be referred to the premolars and molars on the affected side. Teeth in the involved side become sore and painful. Postnasal drip—postnasal drip may cause irritation, stuffiness and nasal discharge. Due to this, patient may get difficulty in breathing. Generalized toxemia—generalized toxemia develops, i.e. fever with chills, dizziness, malaise and nausea. Nasal discharge—nasal discharge is watery in the beginning but later becomes mucopurulent. In cases of sinusitis from infected teeth, the discharge has a foul odor. Nasal mucosa—the nasal mucosa of the anterior nares may show reddening and inflammation and there may be presence of pus. Tenderness on palpation—tenderness to pressure or swelling over the involved sinus. Since the anterolateral and posterolateral sinus walls are thinnest in the area above the tooth root, thumb pressure on the cheek region is the best way to elicit tenderness externally. Premolar and molars of the affected side may be sensitive to percussion. Intraoral finding—intraorally, there may be a mucobuccal swelling, reddening and pain near the sinus region. Postural test—if no pus is seen in the middle meatus, it is decongested with a pledge of cotton soaked with a vasoconstrictor and patient is made to sit with the affected sinus turned up. Examination after 10-15 minutes may show discharge in the middle meatus. Complication—the most common complication is spread of infection to the orbit. Orbital swelling, pain and loss of vision can also occur.
Subacute • Symptoms—It is devoid of symptoms associated with acute congestion such as pain and generalized toxemia. • Discharge—discharge is usually purulent and associated with a nasal voice and stuffiness. • Soreness—soreness of throat is common feature. • Disturbed sleep—patient can not sleep well due to cough that irritates the patient constantly. Chronic • Symptoms—general symptoms of chronic sinusitis include sense of tiredness, low grade fever and feeling of being unwell. Stuffy sensation over the affected side of the face. • Other features—there is nasal obstruction, nasal discharge and headache are the related symptoms.
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Radiographic Features
Diagnosis
• Radiodensity—radiographically, the thickening of the mucous membrane and the accumulation of secretions that accompany sinusitis reduce the air content and it will appear as radiopaque (Fig. 27-4).
• Transillumination test—affected sinus will be found opaque. • Radiograph—Water’s view (Fig. 27-5) and OPG can be taken.
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Fig. 27-4: Opacification seen in right maxillary sinus due to sinusitis ( Courtesy Dr Ashok L).
• Four patterns are seen: • Localized thickening—localized thickening at the base of the sinus. • Generalized thickening—roughly generalized thickening of mucoperiosteum around the entire wall of the sinus. • Complete filling except ostium—complete filling of the sinus except in the region of the ostium on the medial wall. • Complete filling—complete filling of the sinus. • Allergic sinusitis—in the cases of allergy, mucosa will be more lobulated in contrast to that in infection where it is straighter and parallel to the sinus wall. • Chronic sinusitis—chronic sinusitis may result in persistent opacification of the sinus and sclerosis or thickening of surrounding bone. • Antral halo appearance—Sometimes if infected teeth are involved then inflammatory changes may lead to resorption of the antral floor and remodeling to produce the appearance described as an antral halo. • Resolution of sinusitis—resolution of acute sinusitis will appear as small clear areas appear in the interior of the sinus as the thickened mucosa gradually shrinks.
Fig. 27-5: Water’s view showing complete opacification of left maxillary sinus (Courtesy Dr Ashok L).
• Laboratory diagnosis—there is elevated leukocyte count. Lining of maxillary sinus may show a typical acute inflammatory infiltrate with edema of the connective tissue and often hemorrhage. In chronic cases, cellular proliferation is present.
Management • Removal of the cause of dental infection—treatment should be directed to drain the periapical abscess from the root canal or by extracting the teeth. • Antibiotic—most commonly used antibiotic is doxycycline hydrochloride. Doxycycline is given in the dose of 100 mg daily. Penicillin is also the drug of choice as it is effective against most of the anaerobic microorganisms. In some cases, amoxicillin or clotrimazole can be given. • Analgesic and anti-inflammatory drugs—these drug are used to control pain and inflammation. Most commonly used are Ibuprofen or Nimesulide. • Nasal decongestant—Ephedrine nasal drops (0.5%) are most commonly used and give relief for several hours. Xylometazoline (0.1%) is the alternative drugs to Ephedrine but it can lead to more rebound effect.
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• Stem inhalation—it may act by hydrating the mucous layer, making it less viscous and thereby encouraging normal ciliary clearance of the maxillary sinus. The use of volatile aromatic additive, such as menthol or eucalyptus can be used to stimulate cold receptor nerve endings. • Antral lavage—if antibiotics and nasal drops fail to resolve the condition, pus may be removed from the antrum. This procedure is carried out under local anesthesia by inserting hollow trochar and cannula into the antrum through the nasal wall beneath the inferior turbinate. Warmed saline is syringed through the cannula so that the fluid and pus return via the antronasal duct. • Antrostomy—if all the above procedures fail to cure the sinusitis and infection is recurrent then inferior meatal antrostomy and middle meatal antrostomy can be done. • Transnasal endoscopic surgery—endoscopic approach is made to the middle meatus using rigid instrument to visualize the infundibulum and the natural opening of the sinuses.
Cysts Cysts are classified into dental and nondental.
Nondental Cyst Nondental cysts of maxillary sinus are as follows.
Antral Pseudocyst or Benign Mucosal Cyst of Maxillary Antrum It is also called as, ‘retention cyst’, ‘pseudocyst’, ‘lymphangiectatic cyst’, ‘false cyst’, ‘benign mucosal antral cyst’, ‘serous non-secretory retention pseudocyst’, ‘mesothelial cyst’ and ‘intramural cyst’.
Pathogenesis • Inflammatory exudate—severe inflammation around the ducts of mucus glands of the antral lining may alter their integrity. When the patient sneezes, mucus can be expelled into soft tissue through the wall of such injured duct. Once the pathway for extraglandular accumulation of mucus has been established, the process may continue until a cyst has developed. Infection may result from odontogenic source or it may cause due to allergy. • Mechanical factors—because of frequent location of the lesion at the sharp angle between the floor and frontal or lateral aspect of the sinus cavity close to the alveolar process mechanical factors might be involved in the
development of cyst. Mucosal swelling, perhaps the result of a previous common cold may lead to mechanical stress leading to the rupture of sharp angle tissue or its bony attachment. • Proteolytic process—some have also found a low concentration of alpha-antitrypsin in the cystic fluid which suggests the possibility that a proteolytic process could lead to the expansion of the cyst.
Clinical Features • Age and sex—the great majority of cases were found in patients in the age group of 21-30 years. Males are more commonly affected than females in the ratio of 2:1. • Sites—most commonly involved sites are the antral floor and the lateral wall of maxillary sinus. • Symptoms—there may be localized dull pain in the antral region, or fullness and numbness of the cheek. If it is completely filled sinus, it will prolapse through the ostium and cause obstruction and postnasal drip. There may be pain in the teeth and face over or near the sinus. There may be stuffiness, fullness, headache, symptoms of cold, and numbness of upper lip. • Signs—sometimes, antral swelling may also occur. There is copious discharge of yellow fluid from the nostrils. Retention of pseudocyst may enlarge and fill the sinus cavity completely, it frequently rupture as a result of abrupt pressure change caused by sneezing or blowing the nose. Expanding cyst will cause herniation through the ostium into the nasal cavity where it subsequently ruptures.
Radiological Features • Radiodensity—it is homogenous mass that is more radiopaque than the surrounding sinus cavity. • Appearance—It appears as a soft tissue mass rather than a calcified area so that medial and lateral landmarks can generally be visualized through the lesion. • Site—It is found projecting from the floor of the sinus, although some may form on the lateral walls. • Shape—the cyst appears as a spherical, ovoid or dome shaped radiopacity (Fig. 27-6). • Margins—it has a smooth and uniform outline. The smooth curved borders are well defined but not well corticated. • Base—they may have a narrow or broad base. • Size—they vary in size from minute to very large and may occasionally occupy the entire maxillary sinus. Image may be of a fingertip to that of a completely filled sinus making it opaque. • Bone—there is no resorption of adjacent bone and of particular importance is the persistence of thin radiopaque line of the antral cortex.
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• Neoplasm—the neoplasm is less likely to be dome shaped as the retention cyst.
Management • Removal of foci of infection—the adjacent tooth should be treated for any source of infection. • Caldwell-Luc operation—large cysts should be removed through Caldwell-Luc operation.
Sinus Mucocele It is an expanding destructive lesion that begins with the development of mucus retention cyst in a blocked ostium. If mucocele becomes infected, it is called as pyocele or mucopyocele.
Etiopathogenesis Fig. 27-6: Dome shaped radiolucency seen in left maxillary sinus suggestive of antral pseudocyst.
• Mucus type is associated with thickened mucosa while serous type appears normal.
Diagnosis • Clinical diagnosis—dull pain in antral area, discharge of yellow fluid from nostril should suspect this cyst. • Radiological diagnosis—ovoid and dome shaped radiopacity projecting from the floor will diagnose this condition. • Laboratory diagnosis—biopsy shows infiltration of chronic inflammatory cells in connective tissue wall of the cyst. Cystic fluid is thick, tenacious, white translucent and sterile.
Differential Diagnosis • Inflammatory lesions of the sinus—in inflammatory lesions, patient may complain of pain which is absent in case of cyst. • Apical radicular cyst—tooth is not vital. • Odontogenic cyst—mucus retention cyst is dome shaped and does not have thin marginal line representing the hyperostotic borders characterized by odontogenic cyst. Odontogenic cysts are more rounded and tear shaped and most are not so homogenous, as mucus retention cyst. Lamina dura is not intact in odontogenic cysts. • Antral polyp—they are more opaque, more heterogeneous and multiple commonly associated with thickened mucosa. • Surgical ciliated cyst—more rounded and more radiolucent.
• Obstruction of sinus ostium—blockage or obstruction may result from long and tortuous infundibulum, intranasal or intra-antral inflammation, and from polyps and bony neoplasm. This blocked ostium will act as separate cyst like structure lined by epithelium and filled with mucin. • Accumulation of mucin—the cystic lesion continues to accumulate mucus. After it has filled the sinus cavity the pressure increases and the lesion will become destructive by expanding and destroying sinus wall by thinning out the bone wall.
Clinical Features • Site—there is predilection for ethmoid and frontal sinuses due to the relative difficulty as a cyst has protruding through the longer and narrower nasofrontal duct and infundibulum into the nasal cavity, in contrast to the shorter and larger ostium in case of maxillary and sphenoidal sinuses. • Symptoms—it may exert pressure on the superior alveolar nerve in the resorbing sinus wall and cause radiating pain. Sensation of fullness in the cheek may be accompanied swelling over the anteroinferior aspect of the antrum, the area where the wall is thinnest. If the cyst expands inferiorly, it may cause loosening of the posterior teeth in that area. If it expands medially, lateral wall of the nasal cavity is deformed and nasal airway is obstructed. • Signs—if expands towards the orbit, it may cause diplopia and proptosis (protrusion of the globe of the eye).
Radiographic Features • Site—about 90% of the cases are in ethmoidal and frontal sinuses and are rare in maxillary and sphenoid sinuses.
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• Radiodensity—there is opacification of sinus. • Shape—the shape of the sinus is changed into a more circular shape as the mucocele grows. • Effect on surrounding structures—the shape of sinus changes with bony expansion. There is erosion of septa and the bony wall may occur. Borders of the expanding sinus become sclerotic. • Frontal sinus—scalloped borders of frontal sinus become smooth by erosion and intersinus septum may be displaced. • Maxillary sinus—teeth may be displaced or resorbed. • Ethmoid sinus—displacement of the lamina papyracea may occur, displacing the content of the orbit. • Sphenoid sinus—the expansion may be in a superior direction, suggesting a pituitary neoplasm. • Orbit—Bone of supramedial border of the orbit is destroyed or displaced.
Diagnosis • Clinical diagnosis—symptoms of sinus mucocele are severe and consist of radiating pain, diplopia and obstruction of nasal airway. • Radiological diagnosis—opacification of sinus with erosion of septa. Displacement of teeth can also occur.
Clinical Features • Age and sex distribution—the great majority of the patients are in the fourth and fifth decades and their age ranges from 21 to 72 years. There is a preponderance of males to females (2:1). • Symptoms—pain, discomfort or swelling in the cheek or face or intraorally in the palate or alveolus is a common complaint. • Sign—pus may be discharged.
Radiological Features • Site—well defined radiolucency closely related to the maxillary sinus. • Margin—surrounding bone sclerosis is evident in at least a part of the bony margin. There is pneumatization and relatively well defined unilocular radiolucent margins showing marked osteosclerotic changes. • Pressure effect—occasionally, cyst appears to encroach on the sinus itself but lack of communication between the two has been demonstrated by injecting the sinus with a radio-opaque material. As the lesion enlarges, sinus walls become thinned and eventually perforate and may resemble a malignant neoplasm. Resorption of maxillary alveolar processes also occurs.
Differential Diagnosis • Malignancy—any suggestion of a lesion associated with occluded ostium should be mucocele.
Management • Surgical—surgical removal by the Caldwell-Luc operation is traditional method for management of sinus mucocele. • Endoscopic middle meatal antrostomy—nowadays, this treatment module gives good results.
Postoperative Maxillary Cyst This is also type of sinus mucocele which occurs after trauma. It is also called as ‘surgical ciliated cyst of maxilla’. Its name arises from the fact that it has a delayed complication arising within years after surgery involving the maxilla.
Pathogenesis • Trapping of epithelium in wound closure—they are derived from the epithelial lining of the maxillary sinus which is trapped in the wound during closure of the CaldwellLuc incision and subsequently begins to proliferate. Sinus lining will separate from the sinus and epithelium lined cavity is formed in which mucin is secreted. This type of cyst is originated after difficult extraction in which sinus lining is damaged.
Diagnosis • Clinical diagnosis—history of trauma or operation followed by pain and discomfort in the sinus region. • Radiological features—contrast study will help to diagnose this cyst. Well defined radiolucency close to sinus will give clue to diagnose the case. • Laboratory diagnosis—cysts are lined by pseudo-stratified columnar epithelium with squamous metaplasia in chronically inflamed cases. Combination of ciliated, cuboidal and squamous epithelium with varying numbers of mucus cells may be seen.
Management • Enucleation—enucleation through an approach appropriate to the site is the treatment of choice. Recurrence may occur if the wall is very thin and there is perforation of the bone making enucleation difficult.
Dental Cyst These are described in detail in Chapter 13: Cysts of Jaw. • Radicular—those that develop in the maxilla may extend into the maxillary sinus. They may cause elevation of the floor of the sinus resulting in a halo appearance. Large cysts may obliterate the sinus and make differentiation of this form from sinusitis is difficult.
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Disorders of Maxillary Sinus • Dentigerous cyst—when they expand into the sinus, the radiograph shows radiolucency elevating an intact wall or floor of the maxillary sinus. If it is small, it is usually round, dome shaped opacity in the base of the antrum with well defined radiopaque corticated margins to the edge of the meniscus. Sometimes,there may be displacement of the associated tooth (Fig. 27-7). If the cyst is large then there is total opacity of the antral region due to complete compression of the antral cavity. There is also a loss of antral outline. • Cyst in the globulomaxillary area—they may expand so as to obliterate or alter the typical pattern or border of nasal fossa and anterior process of the maxillary sinus.
• Saints triad—it is associated with “Saints triad”, i.e. nasal and antral polyposis, aspirin sensitivity and asthma. • Exacerbation of asthma—polyps may exacerbate the asthma by causing obstruction of the nose. It is most commonly pedunculated, or sessile mass which grows very slowly. After the polyp grows to occupy most of the antrum it frequently herniates into the nasal cavity. This may be brought about by repeated sneezing or nose blowing in about 4-6% cases.
Radiological Features • Appearance—it appear as homogenous soft masses with smooth, outwardly convex borders. Single or multiple lesions may be present. If polyp occurs in the roof of the maxillary sinus in a patient with a history of trauma, the plain film examination may simulate a blow out fracture. • Destruction of walls of sinus—Polyps may cause destruction or displacement of bone. They can displace or destroy medial or lateral wall. • CT features—have mucoid attenuation with mucosal enhancement seen at the polyps’ surface. It appears as smooth homogenous mass. • MRI features—polyps will have low to intermediate T1weighted and high T 2-weighted signal intensities. Mucosa adjacent to polyps will enhance as compared (Fig. 27-8) to polyps.
Fig. 27-7: Dentigerous cyst involving maxillary sinus. Note the displacement of the tooth in the sinus.
Benign Tumor Antral Polyp The thickened mucosa of chronically inflamed sinus frequently form irregular folds called as ‘polyps’. Polypoid atrophy of mucosa may develop into an isolated area or number of areas throughout the sinus.
Clinical Features • Age—it usually occurs in young persons. • Site—maxillary sinus is more involved as compared to other sinus. In maxillary sinus they may arise from any part of the sinus wall and occasionally pass through the ostium to appear in the nose as antrochoanal polyps. • Symptoms—patients present with nasal obstruction, pain is very mild on pressure as mass present inside the nose.
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Fig. 27-8: MRI T2 coronal section image showing well marginated hyperintense area in the floor of the right maxillary sinus (Arrow mark) suggestive of solitary polyp (Courtesy Dr Ashok L).
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Fig. 27-9: Polyp seen in left maxillary sinus as homogenous radiopacity ( Courtesy Dr Bhaskar Patle).
Diagnosis • Clinical diagnosis—saint tried with pain and pressure inside the nasal cavity may give clue to the diagnosis. • Radiological diagnosis—CT and MRI will diagnose the polyp as homogenous radiopaque mass in the sinus (Fig. 27-9).
Fig. 27-10: Homogeneous radiopaque mass with destruction of wall of right maxillary sinus seen due to papilloma.
• Radiological diagnosis—homogenous mass with bone destruction will give clue to the diagnosis.
Management • Excision—surgical excision of tumor should be carried out.
Management • Excision—simple excision is close with endoscopic surgery or Caldwell-Luc operation.
Antral Papilloma It is a rare tumor of respiratory epithelium that occurs in the nasal cavity and the paranasal sinuses.
Osteoma It is most common mesenchymal neoplasm in the paranasal sinus.
Clinical Features
• Age and sex—it is seen in the age group of 20 to 25 years with predominance in males. • Site—usually ethmoid and maxillary sinuses are involved. • Symptoms—there is unilateral nasal obstruction, nasal discharge, pain and epistaxis can occur. Recurring sinusitis and subsequent nasal obstruction on the same side. • Appearance—it has got warty appearance.
• Age and sex—it is more common in 2nd, 3rd and 4th decade. It is more common in male as compared to females and the ratio is 2:1. • Symptoms—it is slow growing and asymptomatic. When symptoms occur, they are as a result of obstruction of the sinus ostium or infundibulum or are secondary to erosion or deformity, orbital involvement or intracranial extension. It may extend in the nose and cause nasal obstruction or swelling on the side of the cheek. • Signs—it may expand into the sinus and produce swelling of the cheek or hard palate. In cases of extension to orbit the patient may have proptosis.
Radiographic Features
Radiological Features
• Site—it appears as isolated polyps in the nose and sinus. • Radiodensity—the neoplasm appears a homogenous radiopaque mass of soft tissue density (Fig. 27-10). • Pressure effect—bone destruction can occur due to pressure erosion.
• Site—they occur more often in frontal and ethmoidal sinuses. The maxillary sinuses are also involved. • Shape—lobulated or rounded homogenous masses of high density are seen. • Margins—they have sharply defined margins.
Diagnosis
Diagnosis
• Clinical diagnosis—warty appearance with recurring sinusitis may suspect this disease.
• Clinical diagnosis—nasal obstruction, proptosis may give some clue to the diagnosis.
Clinical Features
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• Radiological features—lobulated homogenous mass of high density is present.
Management • Excision—this tumor should be surgically removed.
Ameloblastoma It is most common extrinsic tumor affecting the maxillary sinus. It may cause loosening of teeth, nasal obstruction and painless facial deformity. Sinus cavity is invaded at an early stage. There is radiographic appearance equivalent to soft tissue density. Antral cavity is expanded and filled with soft tissue mass. Bony wall is eroded.
Fig. 27-11: Ulceration seen on first molar area due to maxillary sinus malignancy.
Malignant Tumor Squamous Cell Carcinoma It originates from metaplastic epithelium of the sinus mucous membrane lining. It is the most common primary tumor of paranasal sinuses comprising 80 to 90% of cancers in this site.
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Etiology • Idiopathic—Most cases of squamous cell carcinoma of maxillary sinus are without any cause. • Sinusitis—respiratory epithelium is known to undergo squamous metaplasia in the presence of infection and chronic sinusitis can be predisposing factor for antral carcinoma. • Snuff and smoke—the use of indigenous snuff and the smoky atmosphere may be causal factor for carcinoma of paranasal sinus. • Occupational hazards—it is more common in boot and shoe and nickel worker. Adenocarcinoma of the nasal passage is an occupational hazard for furniture workers.
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Epiphora will result if the lacrimal sac or nasolacrimal duct is obstructed. Floor involvement—involvement of the floor of the sinus leads to expansion of the alveolus, unexplained pain, numbness of teeth, loosening of teeth and swelling of the palate or alveolar ridge and malfitting dentures. It may erode the floor and penetrate the oral cavity (Fig. 27-12). Lateral wall involvement—lateral wall involvement leads to facial and vestibular swelling, pain and hyperesthesia of maxillary teeth (Fig. 27-13). Roof involvement—roof involvement leads to diplopia, proptosis and pain over the cheek and upper teeth (Fig. 27-14). Posterior wall involvement—posterior wall involvement leads to painful trismus, obstruction of Eustachian tube causing stuffy ear, referred pain and hyperesthesia over the distribution of second and third division of trigeminal nerve.
Clinical Features • Age and sex—mean age of occurrence is 60 years. Males are commonly affected more than females in the ratio of 2:1. • Symptoms—there is facial pain, swelling, nasal obstruction. Patient also complains unilateral nasal stiffness. When the second division of trigeminal nerve is involved, there is intense pain or paresthesia of midface occurs. • Signs—there is ulceration or mass seen on the hard palate (Fig. 27-11). • Lymph nodes—lymphadenopathy is always present in carcinoma of maxillary sinus. • Medial wall involvement—medial wall involvement leads to nasal obstruction, discharge, bleeding and pain.
Fig. 27-12: Ulceration and perforation seen in hard palate in maxillary sinus malignancy (Courtesy Dr Ashok L).
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Fig. 27-13: Swelling in vestibular region occur due to involvement of lateral wall (Courtesy Dr Ashok L).
Fig. 27-15: Radiopacity seen on right side of maxillary antrum which is obscuring the wall of maxillary sinus.
erosion of the medial wall. There may be destruction of the floor and anterior or posterior walls (Fig. 27-16).
Fig. 27-14: Involvement of roof causes swelling in infraorbital region.
• Nerve involvement—it may involve infraorbital nerve and produces paresthesia of the cheek or erodes blood vessels giving rise to epistaxis. Paresthesia of mandibular nerve can also occur if the tumor invades the cranium.
Radiographic Features Small early lesion • Shape and radiodensity—non-specific well defined round soft tissue opacity within the antrum (Fig. 27-15). • Antral wall—variable destruction of the bony antral wall. Loss of fine linear outline of the lateral wall is a particularly sensitive sign of bone destruction. Large well established lesion • Pressure effect—destructive outline of the sinus destroying bone and causing irregular bony radiolucency with
Fig. 27-16: Destruction of walls of maxillary sinus seen in malignancy.
• Teeth—occasional resorption and displacement of the teeth. There may be bone destruction around the teeth or irregular widening of the periodontal ligament space. • Zygomatic arch—advanced cases involve destruction of the zygomatic arch. • Tomography—on the tomography, there is destruction of the surrounding hard and soft tissue (Fig. 27-17).
Diagnosis • Clinical and radiological diagnosis—ulceration in palate with radiopacity in maxillary antrum may suggest maxillary antrum malignancy.
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Traumatic Injuries to the Paranasal Sinuses Root in Antrum
Fig. 27-17: Destruction of walls of maxillary antrum on left side seen in patient of maxillary antrum malignancy (Courtesy Dr Ashok L).
• Laboratory diagnosis—biopsy features are suggestive of squamous cell carcinoma.
Management • Cytotoxic drugs—local intra-arterial infusion of cytotoxic drugs may be helpful for pain control. • Radiotherapy—it is the main mode of treatment. A course of high voltage radiotherapy or gamma rays are given. • Surgery—if radiotherapy cannot control the disease upto the expectation, excision of the maxilla should be performed. • Reconstruction—after surgery, sophisticated prosthesis should be constructed.
Invasion of the Maxillary Sinus by Local Malignant Disease Tumors of the upper jaw spread easily into the sinus. Pleomorphic adenoma arising in palatal minor salivary gland may bulge into the sinus floor and adenoid cystic carcinoma may invade it.
• Cause—in maxillary posterior teeth, it is possible that fractured root tip may be forced into the maxillary sinus either while extraction or while removing the root tip. Following incomplete extraction of tooth, the apical segment remaining in the socket may be dislodged by injudicious use of elevators. • How to differentiate between root in socket and root in sinus— if root tip is in the socket and superimposed over the sinus, then lamina dura will be intact and if it is in maxillary sinus, lamina dura will be lost. • Perforation of sinus—when root tip is in the sinus and trapped under mucoperiosteum then it will be fixed and it may cause movement when it perforates the sinus. • Removal of root tip—removal of the root tip can be done through the tooth socket or though the canine fossa by Caldwell-Luc approach.
Foreign Bodies • Root fragment and teeth—displaced root fragments or teeth may present in the sinus. • Excess root canal filling—excess root canal filling material forced through the apex of an upper posterior tooth during endodontic treatment. • Oroantral communication—foreign material pushed into the antrum through an existing oroantral communication. • Metallic object—metallic object such as pellets, bullets and fragments of shells or bombs. • Radiological detection—the presence, position and often the nature of the foreign body can be seen by using the radiograph (Fig. 27-18). When roots are present in the socket, it usually reveals root canal but in some cases, there is only root tip present with no root canal seen. If you want to determine it is in the socket or in the sinus then you have to look for the lamina dura and periodontal ligament. If lamina dura and periodontal ligament is present then the root is in the socket.
Sinus Contusion Metastatic Carcinoma of the Maxillary Sinus It is rare site for the secondary tumor deposits. The most common site for the primary disease is kidney followed by the breast in females and the testicle (seminoma) in males.
• Cause—blow to the face produces damage to the lining of paranasal sinuses without fracturing the facial bone. Traumatic force can be transmitted through the bony wall and be absorbed by mucosal lining which suffers damage.
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3 Fig. 27-19: Blow-out fracture showing edema below the eye.
Fig. 27-18: Foreign body seen in maxillary sinus.
• Green stick fracture—it may cause green stick fracture of the sinus with tearing injury to the mucosal lining. • Radiological features—hazy sinus is produced by edema of the mucosa, soft tissue mass that mimics a retention cyst and as a result of intramucosal hematoma, an opaque sinus or fluid level resulting from hemorrhage on mucosal tear. • Difference between sinusitis and sinus contusion—in sinus contusion, there is bloody nasal discharge, extreme tenderness of involved sinus on pressure, rapid resolution of soft tissue changes. Fig. 27-20: Blow-out fracture seen on the CT.
Blow-out Fracture • Cause—blow-out fracture results from sudden increase in intraorbital pressure due to blow to the eye. The pressure of blow forces the inferior orbital content (fat and muscle) through the fracture. • Symptoms—diplopia (double vision) when victim looks upward (caused by entrapment of inferior rectus) and enophthalmos (backwardly depressed eyelid) following reduction of edema (Fig. 27-19) and fat atrophy. • Radiological features—opacification of sinus with or without a fluid level. Soft tissue mass in upper portion of sinus and image of depressed bone fragment (orbital floor in sinus) (Fig. 27-20). It will produce a tear-drop shaped opacity in the upper part of the antrum, the ‘hanging drop appearance’ caused by herniation of the
orbital content downwards into the antrum following collapse of the antral roof. The depression fracture of the orbit is accompanied by fracture of the antrum wall of the maxillary sinus.
Isolated Fracture It involves single wall, which are identified on the radiograph by a bright line. Anterolateral wall of the maxillary sinus is the most common site. Sometimes fracture of the floor of the maxillary sinus occurs into which roots of the posterior teeth are projecting which occurs during tooth extraction.
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Disorders of Maxillary Sinus Zygomatic Complex Fracture The fracture occurs at the line of weakness and passes through the orbital floor, usually medial to the zygomaticomaxillary suture and therefore inevitably involves the maxillary sinus. Fractured zygoma is forced into the sinus. It results in tearing of the lining membrane and subsequent bleeding into the antrum. Antrum will appear cloudy or show a fluid level (Fig. 27-21).
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• Fig. 27-21: Zygomatic complex fracture resulting in the haziness seen in the sinus.
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Fractured Tuberosity
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Apices of upper posterior teeth are within 3 mm of the cortical floor of the maxillary sinus or sometimes they may be inside the maxillary sinus. Forceps extraction of a solitary isolated premolar or molar in an edentulous part of the arch is also prone to cause disruption of the sinus floor. Blind instrumentation—blind instrumentation without adequate surgical exposure, in an attempted retrieval of retained apices in the upper posterior quadrant can cause oroantral fistula. Surgery—oroantral opening can occur in cases of removal of cysts and benign tumors in upper posterior region. Facial trauma—oroantral fistula may occurs following massive trauma to the middle third of the facial skeleton, especially if the face is struck by missile or sharp object which is driven through the mouth into the maxillary sinus. Malignant tumor—malignant tumors of the maxillary sinus may penetrate the lateral bony wall of maxillary sinus or it may erode through the floor of the sinus into the mouth producing oroantral communication. Osteomyelitis—it is rare, unless there is underlying systemic disease like leukemia, diabetes. A severe osteitis with bone loss could lead to the formation of an oroantral fistula of one or both maxillary sinus. Syphilis—gummata of the palate may result in a massive oroantral fistula due to destruction of the intervening bone. Inadequate blood clot formation—inadequate blood clot formation in the alveolus after violation of the maxillary sinus may lead to oroantral communication. Implant denture—there is destruction of the antral floor in a patient fitted with an implant denture in maxillary region. Malignant granuloma, Wegener’s granulomatosis and lymphosarcoma—when the invasive process spreads to the palate, expansive perforation or ulceration may occur leading to huge fistula. Periodontal problems—deep periodontal pockets along the side of the upper molar can destroy the bone, which separate the root from the antrum.
Tuberosity fracture inevitably involves the maxillary sinus. It occurs most frequently when extracting a lone standing upper third molar. If the bone is found to be moving with tooth during extraction the operator should stop immediately. Antibiotics, nasal drops and inhalation are therefore prescribed to help and prevent development of a chronic oroantral fistula.
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Oroantral Fistula
Clinical Features
It is a pathological pathway connecting oral cavity and maxillary sinus. If there is no pathological lining present, it is called as oroantral opening which is seen after tooth extraction.
• Opening—oroantral opening can be seen immediately after extraction of the tooth. • Immediate symptoms—there is passage of fluid from oral cavity into the nose. Patient also notices inability to blow out cheek and smoke cigarettes. Unilateral epistaxis, due to blood in the maxillary sinus escaping through the nasal ostium is present. There may be escaped of air from the mouth into the nose and an alteration in vocal resonance.
Causes • Extraction of teeth—teeth which is having periapical infection. Inappropriate or incorrect use of elevators during root or tooth removal may lead to oroantral fistula.
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• Delayed symptoms—the reason for the delayed response is that, at first instance the oroantral defect was completely occluded by blood clot and it is only when this plug disintegrates as a result of infection than an oroantral communication is firmly established. There may be foul, sweetish, fetid or salty taste in mouth. Facial pain or headache which is of throbbing nature and is exacerbated by movement of the head. There may be painless lump on the gum at the site of extraction socket. • Unilateral nasal discharge—unilateral nasal discharge accompanied by sensation of nasal obstruction or nocturnal coughing resulting from draining of exudate into pharynx. • Postnasal drip—postnasal drip will often lead to an unpleasant taste which is accompanied by nocturnal cough, hoarseness, earache or catarrhal deafness. • Acute exacerbation—inadvertent entry of food particles, chewing gum, fluids, impression materials, dressing and packs may provoke acute exacerbation of the inflammatory disease. • Signs of recent fistula—after forceful extraction, floor of sinus seen with root of the teeth. Sudden disappearance upper molar root while extraction (Fig. 27-22). There may be water running out of the nose while rinsing. • Signs of established fistula—a simple dimple on the alveolar ridge may be the only sign. Invasion of antral polyp through fistula resulting in sudden appearance of exophytic mass on the alveolar crest. There is also aspiration of air into mouth through the tooth socket. Tenderness is positive over the maxillary sinus. • Sinusitis—sinusitis occurs with varying intensity depending on diameter of fistula. Patient exhibits swelling and redness covering the sinus and molar eminence as well as pain beneath eye.
Radiographic Features • Break in continuity of maxillary sinus—radiograph will show break in continuity of maxillary sinus. In some cases there is disalignment of a small portion of the cortical layer of bone. • Features of sinusitis—there are also characteristic features of acute or chronic sinusitis due to ingress of bacteria. • Second view should be taken by tilting the head to know location—evidence of displaced root or tooth and second view of the antrum with the head in a different position may be required to ascertain the exact location of the displaced object. • Silver probe examination—confirmation of presence of fistula can be done by introducing silver probe into the orifice, followed by taking the radiograph.
Diagnosis • Clinical diagnosis—all extracted upper posterior teeth should be examined, not only to ensure they are intact but also for indication of a sinus contamination. If the root is covered with a thin plate of bone or adherent sinus mucosa a communication may be present. • Air blow technique—the patient should be asked to blow air into the pinched nose with the mouth open. This forces the air into the sinus via ostium. If an oroantral opening is present, bubbles appear in the extraction socket. • Probing of sinus—Gentle probing of the socket with a blunt instrument, such as ball ended periodontal probe or small amalgam plugger will confirm the bone defect without perforating an intact lining. • Radiological diagnosis—CT will be able to confirm the diagnosis of oroantral fistula (Fig. 27-23).
Management
Fig. 27-22: Oroantral fistula presented as an opening intraorally (Courtesy Dr Ashok L).
• Drug therapy—antibiotic therapy for 1 week. Most commonly given antibiotics is amoxicillin. Decongestants are given for 1 week. • Drainage—to promote drainage, the oroantral fistula can be enlarged by excising a margin of surrounding mucosa, by cauterizing any granulation tissue and polyps protruding from the sinus with electrocoagulation or simply by cautious application of a chemical agent such as trichloroacetic acid. The patient is provided with a syringe and blunted wide bore needle or a plastic irrigating tube, to wash out the sinus with warm salt water three or four times daily. In some cases, antral lavage and antrostomy is done to help drainage. • Prevention from dislodging clot—if opening is small, great care is to be exercised such as avoidance of use of irrigation, vigorous mouth washing and frequent lusty
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Etiology • Endogenous nidus—endogenous nidus is usually root tip or may be simply fragment of soft tissue, bone, blood or mucus. • Exogenous nidus—exogenous nidus are consisting of snuff or paper.
Clinical Features • Age and sex—it can occur at any age in either sex. • Symptoms—it is usually asymptomatic. But if they continue to grow the patient may complaint of bloodstained nasal discharge, nasal obstruction or facial pain.
Radiographic Features
Fig. 27-23: Oroantral fistula seen as an opening on the CT scan (Courtesy Dr Ashok L).
blowing of the nose. In majority of the cases, good clot will form and normal healing will occur. • Closure of opening—if large accidental opening is present, its immediate closure can be achieved in the following ways: • Rising of mucoperiosteum—mucoperiosteum is raised both buccally and palatally and the height of the alveolar ridge is reduced at the site of opening. Edges of soft tissue are freshened up. A periosteal elevator should be used to raise palatal mucoperiosteum so that approximation of mucosal edges is made possible. • Relaxing incision—relaxing incision is made over the palate avoiding the palatine artery. • Suturing—flaps are then sutured without tension. • Shrinkage of nasal mucosa—nasal drops should be given to shrink nasal mucosa and promote drainage.
• Radiodensity—they may have a homogenous or heterogeneous density. • Internal structure—there is alternating layer of radiolucency and radiopacity in the form of lamination. • Margins—outline may be ragged or smooth. • Shape—shape may be round (Figs 27-24A and B), oval or irregular and it is attached to the wall of the sinus.
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Calcification Antroliths These are calcified masses found in the maxillary sinus. It is defined as a complete or partial calcific encrustation of an antral foreign body, either endogenous or exogenous which serves as nidus. There is calcification of masses of stagnant mucus in site of previous inflammation, root fragments or bone chips or foreign body.
B Figs 27-24A and B: Antroliths seen as round shaped radiopacity in the maxillary sinus (Courtesy Dr Ashok L).
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Diagnosis • Clinical diagnosis—it is not possible to make confirmed clinical diagnosis. • Radiological diagnosis—round shaped radiopaque structure in the sinus will give clue to the diagnosis.
Differential Diagnosis
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• Root fragments—pulp canal is seen and it is moved in different direction if head position is changed.
Management • Removal of antroliths can be done if it is symptomatic.
Suggested Reading 1. Adekeye EO, Ord RA. Giant frontal sinus mucocele. Report of two cases. T. Maxillofac Surg 1984;12(4):184-7. 2. Allard RHB, van der Kwast WAM, van der Wall I. Mucosal antral cyst: review of the literature and report of radiographic survey. Oral Surg, Oral Med, Oral Pathol 1981;51:2-9. 3. Aygyn N, Ozuner O, Zinreich SJ. Staging system for sinusitis. Otolaryngol. Clin North Am 2005;38(3). 4. Ballenger JJ. Diseases of the Nose, Throat, Ear, Head and Neck. 14th ed. 1991, Lea and Febiger, Philadelphia. 5. Bavsley RE, Thunthy KH, Weir JC. Maxillary sinus mucocele report of an unusual case. Oral Surg Oral Med Oral Pathol 1984; 58(4):499-505. 6. Blitzer A, Lawson W. Fungal infection of nose and paranasal sinuses. Part i. Otolaryngol Clin North Am 1993;26:114-6. 7. Bowerman JE. The maxillary antrolith. J Laryngol Otol 1969;83: 873-82. 8. Breiman A, Sadowsky D, Friedman J. Mucosmycosis—Discussion and a report of case involving the maxillary sinus. Oral Surg Oral Med Oral Path 1981;52(4):375-8. 9. Brook I. Aerobic and Anaerobic bacterial flora of normal maxillary sinuses and sinusitis. Laryngoscope 1981;91:372-6. 10. Brook I. Bacteriologic features of chronic sinusitis in children. JAMA 1981;246:967-9. 11. Cohen MA, Packota GV, Hall MJ, Steinberg J. Large asymptomatic antrolith of the maxillary sinus. Report of a case. Oral Surg, Oral Med, Oral Pathol 1991;71:155–7. 12. Cummings LW, Fredrickson JM, Harker LA, Krausing LT, Schuller PE. Otolaryngology head and neck surgery. II ed. Vol. I. 1993, Mosby Philadelphia. 13. Daghistani K, Jamal T, Zaher S. Allergic aspargillus sinusitis with proptosis. J Laryngol Otol 1992;106:799-803. 14. Dhingra PL. Diseases of Ear, Nose and Throat. IIIrd ed. 2005. Churchill, BI Livingstone. 15. Donald C. Lanza, Kennedy WD. Current concepts in the surgical management of frontal sinus diseases. Otolaryngol Clin North Am 2001. 16. Esser WJ. Calculus formation in the maxillary sinus. Oral Surg, Oral Med, Oral Pathol 1965;19:755. 17. Evans J. Maxillary antrolith: a case report. Br J Oral Surg 1975;13:73–7. 18. Evans OF. Sinusitis of the maxillary antrum. N Engl J Med 1975; 293:735-9.
19. Evans OF. Sinusitis of the maxillary antrum. N Engl J Med 1976; 293:735-8. 20. Forman AG, Baker I. Mucus cyst of the sphenoid sinus. Dentomaxillofac Radiol 1990;19(4):178-80. 21. Frederick J, Braude AL. Anaerobic infection of the paranasal sinuses. N Engl J Med 1974;200:135-9. 22. Freguson BJ. Fungus balls of the paranasal sinuses. Otolaryngol Clin North Am 2000;33(2):389-98. 23. Gardner DG. Pseudocyst and retention cysts of the maxillary sinus. Oral Surg, Oral Med, Oral Pathol 1984;58:561-7. 24. Gardner PG. Cullane PJ. Mucoceles of the maxillary sinus. Oral Surg Oral Med Oral Path 1986;62(5):538-43. 25. Ghom Anil. Textbook oral radiology: Elsevier publication, New Delhi: 2008. 26. Giri SP, Reddy EK, et al. Management of advanced squamous cell carcinoma of the maxillary antrum. Cancer 1992;69:657-61. 27. Hav-El G. Management of the paranasal sinus mucocele. J Oral maxillofacial Surg 2001;59(2): 246-7. 28. Hyams V. Papillomas of the nasal cavity and paranasal sinuses. A clinicopathologic study of 315 cases. Ann Otol Rhinol Laryngol 1971;80:192-206. 29. Kaneshiro S, Nakajima T, et al. Postoperative maxillary cyst: a report of 7 cases. J Oral Surg 1981;39:191-8. 30. Karma P. Bacteria in chronic maxillary sinusitis. Arch Otolaryngol 1979;105:386. 31. Kurihara K, Saiki T, Takeda K, Kobayashi J. Epitheloid heman-gioma of the maxillary sinus. A case report of J Oral Maxillofac Surg 1995;53(10):1221-3. 32. MacArthur CJ, Lindbeck E, Jones Dt. Paranasal phycomycosis in the immunocompetent host. Otolaryngol. Head Neck Surg 1992; 107:460-2. 33. Moran PR, Morrison WV. Complications of frontal and ethmoid sinusitis. Laryngoscope 1980;90:661-6. 34. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology (2nd edn), 2004: Saunders Elsevier. 35. Ogata Y, Okinaka Y, Takahashi M. Antroliths associated with Aspergillosis of maxillary sinus: a report of case. J Oral Maxillofac Surg 1997;55:1339-41. 36. Ruoppi P, Seppa J, Pukkila M, Nuutinen J. Isolated sphenoid sinus disease report of 39 cases. Arch Otolaryngol Head Neck Surg 2000;126(6):777-81. 37. Ruprecht A, Batniji S, el-Neweishi E. Mucous retention cyst of the maxillary sinus. Oral Surg Oral Med Oral Path 1986;62(6): 728-37. 38. Sadoff RS, Rubin MM. Bilateral antral mucocele a report of a case. J oral Maxillofacial Surg 1991;49(2):193-6. 39. Som P, Curtin H. Chronic inflammatory sinonasal diseases including fungal infections. The role of imaging. Radiol Clin North Am 1993;31:33-44. 40. Som PM, Curtin HP, Head and Imaging, (4th edn). Vol. I, 2003. Mosby, Philadelphia. 41. Van Dis ML, Miles DA. Disorders of maxillary sinus. Dent Clin North Am 1994;38(1):155-66. 42. Wald E. Acute maxillary sinuits in children. N Engl J med 1981; 304:749-53. 43. Weissman J, Tabor E, Curtin H. Sphenochoanal polyps evaluation with CT and MR imaging. Radiology 1991;178:145-8. 44. Whaites E. Essentials of Dental Radiography and Radiology (2nd edn), Churchill Livingstone, Philadelphia, 1998. 45. White SS, Pharoah MJ. Oral Radiology. Principles and Interpretation (5th edn). Mosby. A. Hartcourt Health Sciences Company, St.Louis, Missouri, 2003. 46. Zinreich S, Kennedy D, Malat J. Fungal sinusitis, diagnosis with CT and MR imaging. Radiology 1988;169:439-44.
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Traumatic Injuries of Oral Cavity 697
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Traumatic Injury of Soft Tissue Traumatic Erythematous Macule or Hematoma Traumatic macule is induced by low grade, usually chronic, physical insult.
Clinical Features • Site—common sites are anterior and lateral border of tongue (Fig. 28-1), floor of mouth, posterior palate, buccal mucosa and mucosal surface of lip. • Symptoms—mild to considerable pain and it regresses after the cause is removed. • Signs—it may blanch when digital pressure is used. • Size—size of red zone corresponds closely to size of traumatic agent. • Margins—margins may or may not sharply define.
• Laboratory diagnosis—inflamed lamina propria covered with thin or eroded stratified squamous epithelium that is completely non-keratinized.
Management • Removal of irritant—mechanical irritant is identified and should be removed.
Ecchymosis and Purpuric Macule (early stage) It is produced by blunt traumatic insult of sufficient force, on the mucosa of skin to cause superficial extravasation of blood (Fig. 28-2).
Fig. 28-2: Soft tissue injury due to trauma. Fig. 28-1: Traumatic hematoma of the tongue occur due to tongue biting.
Diagnosis
Clinical Features
• Clinical diagnosis—red lesion with history of trauma may give clue to the diagnosis.
• Site—palate, buccal mucosa, upper lip (Fig. 28-3) and floor of mouth are common site.
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• Size—size varies according to size and force of physical agent inflicting the damage. • Margins—borders are poorly demarcated and blend imperceptibly with surrounding normal tissue. • Signs—it does not blanch on pressure as RBCs are within the tissue rather than in the vessel.
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Clinical Features • Symptoms—patient complains of pain and ‘bubbling’ sensation while palpating the tissue and often difficulty in breathing. • Appearance—it is manifested as unilateral swelling of the tissues of face and/or neck which occurs very rapidly. • Crepitus—it can be felt while auscultating the swelling. • Mediastinal involvement—spread to mediastinum will result in dysphonia, dysphagia or dyspnea. • Hamman’s crunch—cardiac auscultation reveals crepitus synchronous with the heart beat in case of mediastinum involvement. • Pneumoparotid—it occurs when air enters parotid duct. It appears as unilateral enlargement of the parotid. Milking of parotid duct produce frothy air filled saliva.
Diagnosis • Clinical diagnosis—history and presence of crepitus on palpation are two important diagnostic indicators for cervicofacial emphysema. Fig. 28-3: Macular lesion seen on upper lip due to blunt trauma.
Diagnosis • Clinical diagnosis—macular lesion with history of blunt trauma.
Management
Management • Antibiotics therapy—usually broad spectrum antibiotics are prescribed for dental related cervicofacial emphysema. It usually resolves in 2 to 5 days of time. • Management of pneumoparotid—these are treated with antibiotics, massage, hydration, sialogogues and warm compress.
• It is not required, if the diagnosis is confirmed.
Factitious Injury Cervicofacial Emphysema It is a swelling occurs due to introduction of gas or air in the interstices of the connective tissue. In orofacial region, forced air may spread to mediastinal and retropharyngeal area.
Etiology • Dental procedure—it follows variety of oral and dental procedures like tooth extraction, blowing of compressed air into the root canal during endodontic treatment or into a periodontal pocket, blowing of air from high speed air rotor machine. • Fracture—it can also follow mid facial fractures. • Surgical procedure—it can occur spontaneously as a result of patient’s breathing actions following some type of surgical procedure with the break in tissue permitting air to enter the connective tissue space. In some cases, while surgical operation, compressed air may be forced in small intraoral laceration.
Factitious disorders are characterized by physical or psychological symptoms produced intentionally to assume the sick role. A symptom can be considered intentionally produced if there is direct evidence or if other causes for the symptom have been excluded. A patient presenting with a factitious illness typically has a personality disorder with prominent borderline traits. These patients, when confronted with the possibility that their illness was selfinflicted, typically deny the accusations, become angry. Treatment of this disorder is difficult. Perhaps the best treatment may be recognized that it exists so that unnecessary procedures can be avoided. A factitious patient will rarely seek psychiatric treatment. When our patient was confronted with the possibility that her problem was self-inflicted, she vehemently denied the accusations. Self-inflicted injury is the most common in subcutaneous emphysema. Therefore, when a patient presents with unexplained recurrent subcutaneous emphysema, one should suspect self-infliction and examine for puncture marks.
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Traumatic Injuries of Oral Cavity 699 There may be circular purpura around the mouth. In some cases patient give injury to area to get relief from the pain (Fig. 28-4). This is more common in rural population.
Fig. 28-4: Factitious injury seen on the neck of patient to get relief from the pain.
Traumatic Injury to Teeth There are various causes of traumatic injuries to teeth like falls, collisions, sporting activities, domestic violence, automobile accident and assault.
Factors Affecting Trauma to Teeth • Energy of impact—this factor includes both mass and velocity. Low velocity blows cause the greatest damage to the supporting structure whereas the high velocity blows are usually not associated with damage to the supporting structure. • Resiliency of impacting object—if the tooth is struck with cushioned object or if the lip absorb and distribute the impact, the chances of crown fracture are reduced while the risk of luxation and alveolar fracture is increased. • Shape of impacting object—a sharp impact favors clean crown fracture with minimum displacement of the tooth because the energy is spread rapidly over a limited area. On the other hand, a blunt impact increases the area of resistance and force in the crown is transmitted to the apical region causing luxation or root fracture. • Direction of the impacting force—impact can meet the tooth at different angles, most often hitting the tooth facially, i.e. perpendicular to the long axis of the root. Depending upon on the direction of the impacting force the type of fracture properties of enamel and dentin; it was seen that enamel is weakest in region parallel to the enamel rods and that dentin is easily fractured when force is perpendicular to the dentinal tubules.
Classification Ellis and Davey’s classification • Class I—simple fracture of the crown involving enamel. • Class II—extensive fracture of the crown, with considerable amount of dentin involved but no pulp exposure. • Class III—extensive fracture of the crown with considerable amount of dentin involved with pulp exposure. • Class IV—traumatized tooth becomes nonvital (with or without loss of crown structure). • Class V—tooth lost due to trauma. • Class VI—fracture of root with or without loss of crown structure. • Class VII—displacement of the tooth without crown or root fracture. • Class VIII—fracture of crown and mass. • Class IX—fracture of deciduous teeth. Classification by Andreessen This classification is based on a system adopted by WHO in its application of the international classification of disease to dentistry and stomatology. • Injuries to the hard dental tissues and pulp • Crown infraction—an incomplete fracture of the enamel without loss of the tooth substance. • Uncomplicated crown fracture—it is restricted to enamel or involves enamel and dentin, but does not expose the pulp. • Complicated crown fracture—a fracture involving enamel and dentin and exposing the pulp. • Complicated crown root fracture—a fracture involving enamel, dentin and cementum and exposing pulp. • Root fracture—a fracture involving dentin, cementum and the pulp. • Injuries to the periodontal tissue • Concussion—an injury to the tooth supporting structures without abnormal loosening or displacement of the tooth, but with marked reaction to percussion. • Subluxation—an injury to the tooth supporting structure with abnormal loosening but without displacement of tooth. • Intrusive luxation (central dislocation)—displacement of the tooth into alveolar bone. This injury is accompanied by comminution or fracture of the alveolar socket. • Extrusive luxation (peripheral dislocation)—partial displacement of the tooth out of its socket. • Lateral luxation—displacement of the tooth in a direction other than axially. This is accompanied by comminution or fracture of the alveolar crest. • Extra-articulation (complete avulsion)—complete displacement of the tooth out of its socket.
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• Injuries of the supporting bone • Comminution of alveolar socket—crushing and compression of the alveolar socket. This condition was found with intrusive and lateral luxation. • Fracture of the alveolar socket wall—a fracture contained to the facial or lingual socket walls. • Fracture of the alveolar process—a fracture of the alveolar process which may or may not involve the alveolar socket. • Fracture of mandible and maxilla—a fracture involving the base of the mandible or maxilla and often the alveolar process. The fracture may or may not involve the alveolar socket. • Injuries to gingiva and oral mucosa • Laceration of gingiva or oral mucosa—a shallow or deep wound in the mucosa resulting from a tear and usually produced by a sharp object. • Contusion of gingiva or oral mucosa—a bruise usually produced by impact from a blunt object and not accompanied by a break of the submucosal hemorrhage. • Abrasion of gingiva or oral mucosa—superficial wound is produced by rubbing or scrapping of the mucosa leaving a raw bleeding surface. Classification by Garcia Godoy • 0—Enamel crack. • 1—Enamel fracture. • 2—Enamel, dentin, fracture without pulp exposure. • 3—Enamel, dentin fracture with pulp exposure. • 4—Enamel dentin cementum fracture without pulp exposure. • 5—Enamel dentin cementum fracture with pulp exposure. • 6—Root fracture. • 7—Concussion. • 8—Luxation. • 9—Lateral displacement. • 10—Intrusion. • 11—Extrusion. • 12—Avulsion.
Radiographic Features • PDL space widening—widening of periodontal ligament space in the apical portion. • Reduce pulp canal size—reduction in the size of the pulp canal after a year following the trauma.
Management • Conservative—adjustment of opposing teeth should be done to avoid pain.
Luxation It is the dislocation or disarticulation of teeth which are abnormally mobile and are displaced. There may be complete or partial necrosis of the pulp.
Types • Subluxation—it denotes abnormal loosening of teeth without frank dislocation. • Intrusive luxation—displacement of teeth into the alveolar bone. • Extrusive luxation—partial displacement of teeth out of the socket. • Lateral luxation—movement other than axial displacement.
Clinical Features • Site—teeth commonly involved are maxillary incisors in both dentitions. • Symptoms—teeth are abnormally mobile. Pain is also present. • Signs—bleeding from the gingival crevice indicating periodontal damage. Tooth is extremely sensitive to percussion and masticatory force. Clinical crown may appear shortened in case of intrusive luxation. • Sequelae of luxation—there may be external root resorption, ankylosis of tooth, obliteration of root canals, pulp necrosis and marginal bone loss.
Concussion
Radiographic Features
In this case, there is some injury to the supporting structures without abnormal loosening or displacement of teeth and occurs due to crushing injury to the vascular structure at apex and to the periodontal ligament with resulting inflammatory edema.
• Tooth elevation—elevation of traumatized tooth. • PDL space widening—widening of apical portion of periodontal ligament space. • Pulp chamber obliteration—in intrusion, partial or complete obliteration of pulp chamber may occur.
Clinical Features
Management
• Symptoms—traumatized tooth is sore. • Signs—it is sensitive to horizontal and vertical percussion and biting force.
• Subluxation—if several teeth are traumatized or subluxated, a splint may be placed to stabilize the involved teeth during the healing phase. Follow-up care
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Traumatic Injuries of Oral Cavity 701 is mandatory for these injuries because of the greater potential for pulpal necrosis. A splint can be removed within 7-10 days. • Extrusive luxation—the clinician first repositions the luxated tooth into its alveolar socket. If a clot has formed apical to the displaced tooth, the tooth may be more difficult to reposition and more manipulation and pressure may require. It requires splint to be used to stabilize the tooth during the healing process for 2 to 3 weeks. The tooth should be examined clinically and radiographically at monthly interval. If the periapical lesion appears or a fistula is present, endodontic therapy becomes a major consideration. • Lateral luxation—the repositioning of laterally luxated tooth requires a more forceful degree of reduction because of the type or displacement that has occurred. Manipulation with the thumb and index finger can often reduce the injured tooth. The laterally luxated tooth should be repositioned, first by forcing the displaced apex out of its locked position within the labial bone, allowing the clinician to place axial pressure in an apical direction and to manipulate the tooth into its natural position. Splinting is required routinely after reduction of lateral luxation injuries. Maintain the splint for minimum of 14 days and remove it when no abnormal mobility is associated with the tooth. • Intrusive luxation—the best policy is to wait and watch for the tooth to re-erupt on its own accord. Surgical and orthodontic extrusion should be done. Root canal therapy must be anticipated in almost all intrusive luxation injuries.
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B Figs 28-5A and B: Missing tooth from the arch in Figure A and sample tooth is kept in saline solution in Figure B ( Courtesy Dr Shetty).
Management
Avulsion It is complete displacement of tooth from its alveolus.
Clinical Features • Age—encountered in a relatively younger age • Site—maxillary central incisors are commonly affected. Teeth may be missing from the arch (Fig. 28-5A). • Associated signs—fracture of the alveolar wall and lip injuries are frequently seen.
Radiographic Features • Socket without tooth—presence of dental socket without correspondent tooth. Tooth may be located in the adjacent soft tissue. • Noticeable lamina dura—if recent wound is seen, lamina dura will be noticeable. • Socket sclerosis—socket sclerosis occurs.
• Management at site of injury—replant immediately, if possible. If contaminated, rinse with water before implanting. When immediate implantation is not possible, place the tooth in the transport Medias like milk, saline (Fig. 28-5B), saliva and if none of the above is present, use water. • Replantation of tooth—it refers to the insertion of a vital or non-vital tooth into the same alveolar socket from which it was removed or otherwise lost. If extra-oral dry time is less than 2 hours, replant immediately and of extraoral dry time is greater than 2 hours then soak in a topical fluoride solution for 5-20 minutes, rinse with saline and replant. If tooth has been in physiological storage media, then replant immediately. • Management of the root surface—keep the tooth moist at all times and do not handle the root surface. If the root surface is contaminated, rinse with saline and if persistent debris remains on the root surface then use
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cotton pellet to remove the remaining debris and/or gently brush off the debris with a wet sponge. Management of socket—gently aspirate without entering the socket. If a clot is present, use light irrigation with saline. Do not make surgical flap unless bony fragment prevents replantation. Root canal treatment—mature tooth with complete root formation must have root canals filled before implantation or else pulp necrosis will result. If root canals are not filled, there is gradual obliteration of the pulp chamber and canals by calcification. Splinting—splinting can be done by using a variety of appliance including stainless steel wires, acrylic splints, orthodontic banding and arch wires with wire ligatures and even surgical cements with gauze. In some cases root resorption begins within a week or to a few months or as long as 10 years. Transplantation of teeth—it is the replacement of teeth which is damaged beyond repair by caries or by means of other teeth. Usually, mandibular first molar is replaced by developing third molar. Transplanted teeth have to be esthetically acceptable with no periapical or lateral lesions, sharing adequately in the maintenance or physiologic maxillomandibular and muscular relations. Homologous transplants of preserved frozen teeth have also been proposed to simplify the process.
Bruxism The word bruxism is taken from the Greek word brychein: gnashing of teeth. Although the term bruxism is not generally known to lay people, it is shorter and more convenient than teeth clenching or grinding. Bruxism can perhaps be best defined as the involuntary, unconscious and excessive grinding, tapping, or clenching of teeth. When it occurs during sleep, it may be best called as sleep or nocturnal bruxism. A few people, on the other hand, brux while they are awake, in which case the condition may be called wakeful or diurnal bruxism. All forms of bruxism entail forceful contact between the biting surfaces of the upper and lower teeth. It is also called as ‘night grinding’ or ‘bruxomania’. It is a habitual grinding of the teeth, either during sleep or as an unconscious habit during waking hours. It is the term used both for clenching habit during which pressure is exerted on the teeth and periodontium by the actual grinding or clamping of the teeth and, also to repeated tapping of the teeth.
• Systemic factors—gastrointestinal disturbances, subclinical nutritional deficiency and allergy or endocrine disturbances have been reported to be the causative factors. • Psychological factors—emotional tension in which patient is unable to express his emotion due to fear, rage, rejection and it becomes hidden in subconscious and later expressed by variety of way like by grinding the teeth. • Occupational—like in cases of watchmaker, persons who chew gum, tobacco or objects such as toothpicks or pencils.
Clinical Features • Symptoms—in grinding and tapping, this is contact which involves movements of the lower jaw and unpleasant sounds which can often awaken housemates. Clenching (or clamping) on the other hand, involves inaudible, sustained, forceful teeth contact unaccompanied by mandibular movements. Long-term bruxers sometimes experience jaw tenderness, jaw pain, fatigue of facial muscles, headaches, neckaches, earaches and hearing loss. • Teeth—chronic bruxism may lead to sensitive, wornout, decayed, fractured, loose or missing teeth. Grinding or clenching breaks down the enamel; sometimes in long-term bruxers, the teeth height is reduced to stumps (Fig. 28-6). Instead of a white enamel cover, one often sees the more yellowish and softer dentin. The posterior teeth of some chronic bruxers often loose their cusps and natural contours, appearing instead flat, as if they had been worked over with a file or sandpaper. When anterior teeth are affected, their biting surfaces are damaged.
Etiology • Local—mild occlusal disturbances, unconscious attempt by the patient to establish a greater number of teeth in contact or to counteract a local irritating situation.
Fig. 28-6: Attrition seen lower anterior region in chronic bruxers.
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Traumatic Injuries of Oral Cavity 703 • Dental caries formation—the absence of enamel makes it easier for the bacteria to penetrate the softer part of the teeth and produce cavities. With time, the condition may lead to bridges, crowns, root canals, implants, partial dentures and even complete dentures. As long as bruxism continues, the situation keeps getting worse. Thus, by 40 or 50 years of age, most patients have worn their teeth to the degree that extensive tooth restorations have to be performed. • Appearance—as the teeth wear out, they become shorter. As a result, when the mouth is closed, the upper and lower jaws are nearer than they used to be and hence the nose and chin. The skin now may bag below the eyes and curl around the lips, causing the lips to seemingly disappear. The chin recedes and the person looks comparatively old. • Facial muscles—bruxism involves excessive muscle use leading to a build-up or enlargement (hypertrophy) of facial muscles, especially those of the jaws where the masseter muscle (the muscle that raises the lower jaw and enables closing the jaws) is located. In long-term bruxers, this build-up may lead to a characteristic square-jaw appearance. Some patients resort to removing part of the masseter muscle by surgery or injections of toxic materials to reduce muscle size and thus partially regain their former, more aesthetically pleasing look. • Salivary glands—another example of this spiral involves the occasional inflammation and blockage of some salivary glands. In this case, the masseter muscle becomes disproportionately overdeveloped and blocks the opening of the nearby parotid glands. They, thus interfere with the flow of saliva into the mouth, causing the saliva to accumulate in the glands. This in turn may lead to periodical swelling, pain, inflammation and abnormal dryness of mouth. • TMJ—bruxism may also damage the temporomandibular joints. First few signs of temporomandibular joint disorders are TMJ discomfort or pain, soreness of jaws and muscles, clicking or popping sounds when opening the jaws or while chewing and difficulties in opening the mouth fully. • Malocclusion—malocclusion or bad bite is more common among bruxers than in the general population. Bruxism may often involve more pressure on one side of the mouth than on the other, thereby causing malocclusion. As the teeth wear out (Fig. 28-7), the distance between the upper and lower jaw decreases and overclosure may develop. • Effect on periodontium—There may be loss of integrity of the periodontal structures resulting in loosening or drifting of the teeth and even gingival recession occurs.
3 Fig. 28-7: Severe destruction tooth seen in bruxism patient.
Management • Psychotherapy—the belief that bruxism is traceable to stress and other emotional and psychological factors give rise to a variety of psychotherapeutic approaches. For instance, listening to progressive relaxation or autosuggestion tapes just before going to sleep may foster calmness and self-confidence. • Wakeful EMG Feedback—another psychological approach to stress reduction resorts to instrumentation. During bruxing, the relevant muscles are active and this increased activity or tension can in turn be measured with an electromyograph (EMG: electro—electric; myo— muscle; graph—record). During treatment sessions at home or the laboratory, the patient sits or reclines comfortably. One or more pairs of recording electrodes are then attached to the surface of the skin in close contact to appropriate muscles (e.g. masseter muscles). These electrodes transmit information about the level of muscle activity to a computer monitor. The patient is instructed to consciously lower that level below a threshold line (also visible on the screen). Gradually, by becoming alert to the presence of muscle tension, patients may develop techniques for reducing that tension and hence, bruxism. • Exercise—Quinn suggested isokinetic and stretching exercises of the mandible. Such exercises may or may not help alleviate bruxism, but perhaps may be used to complement other approaches. However, but it seems unlikely that they could ever be used as the sole therapeutic approach. Evidences that this approach is effective and non-existent. • Drugs—both, the stress and brain malfunction etiological theories give at times, rise to the use of anti-anxiety agents, muscle relaxant and other drugs. Most authorities, however, feels that at best, drugs in use now are of limited value in the treatment of great majority of
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chronic bruxers and that they often involve moreover untoward side effects. Evidence that this approach is effective and are non-existent. • Equilibration therapy—some people believe that bruxism is traceable to malocclusion (bad bite). They therefore suggest eliminating this cause through orthodontic adjustment. • Splints—by far, the most common treatment regimen for bruxism relies on the time-honored procedure of splints like nightguards, biteguards, occlusal splints, biteplates, removable appliances or interocclusal orthopedic appliances and use of manufactured customized appliances. Removable splints are worn at night to guide the movement so that periodontal damage is minimal.
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Fracture of Teeth (Fig. 28-8) Dental Crown Fracture Anterior teeth are commonly involved. It may be caused by fall, accident and blows from foreign bodies.
B Figs 28-9A and B: Uncomplicated fracture of crown of teeth (Courtesy Dr Shetty).
Fig. 28-8: Injuries to hard dental tissues and pulp.
Types • Enamel infraction or crack—fracture that involves only enamel without loss of enamel substance. • Uncomplicated fracture—fracture involving enamel or enamel and dentin with loss of tooth substance without pulpal involvement. • Complicated fracture—fracture that extends through enamel, dentin and pulp with loss of tooth substance.
• Uncomplicated fracture—it does not involve pulp and is usually found on mesial or distal corner of maxillary central incisors (Figs 28-9A and B). Dentin involvement is identified by contrast of color between it and peripheral layer of enamel. Exposed dentin is very sensitive to chemical, thermal and mechanical stimulation. • Complicated fractures—there is bleeding from exposed pulp or at least drop of blood oozes from the pinpoint exposure. Exposed pulp will be sensitive to most forms of stimulation (Figs 28-10A and B).
Radiographic Features • Appearance—it will show size and position of pulp chamber, location and extent of exposure and stage of root development.
Management Clinical Features • Cracks—it can be seen in indirect light (directing the beam along the long axis of tooth).
• Crown infraction—no treatment (Fig. 28-11). • Uncomplicated fracture—small defect is corrected by grinding. Oblique fracture has worse prognosis than
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Traumatic Injuries of Oral Cavity 705 • Complicated fracture—pulp capping, pulpotomy and pulpectomy can be done. In immature tooth: Perform pulp capping or partial pulpotomy with calcium hydroxide and bacteria tight coronal seal. In mature tooth: Same as with immature tooth or pulpectomy.
Dental Root Fracture Clinical Features • Sites—it is common with maxillary central incisors. • Coronal fragment—coronal fragment is displaced lingually and is slightly extruded. If fracture line is close to the apex then tooth will be more stable (Fig. 28-12A). • Signs—if only movement of crown is detected, root fracture is likely to be considered. • Symptoms—temporary loss of sensitivity. It returns to normal within 6 months.
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B Figs 28-10A and B: Complicated crown fracture of upper central incisor (Courtesy Dr Shetty).
Fig. 28-12A: Root showing fracture at the apex of root (Courtesy Dr Soni).
Radiographic Features • Appearance—if the X ray beam is projected parallel with the plane of the root, sharp radiolucent line between the fragments can be seen (Fig. 28-12B) . If the X-ray beam is not parallel, it will look as poorly defined gray shadow. • Fracture line—fracture line may be transverse or oblique. • Obliteration of pulp chamber—calcification and obliteration of pulp chamber can be seen in due course of time. Fig. 28-11: Crown fracture involving the enamel and dentin.
Differential Diagnosis • Soft tissue image—it extends beyond tooth margin.
horizontal fracture. Provide a temporary glass-inomer cement bandage or permanent restoration using a bonding agent and composite resin. If very close to pulp, consider Ca(OH)2 base. If an intact fragment exists, a bonding procedure may be carried out.
Management • Fracture in middle or apical third of root—teeth mainly restored to their proper position and securely immobilized. • Fracture at coronal/cervical area—extraction is indicated.
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Textbook of Oral Medicine Management • Removal of coronal fragment—this can be done and after this, dowel crown should be prepared. • Extraction—if 3 to 4 mm of root is remaining, extraction is indicated. • Uncomplication fracture—uncomplicated fracture is to be restored.
Vertical Root fracture
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It is also called as ‘Cracked tooth syndrome’. It runs lengthwise from crown towards apex of tooth.
Causes
Such fracture is likely to be intra- and extra-alveolar. They are result of direct trauma.
• Iatrogenic—they are iatrogenic in origin, i.e. after insertion of pin or retention screws into vital and non-vital teeth. • Endodontically treated tooth—it also occurs in endodontically treated tooth as there is weakening of tooth in such cases. • Traumatic occlusion—it may be caused by traumatic occlusion.
Clinical Features
Clinical Features
• Site—they have labial margin in the gingival third and course obliquely to exist below the gingival attachment on the lingual surface. It frequently involves pulp (Fig. 28-13). • Symptoms—there is pain during mastication. • Signs—tooth is sensitive to occlusal force.
• Site—it is usually seen in posterior teeth in adults, especially in mandibular molars. • Symptoms—dull pain of long duration which may vary from non-existent to mild. • Signs—it may have periodontal lesions resembling chronic lesion. • History—history of repeated failure of endodontic treatment.
Fig. 28-12B: Fracture root in apical region.
Crown/Root Fracture
Radiographic Features • Appearance—if central X-ray lies in the plane of the fracture, it may be visible as a radiolucent line. • PDL thickening—after bacterial invasion, radiograph will show thickening of periodontal ligament space or a diffuse radiolucent lesion.
Management
Fig. 28-13: Crown/root fracture of upper central incisor due to severe attrition of tooth.
• Extraction—extraction of single rooted teeth. • Hemisection—hemisection for multi-rooted tooth followed by extraction of involved half and the remaining half is restored with endodontic therapy.
Perforation of the Root Radiographic Features • Appearance—most crown/root fractures are perpendicular to the direction of the beam.
The root canal is sometimes penetrated during operative procedures and injury may extend to cause a perforation of the root. The usual site of it is at the apex and the side of the root, but the floor of the pulp chamber and even the side of
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Traumatic Injuries of Oral Cavity 707 the crown; near the neck of the tooth may be perforated (Fig. 28-14). Radiographically, it is visible if some smooth metal broach or piece of wire or some opaque substance is inserted in the abnormal passage to make it visible. In some cases, the shadow of root canal can be seen approaching the side of the root and this can be the evidence of a perforation. Rarefying osteitis at the side of a tooth is always suggestive of perforation, particularly if there has been root canal therapy.
Radiological Features • Loss of PDL space—it may be visible on the radiograph as loss of the normal thin radiolucent line representing the periodontal ligament. • Sclerosis—there may be mild sclerosis and apparent blending of the bone with the tooth root.
Management • It has good prognosis and as such no treatment is required.
Traumatic Injury to Facial Bone When patient is subjected to injury, there is chance that jaws may be fractured. Even in some cases, minor trauma may result in bone damage.
Radiographic Features of Fracture
Fig. 28-14: Root perforation seen in the central incisor (Courtesy Dr Soni).
Tooth Ankylosis Ankylosis between tooth and bone is an uncommon phenomenon in the deciduous dentition and even more rare in permanent teeth.
Causes • Partial root resorption—it occurs when partial root resorption is followed by repair; with either cementum or bone that unite the tooth root with alveolar bone. • Occlusal trauma—ankylosis can occur after traumatic injury particularly due to occlusal trauma. • Following root canal therapy—it may follow root canal therapy, if the apical periodontal ligament is irritated or seriously damaged.
Clinical Features • Symptoms—it seldom manifests any clinical symptoms unless there is concomitant pulp infection. • Dull muffled sound—if the extensive area of the root surface is involved, the tooth gives a dull muffled sound on percussion rather than the normal sharp sound. • Difficulty in extraction—there is considerable difficulty while doing extraction of the teeth, sometimes necessitating surgical removal.
There are mainly following features seen in fracture of jaws: • Fracture line—dark line which results from the passage of rays through the line of cleavage has been termed as the fracture line. Fracture line is very dark, when the rays pass freely between the fragments and less dark when the rays pass through small part of the fracture line. • Displacement of the fragment—in it, instead of normal continuity of the surface of bone, there is dis-alignment of the two fragments. In mandible, action of temporalis muscle pulls the posterior portion of the mandible upward is the common cause of displacement. • Deformity—it is alteration in shape of bone as a result of injury in the cortex. The abrupt angulations of bone are indication of deformity. • Radiopaque line—a fracture that has become impacted does not have any space between the fragments and the line of cleavage is obscured by superimposition of bony trabeculae at the site of impaction. In this case, there is slight increase in density at the fracture line due to double number of trabeculae. • Double fracture line—many fractures pass slight obliquely across the bone. When the line of cleavage of inner and outer cortices does not superimpose, it gives an impression that there are two fractures. • Relationship of teeth to fracture line—a fracture may enter the apical end of the tooth socket and disappear. If the line of fracture extends along a lateral aspect of the tooth, the tooth may obscure it. Fracture through the angle of the jaw frequently appears to extend from the apices of the 3rd molar but it has actually started at the alveolar margins of bone. An unerupted tooth may sometimes be present in the fracture line, which might play as predisposing factor in fracture and its presence may
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affect the treatment. With fracture, a tooth may be forced from its follicle into the adjacent bone, soft tissue or between the fragments; causing its separation.
Indication for Removal of a Tooth from the Fracture Line
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Longitudinal fracture involving the root. Dislocation or subluxation of the tooth from the socket. Presence of periapical infection and infected fracture line. Acute Pericoronitis, advanced periodontitis.
Dentoalveolar Fractures These are defined as those in which avulsion, subluxation or fracture of teeth occur in relation with fracture of the alveolus. Anterior alveolar fractures are most common. Labial plate is more prone to fracture than palatal plate. Fracture line is most often horizontal.
Fig. 28-15: Fracture of maxillary tuberosity showing detachment.
Clinical Features • Site—alveolar process of maxilla is more commonly fractured than that of mandible. The most common sites are the upper incisor and cuspid regions and region of tuberosity. • Lip—there is full thickness wound of the lower lip or ragged laceration on its inner aspect caused by impaction against the lower anterior teeth. There may be local bruising and portions of teeth or foreign bodies may get lodged in soft tissue of lip. • Gingiva—there may be laceration of gingiva and deformity of alveolus. • Teeth—there may be fracture of crown and root portion of teeth. Teeth in fractured fragment will have recognizable dual sound when percussed. • Occlusion—marked malocclusion along with displacement and mobility. • Alveolar fracture—a complete alveolar fragment may be displaced into the soft tissue of the floor of mouth and can be covered by mucosa. There may be gross comminution of alveolus occurs. • Maxillary tuberosity fracture—the detached bone may include the floor of maxillary sinus (Fig. 28-15); which is indicated by discharge from the nose on the involved side. Ecchymosis of buccal vestibule can also occur. • Cracked pot noise—impacted alveolar fracture may be virtually immobile. Sometimes crepitations can be detected on palpation and a ‘cracked pot’ noise is detected when the teeth within the alveolar fracture are purcussed.
Radiological Features • Radiologically, fracture line is seen above the apices of root of teeth.
Fig. 28-16: Dentoalveolar fracture showing line distal to central incisor.
• Damage to roots of the adjacent teeth is common with fracture of alveolus (Fig. 28-16). Fracture of alveolar process is well delineated. Posterior palatal fracture is best demonstrated on occlusal radiograph.
Management • Fracture of maxillary tuberosity—if the tuberosity is completely detached from the periosteum, it should be carefully dissected out and the resulting soft tissue defect are sutured to prevent any residual opening into the maxillary sinus. • Extensive fracture of alveolus with teeth attached—splinting of teeth and anchoring to teeth elsewhere in the upper jaw.
Mandibular Fractures Fracture of mandible occurs more frequently than any other fracture of the facial skeleton. It is more common than middle third fracture. The most common facial fractures are mandible (61%), followed by maxilla (46%), the zygoma
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Traumatic Injuries of Oral Cavity 709 (27%) and the nasal bones (19%). Most common cause of mandibular fracture is road traffic accidents. Other causes are assault, falls, industrial trauma and sport injury.
Classification • According to type of fracture: • Simple—it includes closed linear fracture of the condyle, coronoid, ramus and edentulous body of the mandible. Greenstick fracture occurring in children is also included in it. • Compound—fracture of tooth bearing portions of the mandible are nearly always compound into the mouth via the periodontal membrane and some severe injuries are compound through the overlying skin. • Comminuted—direct violence to mandible from penetrating sharp objects and missiles are usually compound and may be further complicated by bone and soft tissue loss. • Pathological—when fractures result from minimum trauma to mandible which is already weakened by pathological conditions like osteomyelitis, neoplasm and generalized skeletal diseases. • According to site of fracture: • Dentoalveolar • Condyle • Coronoid • Ramus • Angle • Body (molar and premolar) • Parasymphysis • Symphysis • According to cause of fracture: • Direct violence—fracture occurs at the site of trauma. • Indirect violence—fracture occurs away from the site of trauma. • Excessive muscular contraction—occasionally, fractures of coronoid process occur because of sudden reflex contracture of temporalis muscle. • According to treatment plan • Unilateral—it is more frequently caused by direct violence. • Bilateral—it occurs due to combination of direct and indirect violence. • Multiple—it is also associated with direct and indirect violence. Most common fracture of this type is Guardsman fracture when soldier faints on parade at midpoint of chin causing fracture of symphysis and both the condyle. • Comminuted—it is usually seen in war missile injury (Fig. 28-17). • Fry and colleagues classified, in descriptive manner, the different directions of the fracture:
Fig. 28-17: Comminuted fracture of body of mandible.
• Horizontal favorable: if the direction of the fracture is such that it resists the action of the elevator muscles in pulling the ramus segment upwards when viewed from side, or horizontal plane called as horizontally favorable fracture. • Horizontally unfavorable: when the direction of fracture line is reversed and posterior fragment is elevated by the muscle pull, the fracture called as horizontally unfavorable (Fig. 28-18). • Vertically favorable: when viewed from above or in the vertical plane, the buccolingual direction of the fracture line is such that it prevents the displacement of the segment lingually by resisting the pull of the medial pterygoid muscle called as vertically favorable. • Vertically unfavorable: when the opposite is the case, in which the segment can be pulled lingually because of the unopposed action of the medial pterygoid, the fracture is termed as vertically unfavorable.
Fig. 28-18: Horizontally unfavorable fracture of the angle of mandible and parasymphyseal fracture involving the teeth in fracture line.
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Clinical Features of Mandibular Fracture
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• Changes in the occlusion—any change in the occlusion is highly suggestive of the mandibular fracture. A change in the occlusion can result from fractured teeth, a fractured alveolar process, a fractured mandible at any location, and trauma to the temporomandibular joint and muscles of mastication. Posttraumatic premature posterior dental contact or anterior open bite may result from bilateral fractures of the mandibular condyle or angle as well as from maxillary fractures with inferior displacement of the posterior maxilla. Posterior open bites may occur with the fractures of the anterior alveolar process or parasymphyseal fractures. Unilateral open bite may occur owing to ipsilateral angle and parasymphyseal fracture (Fig. 28-19). Posterior cross bite can result from midline symphyseal and condylar fractures with splaying of the posterior mandibular segments.
Fig. 28-19: Step deformity seen in the fracture of mandible in the symphysis region.
• Anesthesia, paresthesia, or dysesthesia of the lower lip— Numbness in the distribution of the inferior alveolar nerve after trauma is almost pathognomonic of a fracture distal to the mandibular foramen. • Abnormal mandibular movement—most patients presenting with a fractured mandible have limited opening and trismus owing to guarding of muscles of mastication. Certain mandibular fractures result in predictable abnormal mandibular movements like deviation on opening towards the side of a mandibular condylar fracture (Fig. 28-20). Because lateral pterygoid muscle function on the unaffected side is not counteracted on the opposite side by the nonfunctioning of lateral pterygoid muscle, deviation results. Inability to close the jaws can be the result of fractures of the alveolar process, angle, ramus, and symphysis, causing
Fig. 28-20: Fracture mandible showing deviation on opening.
premature dental contact. Lateral mandibular movements may be inhibited by bilateral condylar fractures and fracture of ramus with bone displacement. • Change in facial contour and mandibular arch form—facial asymmetry should alert clinician to the possibility of mandibular fracture. A retruded chin can be caused by bilateral parasymphyseal fracture. The appearance of an elongated face may be the result of bilateral subcondylar, angle, or body fracture, allowing the anterior mandible to be displaced downward. If there is a deviation from the normal U-shaped curve of the mandible, fracture should be suspected. • Lacerations, hematoma and ecchymosis—trauma significant enough to cause loss of skin or mucosal continuity or subcutaneous-submucosal bleeding certainly can result from trauma to the underlying mandible. Lacerations should be carefully inspected before closure. The direction and type of fracture may be visualized directly through the laceration. In rare cases of animal bites there may be the loss of soft as well as hard tissue. The diagnostic sign of ecchymosis or hematoma in the floor of the mouth indicates mandibular body or symphyseal fracture.
Radiographic Features • Technique required—following types of radiographs are helpful in the diagnosis of mandibular fractures, i.e. panoramic (Figs 28-21 and 28-23) radiograph, lateral oblique radiograph, posteroanterior radiograph, occlusal view, periapical view, reverse Towne’s view, CT scan. • Margin of fracture—the margins of the fractures usually appear as sharply defined radiolucent lines of separation that are confined to the structure of the mandible. Occasionally the margins of the fracture overlap each other, resulting in the area of increased radiopacity at the fractured site.
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Fig. 28-23: Fracture at symphysis and angle of mandible.
Fig. 28-21: Fracture at angle of mandible on left side.
Fig. 28-22: Fracture at body of the mandible.
• Step—displacement of the fracture results in the cortical discontinuity or “step.” • Double fracture line—an oblique fracture that involves both cortical plates may show two fracture lines if the fracture lines in both buccal and lingual plates are not superimposed. In this case, a right angle view such as occlusal view and the fact that the two fracture lines are meeting at same point on the inferior border of the mandible helps in correction of diagnosis. • Lateral oblique view—the lateral oblique view of the mandible can be helpful in the diagnosis of ramus, angle and posterior body fractures (Fig. 28-22). • PA view—the posteroanterior view demonstrates any medial or lateral displacement of the fractures of ramus, angle, body or symphysis (Fig. 28-24). • Occlusal view—the mandibular occlusal view demonstrates displacement in the lateral or medial direction of the body fractures and also shows the anterior or posterior displacement of the symphyseal fracture. • Reverse Towne’s view—the reverse Towne’s view is ideal for showing medial displacement of the condyle and
Fig. 28-24: PA view showing multiple fractures of the mandible.
condylar neck fracture. Periapical dental film shows the most detail and can be used for the nondisplaced linear fractures of the body as well as alveolar process and dental trauma. • CT scan—the CT scan is ideal for the condylar fractures that are difficult to visualize. The greater expenses and radiation exposure limit its use in cases that cannot be diagnosed with conventional radiograph (Figs 28-25A to 28-26).
Differential Diagnosis • Soft tissue shadow of space between tongue and soft palate— in lateral radiograph of normal mandible, it is possible to see the gray shadow of tongue which has curved upper and posterior borders. Immediately behind lies the soft palate, which presents a shape somewhat similar to an inverted triangle. In many radiographs, there is a dark line situated between these two shadows which is
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Fig. 28-26: 3D CT of fracture of mandible (Courtesy Dr Meshram).
plane and X-rays are directed in an appropriate manner, to produce excellent radiographs of this region.
Management
B Figs 28-25A and B: 3D CT image of mandibular fracture at symphysis region (Courtesy Dr Amit Parate, Lecturer, GDCH, Nagpur, India)
produced by presence of air between the tongue and soft palate. This thin dark line is carried down over the shadow of the mandible in the region of the angle and sometimes gives resemblance to a fracture. Careful study shows that the dark line is continued on the bone. • The shadow of hyoid bone—in lateral radiograph of jaws, the shadow of neck intervenes over the some part of the bone and where it ends anteriorly, there is difference in the radiographic density which is quite marked in some cases. There is greater likehood of making error when there is thin dark line present which infact represents the subcutaneous fat on anterior aspect of the neck. In either case, there is evidence of shadow continuing on the bone and no fracture can produce such an effect. • The intervertebral disc space—it presents as dark shadow and can be mistaken for fracture. In this case, intraoral occlusal film can be placed in the mouth in occlusal
Preliminary management • Examination—the first aid required consists of careful examination of mouth and removal of all fragments of teeth, broken filling and dentures. • Airway—if there is danger of falling tongue back, then dorsum of the tongue should be sutured. • Hemorrhage—obvious bleeding point such as facial vessels should be secured with artery forceps and temporary dressing should be applied. • Soft tissue laceration—soft tissue wound should be sutured within 24 hours of injury. • Antibiotics—benzyl penicillin should be administered IM injection or 1 mega unit every 6 hours for first 2 to 3 days and oral penicillin should be continued for further one week. In recent, oral metronidazole 400-800 mg BD is given to all patients with mandibular fracture. Planned management • Reduction—reduction of fracture means the restoration of functional alignment of bone fragments. • Immobilization of fractured bone—the fracture site must be immobilized to allow bone healing to occur. Immobilization can be done with intermaxillary fixation and bone plating.
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Traumatic Injuries of Oral Cavity 713 • Minimally displaced fracture—close reduction and intermaxillary wiring (Fig. 28-27). • Severely displaced fracture—open reduction and intermaxillary fixation.
If the tip of the coronoid process is ditched, the fragment is pulled upwards towards the infratemporal fossa by the temporalis muscle. There may be tenderness over the anterior part of the ramus and hematoma. Painful limitation of movement, especially on protrusion of mandible may be found.
Middle Third Fractures Classification
Fig. 28-27: Fracture with interdental wiring is seen.
Postoperative Care • Sitting position—patient with fracture of mandible finds it more comfortable if they are in sitting position with chin forward, provided that there is no contraindication to this posture such as fracture of vertebra. • Drugs—morphine and its derivative are contraindicated in patients with maxillofacial injuries as these drugs depress the respiratory center and cough reflex. Prophylactic antibiotics should be administered to control the infection. Maintenance of good oral hygiene is essential for prevention of infection.
Coronoid Fracture It is rare. It usually results from the reflex contracture of the powerful anterior fibers of temporalis muscle. During operation on large cyst of ramus, coronoid may get fracture (Fig. 28-28).
Fig. 28-28: Fracture of coronoid is also seen in association with fracture of condyle and mandibular body.
• Central middle third fracture • Le Fort’s type-I—bilateral detachment of the alveolar process and palate or the low level subzygomatic fracture of Guerin. • Le Fort’s type-II—pyramidal subzygomatic fracture of the maxilla. • Le Fort’s type-III—high level suprazygomatic fracture of central and lateral part of face. • Fracture of zygomatic complex • Zygoma depressed with fracture at several sites • Fracture of zygomatic arch • Fracture of naso-ethmoidal complex • Fracture of orbit • Fracture of orbital rim • Orbital blow out fracture Midfacial fracture It may involve the frontal, nasal, lacrimal, zygoma, ethmoidal and sphenoid bones. They are classified by Rene Le Fort. Le Fort I It is also known as low level fracture/Horizontal fracture of Maxilla/Guerin fracture/Floating fracture. • Horizontal fracture above the level of Nasal floor (Fig. 28-29).
Fig. 28-29: Diagrammatic representation of Le Fort I fracture.
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• Fracture line extends backward from the lateral margin of the anterior nasal aperture below the zygomatic buttress to cross the lower 3rd of the pterygoid lamina. • Fracture also passes along the lateral wall of the nose and the lower 3rd of nasal septum to join the lateral fracture behind the tuberosity.
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Le Fort II It is also called as ‘Pyramidal or Subzygomatic fracture’. There is a pyramidal appearance of fracture in PA skull view (Fig. 28-30). • This fracture runs from the thin middle area of the Nasal Bones down to either side crossing the frontal processes of maxilla into the medial wall of each orbit. • Within each orbit, the fracture line crosses the lacrimal bone behind the lacrimal sac before turning forward to cross the infraorbital margin slightly medial to or through the infraorbital foramen. • The #(fracture line) now extends downwards and backwards across the lateral wall of the antrum below zygomatico-maxillary suture and divides the pterygoid laminae about halfway up. Separation of block from the base of skull is completed via the nasal septum and may involve the floor of the anterior cranial fossa.
Fig. 28-30: Le Fort II fracture—A diagrammatic representation.
Le Fort III It is also called as ‘High transverse or Suprazygomatic fracture’. It completely separates the middle third of the facial skeleton from the cranium (Fig. 28-31). • The fracture line runs from near the frontonasal suture transversely, parallel with the base of the skull and involves the full depth of the ethmoid bone, including the cribriform plate. • Within the orbit, the fracture line passes below the optic foramen into the posterior limit of the inferior orbital fissure.
• From the base of inferior orbital fissure, the fracture line extends into two direction • Backwards across the pterygomaxillary fissure to fracture line the root of the pterygoid laminae. • Laterally across the lateral wall of the orbit separating the zygomatic bone from the frontal bone.
Fig. 28-31: Le Fort III fracture—A diagrammatic representation.
Clinical Features Le Fort I • Location—it may be unilateral or bilateral. • Symptoms—in recent injury, there may be slight swelling of upper lip. Some fractures are so mobile that the patient has to keep the mouth slightly open to accommodate the increased vertical dimension of bite. Paresthesia presents over the distribution of infra-orbital nerve and pain over nose and face. • Signs—ecchymosis is present in the buccal sulcus beneath the zygomatic arch. Occlusion is disturbed and variable amount of mobility may be found in the tooth bearing segment of maxilla. If the fracture line is at high level, the fragment will include the pterygoid muscle attachment. It will pull the fragment posteriorly and depress its posterior margin. Due to this, posterior maxillary teeth will force the mandible open resulting in open bite, retruded chin and long face. • Cracked pot sound—in impacted type of fracture, there may be damage to cusps of individual teeth caused by impaction of the mandibular teeth against them. Percussion of upper teeth results in a distinctive ‘Cracked pot’ sound. • Flattening of face—in some cases, there is flattening of middle of the face and epistaxis. • Palpation—manipulation will reveal mobile maxilla and crepitation. Le Fort II • Moon face appearance—there is massive edema that cause marked swelling of the middle third of face giving rise to ‘moon face’ appearance.
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Traumatic Injuries of Oral Cavity 715 • Hemorrhage • Bilateral circumorbital ecchymosis—ecchymosis about the eye which develops within minutes of injury (Fig. 28-32). • Subconjunctival ecchymosis—the conjunctivae over the inner quadrant of eye are blood shot and if the zygomatic bone is involved, this subconjunctival ecchymosis will also be over the outer quadrant. • Periorbital hematoma—it causes swollen conjunctiva to bulge out from between the eyelids.
Fig. 28-32: Circumorbital edema seen in maxillary fracture.
• Eye—there may be variation in the size of pupil which may occur due to peripheral damage to the oculomotor nerve. There may be diplopia and ocular movements may be limited. • Nose—there may be lengthening of the nose. There may be bleeding from the nose. • Face—there is ‘dish-face’ deformity of the face with occasional lengthening of the face. • Nerve damage—as the fracture line passes across the inferior orbital rim, there may be injury to the infraorbital nerve resulting in anesthesia or paresthesia of cheek. • Step deformity—there is step deformity at infraorbital margin. By applying the pressure between the bridge of the nose and the palate, pyramid of bone can be moved. • Cerebrospinal fluid rhinorrhea—it is sometimes appreciated by salty taste in the mouth. • Intraoral finding—retropositioning of the maxilla, so that anterior teeth do not meet and there is gagging on the posterior teeth. There is mobility of the upper jaw. Occasional hematoma of palate, which will cause patient considerable discomfort. Cracked pot sound on tapping the upper teeth. Le Fort III • Location—superficially, it appears similar to Le Fort II but injury is much more severe. It is very unusual to find Le Fort III fracture occurring in isolation.
• Edema—it is more extensive and massive. • Signs—there is tenderness and often separation at the frontozygomatic sutures. The facial skeleton will be tilted to the side opposite to the direction of the fracturing force. There may be mobility of whole of the facial skeleton as a single block. • Nose—nose often blocked with blood clot. There may be cerebrospinal fluid (rhinorrhea). There may be lengthening of nose. • Cerebrospinal fluid rhinorrhea—it will be profused as compared to Le Fort II. • Hooding of eye—there is lowering of the ocular level, due to the fracture line passing above the Whitnall’s tubercle, removing the support given to the eye by Lockwood’s suspensory ligament. As one or both eye drops, the upper lid follows the globe down, producing unilateral or bilateral ‘hooding’ of the eyes. • Hemorrhage—bleeding into periorbital tissues. • Face—there is separation of both frontozygomatic sutures which produces lengthening of face. • Step deformity—flattening and step deformity at infraorbital margin. • Intraoral findings—the entire occlusal plane may drop producing anterior open bite. There is gagging of occlusion in the molar area.
Radiographic Features • Le Fort I—it is identified on PA, lateral skull and Water’s projection (Fig. 28-33). Both the maxillary sinuses are cloudy and may show air filled level. Lateral view shows slight posterior displacement of fragment.
Fig. 28-33: Water’s view showing Le Fort I fracture with fracture of zygomatic bone.
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• Le Fort II—it will reveal the fracture of the nasal bone and both, frontal processes of maxilla and infra-orbital rims on both sides or separation of zygomatic sutures on both sides. Deformities and discontinuation of lateral walls of both sides of maxillary sinus (Fig. 28-34). There is thickening of the lining mucosa and clouding of maxillary sinus. • Le Fort III—hazy appearance due to soft tissue swelling. Separation of sutures, i.e. of nasofrontal process, maxillofrontal, zygomatico-frontal and zygomaticotemporal. Nasal bone, frontal process of maxilla, both orbital floors and pterygoid plate show radiolucent lines and discontinuity. Ethmoidal and sphenoid sinuses are cloudy.
Fig. 28-35: Extensive soft tissue injury associated with fracture of zygomatico-maxillary complex.
Fig. 28-34: CT scan showing the fracture at anterior and posterior wall of maxillary sinus.
Management • Le Fort I—Low level—intermaxillary fixation. High level— intermaxillary fixation and cranio-maxillary fixation. • Le Fort II—reduction followed by intermaxillary fixation. Open reduction and inter-osseous wiring of infraorbital rims. Antibiotics should be given to the patient. • Le Fort III—control hemorrhage and maintain airway. Surgery should be delayed until edema subsides. External immobilization should be done.
Zygomaticomaxillary Complex Fracture The most common causes of ZMC fractures include interpersonal altercations, falls, motor vehicle accidents, and sports injuries. 25% of patients have other associated facial fractures (Fig. 28-35).
Classification • Class I—Fracture of zygomatic bone with minimum or no displacement.
• Class II—Fracture of zygomatic bone with displacement. • Type A—Rotation around a vertical axis • Inversion of the orbital ring • Eversion of the orbital ring • Type B—Rotation around a longitudinal axis • Medial displacement of frontal process • Lateral displacement of frontal process • Class III—Enbloc displacement of the bone • Medial displacement • Inferior displacement • Lateral displacement • Class IV—Comminution of the zygomatic bone • Class V—Fracture of zygomatic arch alone
Clinical Features • Sign—flattening of the cheek, swelling of the cheek, periorbital hematoma, subconjunctival hemorrhage (Fig. 28-36) and limitations of ocular movements, diplopia, ecchymosis and tenderness intraorally over zygomatic buttress, enophthalmos. • Symptoms—lowering of pupil level, tenderness over orbital rim and frontozygomatic suture, epistaxis. Limitations of mandibular movements. Anesthesia of cheek, temple, upper teeth and gingiva. Possible gagging of back teeth on injured side. • Others—step deformity of infraorbital margin. Separation of frontozygomatic suture.
Radiological Features • Traditional facial radiographs like submentovertex view offers excellent resolution of the zygomatic arches (Fig. 28-37).
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3 Fig. 28-38: Water’s view showing the fractured zygoma.
Fig. 28-36: Subconjunctival hemorrhage seen in Zygomatico-maxillary complex fracture.
Fig. 28-39: CT scan, axial section showing the fracture of the anterior wall of maxillary sinus.
Fig. 28-37: Zygomatic arch fracture.
• Other views like Towne’s, Water’s and the AP views also offer significant information. The occipitomental or Water’s view provide good visualization of whole of the zygoma and the maxillary sinus (Fig. 28-38). • CT scans are considered as the standard criteria for the diagnosis of ZMC fractures. The CT scan helps the surgeon to make a more accurate preoperative diagnosis and helps to formulate a treatment plan (Figs 28-39 and 28-40).
Fig. 28-40: CT scan coronal section showing the lateral displacement of fractured zygomatic bone fragment.
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Management
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• Reduction—the treatment objective of the management of the zygomaticomaxillary complex fracture is to restore the premorbid malar and orbital configuration. The fracture of the arch and zygoma may be reduced through intraoral or extraoral approach. Three-point reduction is necessary for proper anatomic alignment of the pyramid—shape malar fragment in all planes and adequate fixation must be followed to keep the alignment stable. When there is minimum displacement of the zygomatic bone or arch, no cosmetic deformity or impairment of the eye movement no treatment may be required (Fig. 28-41).
represents suture line between the malar bone and maxilla. But in it, there is a thin white line on each side of the dark one and these represent the cortex of the suture. • Normal vascular channels—in intraoral periapical(IOPA) radiograph of the posterior teeth, thin dark lines are often seen in the antral shadows. These represent the normal vascular channels and must not be mistaken for fracture. They all show thin white borders which the fractures do not. • Lip line—in the upper cuspid region, lip line can lead to confusion for fracture line. The lip is retracted at the time that the radiographs are made, adding an extra thickness of tissue in the region where the lip is superimposed.
Greenstick Fracture It occurs in young people. Rare in maxilla and mandible. Radiologically, there is sharp angulation present at the site of fracture. There may be one or more linear dark streaks running some distance along the length of the bones from each side of the angulation. Small spicules of bone may be seen standing away from the surface, which had been stripped away at the time of fracture.
Nasoethmoidal Injuries An area behind which lies the interorbital space, which is situated between the medial walls of orbits (Fig. 28-42). Fractures in this region are invariably comminuted. Fig. 28-41: Postoperative radiograph of the patient of zygomatic fracture.
• Open reduction—the indications for the open reduction of the zygomaticomaxillary complex fracture are orbital deformities causing ocular disturbance, diplopia, facial asymmetry, multifragmentation and trismus.
Radiological Differential Diagnosis of Fractures of Maxilla • Infraorbital foramina—it often leads to difficulty in diagnosing maxillary fracture when there is a history of blow. The foramen is situated sufficiently below the margin of orbit to form continuous line of bone between the orbit and margin of the foramen. But sometimes, the shadow of the actual canal is thrown over inferior orbital margin and this dark line suggests that a fracture is present. But, continuity of margin can be traced. • Suture line between malar bone and maxilla—in PA view, there is often a thin dark line on the outer wall of antrum, vertical in direction and situated where the inferior margin of the malar bones joins the facial bone. It
Fig. 28-42: CT scan showing fracture of nasoethmoidal fracture.
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Traumatic Injuries of Oral Cavity 719 Classification Isolated nasoethmoidal injury • Bilateral—central midface injury resulting from direct blow over nasal bridge. Base of nose is driven backwards into interorbital space and nasal tip becomes upturned. Deep crease at base of nose and skin at base of nose frequently lacerated. CSF rhinorrhea should always be suspected. • Unilateral—unilateral nasal deformity. Side of nose is depressed and there is underlying fracture of ethmoid bone. Combined nasoethmoidal injury plus midface fractures • Bilateral—nasoethmoid complex fracture combined with Le Fort II and Le Fort III fractures. Causes traumatic telecanthus and elongation of midface. • Unilateral—nasoethmoid complex injury plus severe comminution of orbit and zygomatic complex. Unilateral displacement of medial canthal ligament resulting in displacement of eye downwards and laterally.
Clinical Features It includes frontal bone depression, nasal deformity, traumatic telecanthus, CSF fluid rhinorrhea, diplopia, and hemorrhage from anterior or posterior branches of ethmoidal artery.
Management • Closed reduction—the use of transnasal wires and compression plates is often unsatisfactory. • Open reduction—realignment of bony fragments under direct vision especially at early stages gives better results. • Repair of bony skeleton—Nasal bridge re-attached to frontal bone. All bone fragments must be preserved, aligned and either directly wired or plated with micro plates.
Complications of Healing In Fracture • Non-union—it results when callus of osteogenic tissue, over each of the two fragments, fails to meet and fuse or when endosteal formation of bone is inadequate. It can occur due to infection of the fracture site, inadequate immobilization and unsatisfactory apposition of bone. Radiograph shows rounding off and sclerosis of the bone ends, a condition known as ‘eburnation’. It is common in elderly patients. • Fibrous union—it occurs as a result of lack of immobilization of the damaged bone. The fractured ends united
by fibrous tissue but there is failure of ossification. They may produce pseudoarthrosis. • Lack of calcification—it occurs in dietary deficiency or mineral imbalance.
In Extraction Dry Socket It is also called as ‘Alveolitis sicca dolorosa ’, ‘Alveolagia or Postoperative osteitis. It is basically focal osteomyelitis in which blood clot has disintegrated or is lost. It is called as dry socket as after the clot is lost, the socket gives dry appearance because of exposed bone. Etiology • Difficult extraction—difficult or traumatic extraction, usually removal of impacted mandibular 3rd molars. • Dislodgement of clot—dislodgment and disintegration of the clot and subsequent infection of the bone. Clinical Features • Duration of occurrence—it is the most common complication in healing of extraction wound. It arises within the first few days after extraction. • Symptoms—it is extremely painful and odor is foul, but with no suppuration. • Signs—exposed bone is necrotic and sequestration of fragments is common. • Healing—healing of such infected wounds is extremely slow. Prevention • Experiment by placing sulfanilamide—sulfathiazole cones placed in fresh tooth socket of dog can prevent the occurrence of dry socket but it will cause retarded blood clot formation and even cause some breakdown of clot and remarkable delay in epithelialization. • Oxidase cellulose—inserted for hemostatic purpose, produces retardation of healing similar to that of combined sulfonamide. • Sulfathiazole in 60% glycerin base reduces the frequency of occurrence of dry socket. • Aureomycin—causes significant reduction in decomposition of blood clot. There is decreased incidence of postoperative pain and swelling after one week. • Tetracycline hydrochloride—if tablet is placed in extraction sockets, it helps in reduction of dry socket to 0.78%. • Trypsin—digests necrotic tissue and debris and restrains bacterial growth. • Antiseptic mouth rinses—use phenolated antiseptic mouth-rinses prior to extraction. • Little trauma—one should try to cause a little trauma to tissue as possible. So that it helps in normal healing.
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• Myospherulosis—it is the complication of healing of an extraction wound or soft tissue wound into which there is placement of antibiotic ointment with petroleum base. It results in formation of clear spaces within the area of healing and the presence of altered erythrocytes which assume the appearance of solitary or clusters of spherules that have been mistaken for large microorganism.
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Management • Packing material—insertion of packing material containing an obtundent. • Zinc oxide and eugenol pack—idoform gauze with zinc oxide and eugenol.
In Wound Fibrous Healing of a Wound It is an uncommon complication following a difficult, complicated or surgical extraction of tooth. It occurs most frequently when tooth extraction is accompanied by loss of both, lingual and labial cortical plates of bone with accompanied loss of periosteum. It is usually asymptomatic and discovered only on radiological examination. Radiologically, it appears as a well circumscribed radiolucent area at the site of extraction wound. Excision of the lesion for the purpose of establishing the diagnosis and to produce normal healing with subsequent bony repair.
Suggested Reading 1. Al,-Khateen TL, EL-Marsafi. The relationship between the indication for the surgical removal of impacted third molar and the incidence of alveolar osteitis. J Oral Maxillofac Surg 1991;49:1415. 2. Andreasen JO. Traumatic injuries to the teeth (2nd edn), 1981. 3. Catellani JE. A review of factors contributing to dry socket through enhanced fibrinolysis. J Oral Surg 1989;37:42-6.
4. Chayra G A, Meador LR, Laskin DM. Comparison of panoramic and standard radiographs for the diagnosis of mandibular fractures. J Oral and Maxillofac Surg 1985;44:677. 5. Dental traumatology. Essential diagnosis and treatment planning L.K. bakland and jens ove andreasen. Endodontic Topic 2004; 7:14-34. 6. Dolan KD, Ruprecht A. Imaging of midfacial fractures. Oral Maxillofac Surg Clin North Am 1992;4:125. 7. Guidelines for evaluation and management of traumatic dental injuries. Dental Traumatology 2001;17;97-102. 8. Guidelines for evaluation and management of traumatic dental injuries. Dental Traumatology 2001;17;145-8. 9. Guidelines for evaluation and management of traumatic dental injuries: dental traumatology 2001; 17; 193-196. 10. Horowitz I, et al. Demonstration of condylar fractures of the mandible by computed tomography. Oral Surg 1982;54:263. 11. Horowitz I, Hirshberg A, Freedman A. Pneumomediastinum and subcutaneous emphysema following surgical extraction of mandibular third molar: three cases. Oral Surg, Oral Med, Oral Pathol 1987;63:25-8. 12. Josell SD, et al. Traumatic injuries to the dentition and its supporting structures. Pediatr Clin North Am 1982;29:717. 13. Kruger E, Schilli W. Oral and maxillofacial traumatology, vol.1&2 Chicago, Quintessence publishing company, 1982. 14. Lindahl L. Condylar fracture of the mandible I. classification and relation to the age, ocllution,and concomitant injuries to the teeth and teeth supporting structure, and fractures of the mandibular body. Int J oral surg 1977;6:12. 15. Martin-Granizo R, Herrera M, et al. Pneumoparotid in childhood: a report of two cases. J Oral Maxillofac Surg 1999;57:1468-71. 16. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology (2nd edn), Saunders Elsevier, 2004. 17. North AF, Rise J. Computed tomography in oral and maxillofacial surgery. J Oral Surgery 1981;39:199. 18. Raymond J Fonseca. Textbook of oral and maxillofacial trauma (2nd edn). 19. Reznick JB, Ardary WC. Cervicofacial subcutaneous air emphy-sema after dental extraction. JADA 1990;120:417-9. 20. Rowe and Williams: Maxillofacial injuries, London, Churchill Livingstone 1994;1&2. 21. Shahshahani MM, Yousef M, Barikbin B. A case of factitious subcutaneous emphysema. Dermatol Online J 2006;12(4):4. 22. Swanson AE. Prevention of dry socket. Oral Surg, Oral Med, Oral Pathol 1990;70:131-6. 23. Traumatic injuries in primary dentition. Dental traumatology 2002;18:287-98. 24. Zingg M, Laedrach K, Chen J, et al: Classification and treatment of zygomatic fracture. J Oral Maxillofac Surg 1992;50:778.
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Definition
Clinical Features
The deposition of calcium salts, primarily calcium phosphate usually occurs in the skeleton. When it occurs in unorganized fashion in soft tissue, it is referred to as Heterotopic calcification.
Classification of Calcification • Dystrophic calcification • General dystrophic calcification of the oral regions • Calcified lymph nodes • Dystrophic calcification in the tonsil • Cysticercosis • Calcified carotid artery • Idiopathic calcification • Sialoliths • Phleboliths • Metastatic calcification • Ossification of the stylohyoid ligament • Osteoma cutis • Myositis ossificans.
• Location—it is most frequent form of pathologic calcification and found in a wide variety of tissues like areas of tuberculosis, necrosis, and blood vessels in arteriosclerosis, scars and areas of fatty degeneration. In oral cavity, area of dystrophic degeneration is found in the gingiva, tongue or cheek. • Symptoms—it is asymptomatic. • Signs—overlying tissue is enlarged and ulcerated and solid mass of calcium salt palpable.
Radiographic Features • Site—the common sites are long standing and chronically inflamed cyst. • Appearance—appear as fine grains of radiopacities which are sparse and diffuse (Fig. 29-1).
Dystrophic Calcification General Dystrophic Calcification of the Oral Region When calcium salt precipitate into primary site of chronic inflammatory dead and dying tissue, it is called as dystrophic calcification. It is associated with high local concentration of phosphatase, as in normal bone calcification and with anoxic conditions within the devitalized tissue.
Fig. 29-1: Dystrophic calcification seen superimposed on ramus of mandible (Courtesy Dr Parate).
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• Size—may be single or multiple and rarely exceed 0.5 cm in diameter. • Margins—outline is irregular or indistinct.
Calcified Lymph Nodes
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These are types of dystrophic calcification that occurs in lymph nodes following chronic infections. Lymph node calcification is uncommon, and usually results from a previous granulomatous disease. A
Causes • Tuberculosis lymphadenitis—tuberculous lymphadenitis is probably a disease in which calcified lymph nodes occur. • Other diseases—actinomycosis, histoplasmosis, catscratch fever and other chronic inflammatory diseases may also present calcified lymph nodes.
Clinical Features • Site—nodes involved are submandibular or cervical chain. • Symptoms—it is usually asymptomatic. • Number—it may be single or multiple or sometimes chain of nodes. • Size and shape—they are hard, round or oblong masses. Outline is well contoured and well defined. • Fixity to underlying tissue—they are mobile during palpation.
Radiographic Features • Site—it is most commonly seen behind or below the angle of the mandible (Fig. 29-2A). In some cases, it is seen in more inferior location when cervical lymph nodes are involved (Fig. 29-2B). In rare cases, calcified node is found posterior to the ramus. • Radiodensity—it is opaque and well defined. In some cases radiodensity is variable showing both opaque and radiolucent appearance. • Appearance—it may have laminated appearance. Radiopacity often exhibits a patchy pattern with a reticular arrangement of radiolucent lines or gaps. • Mass of coral appearance—sometimes, irregular heterogeneous opaque masses are seen which appear to resemble a mass of coral. • Margins—well defined and usually irregular, occasionally having a lobulated appearance similar to outer shape of cauliflower.
Diagnosis • Clinical diagnosis—it is not possible to make clinical diagnosis.
B Figs 29-2A and B: Calcified lymph nodes, cervical lymph nodes that is cauliflower shaped and chainlike (Courtesy Dr Enzio Rovigatti).
• Radiological diagnosis—mass of coral appearance and in some cases, laminated appearance.
Differential Diagnosis • Sialoliths—it is painful and has a smooth outline whereas calcified lymph nodes are usually irregular and sometimes lobulated. • Phleboliths—they are smaller and have concentric radiopaque and radiolucent rings.
Management • Surgical removal—large calcified lymph nodes should be surgically removed.
Tonsillolithiasis It is dystrophic calcification in the tonsil. It is also called as ‘Tonsillar calculi’, ‘Tonsil concretions’, and ‘Tonsilloliths’. The mechanism is similar to that of calcified lymph nodes. It occurs due to recurrent inflammation of tonsil.
Clinical Features • Age and sex distribution—it is common in older age groups between 20 to 68 years of age. Women are more commonly affected. • Location—it can be unilateral or bilateral.
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Soft Tissue Calcifications 723 • Symptoms—small calcification produce no symptoms but larger calcification can produce pain, swelling and dysphagia. • Recurrent tonsillitis—it is also common feature of tonsillar calculi. • Palpation—there is hard, yellow submucosal mass of the affected tonsil.
Radiographic Features • Site—it is seen in middle portion of the mandibular ramus in the region where the image of the dorsal surface of tongue crosses the ramus. • Appearance—it can produce ‘speckled’ appearances of multiple radiopaque superimposed bilaterally on the images of the mandibular rami in a panoramic radiograph. • Size—it may reach the size of 0.5 cm to 14.5 cm. • Margins—multiple small ill defined radiopacities are seen. • Internal structure—it appears more radiopaque than the cancellous bone and same as cortical bone (Fig. 29-3).
Management • Enucleation—larger calcifications with associated symptoms are removed surgically.
Cysticercosis When eggs or gravid proglottids from Taenia sodium (pork tapeworm) are ingested by human, their covering is digested in stomach and larval form (Cysticercus cellulosae) of the parasite is hatched. Larvae penetrate the mucosa, enter the blood vessels and lymphatics and are distributed in the tissue all over the body. After the larva die, the larval spaces are replaced with fibrous connective tissue, which may become calcified.
Clinical Features • Mild cases—they are completely asymptomatic. • Severe cases—there is mild to severe GIT upset with epigastric pain, severe nausea and vomiting. • Nervous system—convulsion, irritability and loss of consciousness. • Size—palpable firm mass upto 1 cm in diameter. • Oral finding—multiple small nodules may be felt in the region of masseter and suprahyoid muscles and in buccal mucosa or lip.
Radiographic Features • Site—the muscle of mastication and facial expression, the suprahyoid muscle and the postcervical musculature. • Margins—the margins are well defined. • Shape—the shape is elongated, elliptical or ovoid. • Internal structure—it is homogenous and radiopaque.
Diagnosis Fig. 29-3: Tonsillitis is present (red arrow) on CT scan (Courtesy RS Kamikawa).
Diagnosis • Clinical diagnosis—recurrent tonsillitis is common features • Radiological diagnosis—speckled appearance with multiple radiopaque image on ramus area.
• Clinical diagnosis—Gastrointestinal problems are present. Small nodules seen in masseter region will give clue to the diagnosis. • Radiological diagnosis—homogenous radiopaque mass is present.
Differential Diagnosis • Salivary stone—it is not multiple as compared to cysticerci.
Differential Diagnosis • Radiopaque lesion in mandibular ramus—in it right angle view such as PA skull or open Towne’s view may show that calcification lies to the medial aspect of the ramus.
Management • Medical management—medical management by the physician.
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Calcified Carotid Artery It is also called as ‘atheroma’. Arterial wall may calcify in all forms of arteriosclerosis with deposition of calcium salts within the medial coat of the vessels.
Causes
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• Inflammatory process—it is sequelae of inflammatory process affecting the wall. • Other causes—it is also found in Sturge-Webber syndrome and diabetes mellitus.
Clinical Features • Usually no clinical sign or symptoms develop.
• Appearance—a pair of thin opaque lines that may have either a straight course or a tortuous path. They may appear as amorphous or punctuate calcifications. • Internal structure—the calcified wall appear as radiopaque circle. • Stroke—in patient who is suffering from diabetes mellitus and having calcification in the region of carotid artery leading to macrovascular atherosclerosis can cause stroke.
Diagnosis • Clinical diagnosis—it is not possible to make clinical diagnosis. • Radiological diagnosis—calcified deposit seen on walls of artery.
Radiographic Features • Site—calcification with the carotid artery are located in the soft tissue below the angle of the mandible and between the hyoid bone and the image of the cervical spine (Figs 29-4A and B). • Margins—calcific deposits on wall of artery will outline the image of the artery.
Differential Diagnosis • Other calcific deposits—usually, the linear nature of the calcified arterial wall indicates the nature of this condition.
Management • This disease requires no treatment. Only special care should be taken for stroke.
Idiopathic Calcification The deposition of calcium in normal tissue despite normal serum calcium and phosphate level is referred to as ‘Idiopathic calcification’.
Sialoliths It is described in Chapter 26: Salivary Gland Disorders.
A
Phleboliths These are thought to be formed in older thrombi in veins or hemangiomas with slow blood flow. The thrombus organizes into granulation tissue and occasionally mineralizes with the deposition of calcium phosphate and calcium carbonate.
Clinical Features
B Figs 29-4A and B: OPG showing calcification in the carotid artery (Courtesy Dr Fábio de Lima Cravo).
• Appearance—the involved soft tissue may be swollen or discolored by the presence of veins or a soft tissue hemangioma. • Pressure application—applying pressure to the involved tissue should cause a blanching or change in color if the lesion is vascular in nature.
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Soft Tissue Calcifications 725 Radiological Features
Ossification of the Stylohyoid Ligament
• Site—they are most commonly found in the hemangiomas. • Margins and shape—the shape is round or oval with a smooth periphery. If it is viewed from side resembles a straight or slightly curved sausage. • Internal structure—it may be homogenously radiopaque but more commonly has a appearance of laminations. A radiolucent center seen, which may represent the remaining patent portion of the vessels (Fig. 29-5).
Ossification of stylohyoid is common and when it is associated with discomfort it is called as ‘Eagle’s syndrome’. Ossification usually extends downward from the base of the skull and commonly occurs bilaterally. Bone tissue forms within segments of the stylohyoid ligament.
Clinical Features • Palpation—there is hard pointed structure over the tonsil. • Symptoms—vague pain on swallowing, turning the head and opening the mouth. Patient may describe earache, headache, dizziness or transient syncope which is caused by elongated styloid process impinging on glossopharyngeal nerve. • Signs—there may be visible swelling on the region of the angle of mandible (Fig. 29-6A). • Stylohyoid syndrome—clinical finding without the history of neck trauma constitutes ‘Stylohyoid syndrome’.
Fig. 29-5: Phleboliths showing multiple oval radiopacities (Courtesy RS Kamikawa).
Diagnosis • Clinical diagnosis—swelling swollen tissue over the vein may suspect the disease. • Radiological diagnosis—round shaped radiopacity with radiolucent center will give clue to the diagnosis.
Differential Diagnosis • Sialoliths—sialoliths occur single as compared to phleboliths which is usually multiple.
Fig. 29-6A: Swelling seen in angle of mandible region due to ossification of stylohyoid ligament.
Management
Radiographic Features
• Treatment of underlying cause should be done.
• Site—styloid process appears as long, lapping, thin, radiopaque process between ramus of mandible and mastoid process. Ossification of ligament roughly parallels the posterior border of the ramus (Fig. 29-6B). • Appearance—it appears as long, tapering, thin radiopaque process that is thicker at base and projects downward and forward. • Size—it varies about 0.5 to 2.5 cm in length. • Internal structure—small ossification appear homogenously radiopaque. As the ossification increases in length and width, the outer cortex of its become evident as radiopaque band at the periphery.
Metastatic Calcification In this, calcium salts are precipitated in previous undamaged tissue. This precipitation is due to an excess of blood calcium and occurs particularly in such diseases as hyperthyroidism which depletes the bone calcium and causes a high level of blood calcium. The deposits of calcium occur in the kidney, lungs, gastric mucosa and media of blood vessels.
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Diagnosis
Osteoma Cutis
• Clinical diagnosis—earache, headache, dizziness with swelling at angle of mandible will suspect this disease. • Radiological diagnosis—elongated stylohyoid process is easily identified on the radiograph (Fig. 29-6C).
These are sites of normal bone formation in abnormal locations. The lesion occur secondary to acne of long duration, developing in a scar or chronic inflammatory dermatosis.
Clinical Features Management
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• Amputation—amputation of stylohyoid process should be carried out.
Fig. 29-6B: Calcified Outline of stylohyoid ligament (Courtesy RS Kamikawa).
• Site—face is the most common site followed by lip (Fig. 29-7A) and tongue is the most common intraoral site. • Size—size ranges from 0.1 mm to 5 cm and may be seen as single or multiple. • Color—color may be normal or yellowish white. • Aspiration—needle when inserted is met with stone-like resistance.
Fig. 29-7A: Osteoma cutis seen in lower lip region as slightly pale in color.
Radiographic Features • Site—most commonly appears in the cheek and lip regions. Image can be superimposed over a tooth root or alveolar process. • Margins and shape—smoothly outlined radiopaque washer-shaped image. • Size—they are very small, although size can range from 0.1 to 5 cm. • Internal structure—it may be homogenous radiopaque or may have a radiolucent center that represent normal fatty marrow.
Diagnosis • Clinical diagnosis—There are areas of dense viable bone in the dermis or subcutaneous tissue. • Radiological diagnosis—washer shaped image seen on the periapical radiograph (Figs 29-7B and C).
Differential Diagnosis Fig. 29-6C: Elongated styloid process with nodular mineralization pattern (Courtesy RS Kamikawa).
• Myositis ossificans and calcinosis cutis—osteoma cutis is more superficial than others.
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Soft Tissue Calcifications 727 Localized Myositis Ossificans It is also called as ‘Post-traumatic myositis ossificans’ or ‘Solitary myositis’.
Etiology • Trauma—it is caused by acute or chronic trauma or heavy muscular strains caused by certain occupation or sports. Traumatization of the periosteum of an adjacent bone with the displacement of osteoblasts into the muscle and subsequent formation of bone. • Periosteal implants—activation of periosteal implants already present in muscle by trauma or hemorrhage. • Metaplasia—metaplasia of the pluripotential intermuscular connective tissue into the bone. Metaplasia of fibrocartilage.
B
Pathogenesis • Injury →hemorrhage into the muscle or associated tendon or fascia →the hemorrhage organized and undergoes scarring →during healing process cartilage is formed → calcification of cartilage →ossification of cartilage.
Clinical Features
C Figs 29-7B and C: Multiple miliary osteoma cutis. Patient with history of large quantity of acne for a long period of time. Periapical radiographs showing evidence of ossifications in the soft tissues of the cheek (Courtesy RS Kamikawa).
Management • Surgical removal—osteomas are occasionally removed for cosmetic reasons.
Myositis Ossificans It is a condition in which fibrous tissue and heterotopic bone form within the interstitial tissue or muscle, as well as in associated tendons and ligaments. Secondary destruction and atrophy of the muscle occurs, as this fibrous tissue and bone interdigitate and separate the muscle fibers.
Types • Localized myositis ossificans or traumatic myositis ossificans. • Progressive myositis ossificans or generalized myositis ossificans.
• Age and sex—it can occur at any age, sex and more often in young persons. • Site—the most commonly involved muscles are the masseter and sternocleidomastoid but in some cases, lateral pterygoid muscle can be involved. • Symptoms—site of trauma remains swollen, tender and painful much longer than expected. In some cases, there is a mild discomfort associated with a progressive limitation of motion. • Signs—the overlying skin may be red and inflamed. Intramuscular mass is palpated at 2 to 3 weeks. The lesion may appear fixed or it may be freely movable on palpation.
Oral Manifestations • Site—it involves the muscles of face particularly masseter and temporal following single traumatic injury. • Symptoms—some difficulty in opening of the mouth.
Radiographic Features • Site—radiolucent band can be seen between the area of ossification and adjacent bone and heterotopic bone may lie along the long axis of the muscle. • Internal structure—faintly homogenous opacity. Delicate lacy or feathery internal structure of increased radiodensity develop indicating bone has formed (Fig. 29-8). Sometimes it is accompanied by circumscribed cortical periphery.
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Textbook of Oral Medicine Management • Rest—sufficient rest should be given with limitation of use. • Excision—excision after process becomes stationary.
Progressive Myositis Ossificans It is characterized by formation of bone in tendons and fascia with subsequent replacement of adjacent muscle by expanded bony mass. In some cases, there is history of hereditary and familial pattern.
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Clinical Features
Fig. 29-8: Myositis ossificans. See the increased radiodensity with margins are more radiopaque than internal structure (Courtesy Dr Bhaskar Patle).
• Margins—margins are more radiopaque than the internal structure. • Shape—there is variation in shape from irregular oval to linear streaks running in the same direction as the normal muscle fibers. These pseudotrabeculae are characteristic of myositis ossificans and strongly imply a diagnosis. • It lies close to the surface of the bone. With the passage of time the new bone is resorbed.
Diagnosis • Clinical diagnosis—palpable intramuscular mass with swelling area of trauma may give clue to the diagnosis. • Radiological diagnosis—pseudotrabeculae and more radiopaque margin is present. • Laboratory diagnosis—biopsy shows degeneration of muscle and connective tissue hyperplasia to chondrification and ossification. The trabecular pattern is often extremely bizarre with the cartilage and myxomatous tissue present which may resemble callus formation.
Differential Diagnosis • Ossification of stylohyoid ligament, dystrophic calcification in areas of necrosis, pathological calcification and phlebitis—the form and location of myositis ossificans are enough make the differential diagnosis.
• Age and sex—it usually affects children before 6 years of age. It is seen more in males as compared to females. • Progress—it may advance rapidly or there may be long period of relative inactivity with intermittent bursts of activity. • Site—starts in muscles of neck and upper back and moves to extremities. • Symptoms—soft tissue swelling that is tender and painful and may show redness and heat. • Sign—gradual increase in stiffness and limitation of motion of neck, chest and back and extremities. Ultimately entire groups of muscles become transformed into bone resulting in limitation of movements. • Associated anomalies—it is associated with congenital small first metatarsal and metacarpal bones, small little bone. Interphalangeal joint may be fused. • Facial finding—the masseter muscle is frequently involved so that fixation of jaw occurs. • Petrified man—the patient becomes rigid and called as ‘Petrified man’. • Prognosis—patient dies during 3rd or 4th decades. Premature death is usually results from respiratory embarrassment.
Radiographic Features • Appearance—there is evidence of dense osseous replacement of the greater part or whole of the muscle. • Internal structure—densities of heterotrophic bone vary widely. The bone that is laid down in the muscle does not show structure of normal bone but it is rather structureless mass of variable density. • Linear striae of increase density—coarse linear striae of increased density represent new bone formation in some cases; the streaks follow the long axis of the particular muscle involved. In early stages calcified deposits are granular and fragmentary. • Margins—lesion have smooth or irregular margins, lying in close relationship with the bone.
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Soft Tissue Calcifications 729 • Advanced lesion—the dense masses with passage of time tend to coalesce. Skeleton becomes osteoporotic because of lack of function as muscles atrophy and joints become ankylosed.
Diagnosis • Clinical diagnosis—’Petrified man’ appearance with gradual limitation of movement of the body. • Radiological diagnosis—bone in muscle show structureless mass of variable density. • Laboratory diagnosis—the muscle in this disease is gradually replaced by connective tissue which undergoes osteoid formation and subsequently ossification. In some cases, cartilage formation may become evident.
Differential Diagnosis • Rheumatoid arthritis—in initial stage, it is difficult but as disease progress specific anomalies confirms the diagnosis. • Calcinosis—the deposits of amorphous calcium salts frequently resorb, but in progressive myositis ossificans the bone never disappear.
Management • No effective treatment exists. Nodules that are traumatized and then ulcerated frequently should be excised.
Suggested Reading 1. Appleton SS, Kimbrough RE, Engstrom HIM. Rhinolithiasis: a review. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1988;65:693-8. 2. Basler RS, Watters JH, Taylor WB. Calcifying acne lesions. Int J Dermatol 1977;16(9):755-8. 3. Beder E, Ozgursoy OB, Karatayli Ozgursoy S. Current diagnosis and transoral surgical treatment of Eagle’s syndrome. J Oral Maxillofac Surg 2005;63(12):1742-5. 4. Boulman N, Slobodin G, Rozenbaum M, Rosner I. Calcinosis in rheumatic diseases. Semin Arthritis Rheum 2005;34:805-12. 5. Boylan PA. Rhinolith. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1973;36:290. 6. Carter LC. Discrimination between calcified triticeous cartilage and calcified carotid atheroma on panoramic radiography. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 2000;90(1):10810. 7. Conlin PA, Jimenez-Quintero LP, Rapini, RP. Osteomas of the skin revisited. A clinicopathologic review of 74 cases. The American Journal of Dermatopathology 2002;24(6):479-83. 8. Cooper MM, Steinberg JJ, et al. Tonsillar calculi: report of a case and review of the literature. Oral Surg, Oral Med, Oral Pathol 1983;55:239-43.
9. Cooper MM, Steinberg JJ, Lastra M, Antopol S. Tonsillar calculi. Report of a case and review of the literature. Oral Surg, Oral Med, Oral Pathol 1983;55:239-43. 10. Correll RW, Jensen JL, Taylor JB, Rhyme RR. Mineralization of the stylohyoid-stylomandibular ligament complex. Oral Surg, Oral Med, Oral Pathol 1979;48(4):286-91. 11. Diamond LH, Cottrell DA, Hunter MJ, Papageorge M. Eagle’s syndrome: a report of 4 patients treated using a modified extraoral approach. J Oral Maxillofac Surg 2001;59(12):1420-6. 12. Elidan J, Brama I, Gay I. A large tonsillolith simulating tumor of the tonsil. Ear Nose Throat J 1980;59(7):296-7. 13. Ennis LM. Roentgenographic appearance of calcified acne lesions. J Am Dent Assoc 1964;68:351-7. 14. Eyre WG, Reed WB. Albright’s hereditary osteodystrophy with cutaneous bone formation. Arch Dermatol 1971;104:635-42. 15. Fini G, Gasparini G, Filippini F, Becelli R, Marcotullio D. The long styloid process syndrome or Eagle’s syndrome. J Craniomaxillofac Surg 2000;28(2):123-7. 16. Friedlander AH, Baker JD. Panoramic radiography: an aid in detecting patients at risk of cerebrovascular accident. J Am Dent Assoc 1994;125(12):1598-603. 17. Friedlander AH, Lande A. Panoramic radiographic identification of carotid arterial plaques. Oral Surg, Oral Med, Oral Pathol 1981;52(1):102-4. 18. Friedlander AH, Maeder LA. The prevalence of calcified carotid artery atheromas on the panoramic radiographs of patient with type 2 diabetes mellitus: Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 2000;89:420-44. 19. Friedlander AH, Manesh F, Wasterlain CG. Prevalence of detectable carotid artery calcifications on panoramic radiographs of recent stroke victims. Oral Surg, Oral Med, Oral Pathol 1994; 77(6):669-73. 20. Hiranandani LH. A giant tonsillolith. J Laryngol Otol 1967;81(7): 819-22. 21. Hirschfeld JJ. Calcification in lymph nodes. Oral Surg, Oral Med, Oral Pathol 1986;61(4) 412. 22. Hoffman H. Tonsilloliths. Oral Surg, Oral Med, Oral Pathol 1978;45:657-8. 23. Kamikawa RS, Pereira MF, Fernandes A, Meurer MI. Study of the localization of radiopacities similar to calcified carotid atheroma by means of panoramic radiography. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 2006;101(3):374-8. 24. Lewis DA, Brooks SL. Cartoid artery calcification in a general dental population: a retrospective study of panoramic radio-graphs. Gen Dent 1999;47(1):98-103. 25. Marshall WG, Irwin ND. Tonsilloliths. Oral Surg, Oral Med, Oral Pathol 1981;51:113. 26. Monsour PA, Young B. Variability of the styloid process and stylohyoid ligament in panoramic radiographs. Oral Surg, Oral Med, Oral Pathol 1986;61(5):522-6. 27. Monteiro MR, Koblenzer CS. Multiple osteoma cutis lesions associated with acne. Int J Dermatol 2000;39(7):553-4. 28. Moritz DL, Elewski B. Pigmented post-acne osteoma cutis in a patient treated by minocycline: report and review of the literature. 29. Neshat K, Penna KJ, Shah DH. Tonsillolith: a case report. J Oral Maxillofac Surg 2001;59(6):692-3. 30. Neville, Damm, Allen, Bouquot: oral and maxillofacial pathology (2nd edn), Saunders Elsevier, 2004. 31. Paquette M, Terezhalmy GT, Moore WS. Calcified Lymph nodes.Quintessence Int 2003;34(7):562-3 32. Sezer B, Tugsel Z, Bilgen C. An unusual tonsillolith. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 2003;95(4): 471-3. 33. Stirling AW. On bony growths invading the tonsil. JAMA 1896; 27:734-5.
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Bacterial Infections
Introduction
Etiology
The literal meaning of the word ‘disease’ is ‘loss of ease’. The oral cavity reflects the state of systemic health more frequently than other parts of the body. Even in ancient time, examination of mouth and tongue was given great importance. The oral tissues are in direct physical continuity with rest of the body and they are also related via blood, lymphatics and nerve pathways. Furthermore, systemic influence such as endocrinological, immunological and psychological factors has an important role in the balance between oral health and disease. During both, development and maintenance, local and systemic factors are concerned in disease process of mouth. Oral health must be considered in relation to general health. The dentist’s role in general health is based on the fact that, he is the first person to see the oral lesion. In preventive dentistry, the utmost principle is of early diagnosis. Dentist has an important role in preventive medicine as many systemic diseases have primary oral manifestations.
Infections Caused by Bacteria The following diseases are caused by bacteria.
Syphilis It is also called as ‘lues’. The incidence of syphilis is decreased after introduction of penicillin in late 1940s. Patient infected with Treponema pallidum and HIV may exhibit a malignant form of syphilis with slow development of standard serological response to syphilis. The tertiary manifestations lead to considerable morbidity and mortality.
• Sexual contact—it occurs most exclusively by venereal contact. • Maternal transmission—infection may transfer from mother to fetus. • Drug user—incidence of syphilis is increased nowadays in crack cocaine abuse and barter of illegal drugs for sex. • Predisposing factors—overcrowded living and primitive housing conditions are the predisposing factors for syphilis.
Classification • Acquired syphilis—contacted primarily as venereal disease due to sexual intercourse with infected partner. • Primary—it is evident clinically 3 to 90 days after the exposure. • Secondary—it is discovered 4 to 10 weeks after primary stage. • Tertiary—this stage develop after the latent phase. • Quaternary syphilis—the atypical malignant progression of tertiary neurosyphilis in immunocompromised HIV individuals is referred as quaternary syphilis. • Latent phase—this appear after secondary stage and in this stage, there is no sign and symptoms are present. Serological test is positive in this stage. • Congenital—this is secondary to fetal infection. • Early syphilis—primary syphilis, secondary syphilis and the early latent phase of the disease are grouped as early syphilis. Early syphilis may last up to two years and is infectious. • Late syphilis—while late latent and tertiary are grouped as late syphilis. Late syphilis is locally destructive and non-infectious.
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Primary Syphilis
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Clinical features • Incubation period—lesion develop at the site of inoculation approximately 3 to 90 days after the inoculation. • Site—it occurs most frequently on penis in males and vulva or cervix in females. Recently, occurrence on extragenital sites have increased as a result of increase in orogenital sex and increased contact among the infected homosexuals. Extragenital sites of involvement include fingers, perianal region, nipples, lips, tonsils and intraoral structures such as tongue and palate. • Chancre—it is slightly raised, ulcerated, non-tender, nonbleeding, firm plaque which is usually round, indurated and with rolled raised edges. • Size—it varies in size from 5 mm to several centimeters. • Symptoms—it is painless, unless superinfected. It disappears without therapy after 10 days. • Lymph nodes—regional lymph nodes become firm enlarged, rubbery in consistency and non-tender. Oral manifestations • Site—oral lesions of primary syphilis are rare and occur at the site of entry of treponema. Chancre has been described on lips, oral mucosa, lateral surface of tongue, soft palate, tonsillar area, pharyngeal area and gingiva. • Transmission—transmission can occur during kissing as a consequence of sexual practice among homosexual and heterosexuals, or by contact with objects such as mouth piece of musical instruments and medical or dental instruments. • Appearance—it has narrow copper colored, slightly raised borders with reddish brown base in center. • Symptoms—intraoral chancres are slightly painful due to secondary infection and are covered with grayish white film. • Size—it measures from 0.5 to 2 cm in diameter. • Signs—occasionally, it retains white sloughy material. In some cases, there is proliferation that resembles pyogenic granuloma. • Tonsils—primary involvement of tonsils is manifested by considerable edema, redness, ulcerated and eroded lesion. • Lymph nodes—regional lymphadenopathy occurs. • Extraoral lip chancre—extraoral lip chancre may have more typical brown crusted appearance which may be multiple. Lower lip involved more frequently (Fig. 30-1). • Healing—oral chancre heals spontaneously in 3 to 8 weeks leaving small scars.
Secondary Syphilis Clinical features • Spread—organisms proliferate and spread by the way of bloodstream to produce lesions elsewhere.
Fig. 30-1: Chancre present on the lower lip in male patient which has got slightly raised border (Courtesy Dr Jitu Sachdeo).
• Incubation period—it usually appears within 4 to 10 weeks after primary lesion. • Symptoms—fever and generalized lymphadenopathy, which is painless, discrete and non-adherent to the surrounding tissues, may be seen. Headache, anorexia, pain in joints and muscles also occurs. • Skin—when appear on skin, they manifest as fine macular or papular rash, sometimes accompanied by alopecia. The skin rash may resolve completely or leave residual areas of hypo- or hyperpigmentation. • Face—circinate lesions on face are characteristic of secondary syphilis. • Mucus patches—mucus patches are small, smooth, erythematous areas or superficial grayish erosions found on mucus membrane of vulva, penis, or in oral cavity, on palate and tonsils. They are described as snail track ulcers. • Condyloma latum—condyloma latum are grayish, moist, flat topped, extra large plaque which sometimes coalesce into larger plaques, found on moist mucocutaneous surfaces such as vulva, anus, scrotum, thigh and axilla. • Split papule—spilt papule is a double papule which occurs at skin folds and angle of mouth. • Lues maligna—this is explosive and widespread form occurs in compromised immune system. It is characterized by formation of necrotic ulceration. • Lymph nodes—generalized symmetrical enlargement of the lymph nodes in posterior cervical, suboccipital, supratrochlear and inguinal regions. • Latent phase—patient may enter the phase of latency without treatment. Oral manifestations • Mucus patches—it is mucous membrane analogue of papular or macular skin eruptions. • Site—it is found on tongue, buccal mucosa, tonsillar and pharyngeal region, and lips.
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Bacterial Infections 735 • Appearance—it appears as slightly raised grayish white lesions surrounded by erythematous base. • Surface—they are covered by grayish white membrane. Trauma results in raw bleeding surface. • Snail track ulcers—confluence and coalescence of these glistening mucous patches gives rise to the so called ‘snail track ulcers’. • Symptoms—it is often painless but mild to moderately painful. • Split papule—they are highly infectious. • Site—split papule is a raised papular lesion developed at the commissure of lip and with a fissure separating the upper lip portion from lower lip portion. • Appearance—they are called as split papules as they are cracked in the middle giving a ‘split pea appearance’. • Condyloma latum—they are flat silver gray wart like papule, sometimes having ulcerated surface. They are painless. Regional lymphadenopathy is usually present.
Tertiary Syphilis Clinical features • Incubation period—it may occur at any age from the third year upto the patient’s life. • Forms—in tertiary syphilis, 1/3rd develop benign or gummatous form, 1/3rd cardiovascular form and 1/3rd neurosyphilis, i.e. general paresis and tabes dorsalis. • Gumma—gumma is due to a chronic destructive granulomatous process which occurs anywhere in the body. Gumma is the result of hypersensitivity reaction between hyperergic host and treponema. Single cerebral gumma may produce symptoms suggestive of brain tumor • Types—there are two types of gumma, i.e. central and cortical. • Appearance—the characteristic gumma appear as chronic granulomatous localized lesion, which ulcerates. It is nodular in appearance. • Signs—punched out ulcer with vertical walls and dull red granulomatous base is the typical clinical feature of ulcerative gummatous lesion. • Cutaneous lesions—cutaneous lesions heal slowly and leave behind tissue paper-like scars. • Neurosyphilis—it occurs due to obliteration of small vessel artery involving vasa vasorum of aorta and other large vessels of the central nervous system (neurosyphilis). Neurosyphilis is manifested as tabes dorsalis and general paresis. Tabes dorsalis is the syphilitic involvement of dorsal column of spinal cord and dorsal root ganglion. General paresis is syphilitic involvement of cerebral tissue.
• Tabes dorsalis • Symptoms—patient looses the positional sense of his lower extremities and walks with a slapping step. Burning and pricking sensation of the extremities, paresthesia, or actual anesthesia of the part may accompany the characteristic gait. • Positive Romberg’s sign—person is unable to stand erect unaided with his eyes closed. • Tabetic crises—short, shooting, knife-like pains may be experienced in the abdominal region called ‘tabetic crises’, which results from involvement of the dorsal root ganglion. • Charcot’s joint—trophic changes consist of deep perforating ulcers and painless destruction of larger joints. • General paresis • Argyll Robertson pupil—pupils that react to accommodation but not to light. • Symptoms—increased irritability, fatigue, mental sluggishness and carelessness in personal habits. • Signs—loss of fine muscular coordination is indicated by inability to enunciate clearly or to perform delicate tasks with the hands. • Spinal cord involvement—involvement of spinal cord is late manifestation characterized by paresthesia, burning and prickling sensation in the extremities. • Patient may get unrealistic ideas of wealth or ability. • Cardiovascular syphilis—it occurs in 10% cases of late syphilis. Involvement of CVS in tertiary syphilis affects aorta and aortic valve and 80% of deaths occur due to it. There is medial necrosis and destruction of elastic tissue occurs in the wall of large blood vessels. Dilatation and aneurysm occurs. • Tertiary syphilis in HIV patient—a recent feature has been an apparent alteration in the behavior of syphilis in HIV positive patients. Natural history of syphilis may be altered in HIV positive patients and this group is at high risk for the development of tertiary syphilis. Genital ulcerations due to syphilitic infection allows a portal of entry for the viral particles and may lead to greater risk of infections in these patients. Oral manifestations • Site—gumma can occur anywhere in the jaw but are more frequently on palate, mandible, and tongue. • Gumma • Appearance—gumma may manifest as solitary, deep, punched out mucosal ulcer. • Symptoms—breathing and swallowing difficulty may be encountered by the patient. • Progress—it usually starts as small, pale, raised, nodular mass in the midline of the palate which ulcerates and rapidly progresses to the zone of necrosis.
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• Signs—it may cause perforation of palatal vault. • Punch out defects—lesion is sharply demarcated and the necrotic tissue at the base of the ulcer may slough away leaving punched-out defects. • Tongue—numerous small healed gummata in tongue results in series of nodules or scars in deeper areas of the organ, giving the tongue an upholstered or tufted appearance. • Leutic glossitis—complete atrophy of papillary coating and firm fibrous texture seen. It is called as leutic glossitis. Initially, it is thought to be precancerous but nowadays, this concept is disputed. Loss of papillae is probably due to endarteritis leading to circulatory deficiency of lingual vasculature. • Chronic superficial interstitial glossitis—the tongue may involve diffusely with gumma and appear large, lobulated and irregularly shaped. This lobulated pattern is called as chronic superficial interstitial glossitis.
Radiographic Features of Syphilis Bones are not known to be involved in the primary stage. Bone involvement usually occurs in tertiary stage and in some cases, in secondary stages.
Gummatous Lesion of the Bone • Site—skull is one of the usual sites of gummatous involvement frequently involving frontal, parietal, and temporal bone. Maxilla is affected more than the mandible, the common site being the hard palate particularly the central portion. It begins as extension of gumma from the palatal mucosal aspect or from the floor of nose. Multiple gummas of oral structure may invade the coronoid process and medial pterygoid muscle. • Central gumma—there is radiolucent area with ill-defined margins which merge with the normal bone or there are multiple areas of greater radiolucency. These areas are separated from one another by normal looking bone. With the passage of time, radiolucent areas are fused and appear as one dark shadow which is caused by perforation of the palate. • Cortical gumma—it starts on the surface of bone and destroys a wide area of the cortical covering. The deeper cancellous bone is involved later and destroyed. The result is that there is a well-marked area of bone destruction, open to the surface of the bone and has sharply defined margins, which are devoid of rarefaction. • Diffuse gummatous infiltration—it is usually found in the vault of the skull in the vicinity of the intramedullary gummata. Mandible is involved more often than maxilla. Suppuration and sequestration are always present. Radiographic appearance suggests widespread
osteomyelitis which has not been treated. There are many islands of bone with widely varying shape and size, many with grossly irregular borders, which are well defined. The density of the islands of bone varies from normal bone to rarefied bone.
Syphilitic Periostitis It is the most common manifestation of congenital syphilis and may also be seen in secondary stage of acquired syphilis. The lesion may develop very late in the disease process and is characterized by periosteal reaction, which may either be limited and circumscribed or extensive. • Site—it involves mandible more commonly and it appears as a single layer or several layers of new bone, more or less parallel with the margins of jaw. The calvarium is one of the usual sites of involvement in this manifestation of syphilis. • Network of lattice—a rare manifestation of syphilitic periostitis is new bone arranged with trabeculae forming a loose type of pattern which is best described as a gross caricature of a network of lattice. There is often a dark line between the new bone and jaw and between the layers of new bone. • Syphilitic osteitis—there are small superficial areas of rarefaction, in the underlying bone, due to syphilitic osteitis.
Congenital Syphilis It is infection of fetus established by the passage of spirochetes from mother, through the placenta. Transplacental infection after 18-week gestation is related to development of immune complement rather than any toxic effect on organism. Congenital syphilis has got three diagnostic features called as Hutchinson’s triad which includes hypoplasia of permanent incisors and 1st permanent molars, eight nerve deafness and interstitial keratitis. Clinical features • Early manifestations—it is manifested within the first 2 years of life (neonatal congenital syphilis) as rhinitis and chronic nasal discharge with maculopapular eruptions, other than mucocutaneous lesion and loss of weight. The lesions can be seen in spleen, kidney, bones and CNS. Bullae, vesicle and superficial desquamation with cracking and scaling of reddened soles and palms, petechiae, mucus patches and condyloma latum also occurs. • Late manifestations—after 2 years, interstitial keratitis (opacification of corneal surface with resultant loss of vision), vascularization of cornea, 8th nerve deafness, arthropathy, signs of congenital neurosyphilis, gummatous destruction of palate and nasal septum develop. There are also saber shins or anterior tibial bowing.
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Bacterial Infections 737 • Higoumenakis’s sign—irregular thickening of sternoclavicular portion of clavicle. Oral manifestations • Postrhagadic scarring and syphilitic rhagades—postrhagadic scars are linear lesions found around oral and anal orifices. They result from diffuse leutic involvement of the skin in these areas from 3rd to 7th week after birth. They appear as red or copper colored linear areas covered with a soft crust. Rhagades are said to be more frequent on the lower lip. Healed syphilitic rhagades appear as ordinary cicatrices. • Linear scars—the linear scars are radially arranged and perpendicular to the mucocutaneous junction, which are more prominent on lower lip near angle of mouth. • Changes in dentition—retarded root resorption of deciduous dentition. There may be ‘marring’ of permanent incisors present in congenital syphilis. 6 to 28% of the incisors and 3 to 37% of the molars have hypoplasia. Spacing between cuspid and incisors is present. Malocclusion and open bite is present. • Molar features—the crown of the first molar in congenital syphilis is irregular and enamel of the occlusal surface and occlusal third of the tooth appears to be arranged in agglomerate mass of globules, rather than in well formed cusp. • Screw driver shaped incisors—constriction of crown toward incisal edge screw results in driver or peg shaped incisor. In addition, incisal edge is usually notch which may be due to the absence of central tubercle or calcification center. Rounding of mesial and distal incisal line angles. • Moon molars—in molars, positioning of the cusps toward the central portion of the crown, gives the tooth a bud shaped or a shrunken occlusal form called as mulberry molars or Moon’s molars. Affected molars are dirty yellow in color due to hypocalcification. • Carabelli cusp—prominent accessory mesiolingual cusp of upper molar (Carabelli cusp). • Jaw bones—defective maxilla which is hypoplastic and short with relative mandibular prognathism. Frontal bossing and saddle nose deformity occurs. Diagnosis of syphilis The presence of clinical manifestations together with history of a sexually active person should give clue to the diagnosis of acquired syphilis. • Dark field examination microscopy—It is the most useful method of identifying spirochete in primary acquired and occasionally, secondary syphilis. Not reliable for oral lesions, since the normal flora contains nonpathogenic treponema which are difficult to distinguish from T. pallidum.
• Lesion biopsy—histopathological examination of suspected lesion, stained by silver impregnation technique, is useful particularly when the lesion contains few organisms, as may be in case of tertiary lesion. For oral lesions, this technique is of considerable value. • Treponemal antigen test—Treponemal test is of value in making a confirmatory diagnosis while non-treponemal test is of value in assessing the efficacy of the therapy. • Non-treponemal (antigen) test—commonly used nontreponemal test is Venereal Disease Research Laboratory (VDRL) and rapid plasma reagin (RPR) test. Both tests are inexpensive, simple and rapid to perform but require competent experienced laboratory to minimize the risk of false positive or false negative results. Management • Antibiotics—patient should give benzathine penicillin (2.4 million units IM) aqueous crystalline penicillin, tetracycline hydrochloride (500 mg orally 4 times a day for 15 days). Patients who are allergic to penicillin erythromycin (500 mg by mouth 4 times a day for 15 days). T pallidum disappears from infectious lesion within 24 hours of instituting therapy. • Follow up—patient should be followed with repeated physical examination and repeated VDRL is to be done at 1, 3, 6, 9, 12, 18 and 24 months. At the end of 24 months, if VDRL is negative, patient is said to be cured. • Prevention—there is no dependable prophylactic measure other than sexual abstinence with infected partner. The use of prophylactic antibiotics locally is beneficial in pregnant women suspected to exposure. Prevention of congenital syphilis can be achieved by subjecting pregnant women to antenatal and postnatal check up.
Non-venereal Treponematoses Endemic syphilis is also called as ‘bejel’ which is caused by spirillar form of Treponema palladium, yaws which is caused by Treponema pertenue and pinta which is caused by Treponema carateum are most non-venereal treponematoses which occur in children and causes destructive skin and bone diseases. These diseases run a milder course compared to venereal treponematoses.
Endemic Syphilis It is also called as ‘bejel’ and most commonly occurs in childhood. Transmission • Direct transfer—direct transfer is through lesion to skin contact. • Indirect transfer—indirect transfer is through the common use of drinking, bowls, or possibly by flies.
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Clinical features • Age—the disease is primarily seen in children, although adult cases are often reported. • Early stage—the early stage disease is characterized by the appearance of mucus patches in the oronasopharyngeal region, angular stomatitis, skin rashes, pigmentary changes and tenderness of the long bones and regional lymphadenopathy. • Oral patches—oral mucus patches are shallow, relatively painless lesions, initially seen as white which soon become erosive. The lesions are usually found on the lips, tongue and other intraoral surface. • Skin lesion—skin lesions may be papular, papillomatous, macular, papulosquamous, annular or circinate. • Sabre tibia—osteoperiostitis usually involving long bones is the most common manifestation which may cause nocturnal pains in the legs. Long standing osteitis and periostitis may eventually lead to forward bowing of tibia known as ‘sabre tibia’. • Late stage—it is seen where early endemic syphilis remains untreated for 6-9 months or even longer as an alteration in about 1/3rd of the patients or as tertiary state of the disease. Late lesions are mainly of gummatous type, involving skin, mucous membrane and bone. Skin lesions are usually extensive, chronic, destructive, scarring and with depigmentation. Gummatous destruction of nasal septum is common. • Rhinopharyngitis mutilans—destruction of the lips, soft palate and nasopharynx can occur leading to gross deformity of the face. Diagnosis • Clinical diagnosis—Rhinopharyngitis mutilans with sabre tibia will give clue to the diagnosis. Management • Penicillin—it is the drug of choice and where penicillin is contraindicated; drugs such as tetracycline and erythromycin can be given. • Surgical correction—surgical correction of the defects of face should be carried out for aesthetic purpose.
Pinta It is almost exclusively confined to the Western hemisphere. The mode of transmission is either by direct or indirect contact. Clinical features • Incubation period—the incubation period is usually 2-3 weeks, after which the disease is clinically manifested. Infection is seen in young adults of 15-30 years of age. • Subcutaneous lesion—the basic lesion of pinta is a solely developing subcutaneous granulomatous lesion.
• Primary lesion—it is believed to occur at the point of contact. They begin as small erythematous papule which enlarges within a year or two. In early lesion, pigment is lost from the germinal layer of epidermis and may become concentrated in upper layer. The primary lesion may be found on trunk, leg, face and around the anus and may be surrounded by satellite lesions. • Pintides—secondary lesion of pinta is known as pintides, which appear after a period of months of years. It starts as papular lesion and develops into plaques with scaly and centrally pigmented areas. These lesions tend to be become eventually depigmented. Lesions are itchy and painless. Moderate lymph node enlargement is often seen mostly due to accompanying secondary infections. • Late lesion—over the period of time primary and secondary lesions become depigmented and the skin over these lesions become atrophic. Hyperkeratosis of the palms and soles accompany the formation of the achromic lesion at this stage. Diagnosis • Clinical diagnosis—skis lesion with pintides and subcutaneous granulomatous lesion will give clue to the diagnosis. Management • Penicillin is the drug of choice. Patients who are allergic to penicillin, tetracycline can be given.
Yaws It is also called as ‘framboesia’ or ‘buba’. It is caused by Treponema pertenue, which is pathogenic for monkeys, rabbits and hamsters. It is transmitted either by direct contact with the exudates of the early infectious lesion or indirectly by contaminated utensils. Clinical features • Primary stage—the incubation period is between 9 to 90 days. The initial lesion, a papule, appears at the site of entry of the Treponema. It occurs usually through an abraded or lacerated site. The lesion may ulcerate and infection can spread via bloodstream. Regional lymph nodes are usually palpable. Children with only primary lesion may complain of pain. • Secondary stage—usually 1 to 3 months after the appearance of the papular primary lesion, infection spreads and a painless papilloma or frambesial granuloma appears. Lesions in the secondary stage are usually found in warm and moist sites such as axilla, groin and the skin around the natural orifices, including the mouth. They may be multiple and condylomatous in appearance. Partially, healed skin lesions often have an annular or
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Bacterial Infections 739 circinate appearance. Skin lesions may spontaneously heal in about 3 to 6 months. Bone and cartilage are involved. Lesions include osteitis, periostitis and dactylitis. In infected growing children, ‘sabre tibia’ develop. Plantar and palmar hyperkeratosis is also seen. • Tertiary stage—tertiary lesion may occur after 5 years of primary lesion. The stage is characterized by gummatous nodular ulcerative lesion. Gummata of the skin start as subcutaneous nodules which eventually ulcerate. Osteoperiostitis, area of rarefaction and necrosis occur in long bones.
sexual intercourse, they penetrate through the intercellular spaces of the epithelium and reach the subepithelial connective tissue. • Inflammatory reaction—within 2 to 3 days of infection, an intense inflammatory reaction occurs resulting in characteristic mucopurulent discharge through urethral lumen. • Chronic stage—a chronic stage may be reached, if untreated and spread is either by direct extension through lymphatics or hematogenous route.
Oral manifestation • Lips—during secondary stage, mucosal surface of lips may involve due to direct extension of the lesion present at the mucocutaneous junction. • Goundou—secondary changes of the nasal processes of maxillary bone have been reported during the secondary and tertiary stages of the disease. These result in thickening of the face on either side of the bridge of the nose, gives rise to a characteristic facial appearance called ‘goundou’. • Gangosa or saddle nose defect—in some cases, the lesion starting either on the soft palate, uvula or hard palate, eventually invades and destroys soft and bony parts of nose which is called as ‘Gangosa’ thereby causing ‘saddle nose defect’. Diagnosis • Clinical diagnosis—saddle nose defect with sabre tibia goundou shape appearance gives clue to diagnosis.
• Age and sex—it is primarily a disease of young adults between the ages of 15 to 24 years and is more common in males, as compared to females. • Location—it is seen on genital site. Occasionally, it can involve extra-genital sites. In male, urethra is involved and in females, cervix is involved. • Incubation period—incubation period is 2 to 5 days. • Symptoms—there is profuse purulent urethral discharge with frequent micturition, followed by dysuria. In some of the patients, there may be fever and headache. • Gonococcal septicemia—features of this include myalgia, arthralgia, polyarthritis, dermatitis, fever, endocarditis, meningitis and oral manifestation. • Skin lesion—dermatologic manifestation includes discrete papules and pustule that often contain of hemorrhagic component. • Gonococcal ophthalmia neonatorum—this is the infection of infant eye which is transferred from infected mother. It may cause blindness. • Complication—Cooper abscess (inflammation of periurethral glands), urethral stricture (difficulty in passing urine), arthritis, meningitis, endocarditis, epididymitis (painful swollen testicle), salpingitis or pelvic inflammatory disease (lower abdominal pain, metrorrhagia and pelvic tenderness on vaginal or rectal examination). • Diagnosis—in all forms of it, including those of oral cavity and pharynx, the diagnosis rests on the identification of organism. Methods which are used include, gram stained smear, culture studies and direct fluorescent antibody test.
Management • Penicillin—it is the drug of choice.
Gonorrhea It is primarily an infection of the genitourinary tract mucosa. It is caused by gram –ve intrabacillary located diplococcus Neisseria gonorrhoeae. It is an oval, paired, gram-negative microorganism. Local infection may occur at extra-genital site (Rectal and pharyngeal gonorrhea). Rectal mucosa is affected in 30% to 50% of women with urogenital gonorrhea. Uncomplicated local infection at other extra-genital sites is rare in adults. Early sexual awakening, prostitution and varied sexuality are believed to be responsible for the increase incidence of gonorrhea.
Pathogenesis • Penetration of gonococci—once the gonococci are directly deposited on the genitourinary tract mucosa during
Clinical Features
Oral Manifestations • Pharyngeal gonorrhea—Pharyngeal gonorrhea is a term used for patients in whom neisseria gonorrhea is isolated from nasopharynx. It is higher in pregnant women, sexually active homosexuals and heterosexuals practicing oral sex. History of fellatio is more associated with pharyngeal gonorrhea. Patient also noticed sore throat and evidence of pharyngitis.
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• Gonococcal stomatitis—incidence is very rare and often shows multiple, painful and round elevated gray white eroded spots, with or without pseudomembrane formation. Regional lymphadenopathy may be seen. The wide range of lesion may develop in gonococcal stomatitis i.e. isolated ulcers, gingivitis and membranous gingivostomatitis. • Gingivitis—acute gingivitis develops around extraction site in patient who practices fellatio repeatedly for days after extensive dental extraction. Gingiva may become erythematous, with or without necrosis. • Lips—lips may develop acute painful ulcerations, limiting the motion. • Tongue—the tongue may present red, dry ulcerations or become glazed and swollen with painful erosion with similar lesions on buccal mucosa and palate. • Temporomandibular joint involvement—gonococcus infection involving articulating joint is the most common form of extragenital gonorrhea. Any joint may be affected, the commonest being knee, ankle and wrist. TMJ is affected in 14% of patients. It occurs as a result of hematogenous spread. Patient noticed difficulty in jaw movements due to pain and swelling of single or both joints is the presenting symptom. Rarely, perforation to the tympanic plate occurs. It may lead to fibrous ankylosis because articular cartilage is destroyed. • Types of gonococcal arthritis—Wright has divided Gonococcal arthritis in two different categories: • Category I—Definite gonococcal arthritis—gonococci recovered in an aspirate from the affected joint. • Category II—Probable gonococcal arthritis. No gonococci recovered from the joint, but each of the following conditions exist. • Presence of gonococcal urethritis proven on smear or culture. • Arthritis occurring within 3 weeks of probable gonococcal infection. • Articular manifestations responding rapidly to antigonococcal therapy.
• Tuberculosis ulcer—undermined, flabby border—usually painless, tuberculin test positive.
Management • Antibiotics—single dose of the broad-spectrum cephalosporin antibiotic ceftriaxone 125 to 250 IM plus doxycycline 100 mg orally, twice a day for 7 days. In case of patient allergic to above drug, sepectinomycin 2 gm IM plus doxycycline. In some cases, orally or intramuscular administered fluorinated Quinolones may be helpful. • Prophylactic treatment—prophylactic ophthalmic erythromycin should be given to prevent gonococcal ophthalmia neonatorum. • Recurrence—without adequate treatment, disease will recur.
Streptococcal Tonsillitis and Pharyngitis The most common cause of this condition is beta hemolytic streptococci, adenoviruses, enteroviruses, influenza and parainfluenza.
Clinical Features • Symptoms—sudden onset of sore throat, fever, dysphagia. • Signs—redness of oropharynx and tonsils (Fig. 30-2), palatal petechiae and yellowish tonsillar exudate. • Lymph nodes—there is cervical lymphadenopathy. • Systemic features—headache, anorexia, abdominal pain and vomiting can also occur.
Radiographic Features Radiologically, the joint reveals no abnormalities. Rarely, perforation through the tympanic plate may occur.
Diagnosis • Clinical diagnosis—purulent urethral discharge with pharyngitis with TMJ involvement can give clue to diagnosis.
Differential Diagnosis • Primary syphilitic lesion—painless indurated edema, painless lymph node swelling, causative agent in lesion.
Fig. 30-2: Inflammation of pharynx and tonsil seen in streptococcal pharyngitis and tonsillitis.
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Bacterial Infections 741 Diagnosis • Clinical diagnosis—tonsilits with cervical lymph adenopathy will lead to diagnosis.
Management • Antibiotics—penicillin and cephalosporin should be given. Erythromycin should be used in patient who is sensitive to penicillin. • Analgesic—analgesic should be given to control pain and inflammation. • Warm saline gargle—it is also effective treatment in case of tonsillitis.
Leprosy (Hansen Disease) It is a chronic infectious disease which has predilection for the skin, nerves and mucous membrane. It probably originated in tropic and spread to the east. Leprosy has always been considered in superstitious dread and the person suffering from leprosy was considered unclean and socially outcasted. It is caused by the leprae bacillus, Mycobacterium leprae, first observed by Hansen in 1868. It is not been possible to grow the bacillus in culture media. It is an acid fast, gram positive, non-motile bacteria with affinity for Schwann cells and cells of reticuloendothelial system.
Pathogenesis • Multiplication of bacteria—after entry in the body the bacilli reach the lymphatic and bloodstream and are taken up by Schwann cells in peripheral nervous system, where they start multiplying. If the host cell mediated immunity is adequate, bacilli are destroyed and there is no disease. In the host, immunity is unstable and suboptimal, there will be some restricted multiplication of bacilli and lesion will develop. • Effect of immunity—the variable status of host cell mediated immunity is reflected in the different clinical types of leprosy. When there is relatively good immunity but not enough to eliminate the infection, a localized type of disease called as tuberculoid type, is seen. When the host cell immunity is deficient a generalized form of the disease lepromatous leprosy develops. • Borderline variety—in between these two polar varieties of the disease, there is a wide spectrum of manifestations, categorized as borderline leprosy.
• Lepromatous leprosy—this is present in reduce cell mediated immune response. • Borderline leprosy—it can be tuberculoid borderline or lepromatous borderline. • Polyneuritic—in this, multiple nerves are involved by the bacteria. • Indeterminate—no specific lesion is found in this type of leprosy. • Erythema nodosum leprosum—this is the severe form of leprosy. • Paucibacillary leprosy—it corresponds to tuberculoid type of leprosy and lesions are limited to skin. • Multibacillary leprosy—this corresponds to lepromatous type and involves multiple organs.
Clinical Manifestations Tuberculoid type or paucibacillary type • Incubation period—incubation period of 2 to 5 years during which patient passes through silent or latent period. • Sex—males are affected more commonly than females with ratio of 3:1. • Skin—lesions are hypopigmented, erythematous and flat or raised cutaneous lesions. Nerve involvement with loss of different types of sensation is also manifested. • Early tuberculoid leprosy—it is manifested by hypopigmented macules which are sharply demarcated and hyperesthetic. • Intermediate tuberculoid lesion—later, the lesions are larger with elevated and circinate margin. There is peripheral spread (Fig. 30-3) and central healing. At the end of this stage, the symptoms are those of irritation of nerve ending in the skin, persistent or recurrent paresthesia and numbness localized to certain area with no accompanying visible alteration in the corresponding skin lesion.
Types • Tuberculoid leprosy—it develops in patient with high immune reaction. It is localized. It is a benign form of leprosy involving the skin, nerves and regional lymph node.
Fig. 30-3: Lesion of tuberculoid leprosy showing peripheral spread (Courtesy Dr Pincha).
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• Fully develop lesion—in this, lesions are densely anesthetic and loose normal skin organs (sweat glands and hair follicles). There may be severe neuritic pain. Loss of eyebrows and eyelashes are prominent features of later involvement. • Peripheral nerve—the sequelae of peripheral nerve involvement may develop in some cases and this may give rise to muscle atrophy, like contracture of hands and feet, loss of phalanges, lagophthalmus, exposure keratitis and corneal ulceration leading to blindness.
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Lepromatous type or multibacillary leprosy • Age and sex—this form is more commonly seen in children and females are affected more as compared to males. • Site—this malignant form of the disease produced widespread involvement of body skin, peripheral nerves, mucous membrane, lymph nodes, eyes, skeleton, testes and other internal organs. It runs chronic course and seldom causes sudden death. • Appearance—it develops early as erythematous macules (Fig. 30-4) or papules without subsequently lead to progressive thickening of skin and the characteristic nodules. • Margins—the borders of the lesion are ill defined and centers of the lesion are indurated and convex. • Eyes—loss of lateral portion of eyebrows is common. • Lymph nodes—painless inguinal and axillary lymphadenopathy is common along with sterility and gynecomastia. • Nerve involvement—nerve involvement is a late phenomenon.
Fig. 30-4: Macular lesion seen on the leg of patient in lepromatous leprosy.
• Claw hand—this is one of the typical features of leprosy (Fig. 30-5).
Fig. 30-5: Claw hand seen in lepromatous leprosy.
Erythema nodosum leprosum (ENL) • Occurrence—they occur in lepromatous and borderline lepromatous patients, most frequently in the latter half of the initial year of treatment. • Signs—tender, inflamed subcutaneous nodules develop, usually in crops. Each nodule lasts a week or two, but new crop may appear. • Symptoms—low grade fever, lymphadenopathy and arthralgia can accompany severe ENL. • Leporma—this is common feature of erythema nodosum leprosum (Fig. 30-6). Facial manifestations • Prevalence—depending on the type and duration of the disease, all patients with lepromatous leprosy show facial and oral manifestations and it is rare in tuberculoid and borderline leprosy. • Leonine facies—the skin of face and forehead become thickened and corrugated giving a patient distorted facial appearance (leonine facies) (Fig. 30-7).
Fig. 30-6: Leproma in erythema nodosum leprosum presented as inflammatory swelling.
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Bacterial Infections 743
Fig. 30-7: Facial appearance in leprosy (note the saddle nose).
• Ear—earlobe becomes pedunculous due to lepromatous infiltration of the helical and lobes of ear. • Symptoms—there is nasal stiffness, epistaxis, hoarseness. • Appearance—the lesions are macular or raised, well defined, hypopigmented, unhydrotic and hyperaesthetic or anesthetic. • Advanced cases—advanced cases are characterized by nodular involvement of facial, cutaneous and subcutaneous structure. • Neural changes—peripheral nerves such as facial and trigeminal nerves are frequently involved. Facial paralysis is observed in 3% of cases, complete or partial facial paralysis may occur either unilaterally or bilaterally. Paralysis of the orbicularis muscle results in facial disfigurement, difficulties in phonation and mastication as well as drooling. Involvement of trigeminal nerve results in hypoesthesia and anesthesia. • Facies leprosa—rhinomaxillary changes termed facies leprosa consist of atrophy of anterior nasal spine, atrophy and recession of the maxillary alveolar process confined to the incisor region and endonasal inflammation. • Saddle nose—from nasal mucosa, granulomatous tissue invade cartilage and bone resulting in nasal collapse. The appearance is called as saddle nose (Fig. 30-7). • Chronic osteomyelitis—destruction of facial cartilage and bone is caused by direct infiltration and secondary infection which results in chronic osteomyelitis. Oral manifestation • Prevalence—it is more commonly seen in lepromatous • Site—involvement of oral mucosa, pre-maxilla, soft palate, uvula, tongue, gingiva and periodontium has been reported.
• Lepromas—small tumor like masses called as lepromas develop on the tongue, lips or hard palate. These nodules have a tendency to break down and ulcerate. Continuous infection may lead to scarring and loss of tissue. • Gingiva—gingival hyperplasia with loosening of teeth have been also reported. • Tooth size and shape—in association with severe and granulomatous infiltration of pre-maxilla in childhood, the tooth diameter is suddenly and concentrically reduced, while the less marked cases exhibit a well demarcated, tapering and shortening of root. • Enamel hypoplasia—transient interruption of odontogenesis results in slight, circumferential hypoplasia of enamel and cementum. • Pulpal necrosis—in long standing lepromatous leprosy, invasion of the pulp by granulomatous tissue causes pulpal necrosis leading to a pinkish discoloration of crown. Anterior teeth are most commonly affected.
Diagnosis • Ziehl-Neelsen stain—skin smears should be examined as a routine with Ziehl-Neelsen stain. The percentage of solid bacilli in a smear is known as morphological index. • Biopsy—skin, mucosal and nerve biopsy for histopathological examination are helpful in doubtful cases. • Lepromin test—lepromin test is non-specific test to determine the hypersensitivity reaction and is useful in determining the immunological status of patient for classification of leprosy.
Differential Diagnosis • Gummatous lesion of syphilis—VDRL test should be performed. • Ulcerative proliferative lesion of coccidioidomycosis and sporotrichosis—peripheral nerve involvement is common in leprosy.
Management • Paucibacillary leprosy—it is treated with 6 month regimen of rifampin and dapsone. Patient allergic to rifampin are treated with clofazimine, ofloxacin and minocycline. • Multibacillary leprosy—this is treated with 24 months therapy of rifampin, dapsone and clofazimine. • Reconstructive surgery—reconstructive and plastic surgery is essential for deformities of the hand and face • Vaccine—BCG vaccines provide some protection against non-lepromatous leprosy. • Social development—environmental changes with social and economic development are useful.
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Tuberculosis
Types
It is a systemic infectious disease of worldwide prevalence and of varying clinical manifestations. It is an infectious granulomatous disease caused by acid-fast bacilli Mycobacterium tuberculosis or rarely, Mycobacterium bovis. It can rarely be transmitted through the placenta from the diseased mother to fetus.
• Primary tuberculosis—it occurs in previously unexposed person and it involve lung. • Secondary tuberculosis—in this reactivation of bacteria and it occur in, compromised host defense. • Miliary tuberculosis—it spreads through bloodstream and there is wide involvement of many organs like kidney, liver and is called as miliary tuberculosis. • Pott’s disease—if tubercular involvement of spine occurs in children, it is called as Pott’s disease. • Scrofula—if it spreads by lymphatics to lymph nodes, it is called as scrofula.
Pathogenesis
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• Primary infection—initial tuberculosis usually occurs in lungs but occasionally, occurs in tonsil or alimentary tract. The common cause of primary infection is inhalation. In most of the patients of primary infection, the associated lymph node lesions heal and calcify. • Rupture of caseous tuberculosis foci—in some cases, caseous tuberculosis focus ruptures into vein and produces acute dissemination throughout the body, a condition called as acute miliary tuberculosis. Meningitis often complicates this condition. • Progressive pulmonary tuberculosis—progressive pulmonary tuberculosis may develop directly from a primary lesion or may occur following reaction of an incompletely healed primary focus. • Post-primary pulmonary tuberculosis—post-primary pulmonary tuberculosis is a condition in which, there is a liquefied center of tuberculosis, pulmonary infection is discharged into sinus. Extension of infection into pleura causes tuberculosis pleurisy.
Clinical Features • Age—they are relatively uncommon and seen in middle and older age groups, as cleansing action of saliva and its antibacterial properties, in general also provide protection against tubercle bacilli. • Symptoms—patient may suffer episodes of fever and chills, easy fatigability and malaise. There may be gradual loss of weight accompanied by persistent cough with or without hemoptysis. Local symptoms depend upon the tissue or organs involved. • Signs—tubercular lymphadenitis may progress to acute abscess or remain as granulomatous lesion (Fig. 30-8). In any case, swelling of neck is present which is tender, painful and often show inflammation of the overlying skin. When abscess forms, it perforates and discharges pus.
Etiology • Causative organism—the first member identified as tuberculous bacillus and designate as Mycobacterium tuberculosis. Other microorganisms associated are Mycobacterium bovis, Mycobacterium kanasasi, Mycobacterium xenopi and Mycobacterium malmoense. The organism is anaerobic, non-motile, non-sporing, rod shaped and is stained with special Ziell-Neelsen stain. • Constitutional factor—it is more common in low income group, unhygienic living conditions, malnutrition and overcrowding.
Predisposing Factors for Oral Infection • Systemic factors—systemic factors like lowered host resistance and increased virulence of the organism may lead to oral manifestation in the tuberculosis patient. • Local factors—local factors like poor oral hygiene, local trauma, presence of pre-existing lesion such as leukoplakia, periapical granuloma, dental cyst, dental abscess, jaw fracture and periodontitis are also responsible for oral infection.
Fig. 30-8: Tubercular lymphadenitis showing swelling in the submandibular region (Courtesy Dr Chole).
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Bacterial Infections 745 • Pulmonary tuberculosis—a persistence cough, hemoptysis, abundant sputum are usual features of pulmonary tuberculosis. There is also evening rise in temperature of 0.5o to 2oF. Night sweats is also present. • Scrofula—in glandular form of the disease, there is marked enlargement of the cervical lymph nodes with caseation and frequent breakdown of the gland. Such tuberculous infection is called as ‘scrofula’. It is usually caused by ingestion of unpasteurized infected cow milk. • Cold abscess—the chronicity of the infection and the lack of marked pain or acute inflammatory symptoms have resulted in the term ‘cold abscess’. • Consumption—progressive tuberculosis may lead to wasting syndrome called as consumption as it appear as patient body is consumed or destroyed. • Lupus vulgaris—involvement of skin in tuberculosis is term as lupus vulgaris.
Oral Manifestations • Site—tongue is most commonly affected followed by palate, lips, buccal mucosa and gingiva. • Primary oral lesion—it develops when bacteria is directly inoculated in the oral tissue of a person who has not acquired immunity to the disease. It involves gingiva, tooth extraction socket and buccal fold. • Secondary oral lesion—infection is carried by hematogenous route or through break in the tissue surface, is deposited in the submucosa, subsequently proliferates and ulcerates the overlying mucosa. It occurs more frequently in cases of extra-pulmonary tuberculosis. • Tubercular ulcer—the lesion may be preceded by an opalescent vesicle or nodule, a result of caseation necrosis. It breaks down into an ulcer which is usually superficial or deep and painful. Margin of the ulcer are undermined with minimum induration. It tends to be increased slowly in size. Mucosa surrounding the ulcer is inflamed and edematous. Base of ulcer is yellowish and granular. • Sentinel tubercle—tiny, single and multiple nodules called ‘sentinel tubercle’ may also be seen surrounding the ulcer. • Mucocutaneous junction—at the mucocutaneous junction, tubercular ulcers are usually extremely shallow with granulating base. Crusting and oozing is seen when the lesion involves adjacent cutaneous surface. They are usually painful. • Nodular form—the nodular form of tuberculosis presents as single or multiple nodules of variable sizes, which initially may appear as semitransparent lesion of pinhead size. They are gray in size and of variable consistency.
• Miliary tubercle—miliary tubercle of oral mucosa are occasionally seen in miliary tuberculosis which is a result of acute dissemination of the infection through hematogenous and lymphatic channel. The oral lesion appears as small, gray tubercle with the tendency to break down and ulcerate. • Periapical tissue—tubercle involvement of the periapical tissue and tooth socket have been reported. The socket may be filled with so called tuberculosis granulation tissue, consisting of many small, pink and red elevations. • Tuberculosis gingivitis—tuberculosis gingivitis is an unusual form which may appear as diffuse, hyperemic or nodular papillary proliferation. • Jaw involvement—it may involve maxilla or mandible. Jaw bone involvement occur as a result of either deep extension of a gingival lesion, from infected extraction socket, an extension of tubercular granuloma at the apex of tooth or by means of hematological spread. It may result in more diffuse form of osteomyelitis and is normally more serous than infections from periapical lesion. • Symptoms of jaw involvement—tubercular involvement of jaw bone causes swelling and the symptoms include difficulty in eating, trismus, paresthesia of the lower lip and enlargement of the regional lymph nodes. Fistulae drain either intraorally or extraorally often with blue margins. • Temporomandibular joint—in some cases, destructive involvement may reach to the TMJ area.
Radiographic Features General • Early changes—the chest radiograph in patient with secondary tuberculosis may show fibronodular changes most often in upper lobe. There is also cavity formation and volume loss. The earliest changes usually are ill defined opacity or opacities situated in the upper lobes. • Advanced cases—in more advanced cases, opacities are larger and more widespread and may be bilateral. An area of translucency within the opacities indicates cavitations. • Displacement of trachea—trachea and mediastinal structures are displaced towards the side of the lesion. Oral • It may be described as a localized or diffused with wide variation in size. • Location—mandibles show greater predisposition than maxilla. • Localized lesion—the localized lesion is of rarefying osteitis, while diffuse one is the nature of osteomyelitis. • Diffuse lesion—in diffuse type of tuberculosis of bone, scattered area of bone destruction separated by portions of bone having normal or near normal appearance are seen.
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• Periostitis—in some cases, tuberculosis may result in laying down the bone which resembles periostitis.
Diagnosis
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• Microscopy—a pulmonary TB suspect, should submit 3 sputum samples for microscopy. Morning sample is ideal. • Staining method—Ziehl-Neelsen, carbol fuschin or kinjouncarbol fuschin have been used for staining mycobacterium. • Polymerase chain reaction—this technique amplifies even very small proteins of predetermined target region of Mycobacterium tuberculosis complex DNA. • Tuberculin skin test—the Mantoux test is the preferred skin test for detecting tuberculosis. It involves the injection of 5 Tuberculin unit of purified protein derivatives, usually 0.1 ml intradermal. The skin test is read on the basis of millimeters of induration produced by PPD. 10-15 mm induration is required for the test to be positive.
Dental Considerations • Evaluation of patient—Dental personnels are at constant risk of contacting the disease while treating the patient of tuberculosis. It is known that smallest droplet of contaminated saliva from the patient may be sufficient source of contagion, particularly if they are inhaled by previously uninfected or non-immunized individual. Patient with past history of tuberculosis should be evaluated by the physician to ensure the course of the treatment and follow up. • Delayed dental treatment—if the culture is positive, dental treatment should not be performed unless there is emergency. In emergency dental treatment special precautions should be taken. • Protection of doctors—to avoid aerosolization use of rubber dam and minimum use of ultrasonic scalers and high speed handpieces should be done. The operating air should be vented to the outside, i.e. not recirculated.
Differential Diagnosis • Syphilis—primary lesion is harder and spirochetes are found. • Traumatic ulcer—short duration and history of trauma. • Sarcoidosis—tuberculin test negative, the granuloma of sarcoidosis are of non-necrotizing type. • Lupus erythematosus—histology, causative agent test negative, skin changes. • Leukemia—immature WBCs, prolonged bleeding and clotting time.
Management • Chemotherapy—short term chemotherapy, isoniazid (5 mg/kg with maximum of 300 mg daily or 15 mg/kg two to three times weekly) and rifampicin (10 gm/kg), ethambutol (25 gm/kg daily for not more than 2 months). • Other drugs—other drugs which can be used are streptomycin, para-aminosalicylic acid, pyrazinamide, thiacetazone, ethionamide and cycloserine. • Surgery—surgery is rarely performed nowadays, as most patients respond well to medication. When indicated, it is usually for a persisting pulmonary cavity with acidfast positive sputum despite 6 months of chemotherapy. The usual type of surgery done is segmental resection of lung or a complete lobectomy.
Actinomycosis It is a chronic granulomatous suppurative and fibrous type of disease caused by anaerobic, gram +ve, non-acid fast bacteria. Most common are Actinomycoes israelii, A. nasalundi, A. viscosus and A. odontolyticus. The organism is considered to be transitional form between bacteria and fungi. The term Actinomyces was given by Harz to refer the ‘ray-like appearance’ of the organism in the granule.
Classification • Cervicofacial—it involve facial and cervical region. • Abdominal—it is serious form and involves abdomen. • Pulmonary—in this, there is pleural invasion resulting in empyema. • Cutaneous—there is subcutaneous swelling in this form. • Central—here, the infection is from the tooth or its membrane and is accompanied by radiographic changes. • Peripheral—the peripheral types originate in the soft tissues and do not involve bone.
Predisposing Factors • Trauma—the breach in the continuity of mucosa caused either by trauma or surgery, if the prerequisite for majority of actinomycosis infections. • Local factors—cervicofacial actinomycosis infections are endogenous in origin and occur when dental plaque, calculus or gingival debris contaminate the relatively deep wounds around the mouth. Presence of carious teeth may act as predisposing factors for actinomycosis. • Others—secondary bacterial invasion and hypersensitivity reaction may act as predisposing factors for actinomycosis.
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Bacterial Infections 747 Clinical Features Cervicofacial form • Age—it is most common type of actinomycosis and is commonly seen in adult males. • Location—submandibular region is the most frequent site of infection. It usually spreads by direct tissue extension. Cheek and masseter region and parotid gland may also be involved. • Symptoms—trismus is a common feature, before the formation of pus. • Signs—the first sign of infection is characterized by the presence of a palpable mass. Mass is painless and indurated. • Sinus and fistula—development of fistula and sinus is common. Skin surrounding the fistula is purplish (Fig. 30-9). Adjacent tissues have doughy consistency. • Sulfur granules—several hard circumscribed tumors like swelling may develop and undergo breakdown, discharging a yellow fluid containing the characteristic submicroscopic sulfur granules. • Ray fungus appearance—round or lobulated colony meshwork of filaments stain with hematoxylin and peripheral club shaped ends of filaments stain with eosin.
Fig. 30-9: Fistula seen in patient of actinomycosis ( Courtesy Dr Patle).
Abdominal form • Abdominal actinomyces is extremely serious form of the disease. • Precipitating factors—trauma, due to surgery or other causes such as fish bone or chicken bone injury, usually precedes the onset of the disease. • Symptoms—generalized symptoms of fever, chills, vomiting, develop followed by symptoms of involvement of organs, such as liver and spleen. • Sign—there is palpable abdominal mass. Intestinal manifestations develop later. Pulmonary form • Symptoms—it produces findings such as fever and chills, accompanied by a productive cough and pleural pain.
• Signs—pleural invasion resulting in empyema and there may be formation of sinus. Subcutaneous form • Cause—infection result from traumatic transplantation of organism, usually due to human bites. • Signs and symptoms—lesion seen as subcutaneous swelling which enlarges slowly softens and ruptures through the sinuses. Occasionally, these lesions burrow through deeper tissue and invade bones.
Oral Manifestations • Cause—organism may enter the tissue through oral mucous membrane and may either remain localized in the adjacent soft tissue or spread to involve salivary glands, bone or skin of face and neck. • Signs—it produces swelling and induration of tissue. It may develop into one or more abscesses, which tend to discharge upon the skin surface liberating pus, which contains typical sulfur granules. There may be nonhealing tooth socket, exuberant granulation tissue and periosteal thickening of alveolus. Skin overlying abscess is purple red and indurate or fluctuant. • Sinus—it is common for sinus, through which the abscess has drained, to heal but due to chronicity, new abscesses are formed and perforate through skin surface. • Face—there is disfigurement of face. Infection may involve maxilla and mandible. • Periapical granuloma—there is formation of periapical granuloma. • Tongue—on the tongue, the lesion is a painful nodule which eventually ulcerates. Untreated cases may reach to the point where the tongue may become fixed. • Actinomycosis osteomyelitis—it can occur in patient with periodontal infection, nonvital teeth.
Radiographic Features • Appearance—it may appear as an area of bone destruction, which resembles a dental cyst, with a well defined area of radiolucency with cortical lining of dense bone. • Lamina dura—lamina dura is deficient at the apex of tooth. • Rarefying osteitis—scattered area of bone destruction, separated from one another by normal or sclerosed bone, is another manifestation. • Tooth features—the persistence radiolucency of tooth socket with an increased density of adjacent bone may be the first sign of disease.
Diagnosis • Clinical dagnosis—sulphur granules with development of fistula and sinus with fever give clue to diagnosis.
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• Radiological diagnosis—loss of lumina dura with scattered area of bone destruction. • Laboratory diagnosis—typical key fungus appearance is seen.
• Two fold therapy—actinomyces infection produces a reactive inflammatory response which causes an area of necrosis and scar tissue around the abscess. This results in decrease in the vascular supply to the affected region and hence, makes penetration of antibiotics difficult. Therefore, two fold therapy including antibiotics and surgery is necessary. • Surgical—the lesion should be surgically removed and the surrounding area should be thoroughly debride. • Antibiotics—following surgical intervention, antibiotics therapy should be continued. The antibiotic of choice is penicillin which should be given 3 to 4 million IV, every 4 hours for 2 to 4 weeks. This should be followed by 0.5 to 12 gm of penicillin, four times a day for 4 to 6 weeks. In patients allergic to penicillin, tetracycline orally 500 mg given four times a day for 6 months. • Other drugs—other agents used in the treatment of actinomycosis include cephalosporin, clindamycin and lincomycin.
• Sites—common sites are areas of stagnation around fixed bridge or crown. • Onset—the commencement of gangrene is denoted by blackening of skin. • Necrotizing ulcerative mucositis—small ulcers of gingival mucosa spread rapidly and involves the surrounding tissues of jaws, lips and cheeks by gangrenous necrosis. • Symptoms—lesion has foul odor. Patients have high temperature during the course of the disease, suffer secondary infection and may die from toxemia or pneumonia. • Skin—overlying skin is inflamed, edematous and finely necrotic which results in formation of line of demarcation between healthy and dead tissue. • Advanced stage—in advanced stage, there is blue-black discoloration of the skin. As gangrenous process advances, slough appears and soon separated, leaving a perforating wound in the involved area (Fig. 30-10). • Noma neonatorum—it arise in first month of low birth weight infants who are having malnutrition. Infants have lesion on lips, nose, mouth and anal area. • Jaw—large masses may be sloughed out leaving the jaws exposed. • Complication—it includes pneumonia, diarrhea, and septicemia. This can lead to death of patient.
Noma
Diagnosis
It is also called as ‘Cancrum oris’, ‘gangrenous stomatitis, necrotizing stomatitis. Nome is derived from the word nomein meaning to devour (eat greedily). It is rapidly spreading gangrene of oral and facial tissues occurring usually in debilitated or nutritionally deficient person. It is caused by Fusobacterium necrophorum.
• Clinical diagnosis—blue black discoloration of skin with sloughing of tissue will give clue to diagnosis.
Management
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Predisposing Factors • Poverty—it occur in persons who are undernourished. • Debilitated disease—debilitated infections such as diphtheria, dysentery, measles, pneumonia, scarlet fever, syphilis, measles, tuberculosis and blood dyscrasias. • Injury—excessive mechanical injury is also predisposing factors. • Poor oral hygiene—this may lead to growth of the bacteria causing increased susceptibility for the infection. • AIDS—as it is immunological disorders, it can lead to Noma. • Others—miscellaneous factors such as leukemia, sickle cell trait, stress and chemotherapeutic agents can cause noma.
Clinical Features • Age—it is seen chiefly in children, but can be found in adults in certain conditions like in malnourished states.
Fig. 30-10: Blackish discoloration with ulceration seen in case of gangrenous stomatitis (Courtesy Dr Tapasya).
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Bacterial Infections 749 Management
Oral Manifestations
• Control of dehydration and electrolyte balance—parenteral fluid should be given urgently to correct dehydration and electrolyte balance. • Blood transfusion—blood transfusion helps in improving the clinical state of the patient, who is usually anemic and toxic. • Antibiotics—the specific drug of choice is penicillin although sulphonamides also yield good results. Other antibiotics which are used are gentamicin, clindamycin. • Reconstructive surgery—reconstructive surgery is necessary to lead near normal life.
• Stomatitis scarlatina accounts for the chief oral manifestation of scarlet fever. • Palate—mucosa of palate may appear congested. Ulceration may also occur on palate. • Face—the face, especially the temporal region and cheeks are flushed and red, but pale area of circumoral pallor is often seen around the mouth. • White strawberry tongue—tongue exhibits white coating and fungiform papillae are edematous and hyperemic, projecting above the surface as small red knobs and it is called as ‘strawberry tongue’. • Red raspberry tongue—coating of tongue is soon lost, beginning at the tip and lateral margins and the organ becomes deep red, glistening and smooth, except for swollen hyperemic papilla. The tongue in this phase is called as ‘raspberry tongue’. • Teeth—in some cases, hypoplasia of teeth is seen in permanent teeth, if conditions occur at the time of tooth development.
Scarlet Fever Predominately occurs in children during winter months, caused by infection with group-A streptococci of beta hemolytic type that elaborate erythrogenic toxins.
Clinical Features • Incubation period—incubation period is 1 to 7 days. • Symptoms—patient exhibits severe pharyngitis and tonsillitis, chills, fever and vomiting. • Signs—throat becomes highly erythematous and exudation is common. There may be enlargement and tenderness of regional lymph nodes. • Skin rash—characteristic diffuse, bright scarlet to dusky red skin rash which appear on the second or third day of the illness (Fig. 30-11). This rash is also called as ‘sunburn with goose pimples’. Rash is more intense in areas of pressure and skin fold. There is a transverse red streak which is called as ‘Pastia’s line’. After 3 to 4 days, the rash fades. This rash is due to toxic injury to the vascular endothelium which produces dilation of the small blood vessels and consequent hyperemia.
Complications • Hypersensitivity reaction—localized or generalized bacterial dissemination or hypersensitivity reaction to the bacterial toxins. • Systemic complication—peritonsillar abscess, rhinitis, sinusitis, otitis media, mastoiditis, meningitis, pneumonia, glomerulonephritis, rheumatic fever and arthritis. • Oral complication—it includes cancrum oris, ulceration with perforation of palate, osteomyelitis and involvement of the temporomandibular joint.
Diagnosis • Clinical diagnosis—white strawberry and red raspberry tongue are typical of scarlet fever.
Differential Diagnosis • Pernicious anemia—tongue in pernicious anemia is not as red as in scarlet fever. • Atrophic glossitis in vitamin deficiency—swab culture of oropharynx disclose the presence of hemolytic streptococci and antistreptolysin -O titer is elevated.
Management • Antibiotics—penicillin is the drug of choice, since group A streptococci are generally highly sensitive to this antibiotic. The species are also sensitive to other antibiotics like erythromycin, tetracycline and chloramphenicol.
Diphtheria Fig. 30-11: Rash of scarlet fever seen on the skin of the hand (Courtesy Dr Pincha).
It is an acute contagious disease caused by gram +ve bacillus Corynebacterium diphtheriae, also called as Klebs
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Loeffler bacillus. It is transmitted by droplet infection or direct contact.
Pathogenesis
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• Portal of entry—the portal of entry is the upper respiratory tract and rarely skin, genitalia, eye and middle ear. • Incubation of bacteria—the bacilli settle on the mucous membrane or upper respiratory tract and lead to inflammation and necrosis of mucosal cells. The infection may spread to adjacent areas. • Primary area—in the primary invasive region, it forms a thick, firm, leathery, blue white pseudomembrane composed of bacteria, necrotic epithelium, macrophages and fibrin. A narrow zone of inflammation surrounding the area is seen. • Secondary area—when the diphtheria bacteria multiply in the local tissues, they produce powerful exotoxins. This exotoxin diffuses through the body through a hematogenous route. Heart, muscle, kidney, peripheral nerves and adrenal glands are thus involved. Death may be caused by heart failure, airway obstruction which is caused by edema or by the effect of toxin.
• Signs—it tends to adhere and leave a raw bleeding surface on removal. • Soft palate—soft palate temporary paralysis usually during 3rd and 5th week of the disease. The paralysis usually disappears in a few weeks or few months.
Diagnosis • Clinical diagnosis—bull neck, sore throat with edematous larynx will give clue to diagnosis.
Prevention • The disease may be prevented by prophylactic active immunization with diphtheria toxoid.
Differential Diagnosis • Herpes simplex infection—small blisters, small shallow ulceration and history of prodromal symptoms. No patch on soft palate. • Hand-foot-mouth disease—nausea, diarrhea, fever and vesiculoulcerative lesion occur simultaneously in the oral cavity and on hand and feet. No patch is seen.
Clinical Features
Management
• Age—it occurs most frequently in children, during the fall and winter months. • Incubation periods—incubation period is two days. • Symptoms—listlessness, malaise, headache, fever and occasional vomiting. Within a short time, patient complains of sore throat. • Signs—mild redness and edema of pharynx with cervical lymphadenopathy. • Bull neck—there may be swelling of the neck, called as ‘bull neck’. • Nose—soft palatal paralysis can lead to nasal regurgitation of liquids during drinking. • Larynx—larynx is edematous and is covered by pseudomembrane. It produces a mechanical respiratory obstruction and typical croup. • Neural involvement—there is generalized polyneuritis with weakness; paresthesia may follow in the next 10 to 14 days. • Complication—it includes myocarditis, polyneuritis and acute intestinal nephritis.
• Rest—the patient should be isolated and bed rest is very essential. • Antitoxin—it is treated with diphtheria antitoxin. Mild cases treated with 10,000 to 20,000 units of antitoxin. Moderate cases with 20,000 to 40,000 units and severe cases with 50,000 to 100,000 units of antitoxin. • Antibiotics—along with antitoxin antibiotics like penicillin and erythromycin should be given.
Oral Manifestations • Diphtheritic membrane—formation of patchy ‘diphtheritic membrane’ which begins on tonsils and enlarges, becoming confluent over the surface. It is thick and grayish in color.
Cat Scratch Disease It is also called as ‘cat scratch fever’. This is most common cause of chronic regional lymphadenopathy. The etiological agent is unknown. Viral as well as bacterial agents have been proposed as the cause of this disease. Initially, causative organism is named as Rochalimaea henselae but later on, it is named as Bartonella henselae.
Clinical Features • Age—it occur at any age, but predominant in children and young adults. It is thought to arise after traumatic break in skin due to scratch or bite of household cat. • Incubation period—the incubation time of the disease ranges from 3-14 days. • Symptoms—in early stage, low grade fever, headache, chills, nausea, malaise or even abdominal pain may occur.
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Bacterial Infections 751 • Signs—within few days of indolent primary lesion, often papules or vesicle develop at the site of injury. • Lymphadenitis—within one to three weeks, lymphadenitis develops. The nodes are painful and may be several centimeter in diameter. The overlying skin may be inflamed. The lymph nodes gradually become soft and fluctuant, owing to necrosis and suppuration. The lymphadenopathy may persist for one to six months. In dental point of view, there may be involvement of preauricular, submaxillary or cervical chain of nodes. • Parotid pain—when scratch occur in parotid area, infection may become localized parotid lymphoid tissue causing significant parotid pain. • Oculoglandular syndrome of Parinaud—it consist of conjunctival granuloma with pre-auricular lymphadenopathy. It occurs when person touches fur moistened with cat saliva during cleaning. In this case, person touches the eye organism may get transfer into conjunctiva. • Others feature—other manifestations includes nonpruritic macular or maculopapular rash, thrombocytopenia, pneumonia, conjunctivitis and grand mal seizure.
Types • • • • •
Cutaneous Ophthalmic Pleuropulmonary Oral Abdominal
Clinical Features • Incubation period—incubation period is up to seven days. • Symptoms—patient complaint of sudden headache, nausea, bony pain, profuse sweating, vomiting, chills and fever. • Suppurative ulcer—a single cut or sore on the skin develops into a suppurative ulcer. • Lymph nodes—lymphatic vessels become swollen and painful and the lymph nodes are remarkably enlarged. • Eyes—the eyes also become involved with conjunctivitis developing through localization of disease in the conjunctival sac. • Complications—tularemic pneumonia and pleuritis are complications of this disease.
Oral Manifestations Diagnostic Criteria Out of the following four, three should be positive for the diagnosis of cat scratch disease: • Contact with cat with presence of scratch. Dermal and ocular lesion should be present. • Negative results for other cause of lymphadenopathy. • Characteristic histopathological finding of staining of pleomorphic bacilli. • Positive cat scratch disease skin test (no longer widely used).
Management • Self limiting—the disease has a benign course and it is self limiting. • Symptomatic treatment—symptomatic treatment is given in the form of analgesic. • Antibiotics—erythromycin is first choice of antibiotics. Another antibiotic which can be given is Doxycycline. • Node aspiration and drainage—aspiration of the nodes should be done with needle tunneled laterally in the node.
Tularemia It is also called as ‘Rabbit fever’. It is caused by gram negative bacillus Francisella tularensis. It is contacted through infected rabbits, muskrats, ground squirrels and other wild germ, particularly of rodent family.
• Cause—primary infection of the mouth usually occurs from eating infected meat. • Site—it is common on soft palate, tongue, gingiva and angle of mouth. • Symptoms—severe pain is major complaint of the patient. • Diphtheria-like appearance—the appearance of the ulcer is shallow with whitish fibrinous pseudomembrane formation. The tonsil, posterior pharyngeal wall, soft palate, base of the tongue and buccal mucosa may be covered by a grayish white membrane simulating the appearance of diphtheria. • Generalized stomatitis—there may be generalized stomatitis. • Regional lymph nodes—regional lymphadenitis may arise in submaxillary and the cervical groups of nodes. Cervical lymph nodes are tender, enlarged and may suppurate.
Diagnosis • Clinical diagnosis—severe pain with ulcer with systemic symptom of headache, fever may give clue to the diagnosis. • Serology—an agglutination test is used to demonstrate a rising titer of antibody in the serum of patients of F. tularensis. • Skin testing—intradermal injection of an extract of F. tularensis gives a positive delayed hypersensitivity reaction in 1st or 2nd week of illness.
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Management • Antibiotics—antibiotics of choice are streptomycin and tetracycline, either alone or in combination.
Tetanus It is also called as ‘lock jaw’. It is a disease of nervous system characterized by intense activity of motor neurons and resulting in severe muscle spasm.
Pathogenesis
4
• Organism responsible—it is caused by anaerobic gram positive bacillus Clostridium tetany. • Production of toxins—the spores of above organism germinated under the anaerobic condition. This will result in production of exotoxin, tetanospasmin and hemolysis. • Toxins reach the brain—all of the above toxins reach the brainstream and anterior horn of spinal cord via bloodstream. • Increase muscle tone—toxin increases muscle tone and rigidity resulting in muscle spasm and convulsion.
Transmission • Injury—it can enter the body through the most trivial injury. • Intravenous drug user—it is often reported amongst intravenous drug users. • Contamination—it is transmitted through contaminated soil, dust or wood splinters. • Tetanus neonatorum—infection of the cut surface of umbilical cord or circumcision wound, due to use of unclean instruments or dressing, may result in tetanus of the newborn which is called as ‘tetanus neonatorum’.
Types • Local tetanus—muscle spasm at the site of entry is known as local tetanus. • Generalized form—this type of tetanus involve many system of the body. • Cephalic form—this type of tetanus occurs in association with facial palsy. • Neonatal form—this occurs in infant and route of transmission is from mother. • Chronic form—the cause of it is due to the persistence of focus of infection and fibrosis from inadequately controlled spasms.
Clinical Features • Age and sex—it is more common in young males during their accident prone years.
• Incubation period—the clinical manifestations occur within 14 days after incubation period. • Local tetanus—it is characterized by muscle spasm near the site of entry of bacilli. In some cases, it may proceed to generalized form. Mortality rate is less than 1% in this form. • Cephalic form—in this, bacilli are introduced through the wounds in the head and neck region. Cranial nerve palsy occurs with cranial nerve, most commonly the 7th cranial nerve. • Generalized form—entire body may be affected with contraction of all groups of somatic muscles leading to characteristic opisthotonos (spine become arch shaped). Reflex spasm frequently develops after stimuli. The temperature is usually raised due to increase metabolic rate. When spasm of intercostal, pharyngeal and diaphragmatic muscle occurs, adequate ventilation becomes impossible and the resultant anoxia causes death. Death in patients with tetanus is generally related to pulmonary complications including bronchopneumonia and pulmonary embolism. • Neonatal tetanus—the incubation period of neonatal tetanus is 3-10 days. It has high fatality rate. The disease is characterized by difficulty in suckling and excessive crying in early stage. As the disease progresses, variable degree of muscular spasm develops. Death is usually due to inadequate ventilation and asphyxia. • Chronic tetanus—it may persist for many years. Clinically, there are features of generalized tetanus to intermittent spasm of individual muscles.
Oral Manifestation • Rigidity of muscle of mastication—this is usually first manifestation of tetanus. • Risus sardonicus—rigidity of facial muscles may occur, producing the typical ‘risus sardonicus’. In this, corners of mouth are drawn back with protruded lip, wrinkling of forehead not possible. • Symptoms—patient complaint of difficulty in chewing, swallowing and inability to insert denture. • Lock jaw—as spasm of muscle of mastication increase jaw is locked and mouth cannot be open.
Diagnosis • Clinical diagnosis—lock jaw with risus sardonicus and opisthotonus will give clue to the diagnosis.
Management • Antitoxin—neutralizing the toxin is achieved by administered of human tetanus immunoglobulin. Specific therapy includes immediate intravenous injection of immune serum containing 20,000 IU of antitoxin.
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Bacterial Infections 753 • Penicillin—1,000,000 units of penicillin G intravenously, every 6 hours, for 10 days must be administered to kill vegetative form of Clostridium tetani. • Sedation—sedation of patient should be done with diazepam. • Supportive care—supportive care includes providing proper nutrition.
Granuloma Inguinale It is also called as ‘granuloma venereum’ and ‘donovanosis’. It is found in inguinal and anogenital region and is caused by Calymmatobacterium granulomatis a gram negative bacillus with prominent polar granules. It is chronic slowly progressing, mildly contagious disease.
Clinical Features
Rhinoscleroma It is unusual chronic infection caused by bacillus Klebsiella rhinoscleromatis and it is common in Europe and central and South America.
Clinical Features • Age and sex—both sexes are equally affected. Common between the ages of 20 to 40 years. • Site—usually found in upper respiratory tract, often originating from nose, but involvement of lacrimal glands, orbit, skin, paranasal sinus and intracranial invasion have been described. • Rhinitis stage—in this stage, there is nasal obstruction, nasal deformity and epistaxis. There is also swelling of upper lip and sore throat. • Infiltrative stage—it is characterized by nasal obstruction, due to the presence of exuberant granulation tissue. Hoarseness results due to laryngeal involvement. Anesthesia of soft palate is common in this stage. • Nodular stage—the proliferation of nasal masses may produce configuration known as ‘Hebra nose’. Posterior extension of the lesion may produce laryngeal and tracheal obstruction of varying degrees. Complications include scleromatous infiltration of eustachian tube and unilateral scleroma of maxillary sinus.
Oral Manifestations • Site—it is common on lip, soft palate, and tonsil. • Appearance—they appear as proliferative granulomatous lesion of lip, soft palate and tonsil. • Symptoms—there is anesthesia of soft palate, impaired taste, upper lip and uvula enlargement.
Diagnosis • Clinical diagnosis—hebra nose with rhinitis and enlargement of lip, and anesthesia of soft palate will give clue to the diagnosis.
Management • Antibiotics—it should be given to control infection.
• Age and sex—it chiefly affects adult black of either sex, but may occur in any race. • Appearance—lesion begins as a small papule that ulcerates, increases in size and eventually gives rise to velvety, beefy, granulating and spreading ulcerative lesion of inguinal and anogenital region. • Pseudo-bubo—inguinal ulceration is commonly secondary to the genital lesion and arises initially as fluctuant swelling known as pseudo-bubo. • Metastasis—metastatic spread to bone and soft subcutaneous tissue has been reported.
Oral Manifestations • Cause—oral lesion appears to be the most common extragenital form of granuloma inguinale. Oral lesions occur either as a result of autoinoculation through infected fingers or through oral coitus. • Site—it is most commonly found on lips, buccal mucosa or palate or they may diffusely involve the mucosal surface • Lip—lesions of lip are characterized by extensive superficial ulceration with well defined elevated, granulomatous margins. • Multiple sinus—long standing lesion is associated with multiple extraoral sinuses. • Types—may be of three types, i.e. ulcerative, exuberant and cicatricial. • Ulcerative—it is painful, extensive with punched out appearance. It has got smooth red base with tendency of bleeding from the lesion. • Exuberant—it appears as proliferative granular mass. The surface of the lesion is rough due to projection. It has got sharp border and lesion are multiple. The mucous membrane is inflamed and edematous. • Cicatricial—fibrous scar formation may become extensive in nature.
Diagnosis • Clinical diagnosis—ulcerative lesion in the oral cavity which can be multiple and exuberant in variety, will give clue to the diagnosis.
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• Laboratory diagnosis—Donovan bodies present in smears which are recognized as large, gram negative oval bacteria with intense bipolar staining (safetypin appearance). There is granulation tissue with infiltration of polymorphonuclear leukocytes and plasma cells.
regional lymphadenopathy are commonly associated symptoms. • Lymph nodes—cervical lymphadenopathy is present. Skin covering the swollen nodes is violaceous and indurated usually with one or more draining sinuses.
Management
Diagnosis
• Antibiotics—azithromycin is the drug of choice. It should give intermittently. Treatment should continue until healing is complete which usually takes 2-3 weeks. • Wound debridement—in chronic cases, wound debridment followed by antibiotics therapy is helpful. • Plastic surgery—plastic surgery is needed for correction of extensive scarring.
• Clinical diagnosis—groove signs with tongue enlargement with scarring will give clue to the diagnosis. • Laboratory diagnosis—lymph nodes biopsy will show minute intracellular cocci.
Lymphogranuloma Venereum It is a venereal disease caused by one of the three strains of Chlamydia trachomatis.
Management • Antibiotic therapy—it consists of macrolides, tetracycline, and fluoroquinolones. • Surgical management—surgical treatment of bubos and secondary scarring.
Clinical Features
Myiasis
• Incubation period—incubation period is 10 days. • Symptoms—there may be fever, chills, headache and malaise. • Signs—it persists as firm, tender enlargement of inguinal lymph nodes. Nodes are tender and adherent to the underlying tissues. • Groove sign—enlargement of lymph nodes both above and below the inguinal ligament, is characteristic feature called as ‘groove sign’. • Overlying skin—overlying skin becomes reddened and dusky and multiple purulent fistulae develop over enlarged glands. • Females—in females, placenta is frequently involved. Marked scarring and local edema frequently develops secondary to suppurative lymphadenitis.
It is referred to the invasion of living tissues by the larvae of certain species of flies. Myiasis, the term first introduced by Hope (1840), refers to the invasion of living tissues of humans or other mammals by the eggs or larvae (maggots) of Diptera (two winged) flies.
Predisposing Factors • Poor oral hygiene—it has been associated with poor oral hygiene, such as in mouth-breathers, thumb-suckers. • Mentally retarded person—it is common in mentally retarded persons. • Cerebral palsy and hemiplegia—this person cannot maintain normal lip closure or normal level of oral care.
Pathogenesis Oral Manifestations • Causes—results due to orogenital contact or antiinoculation. • Site—tongue is the most common site. • Appearance—lesion consists of small, slightly painful superficial ulceration with non-indurated borders which appear on lip. • Signs—in long standing infection, there is zone of cicatrical refraction, dark red area with loss of superficial epithelium, or opaque lichenoid grayish papules. • Tongue enlargement—tongue may become enlarged with areas of scarring and grooves on its dorsal surface. • Associated symptoms and signs—dysphagia, red soft palate and small red granulomatous lesions accompanied by
• Organism responsible—myiasis is caused by members of the Diptera (two winged fly) family that lay over 100 to 500 eggs at a time—on food, necrotic tissue, open wounds and unbroken skin and mucosa. • Life cycle of larva—the eggs hatch to become maggots in less than 1 week and the life cycle is completed when the maggots turn into flies in about 2 weeks. • Obtaining the nutrition—the larvae obtain their nutrition from the surrounding tissues and burrow deeper into the soft tissues by making tunnels separating the gingiva and mucoperiosteum from the bone. Necrotic tissue, present in advanced periodontal diseases will form a good substrate in which the fly can lay its eggs. The periodontal pockets provide the eggs a warm and moist environment for further development.
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Bacterial Infections 755 Types • Cutaneous or dermal myiasis—it affects skin. • Myiasis of external orifices—it includes nasal, oral, vaginal and anal myiasis. • Myiasis of internal organs—it includes intestinal and urinary myiasis.
Clinical Features • Cutaneous myiasis—it is characterized by papular or migratory lesions. • Symptoms—papular lesions are itchy and occasionally painful. • Open lesions—open lesion may produce serious discharge and larvae may be detected through the opening (Fig. 30-12). • Migratory lesions—migratory lesions are superficial, red tunnel-like lesions, which form creeping eruptions.
4 A
Fig. 30-12: Discharge seen from open lesion in oral myiasis.
Oral Manifestation
B
• Incidence—oral myiasis is a rare condition. • Appearance—it presents as an erythematous, edematous or granulomatous lesion. • Symptoms—itching or pain may be present. • Signs—these lesions may pulsate with movement of larvae. An opening is present from which larvae can come to surface of the lesion (Figs 30.13A and B).
Figs 30.13A and B: Larvae seen in lesion of oral cavity (Courtesy Dr Bhaskar Patle).
Diagnosis • Clinical diagnosis—it is easy to make clinical diagnosing by observing larvae in the lesion.
Management • Irrigation—irrigation of the tissue with hydrogen peroxide will come larvae out the lesion (Fig. 30-14). Treating the defect with ether, mercuric chloride, or turpentine oil, this irritates the parasites forcing them to
Fig. 30-14: Larvae seen in the plate which are removed after patient given hydrogen peroxide (Courtesy Dr Bhaskar Patle).
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come out. Whitehead varnish pack, which contains ether, can be applied to the raw wound for protection during the healing phase. • Surgery—surgical removal of larvae should also be done. • Intestinal myiasis—intestinal myiasis may require purgation with sodium sulphate or antihelminthics.
Suggested Reading
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1. Adekeye EO, Ord RA. Cancrum oris. Principle of management and reconstructive surgery. J Maxillofac Surg 1983;11:160-70. 2. Brightman VI, Guggenheimar IG. Herpetic paronchya- primary herpes infection of finger. J AM Dent Assoc 1970;80:112-5. 3. Chauvin PJ, Ajar AH. Acute herpetic ginginvostomatitis in adults, a review of 13 cases including diagnosis and management. J can Dent Assoc 2002;68:247-51. 4. Chue PWY. Gonorrhea its natural history, oral manifestation, diagnosis, treatment and prevention. JADA 1975;90:1297-1301. 5. Cook TM, Protheroe RT, Handel DM. Tetanus a review of literature. Br J Anesthesia 2001;87:477-87. 6. Edwards MB, Roberts GDD, Storrs TJ. Scleroma (Rhinoscleroma) in Nigerian maxillofacial practice review and case report. Int J Oral Surg 1977;6;270. 7. Eisele DW, Inglis AF, Richardson MA. Noma and noma neonatorum. Ear Nose Throat 1990;5:119-23. 8. Eng HL, Lu SY, et al. Oral tuberculosis. Oral Surg, Oral Med, Oral Pathol 1996;81:415-20. 9. Enwonwu CO, Falker WA jr, et al. Noma (cancrum oris) question and answers. Oral Dis 1999;144-9. 10. Felices RR, Ogbreke Kalu UE. Oral myiasis—report of case and review of management. J. Oral Maxillofac Surg 1996;54:219-20. 11. Ficarra G, Zaragoza AM, et al. Early oral presentation of lues maligna in patient with HIV infection. Oral Surg, Oral Med, Oral Pathol 1993;75:728-32. 12. Flumara NJ. Venereal disease of oral cavity. J Oral Med 1976; 31: 36-40. 13. Giunta JL, Flumara NJ. Facts about gonorrhea and dentistry. Oral Surg, Oral Med, Oral Pathol 1986;62:529-31. 14. Gomez RS, Perdigao PF, et al. Oral myiasis by screwworm Cochliomyia hominivorax. Br J Oral and Maxillofac Surg 2003; 41:115-6. 15. Greenberg M, Glick M, Ship J. Burket’s Oral Medicine (11th edn), BC Decker Inc 2008.
16. Greenberg MS, et al. Oral herpes simplex infection in leukemia patient. J AM Dent Assoc 1987;114:483-6. 17. Joseph BK, Savage NW, MacLeod AWG. Cat scratch disease. Case report. Quintessence Int 1999;30:263-5. 18. Khiyani S M, et al. Tubercular ulcer of alveolar mucosa. A case report. Den Dialogue 1986;11(3): 53-5. 19. Lata J, Kapila BK, Agarwal P. Oral myiasis: a case report. Int J Oral Maxillofac Surg 1996;25:455-6. 20. Meyer I, Shklar G. The oral manifestation of acquired syphilis. A study of eighty one case. Oral Surg, Oral Med, Oral Pathol 1967; 23:45-61. 21. Michaud M, Blanchette G, Tomich C. Chronic ulceration of the hard palate: first clinical sign of undiagnosed pulmonary tuberculosis. Oral Surg, Oral Med, Oral Pathol 1984;57:63-7. 22. Miller CS, Cunningham LL, et al. The efficacy of valacyclovir in preventing herpes simplex infection associated with dental procedure. J AM dent Assoc 2004;135:1311-8. 23. Miller M, Haddad AJ. Cervicofacial actinomycosis. Oral Surg, Oral Med, Oral Pathol 1998;85:496-508. 24. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology (2nd edn), Saunders Elsevier, 2004. 25. Phelan JA, Jimenez B, Tompkins DC. Tuberculosis. Dent Clinics North AM 1996;40:327-41. 26. Reichart JR. Facial and oral manifestation in leprosy. An evaluation of seventy cases. Oral Surg, Oral Med, Oral Pathol 1976;41:385-99. 27. Rendall JR, McDougall AC. Reddening of the upper central incisor associated with periapical granuloma in lepromatous leprosy. Br J Oral Surg 1976;13:271-77. 28. Rooney JF, et al. Prevention of ultraviolet light induced herpes labialis by sunscreen. Lancet 1991;338:1419-22. 29. Scaglione F, Demartini G, et al. Optimum treatment of strepto-coccal pharyngitis. Drugs 1997;53:86-97. 30. Scollard DM, Skinsnes OK. Oropharyngeal leprosy in art, history and medicine. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1999;87:463-70. 31. Scully C, Cawson RA. Medical problems in dentistry (5th edn). Churchill Livingstone an imprint of Elsevier, 2005. 32. Siegel MA. Syphilis and gonorrhea. Dent Clinics North AM 1996;40:369-83. 33. Spruance SL, Rea TL, et al. Penciclovir cream for the treatment of herpes simplex labialis, a randomized multicentric, double bind placebo control trial. JAMA 1997;277:1374-9. 34. Weir JC, Buck WH. Periapical actinomycosis. Report of case and review of literature. Oral Surg, Oral Med, Oral Pathol 1982;54:336-40. 35. Woo SB, Lee SF. Oral recrudescent herpes simplex infection. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1997;83:239-43.
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Viral Infections 757
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Viral Infections
Definition Viruses have been defined as submicroscopic entities which reproduce within the specific living cells. Virus may contain either ribonucleic acid (RNA) or deoxyribonucleic acid (DNA).
Classification RNA Virus Orthomyxovirus • Influenza Paramyxovirus • Measles (rubeola) • Mumps Rhabdovirus • Rabies • Hemorrhagic fever Arenavirus • Lymphocytic choriomeningitis • Lassa fever Calicivirus Coronavirus • Upper respiratory infection Bunyavirus Picornavirus • Poliomyelitis • Coxsackie diseases • Common cold • Foot and mouth disease • Encephalomyocarditis Reovirus Togavirus • Rubella • Yellow fever • St. Louis encephalitis Retrovirus
DNA Virus Herpes virus • Herpes simplex I (herpes stomatitis and herpes labialis) or HHV 1 • Herpes simplex II (genital lesion) or HHV 2 • Herpes zoster (chicken pox and shingles) or HHV 3 • Epstein-Barr virus (EBV) (infectious mononucleosis, hepatitis, oral hairy leukoplakia and nasopharyngeal carcinoma) or HHV 4 • Cytomegalovirus (infectious mononucleosis, hepatitis) or HHV 5 • Human herpes virus –6 (roseola infantum, otitis media, encephalitis) or • Human herpes virus -7 (roseola infantum) • Human herpes virus -8 (infectious mononucleosis, febrile exanthema, Kaposi’s sarcoma) • Simian herpes virus B (mucocutaneous lesions, encephalitis) Pox virus • Small pox • Molluscum contagiosum Adenovirus • Pharyngoconjunctival fever • Epidemic keratoconjunctivitis Parvovirus Iridovirus Papovavirus • Human warts or papillomas • Tumorigenic virus in animals
Infections Caused by Viruses Herpes Simplex Infection HSV is ubiquitous virus. It is the most common viral disease affecting men. Initial infection may be acquired from eyes, skin and mucosa with infected secretion. After acquiring
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the infection, all herpes viruses remain latent in host neural cells, thereby evading host immune response.
Epidemiology
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• HSV I—this virus mainly affect the region above the waist. • HSV II—in this case, infection occurs below the waist usually in the genital lesion. But nowadays due to increased oral sex, HSV II is found in the oral lesions. Both HSV I and II can be transmitted sexually. • Occurrence—it occurs in early childhood. Preschool period is more prone due to frequent exchange of salivary and nasal secretions.
•
•
Pathogenesis Oral Herpes • Primary infection—the virus enters the skin or mucous membrane and reproduces. During this stage, oral signs and symptoms, such as fever, may develop. The virus may cause asymptomatic infections. Asymptomatic infection occurs twice as often as symptomatic disease. • Latency—from the infected site, the virus moves to nerves in the region. There the virus reproduces and becomes inactive. • Recurrence—during certain stresses, emotional or physical, the virus may reactivate and cause new signs and symptoms.
Types • Herpetic genitalis—it is caused by HSV-II and is common in uterine cervix, vagina, vulva and penis. Lesions are more likely to occur on well keratinized areas such as shaft of penis but may progress, more or less rapidly, into superficial erosions that are very painful when touched or contaminated with urine. Urethra may be involved and extremely painful dysuria may develop, especially in women. Regional lymphadenopathy, fever, malaise and anorexia may develop. • Genital herpes in HIV patients—the lesion of genital herpes in immunocompromised patients and HIV infected patients are larger, deeper and are likely to persist and release of virus for periods as long as 30 days. Antibodies to the virus develop 4 to 6 weeks after primary infection. • Herpetic meningoencephalitis—this is serious form characterized by sudden fever and symptoms of increased intracranial pressure. Paralysis of various muscle groups with convulsion and even death may occur. • Herpetic conjunctivitis—swelling and congestion of palpebral conjunctiva, keratitis and corneal ulceration. Recurrent lesions can lead to serious corneal scarring, which may produce blindness. • Herpetic eczema (Kaposi varicelliform eruption)—it is epidermal form of herpetic infections superimposed
• •
upon a pre-existing eczema and is characterized by diffuse vesicular lesions of skin. The patient usually exhibits a high fever coincident with typical umblicated vesicles as well as other systemic manifestation. Disseminated herpes simplex infection of newborn—it is uncommon and they acquired it during passage through the birth canal of mother suffering from herpetic vulvovaginitis. The newborns exhibit a wide variety of signs and symptoms of the disease and with few exceptions; die on the ninth or twelfth day of life. Herpetic whitlow—this is the infection of finger by herpes virus through the break in the skin. Dentist may experience primary lesion of fingers from contact with lesions of the mouth or saliva of the patients who are asymptomatic carriers of HSV; called as ‘herpetic whitlow’. Herpes gladiatorum or Scrumpox—infection of skin spreads through the sport of wrestling. Oral infection—in the oral cavity, there may be primary infection (person who is without circulating antibodies) and recurrent infection (circulating antibodies are already present).
Primary Herpes Simplex Infection It is also called as ‘acute herpetic gingivo-stomatitis’, ‘herpes labialis’, ‘fever blister’, ‘cold sore’ and ‘infectious stomatitis’. It occurs in patients with no prior infection with HSV-1. HSV reaches nerve ganglion supplying the affected area, presumably along nerve pathways and remains latent until reactivated. The usual ganglion involved is the trigeminal for HSV-1 and lumbosacral, for HSV-2.
Transmission • Close contact—it occurs during close personal contact, in which exchange of saliva or other secretion happened. • Newborn infection—primary infection of newborn is believed to be caused by vaginal secretions during birth, which results in viremia and disseminated infection of brain, liver, adrenals and lungs. • Socioeconomic status—incidence varies according to socioeconomic group. Person who is having lower economic status will have earlier exposure.
Clinical Features • Age—it develops in both, children and young adults. It can be seen in high school and college students where it is transmitted by kissing and sexual contact. • Incubation period—incubation period is 5 to 7 days. • Prodormal symptoms—prodormal symptoms precede local lesion by 1 to 2 days and it includes fever, headache, malaise, nausea, vomiting and within a few days, mouth
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Viral Infections 759 becomes painful. There is also irritability, pain upon swallowing and regional lymphadenopathy. • Location—this lesion mainly occurs on the hard palate, attached gingiva and dorsum of tongue. In some cases, lesion may be presented on the skin (Fig. 31-1).
• Lips—in severe cases, excoriation involving the lips (Fig. 31-3) may become hemorrhagic (Fig. 31-4) and matted with serosanguinous fibrin-like exudate and parting of the lips during mastication and speech may become extremely painful and difficult.
4 Fig. 31-1: Showing skin lesion of herpes infection (Courtesy Dr Sanjay Pincha).
• Appearance—after this, small vesicles, which are thin walled, surrounded by inflammatory base are formed (Fig. 31-2). They quickly rupture leaving small, shallow, oval shaped discrete ulcers. • Size—the individual ulcer differs in size from 2-6 mm. As the disease progresses, several lesions may coalesce, forming larger, irregular lesions. • Base—the base of the ulcer is covered with grayish white or yellow plaque. • Margins—the margins of the sloughed lesions are uneven and are accentuated by bright red rimmed, well demarcated, inflammatory halos.
Fig. 31-3: Lip lesion seen along with marginal gingivitis (Courtesy Dr Chole).
Fig. 31-4: Excoriation of lip with hemorrhagic lesion seen in herpes infection.
Fig. 31-2: Intact vesicle seen in herpes simplex infection which is thin walled (Courtesy Dr Chole).
• Acute marginal gingivitis—appearance of generalized marginal acute gingivitis is typical feature of herpes simplex infection. Entire gingiva is edematous and swollen and small gingival ulcers are seen (Fig. 31-5). • Pharynx—examination of posterior pharynx reveals inflammation causing difficulty in swallowing. • Lymph nodes—cervical and submandibular lymphadenopathy is present.
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A Fig. 31-5: Acute marginal gingivitis present in the case of herpes simplex infection (Courtesy Dr Chole).
• Healing—the disease is self limiting and lesions begin healing in a week to 10 days and leave no scar. • Herpes simplex infection of adults—it is seen in patients who do not acquire HSV infection and immunity during childhood. In such cases, primary herpes simplex infection is often acquired via new sexual partner and primary HSV gingivostomatitis and pharyngitis can occur. It occurs usually due to HSV I (Figs 31-6A and B) • Histopathological finding—Lipschutz bodies can be seen in HSV infection. In cytologic study, there is presence of multinucleated giant cells, and ballooning degeneration of cells.
Recurrent or Secondary Herpetic Infection In some cases, HSV may be remain latent in epithelium which is the main cause of recurrent infection with HSV. In this case, HSV reactivated at the latent site it moves centrally to the mucosa. When reactivation is triggered, they spread along the nerves to different sites on oral mucosa and skin, destroy the epithelial cells and induce the typical inflammatory response with characteristic lesions of recurrent infection.
B Figs 31-6A and B: Primary infection occurring in adult patient. (A) Ulcer seen with acute marginal gingivitis and (B) Large ulcer seen on the tongue.
•
•
Types
reason for this is herpes virus remain latent in trigeminal ganglion. Immunity—low serum IgA, decreased cell mediated immunity, decreased anti-herpes activity and depression of ADCC (antibody dependent cellular cytotoxicity) and interleukin-2, caused by prostaglandin release in skin can precipitate the attacks. Trauma—trauma to lips, dental extraction can lead to recurrent infection. Infection—in some cases, upper respiratory tract infection can trigger the herpes infection. Others—fever, emotional upset, sunburns, fatigue, menstruation, pregnancy and allergy can be some precipitating factors for herpes infection.
• Recurrent herpes labialis (RHL)—If it occurs on lip, it is called as recurrent herpes labialis. • Recurrent intraoral herpes simplex infection (RIH)—If occurs intraorally it is called as recurrent intraoral herpes infection.
•
Precipitating Factors
Clinical Features
• Surgery—when any surgery which involve trigeminal ganglion, recurrent infection with herpes can occur. The
• Occurrence—recurrent herpes simplex infection may occur at widely varying intervals, from nearly every
•
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Viral Infections 761 month in some patients to only about once a year or even less in others. • Prodormal symptoms—in either location, lesion is preceded by tingling and burning sensation and feeling of tautness, swelling or slight soreness subsequent development of vesicle. • Signs—it is accompanied by edema at the site of the lesion, followed by formation of clusters of small vesicles. • Recurrent herpes labialis—these gray or white vesicles rupture quickly leaving small red ulcerations, sometimes with slightly erythematous halo on lip covered by brownish crust on lips (Fig. 31-7). Sizes range from 1 to 3 mm in diameter, to 1 to 2 cm. But sometimes, it is large enough to cause disfigurement (Fig. 31-8).
small vesicles or ulcers 1 to 2 mm in diameter are commonly found on gingivae, tongue (Fig. 31-9) palate and alveolar region.
4 Fig. 31-9: Recurrent intraoral, herpes infection seen on the tongue (Courtesy Dr Amit Parate).
• Healing—the lesions gradually heal within 7-10 days and leave no scars. • Complication—herpes simplex infection can lead to development of extra-genital lesions, CNS complications and vaginal fungal super infections.
HSV in Immunocompromised Patient Fig. 31-7: Recurrent herpes labialis showing vesicle of the lip (Courtesy Dr Amit Parate).
Fig. 31-8: Extensive lesion of herpes labialis showing disfigurement (Courtesy Dr Amit Parate).
• Recurrent intraoral herpes—in recurrent intraoral herpes (RIH) vesicles break rapidly to form small red ulceration, sometimes with slight erythematous halo. Cluster of
It is described in Chapter 35: AIDS.
Diagnosis • History—negative past history of recurrent herpes labialis and a positive history of close contact with a patient with primary or recurrent herpes is helpful in making the diagnosis. • Typical clinical features—patient is easily diagnosed as having primary herpetic gingivostomatitis; if he/she presents with typical clinical features of generalized symptoms followed by eruption of oral vesicles and acute marginal gingivitis and does not have history of recurrent herpes. • HSV isolation—isolation and neutralization of virus in tissue culture is most positive method of identification. Rabbit kidney and human amnion are sensitive to HSV. • Antibody titer—antibodies to HSV appear in a week and react peak in 3 weeks.
Differential Diagnosis • Hand-foot and mouth disease—in this case, lesion are not clustered and gingiva is not affected. Lesions can also be seen on feet and hand.
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• Herpangina—oropharyngeal and soft palate involvement is more prominent. It affects children in late summer and early monsoon season on soft palate and facial area with fever and malaise. • Chronic recurring aphthae—no stomatitis, no general systemic symptoms and lesions are less numerous and more often found in adults. • Herpes zoster—segmental distribution along the anatomical location of nerve. • Erythema multiforme—it occurs in young adults, as compared to herpes simplex which occurs in children. Gingivitis is not severe and generally limited to anterior part of the mouth. In erythema multiforme skin lesions are present. • Bullous lichen planus—it is painful condition characterized by large blister on tongue and cheek with rupture and it undergo ulceration. • Cheilitis granulomatous—edema appears suddenly without prodormal symptoms and recurrence is absent. • Benign mucosal pemphigoid—no prodormal symptoms; with progression from erythema to swelling to blister to crusting. • Allergic contact dermatitis—sudden appearance with allergen proof.
Management Primary herpes simplex infection Symptomatic • Pain control measures—topical anesthetics like 2% lidocaine, 0.1% diclonine hydrochloride, 0.5% benzocaine hydrochloride are used. Solution of diphenylhydramine hydrochloride (Benadryl) 5 mg mixed with equal amount of milk of magnesia can also reduce the pain. In some cases systemic administration of analgesics is also given. • Topical anti-infective agents—it is given to prevent secondary infection. Agents used are 0.2% chlorhexidine gluconate, tetracycline mouth wash and elixir or diphenylhydramine. • Supportive care—fluid is given to maintain proper hydration and electrolyte balance. Antipyretics can also be given to control the fever. • Good oral hygiene—oral hygiene should be properly maintained to avoid any secondary infection. Specific • Acyclovir—it inhibits DNA replication in HSV infected cells reducing the duration of illness but with few side effects. The optimum oral dosage of acyclovir is 1,000 to 1600 mg daily, for 7 to 10 days. It should be ideally given in a dose of 15 mg/kg five times a day. • Valacyclovir—it is prodrug of acyclovir and it has far better biocompatibility as compared to acyclovir. It should be used in combination with famciclovir.
Recurrent herpes simplex infection • Minimized obvious trigger—recurrent infection can be suppressed by reducing trigger factors. This can be done by applying the sunscreen lotion to lip. • Topical antiviral medication—topical antiviral medication like 5% acyclovir cream, 3% penciclovir cream, 10% docosanol cream are effective. It should be applied three to six times daily. • Topical ammonium chlorides—nowadays, recent formulation of quaternary ammonium chloride, dimethyl carbonal is used and has been marketed. But it is not scientifically proved to effective so its use not recommended. • Systemic antiviral medication—usually Valacyclovir or famciclovir (500-1000 mg three times daily) should be given. • Topical carbon oxolone—it is useful in some cases of herpetic gingivostomatitis.
Varicella Zoster Infection It is an acute disease caused by varicella zoster virus, which is a DNA virus similar to HSV and causes both, primary and recurrent infection. After primary disease is healed, VZV becomes latent in the dorsal root ganglion of spinal nerve or extramedullary ganglion of cranial nerve. VZV becomes reactivated causing lesions of localized herpes zoster. Patients with HIV infection, leukemia and those on immunosuppressive therapy have an increased susceptibility to severe or potentially fatal herpes zoster. Herpes zoster infection can be deep seated and disseminated causing pneumonia, meningocephalitis and hepatitis.
Forms • Chickenpox (Varicella)—it is primary infection with zoster virus. • Shingles (herpes zoster) or zona—it is recurrent infection with zoster virus. It increases with age and occurs in immunocompromised patient. It can be seen in AIDS patient. • Postherpetic neuralgia—it is neuropathic disease resulting from peripheral and central nervous injury by zoster virus. • James Ramsay Hunt syndrome—it is zoster infection of geniculate ganglion.
Chickenpox It is also called as ‘varicella’. It is an acute viral disease occurring in children and most commonly in winter and spring months.
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Viral Infections 763 Clinical Features • Incubation period and mode of transmission—incubation period is two weeks and mode of transmission is by air borne droplet or direct contact with infected persons, with the probable port of entry being respiratory tract. • Age—it is seen in first two decade of life. • Prodromal symptoms—it is characterized by prodromal occurrence of headache, nasopharyngitis and anorexia, followed by maculopapular or vesicular eruptions on skin and low grade fever. • Location—these eruptions usually begin on the trunk and spread to involve the face and extremities. • Onset—there is development of a pruritis, maculopapular rash followed by vesicle. • Dewdrop on rose petal—there is classic presentation of centrally located vesicle surrounded by zone of erythema. This is called as dewdrop on rose petal appearance (Fig. 3110). They occur in successive crops so many vesicles in different stages of formation or resorption may be found. • Healing—the skin eventually ruptures, forming a superficial crust and heals by desquamation. The disease runs its clinical course in a week to ten days, seldom leaving any after effects. • Secondary infection—occasionally, secondary infection of vesicle results in the formation of pustules which may leave small pitting scar upon healing. • Complication—it includes cerebellar ataxia, encephalitis, pneumonia, myocarditis, Reye’s syndrome, sickle cell crisis, hemolytic anemia and hepatitis. • Neonatal chickenpox—this occurs due to infection in pregnancy. This infection may lead to congenital defect in the newborn. • Diagnosis—it is made by virus isolation and typical exanthema present.
• Appearance—the mucosal lesion, initially a slightly raised vesicle with a surrounding erythema, ruptures soon after formation and forms a small eroded ulcer with red margins (Fig. 31-11), closely resembling aphthous lesion.
Fig. 31-11: Intraoral ulceration seen in case of chickenpox infection (Courtesy Dr Sanjay Pincha).
Management • Pain control—patient should be managed with all pain control method which is described in herpes simplex infection. Aspirin is contraindicated as it can lead to Reye’s syndrome. • Control of pruritus—warm baths with soap or baking soda, application of calamine lotion should be done. As VZV is having lipid envelope, it can destroy by soap and detergent. Systemic diphenhydramine is also given to control pruritus. • Antiviral drug—acyclovir should be used in a dose of 800 mg five times daily. It will reduce the severity of lesion. Another antiviral agents use are valacyclovir (1000 mg TDS) and famciclovir (500 mg TDS) for 7 days should be given. • Varicella zoster immune globulin—this is given in case of immunocompromised patient. This will help to reduce severity of clinical manifestation. • Local antiseptic—at the first sign of secondary infection, a local antiseptic should be applied to the skin. If the bacterial infection progresses, appropriate antibiotics should be prescribed. • Prevention by vaccination—live attenuated VZV vaccine should be given in children at 12 and 18 months of age. It should usually combined with MMR (measles, mumps and rubella).
Herpes Zoster Fig. 31-10: Dewdrop like vesicle formation seen on the abdomen of the patient (Courtesy Dr Pincha).
Oral Manifestation • Site—small blister-like lesions occasionally involve the oral mucosa chiefly buccal mucosa, tongue, gingiva, palate as well as the mucosa of pharynx.
It is also called as ‘shingles’ or ‘zona’. It is an acute infectious viral disease of extremely painful and incapacitating nature, characterized by inflammation of dorsal root ganglion, associated with vesicular eruptions of skin and mucous membrane of the area supplied by the affected sensory nerve.
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Predisposing Factors • Trauma—in some cases, trauma in the distribution of trigeminal nerve can lead to herpes zoster infection. • Malignancy—development of malignancy or tumor in the region of dorsal root ganglion can also cause herpes zoster. • Radiation—Local X-ray radiation can also be predisposing factors. • Immunosuppressive therapy—this will lead to reactivation of virus and development of lesion.
Clinical Features
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• Age and sex distribution—it affects adults and there is no sex predilection. • Prodromal symptoms—prodromal period of 2 to 4 days in which shooting pain, paresthesia, burning and tenderness appears along the course of affected nerve. The reason for shooting pain is occurrence of active ganglionitis with resultant neuronal necrosis and severe neuralgia. The pain is present in the area supplied by the affected nerve (dermatome). • Appearance—unilateral vesicles on an erythematous base appear in clusters, chiefly along the course of nerve and giving picture of a single dermatome involvement (Fig. 31-12). This is called as ‘zosteriform’ pattern.
Fig. 31-13: Herpes zoster involving scalp of the patient.
Fig. 31-14: Involvement of ophthalmic division showing involvement of eyes (Courtesy Dr Revent Chole).
• Zoster sine eruptione or zoster sine herpete—it is zoster infection without appearance of dermatomal lesion. • Hutchinson sign—it is cutaneous zoster infection of the side of tip of nose.
Oral Manifestations Fig. 31-12: Intact vesicle seen showing dermatome involvement (Courtesy Dr Pincha).
• Healing—vesicle turns into scab in 1 week and healing takes place in 2 to 3 weeks. • Nerves—nerves commonly affected are C3, T5, L1, L2 and 1st division of trigeminal nerve. It may affect motor nerve. • Involvement of 1st division of trigeminal nerve—involvement of 1st division leads to corneal scarring and blindness (Fig. 31-14) which are presumably related to viral spread, neural damage, vasculitis and inflammatory immune response. 1st division involvement also lead to lesion of scalp (Fig. 31-13).
• Cause of oral lesion—herpes zoster involving 2nd and 3rd divisions of trigeminal nerve lead to oral manifestation. Involvement of 2nd division leads to lesion of midface and upper lip and involvement of 3rd division leads to lesion of lower face and lower lip. • Site—it may be found on buccal mucosa, tongue, uvula, pharynx and larynx. • Symptoms—patient noticed pain, burning, tenderness usually on the palate on one side. • Signs—after several days of symptoms, intact vesicles (Fig. 31-15) appear which soon rupture (Fig. 31-16) to leave areas of erosion (Fig. 31-17).
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Viral Infections 765 • Healing—healing usually takes place within 10 to 14 days (Fig. 31-18).
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Fig. 31-15: Intact vesicle seen on the face by herpes zoster (Courtesy Dr Jitu Sachdeo).
Fig. 31-18: Healed herpes zoster lesion seen on the face (Courtesy Dr Jitu Sachdeo).
• Teeth—trigeminal herpes zoster occurring during tooth formation causes pulpal necrosis and internal root resorption. So in the case of herpes zoster, several nonvital teeth can be seen (Fig. 31-19). In some cases, osteomyelitis can also develop in the patient. Fig. 31-16: Herpes zoster showing ruptured vesicle in the oral cavity.
Fig. 31-19: Multiple non-vital teeth seen 7 years after occurrence herpes zoster (Courtesy Dr Chole).
Diagnosis
Fig. 31-17: Erosion area seen on the palate in case of herpes zoster (Courtesy Dr Chole).
• Clinical diagnosis—lesions along the distribution of nerve will give clue to diagnosis. • Fluorescent antibody testing—in this test, smear is obtained by scraping the lesion and staining it with fluorescent conjugated monoclonal antibody.
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Textbook of Oral Medicine Table 31-1: Difference between herpes zoster and recurrent herpes simplex infection
Herpes zoster
Recurrent herpes simplex infection
Prodromal symptoms—fatigue, hyperesthesia, pain
Prodromal symptoms—tension, burning, itching
Development—edema and erythema, papulovesicular Development—vesiculoerosive lesion in crops and clusters, then vesiculopustular lesions and erosion but not limited to dermatome
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Severe pain
Moderate pain
Lesions limited to the course of a sensory nerve
No skin lesions
Longer course—post-zoster neuralgia
Fast healing without consequence
No recurrence
Recurrent appearance
• PCR—Polymerase chain reaction testing is used to detect viral antigen. • Biopsy—it will show multinucleated giant cells. • Virus isolation—this virus is difficult to culture.
Differential Diagnosis • Recurrent herpes simplex infection—described in Table 31-1. • Herpangina—acute infection, palatal vault is affected.
Etiopathogenesis • Peripheral injury—zoster virus injures the peripheral nerve by demyelination, wallerian degeneration and sclerosis. • Central injury—there is also atrophy of dorsal horn cells in the spinal cord. • Infection—low grade persistent infection of trigeminal ganglion also cause postherpetic neuralgia.
Clinical Features Management • Antiviral drugs—acyclovir 800 mg five times daily which is associated with significantly accelerated healing within 48 hours of the onset of rash. • Symptomatic treatment—antipyretic medication with antipruritics diphenhydramine can be administered to decrease itching. • Prevention of postherpetic neuralgia—intralesional steroids and local anesthetic can be used to decrease healing time and to prevent postherpetic neuralgia. But this comes with many side effects and there are some conflicting reports about the efficiency of steroid in control of postherpetic neuralgia. • Capsaicin—topical capsaicin 0.025% four times a day has been suggested for temporary relief of neuralgia following herpes zoster infection. Capsaicin is derived from red peppers The mechanism of action apparently involves the depletion of substance P in the peripheral sensory neurons causing the skin less sensitive. After treatment patient should wash hand after use and avoid contact with mucosal surface. • Tetracycline rinse—mouth rinsing with tetracycline, three to five times daily, may reduce the pain.
Postherpetic Neuralgia This is complication of zoster infection.
• Age and sex distribution—It affects older age group. Incidence of postherpetic neuralgia is more in women as compared to men. • Symptoms—initially, there is presence of rash which is followed by pain. Pain may continue for weeks to months. If pain occurs more than 6 months of duration is usually called as postherpetic neuralgia. • Other symptoms—there may be paresthesia, hyperesthesia and allodynia. In some cases, there is also presence of sensory deficit.
Management • Prevention—use of live attenuated Varicella zoster vaccine after age of 60 years will reduce the incidence of postherpetic neuralgia. To control postherpetic neuralgia, antiviral drug should be given in early course of disease. • Topical therapy—use of topical agents like lidocaine (anesthetics), capsaicin (an extract of hot chili peppers that depletes the neurotransmitter substance P) should be used. • Drug therapy—the use of TCA (tricyclic antidepressant) like Amitriptyline, nortriptyline, doxepin and desipramine have been used to minimize painful sequelae of this infection. The patient who cannot tolerate TCA due to cardiovascular side effect, the other drug gabapentin and pregabalin should be given. Carbamazepine or phenytoin can also be given to minimize the pain.
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Viral Infections 767 • Surgery—when drug therapy is ineffective then surgery should be carried out at the level of peripheral nerve or dorsal root is indicated. In some cases, sympathetic nerve block is also effective. • Steroid therapy—steroid injection can be given in a patient with age more than 60 years, for the treatment of postherpetic neuralgia. This will help in reducing the pain of the patient.
James Ramsay Hunt Syndrome It is zoster infection of geniculate ganglion with involvement of the external ear and oral mucosa. The clinical manifestation of it is facial paralysis as well as pain of the external auditory meatus and pinna of the ear. In addition, vesicular eruption occurs in the oral cavity and oropharynx with hoarseness of voice, tinnitus, vertigo and occasional other disturbances.
Oral Manifestations • Onset—oral lesions precede 2 to 3 days before cutaneous rash and are pathognomonic of this disease. • Site—the most common site is on buccal mucosa. • Koplik’s spots—intraoral lesions are called as Koplik’s spots and occur in 97% of cases (Fig. 31-20). They are small, irregularly shaped flecks which appear as bluish white specks surrounded by bright red margins. They are described as ‘grains of salt’ on red background. • Other features—there is generalized inflammation, congestion, swelling and focal ulceration of gingiva, palate, and throat may occur.
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Mumps It is described in Chapter 26: Salivary Gland Disorders.
Measles It is also called as ‘Rubeola’ or ‘morbilli’. It is an acute contagious dermatotropic viral infection, primarily affecting children and occurs many times in epidemic form.
Fig. 31-20: Bluish white numerous Koplik spots seen in measles.
Diagnosis
Transmission • Droplet infection—spread of disease occurs by direct contact with a person or by droplet infection, the portal of entry being the respiratory tract.
Clinical Features • Incubation period—incubation period is 8 to 10 days. • Prodromal symptoms—onset of fever, malaise, cough and coryza (running nose). • Eye lesion—there is conjunctivitis, photophobia, lacrimation occurs. • Skin lesion—skin eruption begins on face, in the hair line and behind the ear and spread to neck, chest, back and extremities. They appears as tiny red macules or papules which enlarge and coalesce to form blotchy discolored irregular lesions, which blanch on pressure. Skin lesions fade away in 4 to 5 days with fine desquamation. • Complication—it is the disease which lowers general body resistance and for this, it often leads to complications. Complications include bronchial asthma, encephalitis, otitis media, noma, and Hodgkin’s lymphoma.
• Clinical diagnosis—typical clinical features like Koplik spots and history are important diagnostic criteria for measles. • Laboratory diagnosis—it is done by virus isolation and raised antibody titers. Antibodies appear after 3 days of rash.
Differential Diagnosis • Small pox—high fever, monoform exanthema. • Chickenpox—typical exanthema that follows the intraoral lesion. The diagnosis can be established microscopically (blister swab) and virologically.
Management • Vaccination—best treatment for the measles is vaccination. The widely used vaccine is MMR. One injection of live, attenuated measles virus should be given subcutaneously in children over one year. Second dose of vaccine is given in 12 to 15 months. • Passive immunization—human immunoglobulin given intramuscularly is recommended for the prevention and attenuation of measles, particularly for contact under
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18 months of age and for debilitated children. The dose is 250 mg for children under 1 year and 500 mg for those over this age. • Isolation of patient—the patient should be isolated, if possible. • Symptomatic treatment—analgesic, anti-pyretic should be given to patient to control pain and fever. • Specific drug treatment—no drug has shown any promising results in the management of measles. Drugs which are tried are ribavirin, interferon, immunoglobulin and vitamin A.
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Rubella (German Measles) Rubella it produced by Togavirus. It is milder infection as compared to measles.
Transmission • Droplet infection—it is transmitted through droplet infection in individual who is living in close living condition. • In utero—infants with congenital infection may be present. It may result in birth defect. Infant born with rubella is called as congenital rubella syndrome (CRS).
Clinical Features • Incubation period—incubation time is 14 to 21 days. • Prodromal symptoms—it includes fever, headache, malaise, anorexia, conjunctivitis, coryza, cough and pharyngitis. • Lymphadenopathy—it is seen in suboccipital, postauricular, and cervical chains. • Complication—it includes arthritis, encephalitis and thrombocytopenia. • Rash—the exanthematous rash seen on face and neck. It is discrete pink macule and it fades as it spreads. • Congenital rubella syndrome—it results in deafness, heart disease and cataracts.
Oral Manifestation • Forschheimer’s sign—small, discrete, dark red papules seen on soft palate. • Petechiae—petechiae can also be seen on the palate.
Diagnosis • Clinical diagnosis—it is very difficult to establish clinical diagnosis as clinical presentation is mild and subclinical. • Laboratory—serological analysis should be carried out to establish diagnosis.
Management • Vaccination—this has dramatic results after vaccine was released in 1969. • Human rubella immunoglobulin—it is administered to have passive immunity. If it is given within days after the exposure, it will decrease the severity of infection.
Coxsackievirus Infection They are RNA retroviruses and are named after town in upper New York where they were first discovered. They are divided into 2 groups: • Type A—24 types • Type B—6 types These viruses can cause hepatitis, meningitis, myocarditis, pericarditis and respiratory disease. Three clinical types of infection are important and discuss below. These diseases occur more frequently from June to October (summer and early fall).
Transmission • Fecal oral route—it is major path of transmission. Frequent hand washing will diminish the spread of this virus. • Saliva—virus can spread through saliva during acute condition. • Predisposing factors—overcrowding, poor oral hygiene may aid to infection.
Herpangina It is also called as ‘aphthous pharyngitis’, ‘vesicular pharyngitis’. A4 causes majority of the cases. A4 to A10 and A16 to A22 have also been implicated.
Clinical Features • Age—majority affected are young children aged 3 to 10 years. • Incubation period—incubation period is of 2 to 10 days. • Site—it occur on posterior pharynx, tonsil, faucial pillars and soft palate. • Prodromal symptoms—initially, generalized symptoms of fever, chills, headache, anorexia, prostration, abdominal pain and sometimes vomiting. Sore throat, dysphagia and occasionally, sore mouth can occur. • Ulceration—lesion starts as punctate macule which evolves into papules and vesicles (Fig. 31-21). Within 24 to 48 hours, vesicles get ruptured forming small 1 to 2 mm ulcers. • Base and margins—ulcers show a gray base and inflamed periphery. • Healing—they generally heal without treatment in 1 week.
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Viral Infections 769 • Appearance—oral lesions are more extensive than herpangina. The tongue may become red and edematous. Clinical manifestations last for 3 to 7days.
Diagnosis • Clinical diagnosis—oral lesion in association with skin lesion will aid to diagnosis.
Differential Diagnosis
Fig. 31-21: Ulceration seen on posterior part of oral cavity in case of herpangina.
Diagnosis • Clinical diagnosis—lesions are seen posterior part of oral mucosa.
Differential Diagnosis • Primary herpes simplex infection—herpangina occur in epidemic, and HSV does not. Clinical manifestations of herpangina are generally milder than HSV infection. Lesions of herpangina occur in pharynx and posterior portions of oral mucosa and in case of herpes simplex infection, it occur in anterior part of oral cavity. Herpangina does not cause generalized acute, marginal gingivitis which is typical feature of herpes simplex infection. • Herpes zoster—in this, segmental distribution of vesicle is seen which is absent in case of herpangina.
Hand-Foot-and-Mouth Disease It is caused by A16, A5, A7, A9, A10, B2 and B5.
Clinical Features • Age—it primarily affects children between the age of 6 months and 5 years. • Symptoms—there is anorexia, low grade fever, diarrhea, nausea and vomiting. • Appearance—it is characterized by appearance of maculopapular, exanthematous and vesicular lesions of skin, particularly involving the hands, feet, legs, arms and occasionally buttocks.
Oral Manifestations • Sites—the most common sites for oral lesions are hard palate, tongue and buccal mucosa. • Symptoms—a sore mouth with refusal to eat is one of the most common findings in this disease.
• Herpetic ginginvostomatitis—entire oral cavity is affected. No hand and feet involvement. • Varicella zoster infection—segmental distribution along the anatomical location of nerve (unilateral lesions). • Herpangina—affect children mostly in late summer and early monsoon and lesions are common on soft palate and facial area with fever and malaise. • Allergic stomatitis—sudden appearance, no prodromal symptoms with itching and noticeable erythema. • Chickenpox—in addition to intraoral changes, polymorphous exanthema on the entire body and severe lesions.
Acute Lymphonodular Pharyngitis It is caused by A10 and is same as herpangina. Yellow-white nodules appear that do not progress to vesicles or ulcers. It is self limiting and only supportive care is indicated.
Clinical Features • Age—the disease affects predominantly children and young adults, occasionally older adults can also be affected. • Site—the lesion appears on uvula, soft palate, anterior pillars and posterior oropharynx. • Incubation period—it has got 5 days incubation period and course may run for 4 to 14 days, with local oral lesions resolving within 6 to 10 days. • Symptoms—the chief complain is of sore throat, 41o C temperature, mild headache, anorexia and loss of apetite. • Appearance—it consists of raised, discrete, and whitish to yellowish solid papules of 3 to 6 mm in diameter, surrounded by narrow well defined zone of erythema. • Signs—lesion is non-vascular, non-ulcerated, tender, superficial and bilateral.
Diagnosis • Clinical diagnosis—whitish nodule with sore throat can lead to diagnosis.
Management • Symptomatic treatment—no specific treatment is necessary since the disease is self limiting and generally
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regresses within one to two weeks. Symptomatic treatment directed towards giving anti-pyretic and topical anesthetics. • Nutritional supplement—as eating and swallowing is difficult, patient should be given proper hydration.
Infectious Mononucleosis
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It is also called as ‘glandular fever’ or ‘mono’. It is a benign acute infectious disease caused due to the Epstein-Barr virus, a herpes virus which infects the B-lymphocytes. It is commonly seen in adolescents and young adults. The mechanism of human transmission is not entirely known but one important mean is thought to be through deep kissing so this condition is also called as ‘kissing disease’. EBV is present in oropharyngeal secretions and mixed saliva during active phase.
Clinical Features • Incubation period—it varies from 10 to 40 days. • Age—disease occurs chiefly in children and young adult in 4 to 15 age groups. • Symptoms—the patient usually complaint of sore throat accompanied by fever usually 101°F to 103°F and extreme fatigability. Occasionally, there is a complaint of headache, photophobia, nausea, vomiting, diarrhea and presence of erythematous macular rash (Morbilliform skin rash). • Signs—physical examination reveals enlarged palatine tonsils with copious amount of cheesy yellow exudate filling tonsillar crypt. Patient may also be having splenomegaly and hepatomegaly. • Lymphadenopathy—enlargement of the superficial lymph nodes, particularly the posterior cervical are common manifestations. Lymph nodes are slightly tender on palpation. • Chronic fatigue syndrome—this is controversial whether this is associated with EBV infection. In this, patient noticed chronic fatigue, fever, pharyngitis, myalgia, headache, arthralgia, paresthesia, depression and cognitive defect. • Complications—airway obstruction, splenic rupture, progressive neurological involvement and hemolytic anemia. • Hematological finding—there is an increase in white blood cell count.
Oral Manifestations • Site—lesion present on soft palate, labial and buccal mucosa. • Petechiae—it can be seen on soft palate (Fig. 31-22). They are transient.
Fig. 31-22: Multiple petechiae seen on soft palate in the patient of infectious mononucleosis.
• Ulcerative gingivitis, periodontitis and stomatitis—ulcerative gingivitis, periodontitis and stomatitis may be present and the lesion normality persisting for 3 to 11 days. • Tonsils—intraorally, the most prominent sign is enlargement and inflammation of the tonsils along with sore throat and difficulty in swallowing. Quite commonly the tonsils are covered by a white or grayish pseudomembrane. • Bleeding—1/3rd of the patients with hemorrhagic tendency exhibit oronasopharyngeal bleeding, including bleeding from gingiva.
Diagnosis • Clinical diagnosis—morbilliform skin rash with enlarged palatine tonsil with fever can aid in diagnosis. • Laboratory diagnosis—there is positive Paul Bunnel (test for detecting EBV antibody) and mono spot test.
Management • Symptomatic—the oral lesion of infectious mononucleosis is treated symptomatically. A topical anesthetic may be used in painful ulcers and hydrogen peroxide rinses aid in ameliorating the fusospirochetal gingivitis. Patient should be given antipyretic and antiinflammatory therapy to control fever and pain. • Antiviral drugs—ganciclovir and Alfa interferon inhibit the replication of Epstein Barr virus in vitro. Alpha interferon reduces EBV replication and shedding in organ transplant patient. • Corticosteroid—corticosteroids are indicated only in the presence of complications like airway obstruction, progressive neurological involvement, hemolytic anemia. Normaly corticosteroid should be avoided. • Precaution—patient should avoid sports as it may lead to splenic rupture.
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Viral Infections 771 Cytomegalovirus Infection This virus is also called as HHV-5. It may be clinically expressed or latent. CMV can remain latent in salivary gland cells, endothelium, macrophages and lymphocytes. Cytomegalovirus (CMV) is a double-stranded DNA virus that is fairly common in the general population, with approximately 60% of people being seropositive but asymptomatic.
Transmission • In utero transmission—infants can acquire it in utero from placenta, during delivery. Infant can also acquire infection through breastfeeding. • Sexual transmission—transmission can also occur through exchange of body fluid like saliva, during sexual activity. • Blood transfusion and organ transplantation—blood and transplanted tissues are also potential means of transmission of virus to susceptible individuals.
• Laboratory diagnosis—characteristic “owl’s eye” appearance of cellular inclusions during the histologic examination.
Clinical Features
Management
• Neonatal infection—features of this infection include hepatosplenomegaly, extramedullary cutaneous erythropoiesis, encephalitis and thrombocytopenia. Encephalitis may lead to mental retardation and motor retardation. • Adult’s infection—there is fever, malaise, myalgia, abnormal liver function. Petechial hemorrhages can also occur. Patient may also suffer from pneumonia, microcephaly, cerebral calcification and hearing defect. • CMV chorioretinitis—this is commonly seen in AIDS patient. This may lead to blindness of patient. • CMV colitis—this will lead to bloody diarrhea.
• Prevention—it should be done by passive immunization with hyperimmune gamma globulin. • Antiviral therapy—no specific antiviral therapy is useful. Foscarnet, ganciclovir and alpha interferon can be used which may yield success in some cases. Intravenous ganciclovir will produce resolution of oral ulceration in most instances.
Oral Manifestations • Salivary gland involvement—this can occur in immunocompetent patient. Patient usually present with acute sialadenitis which can involve major and minor salivary gland. Affected gland is painful. Patient may suffer from xerostomia. • Mucosal ulceration—oral ulcer occur in patient with CMV disease. It is more commonly seen in AIDS patient. • Gingival infection and hyperplasia—patient may suffer from gingivitis and gingival hyperplasia (Fig. 31-23). • Dental significance—susceptible dental personnel may acquire CMV infection in the absence of barrier protection.
Diagnosis • Clinical diagnosis—CMV produces deep, penetrating oral ulcerations on the lips, tongue, pharynx, or any mucosal site.
Fig. 31-23: Gingival infection and ulceration seen in the patient with cytomegalovirus infection.
Foot and Mouth Disease It is also called as ‘aphthous fever’, ‘hoof and mouth disease’, ‘epizootic stomatitis’. It is a viral infection which rarely affects man, but does affect hogs, sheep as well as cattle. Transmission of this disease occurs through infected animals in human beings, it is usually through milk from infected animals. It is manifested by fever, nausea, vomiting, malaise and appearance of ulcerative lesions of oral mucosa and pharynx. There is development of vesicle on skin. In some cases, they occur usually on the palms of hands and soles of feet. Intraorally it can occur at any site, but lips, tongue, palate and oropharynx appear to be affected. These lesions being as small vesicles which rapidly rupture, but heal within two weeks.
Condyloma Acuminatum It is also called as ‘genital wart’, ‘venereal wart’ or ‘verruca acuminata’. It is caused by human papillomavirus (HPV). It can be transmitted from mother to infant, at birth and resulting syndrome is called as juvenile onset respiratory papillomatosis.
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Clinical Features
Clinical Features
• Incubation period—it is about 1 to 3 months from the time of sexual contact. • Locations—it is seen on external genitals, perianal mucosae, and adjacent skin as well as in vaginal and anal canal. Wart growth is favored by moist warm environment of perianal skin and mucosal surface. • Appearance—they are a pink, fleshy papillomatous lesion which proliferate and coalesces rapidly to form diffuse papillomatous clusters of varying sizes.
• Age—it is common in children and some cases may be found in middle age. • Site—skin of hand is common site and in case of oral cavity it is commonly present a vermilion border, labial mucosa and anterior tongue. • Appearance—it appear as papular or nodular growth with papillary projection. The color of cutaneous lesion is pink, yellow, or white and oral lesions are usually white in color (Fig. 31-24). • Surface of lesion—rough and pebbly. • Base—base is pedunculated or sessile. • Keratin horn or cutaneous horn—in some cases, extreme accumulation of keratin will result in hard surface projection. This is called as cutaneous horn or keratin horn.
Oral Manifestations
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• Sites—it may involve gingiva, cheek, lip, hard palate, tongue and floor of mouth. • Appearance—small keratotic warts occurring alone or in clusters on oral mucosa can be seen. • Size—the enlargement may be larger than 1 cm in diameter. • Margins and base—the lesion is sharply delineated and may appear sessile and pedunculated.
Diagnosis • Clinical diagnosis—sessile pink pedunculated growth with history of oral sex is important in clinical diagnosis. • Laboratory diagnosis—virus isolation can be done by staining of viral antigen DNA by hybridization restriction, endonuclease analysis and polymerase chain reaction.
Differential Diagnosis • Focal epithelial hyperplasia—in it, fine granular surface texture and plaque-like shape of enlargement while in case of condyloma, there is cauliflower appearance. Fig. 31-24: Common wart seen on finger (Courtesy Dr Pincha).
Management • Surgical—genital warts are treated by excision, electroor cryosurgery, CO2 laser therapy. • Application of chemical agents—application of chemical agents such as podophyllin, cantharidin and 5-fluorouracil can be given. • Immunomodulating agents—immunomodulating agent such as interferon can also be used in case of condyloma acuminatum.
Verruca Vulgaris (Common Wart) Verruca vulgaris is caused by HPV virus type 2,4,6 and 40. It is transmitted by autoinoculation and develops on other part of the body and skin.
Diagnosis • Clinical diagnosis—keratin horn with pedunculated surface pebbly lesion on hand will diagnose this condition. • Laboratory diagnosis—there is proliferation of hyperkeratotic stratified squamous epithelium which are arranged in finger-like projection. There is also cupping effect.
Management • Cryotherapy—liquid nitrogen cryotherapy is the treatment of choice in this condition. Cryotherapy will induce subepithelial blister which lifts the infected epithelium from the connective tissue allowing it to slough away.
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Viral Infections 773 • Surgical excision—surgical excision is usually carried out in case of oral lesion. • Keratinolytic agents—topical application of keratinolytic agents can also be done.
Molluscum Contagiosum Infection It is caused by molluscum contagiosum virus pox group.
Transmission • Skin contact—it occurs due to intimate skin contact. • Sexual contact—there is marked increase at the time of onset of sexual activity. • Predisposing factors—poverty, overcrowding and poor hygiene are predisposing factors for transmission of virus.
Epstein-Barr Virus (EBV) Infection The prevalence of EBV antibodies increase in adolescence and early adulthood due to increased opportunity for exchange of EBV in saliva, associated with adolescent, social activity. In this group, it is often characterized by a syndrome referred as infectious mononucleosis or ‘kissing’s disease’. EBV may occur as blood borne infection. EBV is associated with: • Infectious mononucleosis (discussed in Chapter 37: Blood Disorders) • Anaplastic nasopharyngeal carcinoma • Burkitt’s lymphoma (discussed in Chapter 37: Blood Disorders) • B cell lymphoma (discussed in Chapter 37: Blood Disorders) • Hairy leukoplakia (discussed in Chapter 35: AIDS).
Clinical Features • Incubation period—incubation period is 14 to 50 days. • Age—it is more common in children and young adults. • Sites—it is more common on skin of inner thigh, lower abdomen or external genitals. Some cases may be seen on lips, tongue and buccal mucosa. • Appearance—it manifests as multiple or isolated discrete elevated nodules, or sometimes papules, with depressed centers, which may be keratinized and are normal or pink in color. • Adjacent area—adjacent area is surrounded by the zone of erythema. • Shape and size—these lesions are hemisphere in shape, usually about 5 mm in diameter. • Number—multiple lesions sometimes numbering 100 can also occur. • Healing—it is self limiting and regresses spontaneously within 1 to 2 months.
Diagnosis • Clinical diagnosis—discrete nodule with depressed center is typical of this disease. • Laboratory diagnosis—it shows large eosinophilic intracytoplasmic inclusion bodies known as HendersonPaterson inclusion or simply Molluscum bodies, measuring approximately 25 microns in diameter in the biopsy.
Management • Surgical therapy—it includes curettage, followed by local cautery, cryotherapy. • Topical therapy—topical application of caustic acid and irritants such as phenol, TCA, podophyllin and cantharidin.
Smallpox It is also called as ‘variola’. On December 9, 1979, the WHO global commission for the certification of smallpox declared that smallpox eradication has been achieved throughout the world. Thus, there has been for the first time in history that a disease was totally eliminated from this planet. Previously this disease manifested as occurrence of high fever, nausea, vomiting, chills and headache. The patient is extremely ill and may become comatose during this period. Orally there is ulceration of oral mucosa and pharynx is common. Multiple vesicles appear and rupture to form ulcers of non-specific nature. Immunization is essential in the early period of life.
Chikungunya Chikungunya is a relatively rare form of viral fever caused by an alpha virus that is spread by mosquito bites from the Aedes Aegypti mosquito, though recent search by the Pasteur Institute in Paris claims the virus has suffered a mutation that enables it to be transmitted by Aedes Albopictus (Tiger mosquito). Chikungunya is closely related to O’nyong’nyong virus. The disease was first described by Marion Robinson and W.H.R. Lumbsden in 1955, following an outbreak on the Makonde Plateau, along the border between Tanganyika and Mozambique, in 1952. Chikungunya is not considered to be fatal. However, in 2005-2006, 200 deaths have been associated with this disease on Reunion Island and a widespread outbreak in southern India. Tamilnadu reported the largest no. of cases as of July 2006, specifically in Madurai and Tirunelveli.
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Clinical Features
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• Symptoms—it includes fever which can reach 39 degree Celsius. Fever lasts for 2 days and comes down. There is petechial or maculopapular rash usually involving the limbs and trunk, and arthralgia or arthritis affecting multiple joints which can be debilitating. • Other symptoms—there can also be headache, conjunctival infection and slight photophobia. • Persistent symptoms—however, joints pain, intense headache, insomnia and extreme degree of prostration lasts for about 5-7 days. • Dermatological manifestation—it includes maculopapular rash, nasal blotchy erythema, lymphoedema over acral area, multiple ecchymotic spots, vesiculobullous lesions, sublingual hemorrhage, photo urticaria and acral urticaria • Oral manifestation—lichenoid eruptions, aphthous ulcers (Fig. 31-25), freckle pigmentation over facial area.
Fig. 31-25: Aphthous type ulceration seen in Chikungunya patient.
Management • There is not any treatment available for this disease. Only symptomatic treatment in the form of analgesics can be given.
Suggested Reading 1. Barrett AP, Katelaris CH, et al. Zoster sine herpete of trigeminal nerve. Oral Surg, Oral Med, Oral Pathol 1993;75:173-5. 2. Brightman VI, Guggenheimar IG. Herpetic paronchya—primary herpes infection of finger. J AM Dent Assoc 1970;80:112-5. 3. Buchner A. Hand Foot and mouth disease. Oral Surg, Oral Med, Oral Pathol 1976;41:333-7. 4. Chauvin PJ, Ajar AH. Acute herpetic ginginvostomatitis in adults, a review of 13 cases including diagnosis and management. J Can Dent Assoc 2002;68:247-51. 5. Cohen SG, Greenberg MS. Chronic oral herpes simplex virus infection in immunocompromised patients. Oral Surg, Oral Med, Oral Pathol 1985;59:465-71. 6. Courant P, Sobkov T. Oral manifestation of infectious mononucleosis. J Periodontal 1979;40:279-83.
7. Epstein JB, Scully C. Cytomegalovirus: a virus of increasing relevance to oral medicine and pathology. J Oral Pathol Med 1993;22:348-53. 8. Epstein JB, Sherlock CH, Wolber RA. Oral manifestation of cytomegalovirus infection. Oral Surg, Oral Med, Oral Pathol 1993;75:443-51. 9. Frase-Moodie W. Oral lesion in infectious mononucleosis. Oral Surg, Oral Med, Oral Pathol 1959;12:685-91. 10. Green TL, Eversole LR, Leider AS. Oral and labila Verruca vulgaris, clinical, histological and Immunohistochemical evaluation. Oral Surg, Oral Med, Oral Pathol 1986;62:410-6. 11. Greenberg MS, et al. Oral herpes simplex infection in leukemia patient. J AM Dent Assoc 1987;114:483-6. 12. Greenberg MS. Herpesvirus infection. Dent Clin North AM 1996; 40:359-68. 13. Greenberg, Glick, Ship. Burket’s Oral Medicine (11th edn), BC Decker Inc, Hamilton, 2008. 14. Johnson PA, Avery C. Infectious mononucleosis presenting as a parotid mass with associated facial nerve palsy. Int J Oral Maxillofac Surg 1991;20:193-5. 15. Jones AC, Freedman PD, et al. Cytomegalovirus infection of oral cavity: a report of six cases and review of literature. Oral Surg, Oral Med, Oral Pathol 1993;75:76-85. 16. Kaplan LJ, Daum RS, et al. Severe measles in immunocompromised patient. JAMA 1992;267:1237-41. 17. Langenberg AG, Corey L, Ashley RL, et al. A prospective study of new infections with herpes simplex virus type 1 and type 2. Chiron HSV Vaccine Study Group. N Engl J Med 1999;341(19): 1432-8. 18. MacPhail LA, Greenspan D, et al. Acyclovir resistant Foscarnet sensitive oral herpes simplex type 2 lesion in patient with AIDS. Oral Surg, Oral Med, Oral Pathol 1989;67:427-32. 19. McKenzie CD, Gobetti JP. Diagnosis and treatment of orofacial herpes zoster. JADA 1990;120:679-81. 20. Miller CS, Cunningham LL, et al. The efficacy of valacyclovir in preventing herpes simplex infection associated with dental procedure. J AM dent Assoc 2004;135:1311-8. 21. Mintz SM, Anavi K. Maxillary osteomyelitis and spontaneous tooth exfoliation after herpes zoster. Oral Surg, Oral Med, Oral Pathol 1992;73:664-6. 22. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology (2nd edn), Saunders Elsevier, 2004. 23. Perna JJ, Eskinazi DP. Treatment of oro-facial simplex infection with acyclovir. Oral Surg, Oral Med, Oral Pathol 1988;65:689-92. 24. Rooney JF, et al. Prevention of ultraviolet light induced herpes labialis by sunscreen. Lancet 1991;338:1419-22. 25. Schubert MM, Epstein JB, Lloid ME. Oral infection due to cytomegalovirus in immuno-compromised patients. J Oral Pathol Med 1993;22:268-73. 26. Scully C, Cawson RA. Medical problems in dentistry (5th edn), Churchill Livingstone: an imprint of Elsevier, 2005. 27. Scully C, et al. Are viruses associated with aphthae and oral vesiculo-erosive disorder? Br J Oral Maxillofac Surg 1993;31(3): 173-7. 28. Scully C. Orofacial herpes simplex virus infection: current concept in epidemiology, pathogenesis and treatment and disorder in which virus may be implicated. Oral Surg, Oral Med, Oral Pathol 1989;68:701-10. 29. Simon PA. Oral condyloma acuminatum as an indication as a indication of sexual abuse; dentistry role. Quintessence Int 1986; 112:455-8. 30. Spruance SL, Rea TL, et al. Penciclovir cream for the treatment of herpes simplex labialis, a randomized multicentric, double bind placebo control trial. JAMA 1997;277:1374-9. 31. Whitaker SB. Intraoral molluscum contagiosum. Oral Surg, Oral Med, Oral Pathol 1991;72:334-6. 32. Woo SB, Lee SF. Oral recrudescent herpes simplex infection. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 199783:239-43. 33. Yoshiaki Yura, et al. Recurrent intraoral herpes simplex virus infection. Int J Oral Maxillofac Surg 1986;15:457-63.
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Fungal Infections 775
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Fungal Infections
Introduction Nowadays as patient is receiving broad spectrum antibiotics, radiation, cytotoxic and immunosuppressive drugs, there is increases incidence of fungal disease in the society. Many of the fungal disease are not diagnosed due to lack of diagnostic facility. Fungi belongs to plant kingdom which are non-photosynthetic due to absence of chlorophyll. Pathogenic fungi exists in three forms like yeasts, yeast like and filamentous organism.
Infection Caused by Fungi The spectrum of infection cause by fungi is wide and there is no satisfactory classification of fungal disease. Some important dental point of view fungal disease are described below.
Histoplasmosis It is also called as ‘Darling’s disease’. It is caused by Histoplasma capsulatum, a dimorphic fungus that grows in the yeast form in infected tissue. Infection results from inhalation of dust contaminated with dropping, particularly from infected birds.
Types • Acute primary histoplasmosis • Progressive disseminated histoplasmosis • Chronic cavitary histoplasmosis.
Clinical Features • Acute primary histoplasmosis—primary infection is mild, manifesting as self limited pulmonary disease that heals to leave fibrosis and calcification. There is chronic low grade fever, malaise, headache and productive cough. There may be pleuritic pain. Chest radiograph may
show patchy infiltrate which may exhibit signs of calcification. • Progressive disseminated histoplasmosis—it is seen in children and elders. It is manifested in hepatosplenomegaly and lymphadenopathy. Patients with disseminated form show evidence of bone marrow involvement by anemia and leukopenia. There is also kidney involvement with gastrointestinal and oropharyngeal ulcerative lesions. • Chronic cavitary histoplasmosis—it closely mimics chronic cavitary tuberculosis. The cavitary lesions are bilateral and are found in the upper lung fields. Symptoms include cough, dyspnea and weight loss. • Laboratory diagnosis—the organisms are found in large numbers in phagocytic cells and appear as tiny intracellular structures measuring little more than 1 micron in diameter. Biopsy shows small oval yeasts within macrophages and reticuloendothelial cells as well as chronic granuloma, epithelial cells, giant cell with caseation necrosis.
Oral Manifestations • Sites—it is seen on buccal mucosa, gingiva, tongue, palate or lip. Oral lesions are common in the progressive disseminated form. • Symptoms—patient may complain of sore throat, painful chewing, hoarseness, difficulty in swallowing. • Appearance—oral lesions are nodular, ulcerative or vegetative. If left untreated, it will progress to form firm papule or nodules which ulcerate and slowly enlarge. It resembles malignancy. • Base and surface—ulcerated area covered by nonspecific gray membrane (Fig. 32-1) and is indurated.
Diagnosis • Clinical diagnosis—hepatomegaly, splenomegaly, with oral ulcerative lesion will give clue to the diagnosis.
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Oral Manifestation • Site—it involves mucosa and jaw bones. • Signs—mandibular and maxillary involvement is usually presented as bony resorption, resulting in loosening of teeth.
Diagnosis
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• Clinical diagnosis—multiple cutaneous lesion with loosening of teeth may give clue to diagnosis. Fig. 32-1: Ulcerative lesion seen in female patient in histoplasmosis. It is mistaken as malignancy of mandibular vestibule.
• Laboratory diagnosis—Histoplasma organisms are found in phagocytic cells.
Management • Amphotericin B—amphotericin B is the drug of choice and lesion may require surgical intervention.
Differential Diagnosis
Blastomycosis
• Tuberculosis—sputum examination, tuberculin test. • Blastomycosis—biopsy and culturing the organism from tissue. • Mucormycosis—biopsy. • Cryptococcosis—organisms cultured on Sabouraud’s glucose agar.
It is caused by ‘blastomyces dermatitidis’. Organism is a normal inhabitant of soil and that is the reason for it to be common in agricultural worker. It is transmitted through the respiratory tract. Infection with blastomycosis begins in a vast majority of cases by inhalation. Oral lesion may be primary (local inoculation) or secondary (extrapulmonary dissemination) to some infection elsewhere in the body.
Management • Supportive treatment—patient should be given analgesic and antipyretics to control pain and fever. • Ketoconazole—it should be given for 6 months in nonimmunosuppressed patient. • Itraconazole—this agent is more effective and less toxic than ketoconazole. • Amphotericin B—intravenous amphotericin B should be given in chronic and severe form.
African Histoplasmosis It is caused by fungus Histoplasma duboisii that is larger than Histoplasma capsulatum. The disease, because of its clinically distinct form and geographical distribution is called as African histoplasmosis. The disease exists in two forms, i.e. localized and disseminated.
Clinical Features • Localized form—it is confined to the skin, lymph nodes or localized bony areas. Bones when involved, may show cyst-like lesions.
Types • Primary pulmonary blastomycosis • Cutaneous blastomycosis • Disseminated or systemic blastomycosis.
Clinical Features Primary pulmonary blastomycosis • Age and sex—it is more common in men than women and typically occurs in middle age. • Symptoms—it follows a chronic course with malaise, high grade fever and mild cough. If untreated, shortness of breath, weight loss and blood tinged sputum are encountered. In some cases, it may precipitate adult respiratory distress syndrome. Cutaneous Blastomycosis • Sites—infection of skin, mucosa and bone may also occur, resulting from metastatic spread of organism through lymphatic system. • Appearance—skin and mucosal lesion starts as subcutaneous nodule and progresses to well circumscribed indurated ulcer.
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Fungal Infections 777 • Signs—elevated, verrucous, crusted and single or multiple lesions developing on exposed part of the body, particularly on hands and face. • Margins—lesion leaves a slanted serpiginous border with a tendency towards healing in the center. When the crust is lifted, pus exudes. Disseminated or Systemic Blastomycosis • Cause—it results from the spread of infection from pulmonary form. • Sites—bones are involved in larger number of cases. Liver, kidney, spleen and gastrointestinal tract may be involved. • Signs—cerebral abscess are found, which occur as a result of brain involvement.
Oral Manifestations • Symptoms—oropharyngeal pain is present. • Signs—enlargement of cervical lymph nodes occurs. • Appearance—non-specific, painless verrucous ulcer with indurated borders is present. It is often mistaken for squamous cell carcinoma (Fig. 32-2). Some lesions are hard nodules and appear as sessile, granulomatous appearing plaque.
cultural worker or when review of system reveals pulmonary symptom. • Radiological features—chest radiograph will show pulmonary involvement. • Laboratory diagnosis—diagnosis is made on the basis of biopsy and on culturing the organism from tissue.
Differential Diagnosis • Squamous cell carcinoma—present for weeks or months, palpation shows induration, most common in older patient. • Tuberculosis—undermined flabby borders, usually painless, sputum examination, Mantoux test. • Histoplasmosis—culture and biopsy should be done. • Mucormycosis—biopsy. • Cryptococcosis—organism culture should be done.
Management • Itraconazole—it is generally recommended for the patient of chronic blastomycosis. • Amphotericin B—it is usually given in chronic case of blastomycosis. Intravenous amphotericin B for 8 to 10 weeks causes resolution of the disease. In case of acute blastomycosis, it does not require any treatment.
Mucormycosis It is also called as ‘phycomycosis, zygomycosis’. It is caused by saprobic organism of class Zygomycetes. It is more common in patients with decreased resistance, due to diseases like diabetes, tuberculosis, renal failure, leukemia, cirrhosis and in severe burn cases. It begins with inhalation of fungus by susceptible individual.
Types
Fig. 32-2: Blastomycosis presenting as ulcerative lesion resembling squamous cell carcinoma.
• Superficial—it involves external ear, fingernails and skin. • Visceral • Pulmonary • Gastrointestinal • Rhinocerebral or rhinomaxillary form—it is important with dental point of view.
Radiographic Features • Periosteal reaction—radiograph may show periostitis and sub-periosteal new bone formation. Osteoblastic reaction is usually present in the later stages of disease. • Chest radiograph—chest radiograph show concomitant pulmonary involvement in most of the cases.
Diagnosis • Clinical diagnosis—the index of suspicion is increased when chronic, painless, oral ulcer appears in an agri-
Clinical Features • Locations—infection usually arise in lateral wall of nose and maxillary sinus; may rapidly spread by arterial invasion to involve the orbit, palate, maxillary alveolus and ultimately the cavernous sinus and brain through hematogenous spread and may cause death. • Symptoms—ptosis, proptosis, nasal obstruction, fever, swelling of cheek and paresthesia of face can occur.
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• Intracranial involvement—intracranial involvement may be heralded by cranial neuropathy, especially of the trigeminal and facial nerve. There is increased lethargy, progressive neurologic deficit and ultimately death. • Artery involvement—fungus invades artery to cause fibrosis and ischemia of the supplied area. • Nose—there is appearance of a reddish black nasal turbinate and septum. Nasal discharge caused by necrosis of nasal turbinate.
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• Site—most common site involved is maxillary sinus. Other sites which can also be involved are palate, lip, alveolar bone and gingiva. • Signs—ulceration of palate may occur due to necrosis and invasion of palatal vessels. It is large and deep, causing denudation of underlying bone (Fig. 32-3). Ulcer may be seen on gingiva, lip and alveolar bone. Ulcer on palate may appear black and necrotic. • Massive destruction—it can be seen when the condition is not treated at the earliest.
Fig. 32-4: CT scan showing increased radiopacity due to soft tissue mass in left maxillary sinus (Courtesy Dr Iswar).
• Radiologicalfinding—CTscanwillhelpfulinthediagnosis. • Laboratory diagnosis—organism appear as nonseptate hyphae with branching at obtuse angles.
Differential Diagnosis • Squamous cell carcinoma—indurated, longer history, resistance to therapy, firm borders, older patient, biopsy. • Necrotizing sialometaplasia—rare, limited to hard and soft palate, usually painless. • Aphthous ulcer—short duration, painful, heals in one to three weeks.
Management Fig. 32-3: Mucormycosis showing deep ulceration of the palate (Courtesy Dr Ashok L).
Radiographic Features • Appearance—paranasal sinus may reveal mucoperiosteal thickening of the involved sinus. With disease progression, there is increased nodularity and soft tissue thickening, usually mimics a tumor on radiographical examination. • CT scan features—CT scan is most helpful for detecting the degree of bone destruction and for evaluating disease extension into the orbit and brain (Fig. 32-4).
Diagnosis • Clinical diagnosis—the nose involvement with destruction of palate, neurological finding may give clue to the diagnosis.
• Surgical debridement—radical surgical debridement of infected and necrotic tissue should be carried out. • Amphotericin B—systemic administration of high dose of amphotericin B should be given. • Control of underlying disease—control of predisposing factors such as diabetes should be attempted. • Obturation—prosthetic obturation of palatal defect should be carried out. • Symptomatic treatment—it should be given to eliminate secondary infections and pain relief.
Cryptococcosis It is also called as ‘torulosis’. It is a chronic fungal infection caused by Cryptococcus neoformans and Cryptococcus bacillispora. The causative organism is gram positive, budding, yeast-like cell with an extremely thick, gelatinous capsule, measuring 5 to 20 microns in diameter. Infection
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Fungal Infections 779 occurs due to inhalation of airborne microorganism. It has increased incidence in immunosuppressive patients, most commonly in HIV positive patient.
Clinical Features • Age—there is slight predilection for middle aged males. • Site—the infection usually occurs in lungs. • Symptoms—it may be asymptomatic and in some cases, patient may complain of cough with mucoid expectoration. Occasionally, pleuritic pain and hemoptysis can also occur. • Skin lesion—the skin lesion appears as multiple brown papules which ultimately ulcerate, the clinical picture is nonspecific. • Neurological features—meningoencephalic lesions produce a variety of neurologic signs and symptoms, generally associated with increased intracranial pressure. • Coin lesion—the radiograph of chest shows infiltrates and occasionally ‘coin’ lesion. • Diagnosis—the organisms can be cultured on Sabouraud’s glucose agar.
Oral Manifestations • Locations—lesion of hard palate, soft palate, gingiva, extraction socket, tongue and tonsillar pillar are common. • Appearance—they appear as simple non-specific, single or multiple ulcers. They are nodular and granulomatous, which may ulcerate during the course of disease.
spores of the causative organism, Coccidioides immitis. Symptoms occur usually 14 days after the inhalation of fungus. Infection is common in summer months, especially after periods of dust storm. It is self limiting and runs its course within 10 to 14 days. Lesions of head and neck, including the oral cavity, occur with some frequency.
Types • Primary non-disseminated coccidioidomycosis. • Progressive disseminated coccidioidomycosis.
Clinical Features • Age and sex—it is common in all age groups and predominantly seen in males. • Primary pulmonary coccidioidomycosis—the patient generally develops manifestations suggestive of respiratory disease such as cough, pleural pain, headache and anorexia. Patient may also complain of low grade fever and joint pain. • Primary cutaneous coccidioidomycosis—skin lesions are also present, like erythema nodosum or erythema multiforme. Primary lesions, when they occur, are associated with regional lymphadenopathy. Granulomatous, verrucous or necrotic ulcers exuding thick pus are seen on involved skin surface. • Progressive disseminated coccidioidomycosis—the disease usually runs rapid course and the dissemination extends from the lungs to various viscera, bones, joints, skin and central nervous system, where meningitis is the most frequent cause of death.
Diagnosis • Clinical diagnosis—the brown skin lesion with neurological features and non-specific ulcer seen in oral cavity. • Laboratory diagnosis—gram positive yeast-like cell with gelatinous capsule.
Management • Ketoconazole—mild to moderate cases can be treated with ketoconazole for 6 to 12 weeks. • Amphotericin B—the severe form requires amphotericinB, intravenously for up to 10 weeks. • Combination therapy—combination therapy of amphotericin B and flucytosine is used in many cases to treat the disease. Another combination of fluconazole and itraconazole is also useful in Cryptococcosis infection.
Oral Manifestations • Appearance—the lesions of oral mucosa and skin are proliferative, granulomatous and ulcerated lesions that are non-specific in their clinical appearance. • Healing—these lesions tend to heal by hyalinization and scar formation. • Lytic lesion—lytic lesions of jaw may develop.
Diagnosis • Clinical diagnosis—symptoms suggestive of respiratory disease, granulomatous and ulcerated oral lesion may give clue to the diagnosis. • Laboratory diagnosis—biopsy shows mononuclear cell, lymphocytes, and plasma cells with foci of coagulation necrosis.
Coccidioidomycosis It is also called as ‘valley fever’, ‘desert fever’ or ‘coccidiodal granuloma’. The disease appears to be transmitted to man and animals by inhalation of dust contaminated by the
Management • Amphotericin B—it has been found to be an effective chemotherapeutic agent for the disease. It is given in
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patient who is immunosuppressive, disseminated infection and severe pulmonary infection. Long term therapy is required for complete cure. • Fluconazole—it is given in high doses for extended period of time. • Ketoconazole—it is used as an alternative therapy to amphotericin B.
Paracoccidioidomycosis It is also called as ‘South American blastomycosis’, ‘Lutz disease’. It is caused by Paracoccidioides brasiliensis. It is more commonly seen in farmers.
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• Symptoms—lung involvement produce symptoms of pneumonitis or bronchitis. The expectoration is often tinted with blood.
Oral Manifestations • Appearance—they are similar to candidiasis or thrush (Fig. 32-5), being white, velvety, patch like covering of the oral mucosa, isolated or diffuse in distribution. • Tonsillar lesion—tonsillar lesions are common in association with oral lesions.
Clinical Features • Geographic location—this is more commonly seen in South America. • Age and sex distribution—it is exclusively found in males as compared to females. It is more common in middle age group. • Signs—patient usually present with signs of pulmonary infection. In some cases, adrenal involvement also occur resulting in hypoadrenocorticism.
Oral Manifestation • Site—commonly affected site are alveolar mucosa, gingiva, and palate. Lips can also be affected. • Appearance—oral lesion appear as mulberry-like ulceration. Fig. 32-5: Geotrichosis presenting as candidiasis type lesion on oral cavity.
Diagnosis • Clinical diagnosis—signs of pulmonary infection, with mulberry-like ulceration. • Laboratory diagnosis—size of this organism is larger than North American form.
Management • Sulfonamide—this can be used to treat mild to moderate infection. • Amphotericin B—this is used in severe cases. It should be used intravenously. • Itraconazole and ketoconazole—this can also be used in some cases when the condition is not life threatening.
Diagnosis • Clinical diagnosis—lung involvement with candidal type lesion in debilitated patient. • Laboratory diagnosis—the organism is small, rectangular shaped; spores measuring approximately 4 to 8 microns, often with rounded ends. The tissue reaction is nonspecific and of acute inflammatory type.
Management • Antifungal therapy—it includes topical and systemic application of nystatin and amphotericin B.
Geotrichosis
Sporotrichosis
It is caused by organism Geotrichum candidum. It is found in patients with debilitating diseases.
It is a fungal infection caused by Sporotrichum schenckii. The disease predominantly affects skin.
Clinical Features
Causes
• Location—these are more commonly found in lungs and oral mucosa.
• Exposure to animal—exposure to a wide variety of animals, both domestic and wild.
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Fungal Infections 781 • Accidental injury—accidental injury from the thorns of some plants or bushes. Accidental laboratory or clinical inoculation in hospital workers.
Rhinosporidiosis
Clinical Features
Clinical Features
• Incubation period—the incubation period is from a week to 3 weeks. It involves the skin, subcutaneous tissues and oral, nasal and pharyngeal mucosa. • Skin lesion—the skin lesion often described as sporotrichotic ‘chancre’ appears at the site of inoculation as firm, red to purple nodule which soon ulcerates. • Lymph nodes—regional lymphadenopathy is generally developed and it may ulcerate and drain.
• Location—it is more common on oropharynx, nasopharynx, larynx, skin, eyes and genital mucosa. • Symptoms—initial symptoms include nasal irritation, accompanied by mucoid discharge. • Skin lesion—the skin lesion appears as small verrucae or warts, which ultimately become pedunculated. • Signs—posteriorly, these polypoid masses may extend into the pharynx. The lesions are soft, friable and highly vascular. • Genital lesions—genital lesion resembles condyolomas.
Oral Manifestations • Location—non-specific ulceration of the oral, nasal and pharyngeal mucosa. • Appearance—long standing lesions become granulomatous, vegetative or papillomatous. • Symptoms—pain is present and the cervical lymph nodes are always enlarged.
Radiographic Features • Incidence—it rarely involves the bone, it resembles to those which occur in tuberculosis. • Appearance—in the mandible, there is large destructive lesion in the molar region and ramus. It has a loculated cystic appearance, which causes marked expansion of the inferior aspect of the jaw. • Periosteal reaction—in long bones, sporotrichosis may produce some periosteal new bone, but this reaction is confined to jaws of children.
Diagnosis • Clinical diagnosis—lymph nodes enlargement with non specific ulceration of oral cavity will give clue to the diagnosis. • Radiological diagnosis—periosteal reaction with expansion of inferior portion of jaw. • Laboratory diagnosis—the fungus is small, ovoid branching organism with septate hyphae showing budding form. It is only 3 to 5 microns in diameter and can be cultured on Sabouraud’s glucose agar medium. The tissue reaction is a granulomatous.
Management • Potassium iodide—it includes oral administration of potassium iodide in suitable doses.
It is caused by Rhinosporidium seeberi. It affects oropharynx and nasopharynx.
Oral Manifestations • Sites—the soft palate appears to be the most frequent site of oral involvement. • Appearance—it is accompanied by a mucoid discharge and appears as soft, reddish pink, polypoid growth of tumor like nature which spreads to the pharynx and larynx. The lesions are vascular and bleed readily.
Diagnosis • Clinical diagnosis—pedunculated wart with nasal polypoid mass, with intraoral soft reddish pink growth on soft palate. • Laboratory diagnosis—the organisms appear as sporangia containing large number of round or ovoid endospores with size of 5 to 7 microns in diameter.
Management • Surgical—surgical removal of the growths and application of cautery is the treatment recommended for rhinosporidiosis.
Aspergillosis It is a fungal infection caused either by sensitization to parasitic colonization, or tissue invasion by species of genus Aspergillus. It is second to candidiasis, as an opportunistic infection, in immunocompromised patients. It is more commonly seen in diabetes mellitus patients.
Clinical Features • Sites—the respiratory tract, external auditory canal, nasopharynx, cornea, gastrointestinal tract and occasionally the skin may be the primary sites of infection.
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• Symptoms—in some cases, there may be asthmatic episode in sensitive persons. • Nasal aspergillosis—it may present swelling, ulceration, crusting and necrosis of anterior turbinates, nasal septum and nasal wall. • Allergic fungal sinusitis—in some cases, disease may appear as allergic infection appearing in the sinus. • Aspergilloma—it is mass of fungal hyphae seen in maxillary sinus. • Disseminated form—this type of aspergillosis infection occur in case of immuno-compromised patient. Patient may have chest pain, cough and fever in this case. Prognosis of the patient is poor in this case.
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Oral Manifestation • Sites—it is seen on palate and tongue. Soft palate involvement seems to be more common in upper respiratory tract involvement. • Palatal lesion—a lesion on the palate is manifested as a painful ulcer, surrounded by a ring of black necrotic tissue. • Gingival ulceration—this is also a common feature of aspergillosis infection in oral cavity. The color of ulceration may be gray or violaceous hue. • Antroliths—this is also reported from patient suffering from aspergillosis. • Disseminated infection—oropharyngeal aspergillosis, in patients with hematological malignancies, presents as yellowish-black ulceration of soft palate and posterior part of tongue. These patients complain of intense local pain, oral bleeding and dysphagia.
Diagnosis • Clinical diagnosis—gray color ulceration in oral cavity accompanied by nasal infection, chest pain may give clue to the diagnosis. • Laboratory diagnosis—organism can be seen on biopsy.
Management • Amphotericin B—it is the treatment of choice. It can be given intravenously. • Surgical debridement—disseminated aspergillosis in immunocompromised patients should be treated on an individual basis surgical debridement. • Itraconazole—itraconazole can be given local debridement of the lesion.
Protozoal Infection
Types • Visceral leishmaniasis—it is also called as Kalaazar. It is caused by Leishmania donovani. • Cutaneous leishmaniasis—it is caused by Leishmania braziliensis.
Clinical Features Visceral leishmaniasis • Incubation period—incubation period is 2 weeks to 2 years. • Symptoms—onset may be insidious with a low grade fever or it may be abrupt with sweating and high intermittent fever. Cough and diarrhea can also develop. • Signs—the spleen becomes enlarged, often massively. If not treated, patient will become anemic and wasted. Mucocutaneous leishmaniasis • Incubation period—is 1 week to 1 month. • Age—it is usually seen in young men. • History—there is past history of superficial ulcer of skin, caused by bite of an infected sandfly, which heals with depressed scar. • Nose—nasal mucosa becomes congested and ulcerates. Later, all the soft tissues of nose may be destroyed.
Oral Manifestation Visceral leishmaniasis • Pigmentation of face—there may be increased pigmentation of face. • Gingival finding—there may be spontaneous bleeding, edematous gingiva and loose teeth. Mucocutaneous leishmaniasis • Incidence—mucosal lesion usually occurs 1-2 years after skin lesion. • Site—lips, soft palate and larynx may be involved. • Appearance—the mucosal lesions are long standing, destructive, granulating ulcers which in many instance cause severe mutilation of structure involved. • Lymph nodes—regional lymphadenopathy is common.
Diagnosis • Clinical diagnosis—face pigmentation with edematous gingiva will suspect the disease. • Laboratory diagnosis—organisms can be isolated from the lesion.
Leishmaniasis
Management
It is caused by the genus Leishmania which consist ofthree flagellate protozoa, which cause variety of distinct infections in man and are transmitted by sandfly bites.
• Amphotericin B—it is the drug of choice for visceral leishmaniasis. If the lesions are multiple, parenteral injection of amphotericin B should be given.
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Fungal Infections 783 • Cryosurgery—in mucocutaneous lesion, small lesion may be treated by freezing with liquid carbon dioxide, curettage or infiltration with 1-2 ml sodium gluconate.
Trichinosis It is caused by Trichinella spiralis, which is small, spiral, thread-like organism. Human infection occurs as a result of eating parasitized food, usually pork, which has not been completely cooked.
Clinical Features • Sites—striated muscle, masseter, neck muscle and diaphragm. • Symptoms—there is fever, facial and periorbital edema, muscle pain and eosinophilia.
Oral Manifestations • Site—tongue is the most common site involved. It also occurs in muscles attached to mandible, in mandibular alveolar process and in gingival tissues. • Symptoms—there is trismus, muscular cramps of the facial muscle, jaw and tongue. There is also monotony of speech. • Signs—there may be petechiae of buccal mucosa, palate and floor of mouth. There is also bleeding from gingiva, lips and nose.
Diagnosis • Clinical diagnosis—trismus, monotonous speech with petechiae of buccal mucosa or palate may give clue to the diagnosis.
Management There is no specific treatment for trichinosis and in severe cases, prognosis is poor.
Suggested Reading 1. Bradsher RW. Histoplasmosis and blastomycosis. Clin Infect Dis 1996;22(suppl):102-11. 2. Brightman VI, Guggenheimar IG. Herpetic paronchya- primary herpes infection of finger. J AM Dent Assoc 1970;80:112-5. 3. Damante JH, Flury RN. Oral and rhinoorbital Mucormycosis: a case report. J Oral Maxillofac Surg 1998;56:267-71. 4. Economopoulou P, Laskaris G, Ferekidis E, et al. Rhino cerebral Mucormycosis with severe oral lesion: a case report. J Oral Maxillofac Surg 1995;53:215-7. 5. Einstein HE, Johnson RH. Coccidioidomycosis new aspect of epidemiology and therapy. Clin Infect Dis 1993;16:349-56. 6. Falworth MS, Herlod J. Aspergillosis of the paranasal sinus: a case report and radiographic review. Oral Surg, Oral Med, Oral Pathol 1996;81:255-60. 7. Greenberg, Glick, Ship. Burket’s Oral Medicine (11th edn), BC Decker Inc, Hamilton, 2008. 8. Jones AC et al. Mucormycosis of the oral cavity. Oral Surg, Oral Med, Oral Path 1993;75(4):455-60. 9. Jones AC, Bentsen TY, Freedman PD. Mucormycosis of the oral cavity. Oral Surg, Oral Med, Oral Pathol 1989;68:624-7. 10. Jones AC, Bentsen TY, Freedman PD. Mucormycosis of the oral cavity. Oral Surg, Oral Med, Oral Pathol 1993;75:455-60. 11. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology (2nd edn), Saunders Elsevier, 2004. 12. Oda D, et al. Oral histoplasmosis as a presenting disease in AIDS. Oral Surg, Oral Med, Oral Path 1990;70:631-6. 13. Ogata Y, Okinaka Y, Takahashi M. Antroliths associated with aspergillosis of maxillary sinus: a report of case. J Oral Maxillofac Surg 1997;55:1339-41. 14. Paes De Almeida O, Jorge J, Scully C, et al. Oral Manifestation of Paracoccidioidomycosis (south American blastomycosis). Oral Surg, Oral Med, Oral Pathol 1991;72:430-5. 15. Rose HD, Gingrass DJ. Localized oral blastomycosis mimicking actinomycosis. Oral Surg, Oral Med, Oral Pathol 1982;54:12-4. 16. Samaranayake LP. Oral mycoses in HIV infection. Oral Surg, Oral Med, Oral Pathol 1992;73:171-80. 17. Schmidt-Westhausen A, Grunewald T et al. Oral cryptococcosis in patient with AIDS: a case report. Oral Dis 1975;1:77-9. 18. Scully C, Cawson RA. Medical problems in dentistry (5th edn), Churchill Livingstone: an imprint of Elsevier, 2005. 19. Scully C, Paes De Almeida O. Orofacial manifestation of the systemic mycoses. J Oral Pathol Med 1992;21:289-94. 20. Sposto MR, Mendes Glannini MJ, Moraes RA et al. Paracoccidioidomycosis manifesting as oral lesion: Clinical, cytological and serological investigation. J Oral Pathol Med 1994; 23:85-7. 21. Sugata T, Myoken Y, et al. Invasive oral aspergillosis in immunocompromised patient with leukemia. J Oral Maxillofac Surg 1994; 52:383-6. 22. Young LL et al. Oral Manifestation of histoplasmosis. Oral Surg, Oral Med, Oral Path 1972;33:191-204.
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33 4
Specific System Disorders
Basic Life Support If the patient is unconscious you have to give him a basic life support. Patient may become unconscious in the dental chair and in that situation; you have to manage the patient in your dental clinics. When victim heart ceases its activity, respiratory failure and cardiac arrest ensue. In such cases, administration of CPR within 3 minutes of cessation of activity of heart becomes a must. Basic life support is the attempt to restore lung and heart function. Mainly, you have to follow the ABC of basic life support, i.e. Airway, Breathing and Circulation.
Positioning of the Patient • Supine position—patient should be placed in supine position with the brain at the same level as the heart and the feet elevated slightly at 10 to 15 degree angulation. Head down position should be avoided as of gravity will act to force the abdominal viscera superiorly into the diaphragm, thus restricting movements. • Position of pregnant women—if pregnant women loose consciousness in the dental office, the back of dental chair should be lowered to supine position and patient turn towards her right side, with a blanket or pillow under her back on her left to maintain that position.
Airway Opening the airway and restoration of breathing constitutes the basic steps in life support. Any type of head support on the dental chair should be removed because such support flex the neck and thus making airway maintenance more difficult. • Head tilt—this procedure is accomplished by placing the rescuer’s hand on the victim’s forehead and applying a firm, backward pressure with the palm.
• Head tilt chin lift (Figs 33.1 A and B)—in this, the fingers, of one hand are placed under the body- symphysis region of the mandible to lift the tip of the mandible up, bringing the chin forward. As the tongue is attached to the mandible, it is thereby pulled forward and off from the posterior pharyngeal wall. • Head tilt, neck lift—in this, one hand of the rescuer is placed beneath the victim’s neck to lift and support it. • Foreign material in airway—if there is evidence of foreign matter in the airway, then check for airway patency. Partial airway obstruction produces noise and complete airway obstruction produces silence. If foreign body is suspected, the patient must be rolled on one side with lowering its head below the level of heart. Rescuer should place two fingers in the patient’s mouth and remove anything in the entire oral cavity.
Breathing You have to position your cheek close to victim’s nose and mouth, look towards victim’s chest; then look, listen and feel for breathing (5-10 second) (Fig. 33-2). Exhaled air ventilation can be give by mouth to mouth or mouth to nose. • Mouth to mouth—if not breathing, pinch victim’s nose close and give 2 full breaths into victim’s mouth. This is done by taking a deep inspiration and exhaling in the patient’s mouth and then patient is allowed to exhale passively. This procedure is continued at the rate of 12-14/min. • Mouth to nose—when it is impossible to breathe into patient’s mouth and if the rescuer if unable to adequately seal the mouth, the above technique is followed. In this technique, the rescuer keeps the head tilted backwards, with one hand on the forehead and other hand lifts victim’s mandible, sealing the lips. Taking a deep breath, rescuer seals his lips around the victim’s nose and blows in, until he feels and visualize the expansion of victim’s lungs.
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Specific System Disorders 785 • Postbreathing—after it, atmospheric air ventilation should be delivered to the victim. If breath does not go in, reposition the head and try again to give breath. If still blocked perform abdominal thrust (Fig. 33-3).
A
4 Fig. 33-3: Abdominal thrust should be given to patient if patient is not able to breathe.
Circulation • Carotid pulse checking—you have to check for carotid pulse for 5-10 seconds, at side of victims neck • Rescue breathing—if there is a pulse but victim is not breathing, give rescue breathing at the rate of 1 breath every 5 second or 12 breaths per minute • Technique to give compression to chest (Fig. 33-4)—place heel of one hand on lower part of victim’s sternum; with
B Figs 33-1A and B: Head tilt chins lift method to maintain the airway of the patient.
Fig. 33-2: Patency of air way should be checked.
Fig. 33-4: Technique of describing chest compression.
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your other hand directly on tip of first hand, depress sternum 1.5 to 2 inches. Perform 20 compressions to every 4 breaths (rate 80-100 per minute); check for return of pulse every minute. Continue it uninterrupted until advanced life support is available.
Cardiovascular Disease Symptoms
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• Dyspnea—it refers to breathlessness on physical exertion. • Orthopnea—it is difficulty in breathing while lying down. It is due to rise in pressure in the right atrium and right ventricle leading to more blood flow into the lungs. Stiffness and congestion of lungs lead to breathlessness. • Edema—edema of the feet and ankles is suggestive of cardiac failure due to retention of salt and water. • Pain—causes of pain in chest are cardiac ischemia and pericarditis. • Palpitation—it refers to awareness of the heart beat. It is a feature of anxious patient, paroxysmal tachycardia and atrial fibrillation. • Syncope—it occurs due to decrease in cardiac output, decreased peripheral resistance or combination of the two.
Signs • Anemia—pallor of skin and mucous membrane • Obesity—such patients are more likely to have cardiac disease. • Peripheral cyanosis—it occurs due to impairment of circulation, as in vasoconstriction, low cardiac output or stress. • Central cyanosis—it occurs due to improper oxygen saturation of blood or due to right to left shunt. • Clubbing—it is seen in congenital heart disease and in advanced cases of infective endocarditis (Fig. 33-5). • Temperature—skin may be cold in cardiac failure and syncope. • Arterial pulse—changes in the pulse pattern are noted in arrhythmias, reduced cardiac output, pulmonary embolism and aortic stenosis.
Examination of the Heart • Inspection—enlargement of heart can be seen as a prominence to the left of sternum. • Palpation—apex beat; normally apex beat is palpated within the mid-clavicular line in the 5th intercostal space. Displacement is seen in cardiac enlargement and fibrosis, collapse or removal of lungs.
Fig. 33-5: Clubbing in cardiovascular disease (Courtesy Dr Milind Chandurkar).
• Dullness—it is noted in pericardial effusion and emphysema. • Auscultation—it is done to hear the heart sounds and murmurs. • First heart sound—it is heard loudly at the apex. It occurs due to closure of the mitral valve. Accentuation of 1st heart sound is heard in anxiety and thyrotoxicosis, due to tachycardia and in mitral stenosis. Diminished heart sound is heard in myocarditis, cardiomyopathy and mitral regurgitation. • Second heart sound—it is heard due to closure of the aortic and pulmonary valves. Second heart sound is altered in bundle branch block or increased ventricular stroke volume and form left or right shunt. • Third heart sound—it is heard at the apex in young individuals. In older individuals, it is suggestive of mitral regurgitation and cardiomyopathy. • Fourth heart sound—occurs due to forceful left ventricular distension before the first heart sound. It is suggestive of hypertension, cardiomyopathy, ischemic heart disease and left ventricular hypertrophy. • Murmur—it occurs due to turbulent blood flow. It is heard due to abnormal heart valves. • Blood pressure—it increases due to stress or tachycardia.
Consideration of Prophylaxis in Cardiovascular Disease • Heart disease in which prophylaxis recommended—the disease in which prophylaxis recommended are prosthetic cardiac valve including bioprosthetic and homograft valve, previous bacterial endocarditis, surgically constructed systemic pulmonary shunt, rheumatic and other acquired valvular dysfunction, even after valve surgery, cardiomyopathy, mitral valves
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Specific System Disorders 787 prolapse with valvular regurgitation and most congenital heart malformations. • Heart disease in which prophylaxis is not recommended— the disease in which prophylaxis is not recommended are surgical repair without residual symptoms beyond 6 months of atrial septal defect, ventricular septal defect, patent ductus arteriosus, previous coronary arterial bypass graft surgery, mitral valve prolapse without valvular regurgitation, heart murmurs, previous rheumatoid fever without valvular dysfunction and cardiac pacemaker and implanted defibrillation. • Dental procedure in which prophylaxis is recommended— dental procedures likely to induce gingival or mucosal bleeding, including professional cleaning, surgical operations involving respiratory mucosa (including maxillary sinus), incision and drainage of infected tissues and intraligamentary injection. • Dental procedure in which prophylaxis is not recommended— dental procedures not likely to induce gingival bleeding, injection of local anesthesia, shedding of primary teeth and new denture insertion will not require dental prophylaxis.
Angina Pectoris It is hypoxia of the cardiac muscles, resulting from an imbalance between the oxygen consumption and oxygen supply of the cardiac muscles. It is the name given to paroxysm of pain. If anginal pain persists for more than half an hour, myocardial infarction or some acute abdominal condition should be considered.
Etiology • Coronary artery disease—it is commonly associated with coronary artery disease and coronary artery spasm associated with atherosclerosis. • Oxygen carrying capacity of blood—limited oxygen carrying capacity of blood and excessive oxygen demand. • Predisposing factors—stress, physical or emotional or use of tobacco may predispose to an attack. Stress cause release of catecholamine and tachycardia.
Types • Stable—it occurs with known physical effort and is relieved at rest and on administration of nitrates. It also gets aggravated by cold weather, smoking, emotional upset, high altitude, sexual excitement and straining at stools. • Nocturnal—angina appears in the middle of the night due to left ventricular failure, which may be precipitate by dreams, causing release of catecholamine.
• Unstable—this is also called as peri-infarction angina as 20% of these patients develop myocardial infraction within 4 months. The following types of angina are called as unstable angina. • Recent angina (less than 60 days). • Stable angina in whom symptom are more severe in intensity, frequency and duration. • Angina at rest. • Angina following myocardial infarction. • Prinzmetal’s angina—this occurs in early morning, associated with ST segment elevation on ECG. It responds to nifedipine and nitrates as it is caused by coronary spasm which can be induced by smoking or hyperventilation. • Postinfarction angina—some patients with myocardial infarction develop angina, 2 days to 8 weeks following the infarction.
Clinical Features • Age and sex—it is most common in age range from 45 to 65 years and male to female ratio is 4:1. • Symptoms—there is substernal pain radiating to both arms and ulnar border of the left arm, jaw, teeth, occipital region or epigastrium. The nature of pain is of crushing type. Pain is of short duration, lasting for 3 to 5 minutes. Pressure or discomfort in the substernal region. Patient may feel as if heavy weight has been placed on his chest. There may be breathlessness or fatigue, due to low cardiac output. • Relieving of pain after cessation of exertion—in most of the cases, the pain is relieved by cessation of exertion. For this reason and because of intense pain, the person commonly maintains a fixed position during the attack. • Signs—variation in pulse rate with generalized facial or circumoral pallor with cold perspiration may be exhibited.
Diagnosis • Clinical diagnosis—a typical history of angina itself could give the diagnosis, even in absence of any other abnormalities on investigation or examination. Though physical examination in angina is often normal, certain clues to the presence of IHD may be present like gallop rhythm (third heart sound), left ventricular enlargement, thickened blood vessels and absent pulse, systolic murmur of mitral regurgitation or papillary muscle dysfunction. • Diagnostic tests • ECG—in 50% of patients resting ECG may be normal. • Stress testing—with bicycle ergometer using standard protocols, or treadmill.
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• Thallium stress test—done by injecting thallium, while the patient exercises and then regional myocardial perfusion is assessed by gamma camera. • Echocardiography and Doppler study—this will be helpful to judge the regional wall motion, abnormality and left ventricular thrombus. • Coronary angiograms—to diagnose blockade of coronary arteries and it’s location and severity.
It results from thrombotic occlusion (or sometimes prolonged spasm) of the infarct related blood vessels. Myocardial ischemia and necrosis occurs from subendocardial to subpericardial region. The entire process takes 6 hours to complete. An anginal attack lasting longer than 30 minutes is considered by definition to be myocardial infarction.
Clinical Features
Prevention of Anginal Attack
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Myocardial Infarction
• Modification of life style—avoid exertion and walking uphill is avoided. • Tranquilizer—diazepam 5-10 mg 6-8 hrly, to relieve anxiety. • Coronary vasodilator—nitrates and calcium antagonist. • Control risk factor—obese patients to reduce weight, smoking strictly forbidden. • Antiplatelet drugs—low dose of aspirin should be given to prevent risk.
Management • Nitroglycerine tablet—if the patient experiences an anginal attack in the dental chair, nitroglycerine tablet or sublingual spray (amyl nitrite) should be immediately applied under the tongue. Dose should be 0.5 mg of glycerine tri-nitrate or 5 mg of isosorbide dinitrate. • Prophylactic drugs—in a known case of angina pectoris relatively short acting antianginal drugs such as sublingual isosorbide dinitrate tablet is recommended prophylactically, before initiating the dental therapy or a particularly stressful phase of dental therapy.
Dental Considerations • Difference between anginal pain and pain of dental origin— the pain is usually referred to jaws and teeth, resembling a toothache and causing patient to seek dental attentions. Due to overlapping of the fifth cranial nerve, cardiac pain may be transmitted to jaws and interpreted as dental pain. Anginal jaw pain is characterized by its severity, its onset associated with exertion and its disappearance with rest. These characters differentiate it from the usual pain of dental origin. • Anginal attacks in dental chair—acute anginal attacks may occur as a result of stress associated with dental services, i.e. extraction. If a patient is known to be angina pectoris patient, short acting antianginal drug such as sublingual isosorbide dinitrate is given prophylactically in addition to any long acting nitrate drugs before initiating dental therapy. • Deferring the procedure which require general anesthesia or conscious sedation—any dental procedure which require general anesthesia or conscious sedation should defer for 3 months duration after recent anginal attacks.
• Symptoms—nausea, vomiting, tachycardia, grossly irregular pulse and breathlessness. • Signs—there is pallor, diaphoresis and pulmonary edema. Initially, there is rise in blood pressure which may be followed by a fall, especially if cardiogenic shock occurs. Heart sounds are muffled. On second and third days, mild fever of 38-39° C may occur.
Diagnosis • History—the characteristic history of chest pain and pain radiating to other areas, as described for angina may be the only guide. Patient who presents the history must be carefully evaluated because in early disease history may be the only positive finding. • Clinical symptoms—clinical symptoms of collapse, severe unremitting chest pain, changes in heart rate, hypotension will give clue to diagnosis. • ECG changes—the electrocardiogram shows changes characteristic of or compatible with acute myocardial infarction in only 80% of the cases and therefore cannot be used, always, to exclude the presence of myocardial infarction. Also shows the earliest change in ST segment elevation with the onset of pain. • Nonspecific test—polymorphonuclear leucocytosis with high ESR may be seen in the first week, due to tissue necrosis. • Serum enzymes—there may be elevation in certain enzymes like CPK, SGOT, LDH and AST in the blood. • Radionuclide technique provides accurate information about myocardial infarction. In these, gammas emitting radionuclide are used in making cardiac scintigrams. Normally, perfuse myocardium is labeled by these radionuclide and abnormally perfuse myocardium is not labeled, producing the cold spot on scintigrams. • Positron emission tomography is also very useful nowadays.
Management • Cardiopulmonary resuscitation—in case of cardiopulmonary arrest, cardiopulmonary resuscitation should be immediately begun. • Prophylactic lidocaine—in patients with life threatening acute arrhythmias, usually premature ventricular
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•
•
• •
contraction or ventricular tachycardia, occur in the dental office. Before transportation of the patient to an acute care medical facility, prophylactic 10% lidocaine can be injected IM in the deltoid muscle at the dose of 4 to 6 mg/kg body weight. Control of chest pain is done by sublingual nitroglycerine 0.3-0.4 mg, repeated every 5-10 minutes and morphine hydrochloride 15 mg, subcutaneously. Nitrous oxide in a concentration of 35%, mixed with oxygen has been quite effective in decreasing the pain of acute myocardial infarction. Anticoagulants like heparin 2000-5000 units, every 6-8 hourly. Oral aspirin—oral administration of aspirin daily improves survival but nowadays it is not recommended for daily use.
• Signs—typical subcutaneous nodules may be present. There is involvement of successive joint which are red, tender and painful. Wrist, ankles, elbows and knees are commonly involved (Figs 33-6A and B). Murmur and erythema marginatum, epistaxis and abdominal pain.
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Dental Consideration • Premedication—these patients require special management because they may have decreased ability to withstand stressful conditions. Patients, for whom dental treatment is particularly stressful, should be premedicated before treatment. Oral benzodiazepam are helpful in 5 mg doses. It should be given in a waiting room 45 minute before the procedure. • Patient on anticoagulant therapy—careful history taking is a must in such patients. Patients on long-term anticoagulant therapy should be given instructions with regard to bleeding, if surgical procedures like dental extraction are carried out. Anticoagulant dosage should be decreased by the cardiologist before any surgery. Sudden withdrawal of anticoagulant drugs may result in thrombosis or embolism. • Timing of dental treatment—after acute myocardial infraction all dental procedure should be deferred for 3 weeks and after that simple emergency dental treatment can be carried out but with the opinion from physician.
A
B Figs 33-6A and B: (A) Hand deformity in rheumatoid arthritis (B) same hand in palmar view (Courtesy Dr Milind Chandurkar).
Diagnosis Rheumatic Heart Disease and Fever It is an inflammatory complication that may follow group of streptococcal infection; manifested by one or more of the following arthritis, carditis, and chorea. Rheumatic fever usually comes on 1 to 3 weeks after the streptococcal infection.
Clinical Features • Age—it is usually a disease of childhood occurring most often between the ages of 6 to 16 years with peak of 8 years. • Symptoms—chorea (involuntary movement), the symptoms of acute carditis. The child often complains of sore throat and has a temperature of 38 to 39°C.
• History—history of preceding streptococcal infection and predominate manifestation of arthritis and carditis. • Jones diagnostic criteria—Jones criteria of diagnosis of rheumatic fever. At least of two major criteria should be followed. Major criteria
Minor criteria
• • • • • •
• Fever • Arthralgia • Previous rheumatic fever or rheumatic heart disease • Elevated ESR and positive C-reactive protein • Protein raised
Carditis Polyarthritis Chorea Subcutaneous nodule Erythema marginatum Characteristic ECG change
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Management • Rest—bed rest and sedation during acute episode. • Salicylates—salicylates are almost specific for the pain of rheumatic fever. • Prophylaxis—continued prophylaxis against a beta hemolytic streptococcal infection is indicated and given in the form of a monthly injection of 1.2 million units of benzathine penicillin G or in 200,000 units of oral penicillin, given twice daily or 1 g of sulfadiazine, given orally, once a day. Such prophylactic therapy is discontinued after 20 to 39 years of age.
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Dental Considerations Following are suggestions for prophylactic procedures, for reduction of postextraction bacteremia and the possible development of subacute bacterial endocarditis • History—proper history taking about evidence of rheumatic fever, MV prolapse. If there is history of rheumatic fever, administer prophylactic antibiotic therapy before dental procedure. • Antibacterial mouth rinse—make the patient rinse with antibacterial mouthwash, such as chlorhexidine immediately before the treatment to help reduce the number of microorganisms. • Atraumatic procedure—keep dental procedure atraumatic as best possible. • Refer to physician—if a febrile illness develops within 3 months of the dental procedure, refer the patient to physician.
Hypertension Hypertension is the most common and significant medical condition encountered in dental practice. Normal blood pressure is 120/80 mm Hg.
• Secondary hypertension—it may be caused by factors such as renal parenchymal disease, renal artery disease, pheochromocytomas, adrenal cortical hyperfunction and central nervous system lesion.
Clinical Features • Symptoms—patient may complaint of occipital headache, dizziness, nausea, vomiting, malaise, and shortness of breath and nose bleed. In some cases chest pain occurs. In a milder form, there is extensive intraoperative bleeding. • Signs—blood pressure above 160 /100 mm Hg. There is cardiac enlargement and narrowing of retinal arterioles also occurs. Hypertensive patients may lead to hemorrhage, myocardial infarction, cardiac decompression and renal failure. • Odontalgia—odontalgia is observed in hypertensive patients, which occurs due to hyperemia of dental pulp or congestion of this tissue resulting from increase blood pressure. • Drug side effect—many patients in dental office may be reported with gingival enlargement which occurs due to nifedipine (calcium channels blocker) use in hypertensive patients. Antihypertensive medication like thiazides, methyldopa, propranolol, etc. can cause lichenoid reaction in the oral cavity. ACE (angiotensin converting enzyme) inhibitors can cause taste impairment, burning sensation of mouth called as scalded mouth syndrome. Xerostomia can also occur due to many antihypertensive drugs. • Hypertensive crisis—hypertensive crisis is a sudden rise of arterial blood pressure to a very high level (160/100 or 250/150 mm Hg) with clinical and pathological manifestations. Such patients can pose problems involving heart, brain and kidney.
Stages • Stage I (mild) hypertension—a diastolic pressure of 90-99 mm Hg and systolic pressure of 140-160 mm Hg. • Stage II (moderate) hypertension—diastolic pressure of 100 to 109 mm Hg and systolic pressure 160-170 mm Hg. • Stage III (severe) hypertension—it has diastolic pressure 110-119 mm Hg and systolic pressure of 170-190 mm Hg. • Stage IV (very severe) hypertension—it is also called as malignant hypertension. It has diastolic pressure more than 120 mm Hg and systolic pressure of 190 mm Hg.
Types • Primary or essential or idiopathic hypertension—it occurs due to hereditary or environmental cause. Environmental cause includes high sodium intake, excessive alcohol consumption, physical inactivity, smoking and stress.
Dental Significance • Treatment planning—an elevated blood pressure in a dental patient requires careful consideration in treatment planning, premedication, selection of an anesthetic and determining the duration and extent of operative procedure. • Risk of medical emergencies—undetected hypertension increases the risk of experiencing cardiovascular conditions such as angina, myocardial infarction and cerebrovascular accident while undergoing dental care. • Effects of antihypertensive drugs—oral health care can be affected by the known side effects of antihypertensive drugs and their interaction with other medications. • Care of general health—the dentist can perform a valuable patient service by identifying undetected hypertension.
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Specific System Disorders 791 Dental Management • Identification—the dentist should have equipments in the office to measure blood pressure. • Pain control—effective control of operative and postoperative pain should be done after dental procedure. • Stress and anxiety reduction—elevation of blood pressure caused by nervousness or stressful situations should be minimized in hypertensive patients. The patient should not be permitted to struggle when using inhalation analgesia or general anesthesia and adequate oral and parenteral presedation should be used. Patients with known hypertension should have blood pressure checked at each dental visit, to assure that there is no risk of harm from the stress of dental procedure. Very anxious patient should be given 5 mg of diazepam or 30 mg of oxazepam, night before and one hour before the dental appointment. • Limit the use of epinephrine—epinephrine use should be limited in patient with hypertension. The reason for this many patients of hypertension usually suffer from the cardiovascular disease and epinephrine will cause vasoconstriction in these patients. • Avoidance of drug interaction—many NSAID interacts with ACE inhibitors decreasing the efficacy of antihypertensive agents. Vasopressor drugs can interact with nonselective beta blockers provoking hypertensive episode. • Physician referral—if blood pressure is high, patient should be referred to the physician for further observation and regarding the antihypertensive medication. • Emergency extraction—when extraction is necessary on an emergency basis, the hypertensive patient should be hospitalized and local homeostatic measures should be taken to avoid undue hemorrhage. In these patients, proper premedication should be given. • Hypertensive crisis in dental chair—if it arises intraoperatively, patient should rest in semisitting position. O2 may be administered; if it does not help, diazepam may be administered at very slow rate. If this is not helpful, the patient should be left to the care of medical physician. In the mean time, injection frusemide is given intravenous and 10 ml capsule of nifedipine may be broken and sprinkled sublingually to bring the blood pressure down. • Management of side effects of drugs—xerostomia should be managed by pilocarpine, sugarless mint or gums and minimizing caffeine intake. Gingival overgrowth is reduced by excellent oral hygiene. Lichenoid reaction is treated by topical corticosteroids.
Infective Bacterial Endocarditis It is a serious disorder which is the most common bacterial origin but on occasion, it may be mycotic. Causes of
endocarditis of dental origin are almost always caused by bacteria of low virulence, that slowly attack a previously damaged endocardium, causing subacute bacterial endocarditis.
Pathogenesis • Organism responsible—it is usually caused by oral microorganism like alpha hemolytic streptococci, enterococci, pneumococci, staphylococci and group A streptococci. • Damaged blood flow—in normal patients blood becomes sterile after this transient phase. In patients with damaged heart valves, initially there is formation of a sterile platelet fibrin clot or thrombus on the damaged heart surface. It acts as nidus for bacterial proliferation, subsequently leading to infective endocarditis. • Oral bacteremia—dental procedure can lead to release of bacteria into the blood circulation. The most common type of organism responsible for this oral bacteremia is streptococci viridians which are abundantly found in the mouth. It occurs in person who is having poor oral hygiene and undergoing extraction. • Consequence of infective endocarditis—infective endocarditis will lead to proliferation of bacteria on the damaged heart surface can lead to impaired valvular function, congestive heart failure, abscess of myocardium due to production of pus and release of infectious emboli which can get lodged in organs such as brain, kidney and spleen.
Predisposing Factors • Heart disease—it has marked predisposition for persons with rheumatic or congenital, cardiac or vascular defect, bicuspid aortic valve, leutic aortic valvular disease, idiopathic hypertrophic subaortic stenosis and mitral valve prolapse. • Surgical correction—recent surgical correction of congenital valvular defect within 6 months. • Hypertrophic cardiomyopathy—it can also occur in hypertrophic cardiomyopathy. • Surgical trauma—surgical trauma and dental extraction are commonly related chronologically, to the onset of clinical symptoms.
Clinical Features • Age—it can occur at any age, but most common in middle age group. • Progress—after formation of vegetative lesion (thrombi), they serve as foci of the intermittent dissemination of microorganisms throughout the body. These vegetative lesions are friable and small pieces may break off and form septic emboli.
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• Symptoms—the patients experience progressive weakness, loss of weight, dyspnea, anorexia, muscular and joints aches and pains, with low grade fever. • Signs—Petechial hemorrhage in the conjunctiva and oral mucosa occur due to septic emboli. • Larger emboli can lodge occasionally in spleen, kidney, lungs and brain where they produce symptoms referable to the structure and the organs involved.
should be instructed to consult physician if a febrile illness develops within 3 months of a dental treatment. • Antibacterial mouth rinse—make the patient rinse with an antibacterial mouthwash, immediately before dental treatment, to help reduce the number of oral microorganisms. • Atraumatic dental procedure—keep dental treatment as atraumatic as possible.
Diagnosis
Congestive Cardiac Failure
• Clinical diagnosis—it is frequently made by elimination of other conditions. The disease should be suspected in any patient with valvular heart disease, who has unexplained fever for week or more, or exhibits embolic phenomenon or an unexplained anemia.
It is the condition where the heart fails to maintain an output sufficient for the needs of the body.
Management • Antibiotics therapy—intensive antibiotic therapy, usually 20,000,000 units of penicillin in combination with gentamicin for 2 weeks should be given. • Removal of infected valve—early removal of infected valve should be done with sterile replacement.
Dental Considerations • Oral cavity, a source of infection—organisms responsible for subacute bacterial endocarditis were disseminated commonly through bloodstream, following dental extraction. It was demonstrated that gingival sulcus was an important site from which the bacteria gained entrance into the bloodstream. Actual cauterization of gingival crevice before extraction markedly reduces the percentage of transient bacteremia. Even in the absence of direct dental procedure, bacteremia can be produced secondary to foci of infection in the oral cavity. • Prophylactic measure—every known prophylactic measure should be taken to preclude the possibility of transient bacteremia occurring in patients with known vascular lesions.
Prevention • Proper history should be taken—ask the patient about history of rheumatic fever, heart disease with valvular involvement or heart murmur. • Prophylactic antibiotics therapy—if the heart disease to endocarditis is known to be present, administer the prophylactic antibiotic therapy before the dental treatment. • Physician consultation—if questionable positive history of heart disease is obtained, you have to consult the patient’s physician. All patients who are at risk of developing endocarditis, subsequent to dental treatment,
Classification • Low output cardiac failure—there is a primary lesion in heart which decreases the contractibility of the heart and causes diminished cardiac output. • High output cardiac failure—there is primarily no lesion in the heart, but due to extra cardiac condition, there is increased work load on the heart which causes cardiac failure with increased cardiac output.
Causes • Low output failure—it is caused by myocardial lesions like ischemic heart disease, rheumatoid heart disease, cardiomyopathy, valvular endocarditis, congenital heart disease and vascular lesions like hypertension and aneurysm of aorta. • High output failure—thyrotoxicosis, anemia, hypoproteinemia, beriberi, AV Fistula and cirrhosis of liver can cause congestive cardiac failure.
Clinical Features • Symptoms—there is increased breathlessness following moderate exertion, chronic productive cough associated with blood tinged sputum. Patient also complains of wheezing, anorexia, bronchospasm, and dyspnea. • Signs—pitting edema of lower extremities, hepatic enlargement, and generalized edema. Congestion of the large veins of neck and raised jugular venous pressure. There is also cyanosis of lips, tongue and oral mucosa with ankle edema.
Diagnosis • Clinical diagnosis—breathlessness, generalized edema and raised jugular venous pressure will give clue to diagnosis.
Management • Bed rest—complete bed rest is required. • Digoxin—it should be the first line therapy for heart failure. • Diuretic—in cardiac failure, there is always sodium and water retention, hence diuretics are given.
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Specific System Disorders 793 • Vasodilators—vasodilators are given, e.g. nitroprusside— 5-10 mg/min. • Oxygen—it can be administered for proper circulation. • Massage—massage of lower limb to maintain peripheral circulation.
Dental Considerations • Heart attack in dental office—the dentist should watch for early signs of congestive cardiac failure like cyanosis of lips, tongue. If the patient develops acute pulmonary edema in the dental office, patient should be made comfortable in sitting position or semisitting position and administered 100% O2. Injection frusemide and aminophylline should be given. Physician should be immediately called for.
Congenital Heart Disease Congenital heart diseases are the most common types of anomalies present in child and more common as compared to rheumatic diseases.
Clinical Features • Symptoms—they are variable. Some children manifest breathlessness, inability to thrive, growth retardation and central cyanosis. • Persistent ductus arteriosus—it is failure of closure of ductus arteriosus which plays role in fetal life as most of the blood passes through ductus arteriosus into the aorta. It results in recirculation of blood through the lungs, leading to increased workload on the heart. It occurs commonly in women. Affected individuals may suffer from growth retardation, dyspnea, cyanosis and cardiac failure. Surgical correction is possible in some cases. • Atrial septal defect—it results in shunting of blood from left atrium and then to the right ventricle and pulmonary arteries, leading to progressive enlargement of the right side of the heart and the pulmonary artery with its branches. Females are affected more than males. There is dyspnea, cardiac failure and arrhythmias. It is treated by surgical closure. • Ventricular septal defect—it is usually asymptomatic. • Pulmonary stenosis—it occurs either alone or along with atrial septal defect or ventricular septal defect. Larger pulmonary stenosis results in dyspnea, fatigue or syncope.
Oral Manifestations • Bluish red discoloration—general bluish red discoloration of oral mucosa with severe marginal gingivitis and bleeding.
• Tongue—tongue is often deeply fissured and edematous. • Delayed eruption—both permanent and deciduous teeth are delayed in eruption. • Enamel hypoplasia—this is also frequently present in patient with congenital heart disease. • Skimmed milk appearance—teeth will have bluish white skimmed milk appearance with vasodilation in the pulps.
Diagnosis • Clinical diagnosis—generalized bluish discoloration of oral muscle with symptoms of atrial septal defect and persistent ductus arteriosus.
Management • Antibiotics prophylaxis—antibiotics cover is needed for operative procedure. • Cardiac surgery—this should be done to correct congenital anomalies.
Dental Considerations • Adequate analgesia—adequate analgesia should be given to the patient during oral surgical operation. General anesthesia should be avoided. • Conscious sedation—conscious sedation with nitrous oxide should be given with approval of physician. • Avoid using gingival retraction cord containing epinephrine—gingival retraction cord containing epinephrine should be avoided.
Cardiac Transplantation These patients are on immunotherapy for life. Too little therapy will result in rejection of episode, while too much runs the risk of both infection and neoplasm. Opportunistic infections like fungal, protozoal and viral infection are common in these patients. Dental treatment after transplantation should be carefully planned in view of the patient’s lower immune status with particular attention to WBC count and Hb concentration. Before performing any treatment, the dentist should take consent of the patient’s physician and consider antibiotic prophylaxis. As many of these patients are on long-term steroid therapy, steroid supplements should be given. Prophylactic antibiotic dose and its indications: • Amoxicillin—3 gm orally, 1 hr before the procedure. 1.5 gm 6 hours after the initial dose. • Patients with allergy to penicillin—Erythromycin ethyl succinate 800 mg, Erythromycin stearate 1 gm orally, 2 hours before the procedure. Clindamycin 300 mg 1 hour before the procedure and 150 mg, 6 hours after the initial dose.
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Coarctation of Aorta It is a developmental anomaly characterized by marked diminution in the caliber of aortic arch, just distal to where the left subclavian artery arise. Patient suffers from secondary hypertension and cerebral aneurysm with hemorrhage. Intraorally there is marked enlargement of mandibular arteries and branches leading to individual teeth. Arterial hemorrhage will occur following tooth extraction. Pulp of all the four maxillary incisors were markedly enlarged and funnel shaped, occupying great portion of crown and roots.
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Respiratory Disorders Bronchial Asthma Asthma is a common disease estimated to affect 4 to 5% population. It is initially a spontaneously, reversible, spasmodic contraction of the smooth muscles of bronchi resulting in bronchiolar narrowing. As the attack progresses, resistance to airflow may be further exacerbated by mucosal edema and inflammatory infiltrate of mucosa.
Types • Extrinsic asthma—it is developed by allergic factors. It is also called as allergic asthma. Patient, who is having asthma of allergic origin, often has positive family history of disease and positive atopic history including hay fever, rose fever and eczema. • Intrinsic asthma—it is precipitated by nonallergic factors. It is also called as non-allergic asthma, idiopathic asthma and infective asthma. • Mixed asthma—it is combination of allergic and nonallergic asthma. • Status asthmaticus—it is persistent exacerbation of asthma.
Predisposing Factors Extrinsic asthma • Airborne allergen—house dust, feathers, animal dander, furniture stuffing, fungal spores and a wide variety of plant pollens. • Allergenic food—it includes cow’s milk, eggs, fish, chocolate, shellfish and tomatoes. • Allergic drug—it includes penicillin, vaccines and aspirin. Intrinsic asthma • Infections—respiratory infections, usually viral, are well known initiating factor in the asthmatic patient. • Exercise—some patients have acute asthmatic attack after prolonged exercise.
• Psychological—emotional stress such as nervousness, anxiety can cause asthmatic attack. The dental office is a common site for asthmatic attack. Child may develop asthmatic attack after taken into treatment room and recover after moving out from treatment room.
Clinical Features • Age—it is more common in children, especially boys. It can also occur in older individuals. • Symptoms—patients notice a sensation of fullness in the chest. Predominately, symptoms of acute attack are wheezing, coughing and labored breathing. There is also sneezing and gasping sounds are heard while attempting to breath. • Attack termination—termination of attack is usually heralded by a period of intense coughing with expectoration of thick, tenacious mucous plug which is followed by sensation of relief. • Signs—with severe attack, the patient is extremely anxious and agitated. Heart rate is increased to 130 per minute. Cyanosis of mucous membrane of lips may be visible along with perspiration and flushing of face and upper torso in severe attack. Patient is more comfortable if allowed to sit or stand upright with the back upright and the chest, shoulder and head fixed. • Extrinsic asthma—bronchospasm usually develop within minutes after exposure to allergens. These attacks usually become less frequent and less severe during middle and late adolescence and may disappear entirely. • Intrinsic asthma—attack of intrinsic asthma is usually more fulminant and severe than those of allergic asthma. The long-term prognosis is poorer and the patient eventually exhibits clinical signs and symptoms in interval between acute episodes. • Status asthmaticus—in it, acute asthmatic attack persists in spite of drug therapy. Bronchospasm may continue for hours or even days without remission. Patient more commonly exhibits extreme fatigue, dehydration, severe hypoxia, cyanosis, peripheral vascular shock and drug intoxication from intensive therapy. Chronic partial airway obstruction may lead to death from respiratory acidosis.
Diagnosis • Clinical diagnosis—diagnosis of bronchial asthma is based on the symptoms, pulmonary function test and physical finding of expiratory wheezes during the acute attack. • Laboratory diagnosis—there is raised total IgE and specific IgE antibody concentration.
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Specific System Disorders 795 Management
Chronic Obstructive Pulmonary Disease
• Sympathomimetic amine—use of drugs like terbutaline, isoproterenol and metaproterenol as first line therapy. It dilates and prevents bronchial smooth muscle constriction. • Xanthine derivatives—xanthine derivatives like aminophylline and theophylline can be used. It inhibits the hydrolytic degradation of cyclic AMP. • Corticosteroid—corticosteroids like hydrocortisone and prednisone can also be used. It lessens intensity of antigen-antibody reaction. • Omalizumab—it is recombinant humanized monoclonal anti-IgE antibody, will cause reduction in total serum IgE and thereby decreasing the symptoms of asthma. • Sodium cromoglycate—cromolyn sodium is used. It protects against mast cell destruction. • Combination—inhaled corticosteroids with bronchodilators. • Antihistamine—antihistaminic usually are useful because they produce drying and obstruction of air. • Emergency management—emergency treatment is inhalation of a solution containing 0.1 mg isoproterenol or 1:1000 epinephrines by nebulizer or injection of 0.1 ml of 1:1000 epinephrines. Continuous inhalation by nasal catheter is helpful to relieve the hypoxia. • Hydration—hydration is necessary in the form of 5% glucose in water because there is dyspnea.
It is characterized by airway obstruction and breathlessness.
Dental Considerations • Avoid inhalation anesthetics—patient using betaadrenergic inhaler should be reminded to bring the inhaler with them to dental office; the dentist should avoid inhalation anesthetics or analgesic in asthmatic patient because of the possibility of stimulating an acute asthmatic attack. • Dental work—if attacks are seasonal, routine dental work can be performed during the time when frequency of attack is lowest. Patients on steroids may require additional steroid to avoid serious reaction to stress of dental procedure. • Attacks in dental chair—in case of acute attack occurring on dental chair, following measures should be taken: • Terminate the procedure—terminate the dental therapy and position the patient in any comfortable position. • Administration of bronchodilators—0.5 ml, 1:1000 adrenalines can be injected subcutaneously or intramuscularly. If attack is prolonged, steroids are indicated • Aerosol spray—the onset of aerosol drug is rapid and relief of symptoms occurs within seconds. • Administer oxygen—it may be administered by full face mask, nasalhood or nasal cannula.
Types • Chronic bronchitis—it refers to inflammation of bronchi. It is defined as a condition in which there is mucus producing cough present, for at least 3 months of the year, for more than 2 consecutive years. • Emphysema—it is dilatation of air spaces distal to terminal bronchioles with destruction of alveoli reducing alveolar surface area for respiratory exchange.
Causes • Smoking—the most common cause of COPD is smoking. • Environmental dust—the other factors are chronic recurrent infection, air pollution and occupational inhalants. • Deficiency of antiproteolytic enzyme—deficiency of antiproteolytic enzyme alpha 1-antitrypsin is a rare cause of emphysema.
Clinical Features • Early morning cough—patient shows early morning mucoid cough which becomes purulent during exacerbation. • Pink panter or pink puffer—this is present in emphysema in hyperventilation, occurs to maintain normal blood gases. This will cause vasodilatation and patient will be pink due to CO2 retention. • Cutaneous vasculitis—in some cases of emphysema cutaneous vasculitis may be present (Fig. 33-7).
Fig. 33-7: Cutaneous vasculitis seen in respiratory disease (Courtesy Dr Milind Chandurkar).
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• Blue bloated appearance—this is present in chronic bronchitis. In this patient is unable to maintain hyperventilation and become hypoxic. This will lead to central cyanosis, ankle edema, and raised jugular venous pressure of cor pulmonale to give blue bloated appearance. Wheezing, dyspnea and cough. • Later stage—in the later stage, there can be blood tinged sputum and fever.
Diagnosis • Clinical diagnosis—cutaneous vasculitis with pink panter with blue bloated appearance will aid in diagnosis.
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Management • Stoppage of habit—patient should ask to quit the habit of smoking. • Bronchodilator—bronchodilators are particularly effective in relieving bronchospasm. Bronchodilators used are ipratropium bromide, oxitropium, and theophylline. • Antibiotics—antibiotic therapy should be initiated with earliest sign of chest infection. Antibiotics used are amoxicillin, trimethoprim, or tetracycline. • Oxygen therapy—oxygen is useful both, intermittently on a chronic basis and continuously with an acute exacerbation of disease.
violent attacks of coughing, accompanied by shortness of breath and chest pain are classic symptoms of pulmonary foreign bodies. Dental procedures are directly or indirectly involved in a high percentage of foreign body problems hence, the cooperation of the dentist is essential for the prevention of these accidents. Dentures are important indirect cause of foreign body accident. The tactile sense of the denture patient is severely impaired by the dentures and the foreign body (usually bones) may pass the point of recovery by reflex action before the patient becomes aware of it. Dentures can become embedded in the soft tissue or block the respiratory and alimentary tract, without being detected by the X-ray (as denture material is radiolucent) such as in high velocity automobile accidents. Denture foreign body can be a portion of tooth, a restoration or an operating instrument that is lost during dental treatment, tooth fragment, instrument during surgery and prosthesis lost by the patient. The risk of respiratory tract foreign body can be eliminated almost entirely by the use of the rubber dam or throat packs. Complete and partial dentures should be removed during sleep, unconsciousness and before surgery.
Renal Disorder Renal Failure
Dental Considerations • Upright position—patient should be treated in upright position. If patient is flat there are chances of breathlessness. • Avoid using rubber dam—the patient’s tolerance to partial airway obstructing devices such as rubber dam is less so use of rubber dam should be avoided. • Short treatment time—mucus producing cough, wheezing, and dyspnea in these patients prevent long treatment sessions. This should be taken into consideration while planning the dental therapy. • Inhalation analgesic—inhalation analgesic should be given only when it is necessary and in conjunction with anesthesiologist. • Drug interaction—as patient is taking theophylline, many drugs like epinephrine, erythromycin, clindamycin, etc. should be given cautiously. • Avoid giving general anesthesia—patient should be avoided giving general anesthesia unless it is very necessary.
Pulmonary Foreign Bodies Foreign bodies occluding or obstructing a main respiratory passage will produce cyanosis and asphyxia. Sudden and
Renal failure produces a standard symptom complex, regardless of the underlying cause. It is caused by many diseases.
Etiology • Glomerulonephritis—it represents a heterogeneous group of disease of varying etiologies that produce irreversible impairment of function. The attack of glomerulonephritis is either streptococcal or nonstreptococcal. Chronic glomerulonephritis has usually very slowly, but steadily progressive course, leading to renal failure or uremia in few years to as many as 30 years. • Pyelonephritis—it refers to the effect of bacterial infection in kidney, with E. coli being the cause of infection. Any obstruction of urinary tract can predispose to active pyelonephritis and also can occur due to generalized sepsis in patients with bacterial endocarditis or with staphylococcal infection. Clinically, there is sudden rise of body temperature, shaking chills, aching pain in one or both costovertebral areas or flanks and symptoms of bladder inflammation. • Hemolytic uremic condition—this condition is caused by E. coli.
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Specific System Disorders 797 • Other diseases—other diseases which can cause renal failure are polycystic renal disease, nephrosclerosis, diabetic nephropathy, collagen vascular disease, hereditary nephropathy, analgesic abuse nephropathy, obstructive nephropathy, gouty nephropathy, neoplastic nephropathy, etc.
Diagnosis • Clinical diagnosis—variety of clinical symptoms occur in it with oral manifestation. • Radiological diagnosis—pulpal narrowing with loss of lamina dura can be seen.
Management
Clinical Features • Gastrointestinal—nausea, vomiting, anorexia, parotitis, gastritis and gastrointestinal bleeding. • Neuromuscular—headache, myoclonic jerks, peripheral neuropathy, paralysis, seizures and asterixis. • Hematological and immunological—normocytic and normochromic anemia, coagulation defects, increased susceptibility to infections, decreased erythropoietin production and lymphocytopenia. • Endocrine and metabolic—renal osteodystrophy, secondary hyperparathyroidism, impaired growth and development, loss of libido and sexual function and amenorrhea. • Cardiovascular—arterial hypertension, congestive heart failure, cardiomyopathy, pericarditis and arrhythmias. • Dermatological—pallor, hyperpigmentation, ecchymosis, uremic frost, pruritus, reddish brown distal nail beds.
Oral Manifestations • Incidence—in the study of renal patients, 90% were found to have oral manifestations. • Ammonic taste and smell—patients complain of ammonic taste and smell, particularly in the morning. It is caused by the high concentration of urea in saliva and its breakdown to ammonia. • Xerostomia—the patients may complain of xerostomia which is caused by direct involvement of salivary gland, chemical inflammation, dehydration and mouth breathing. • Erythemopultaceous form—the acute rise in BUN level may result in uremic stomatitis, which appears as erythemopultaceous form, characterized by red mucosa covered with a thick exudate and a pseudomembrane. • Ulcerative form—in some cases, stomatitis may be in ulcerative form which appears as frank ulceration with red and pultaceous coat. • Low caries activity—low caries activity despite of high sugar intake; poor oral hygiene due to increased salivary urea nitrogen. • Enamel hypoplasia—it is frequently seen in patients where renal disease is started at young age. • Other—there is pulpal narrowing and calcification, severe tooth erosion and loss of lamina dura can also be seen.
• Hemodialysis—to remove nitrogenous and toxic products of metabolism from blood by means of a dialysis system. • Peritoneal dialysis—in it, 1-2 liters of dialysate are placed in the peritoneal cavity to remain there for varying intervals of time. Main advantage of this is that there is no risk of air embolism and blood leak. • Drug treatment—Aminoglycoside (gentamicin), antimicrobial (penicillin), analgesic (acetaminophen), narcotic (codeine, morphine), sedative (diazepam), amitryptline, antihistaminic (chlorpheniramine), phenytoin and lidocaine. • Kidney transplantation—it involves surgical removal of a kidney from a donor and implantation into a recipient. This method is for prolonged life in patient with end stage renal failure; the kidney transplantation patient receives a continuous regimen of immunosuppressive medication to ensure graft survival.
Dental Consideration • Many patients who are receiving dialysis have conditions of oral neglect. • Dialysis—if time and patient’s conditions permit, dialysis should be part of the preoperative preparation. Dialysis will return the state of hydration, serum electrolyte, urea nitrogen and creatinine toward normal and will reduce the need for dialysis in the immediate postoperative period. • Control of bleeding—as bleeding is common problems in renal failure patient, hemostatis should be done with the help of desmopressin, cryoprecipitate and conjugated estrogens. • Position of patient in dental treatment—blood flow through the arm should not be impeded by requiring the patient to assume a cramped position or using that arm to measure blood pressure. Patient should avoid sitting for long periods of time with leg dependent. If dental treatment is long, then patient should be allowed to walk for few minutes every hour. • Infective endocarditis—the presence of an access site increases the susceptibility to infective endocarditis. Antibiotic prophylaxis is required for control of infective endocarditis. Start with broad spectrum antibiotic, e.g. amoxicillin 3 g, 1 hr before treatment and 500 mg every 8 hours for 1-2 days.
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• Candidial infection—candidal infection can occur in oral cavity. For candidiasis, administer nystatin mouthwash 5000000u/ml QID, day before the treatment and 2 days after dental treatment. • Medication in dialysis patient—most drugs are excreted at least partially by the kidney. Following are the drugs to be avoided in dialysis patients: • Nonsteroidal anti-inflammatory drugs—it may induce sodium retention and impair the action of diuretics, prevent aldosterone production and cause acidosis. • Tetracycline and steroids—they are antianabolic and increase urea nitrogen to twice the baseline level. • Phenacetin—it is nephrotoxic and puts added strain on an already damaged kidney. • Benzyl penicillin—this has got significant potassium content and can be neurotoxic. So this drug is contraindicated in renal failure. • Others—other drug which should be contraindicated are absorbed antacids, carbenicillin in large doses, ascorbic acid, ammonium chloride and laxatives.
Renal Osteodystrophy It occurs due to defect in hydroxylation of 25-HCC to 1, 25DHCC a process that normally occurs in kidney. Hypocalcemia occurs due to impaired calcium absorption and hyperphosphatemia, due to reduction in renal phosphorous excretion. Hypocalcemia results in secondary hyperparathyroidism with increased level of serum parathyroid hormone. Systemic acidosis is also associated with these conditions. There are symptoms of chronic renal failure.
Clinical Features • Myopathy—muscle cramps are more common; ‘restless leg syndrome’, where patient’s legs jump at night. • Neuropathy—sensory neuropathy may cause paresthesia. Motor neuropathy may present as foot drop. Autonomic neuropathy may cause delayed gastric emptying, diarrhea and postural hypotension. • Endocrine function—there may be hyperporlactinemia and hyperparathyroidism. Amenorrhea is common in females. There is also loss of libido and sexual functions. Growth retardation occurs in children and bone fractures occur frequently. • CVS effects—hypertension results in 80% of patients. This is due to sodium retention and increased secretion of renin, angiotensin-I and aldosterone. Atherosclerosis is common. • Acidosis—there is also acidosis; cellular and humoral immunity are impaired. • Bone—in adults, gradual softening and bowing of bone occurs.
Radiographic Features • Radiodensity—generalized loss of bone density and thinning of bony cortex. • Lamina dura—loss of lamina dura. • Angle of mandible—thickness of cortex of mandibular angle is reduced. • Medullary spaces—increase in medullary space at the expense of trabeculae. Other bones may show areas of sclerosis.
Diagnosis • Clinical diagnosis—myopathy, neuropathy can give clue to diagnosis. • Radiological diagnosis—generalized loss of bone density with thinning of bony cortex will aid in diagnosis.
Management • Vitamin D—plasma Ca++ and K+ are kept as near as normal. • Vitamin D—hypocalcemia is corrected by giving hydroxylated synthetic analogues of vitamin D. • Phosphate binding agents—hyperphosphatemia is controlled by dietary restriction of foods with high phosphate content (like milk, cheese, eggs) and the use of phosphate binding drugs.
Uremia It is a clinical condition caused by the retention of urinary constituents in the blood. The characteristic symptoms are headache, itching, nausea, convulsions, and eventually coma. Patient’s breath may have urinous odor. There is unpleasant taste and dryness of mouth. There is erythematous, pseudomembranous type of uremic stomatitis. If pseudomembrane is removed, it will expose dry, red, swollen mucosa. The oral bleeding tendency, often observed in patients with uremia, is due to uremic thrombopathy. Patient has an increased disposition to develop oral candidiasis.
Kidney Transplantation In order to prolong life in patients with end stage renal failure, renal transplantation is done. It involves surgical removal of kidney from living first degree relative such as sibling, parent, child or a recently expired source. Kidney transplant patient usually receives a continuous regimen of immunosuppressive medication to ensure graft survival.
Clinical Features • Majority of clinical manifestation occur secondary to immunosuppressive drugs.
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Specific System Disorders 799 • Buffalo hump—steroids are responsible for cushingoid effect, characterized by rapidly acquired adiposity about the upper portion of the body, mooning of face and tendency to become round shouldered and develop a ‘buffalo hump’ at the base of neck. • Infection—there is increase susceptibility to fungal infection due to decreased migration and impaired phagocytic function of leukocytes and macrophages. • Hepatic dysfunction—cyclosporine can cause hepatic dysfunction because metabolism occurs exclusively in the liver.
Oral Manifestations • Oral mucosa—pale mucosa with diminished color demarcation between attached gingiva and alveolar mucosa. • Salivary gland—enlarged salivary glands and decreased salivary flow resulting in xerostomia. • Odor and taste—odor of urea on breath and metallic taste. • Teeth—enamel hypoplasia, dark brown stain on crowns, dental malocclusion, and low caries rate. • Gingiva—increase in calculus formation, low grade gingival inflammation and bleeding from gingiva and mouth. • Candidiasis—candidal infection can occur on tongue. • Other—petechiae, ecchymosis, erosive glossitis, burning and tenderness with dryness of mucosa. Dehiscence of wounds also occurs.
Radiological Features • Demineralization of bone—there is demineralization of bone with loss of bony trabeculation. • Ground glass appearance—sometimes, ground glass appearance can be seen. • Other finding—loss of lamina dura, socket sclerosis is other radiological findings.
Diagnosis Diagnosis can be made by history.
• Defer dental treatment—after transplantation, routine dental treatment should be postponed until maintenance dose; of immunosuppressive agents is reached. • General guidelines for managing the kidney transplant patient who is taking corticosteroids: • Always use long acting anesthetics agents such as bupivacaine. • Use mild sedatives for apprehensive patients. Use postoperative pain medications, when indicated. • Patients who are receiving alternate day corticosteroid therapy should be treated on off day. • If the patient is receiving daily therapy, then the dosage of oral steroids should be doubled the day before, the day of and 2 days after treatment. • Alternatively, single dose of 100 mg dose of hydrocortisone hemisuccinate should be given intramuscularly just before the treatment and extra 20 mg dose should be given early that evening. • Following steps should be taken for proper management of renal transplant patients: • The patient’s physician should be consulted to coordinate treatment. • Broad spectrum antibiotics should be used in prophylactic medication of the patient, before dental treatment, because of decreased immune status. • Complete blood count with differential and platelet count should be obtained before any surgical procedure as corticosteroids can cause myelosuppression.
Disorders of Gastrointestinal Tract Hepatitis It is an acute, inflammatory and infective infection caused by hepatitis A, B, C, D and NANB viruses. Dentists are 3 to 4 times more likely to be exposed to hepatitis than with general population.
Types
Dental Considerations • Elimination of source of infection—Oral infection in transplant patients has been reported as frequently as pneumonia or urinary tract infection. Prompt diagnosis of the site and cause of infection in immunosuppressed patient should be on high priority. Identification of pathogens should be performed with culture, sensitivity, smear, aspiration technique or biopsy. The successful management of transplant patient begins before transplantation, with the preoperative elimination of potential sources of infection.
• Hepatitis A—it is also called as infectious hepatitis. It is endemic and occurs in person who lives in poor living condition. Spread of hepatitis A is by orofecal route. The period of infectivity is highest during the week before the onset of clinical symptoms. It is common in children, primary and nursery school age. Once it occurs it gives life long immunity. • Hepatitis B—it is also called serum hepatitis. It is transmitted by parenteral route, for example, blood and blood products and contaminated needles. It can also be transmitted due to close personal contact. It is also found in saliva, semen and vaginal secretions. 5 to10%
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of infected person remain as carriers. Hepatitis B tends to have greater mortality and morbidity than hepatitis A. Hepatitis C—it is caused by hepatitis C virus and it is responsible for sporadic viral hepatitis in intravenous drug user, and in patient with renal dialysis. It has got less clinical severity as compared to hepatitis B. It is associated with lichen planus, lymphoma, and cryoglobulinemia. Hepatitis D—it is called by delta agents or hepatitis D virus. It is incomplete virus carried within hepatitis B virus and will replicate in presence of HBsAg. So this infection occurs in association with hepatitis B infection. It is spread by parenteral route. It has got same clinical features as that of hepatitis B. Hepatitis G—it is caused by hepatitis G virus or GB virusC. Many of this patient is infected with hepatitis C virus. It produces clinical symptoms less severe to hepatitis C. Posttransfusion hepatitis—this is caused by newer hepatitis virus like TTV (transfusion transmitted virus), SEN D and SEN H. These virus are not transmitted during dentistry.
Phases of Hepatitis • Prodromal phase—is of 1-2 weeks; symptoms like anorexia, nausea, malaise and fever occur. • Icteric phase—(6-8 weeks) anorexia, nausea, vomiting and pain in the right upper quadrant of abdomen. Hepatomegaly and splenomegaly may also be seen. • Convalescent (recovery) phase—symptoms disappear, but abnormal liver function values may persist.
Clinical Features • Incubation period—in this, most cases resolve completely within 4 months after onset of symptoms but, some end in fulminating disease and others progress to chronic hepatitis. • Symptoms—systemic complains include malaise, arthralgia, morbilliform skin rash, anorexia, vomiting and myalgia. Patient has high grade fever with tenderness and enlargement of liver. Patient also complains of upper respiratory tract infection, distaste for cigarette, fever and enlargement of liver. • Signs—jaundice, darkening of urine, splenomegaly and whitish stools occurs. • Oral manifestation—icterus of the oral mucosa, which is seen on the palate and in the sublingual region.
Laboratory Findings • Plasma bilirubin level—plasma bilirubin level excess of 3 mg/dl. • SGPT SGOT level—SGPT, SGOT levels increase 10 times in hepatitis.
• Alkaline phosphate level—liver enzymes such as alkaline phosphatase and lactic dehydrogenase show slight elevation. • WBC—WBC shows leukopenia, leukocytosis and atypical lymphocytes. • Australia antigen—demonstration of HBsAg or Australia antigen.
Management • General treatment: • Symptomatic treatment— like bed rest and prevention by isolation of blood, saliva contaminated objects; use of gloves and apron and sterilized instruments are must. • Nutrition—a high calorie diet should be given. It is usually given in morning because many patients experience nausea in evening. • Drugs—there is no specific drug useful for it. But interferon and ribavirin have been tried, with some success in chronic hepatitis. • Prevention—the patient should avoid salivary transmission to others by avoiding kissing, spitting and sharing food, cigarettes, utensils and sexual contact. • Hepatitis A—it is self limiting and resolves with in one month mortality is very low. Treatment is usually symptomatic. • Hepatitis B—chronic hepatitis B infection can be treated with lamivudine or interferon. Treatment is needed for 1 to 3 years. • Hepatitis C—chronic hepatitis C is treated by combination of ribavirin, interferon alpha or pegylated interferon. • Hepatitis D—drug treatment with alpha interferon is effective. • Hepatitis G—alpha interferon is also effective against hepatitis G.
Prevention • Hepatitis A—people who are known to have contact with a patient, such that they may have ingested minute amounts of fecal material or have been injected with as little as 0.0004 ml of infected blood, should be given prophylactic gamma globulin injections. • Hepatitis B—a vaccine has been prepared from the plasma of asymptomatic carriers of hepatitis B. It is composed of non-infectious hepatitis B surface antigen particles. It is recommended in all high-risk groups. • Hepatitis C—there is no vaccine available for this hepatitis. Preventing measure like not sharing personal item with bloodstain, not sharing needle in drug user, avoid having tattoo without strict health precaution.
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Specific System Disorders 801 • Hepatitis D—vaccination against hepatitis B will also give protection against hepatitis D.
Dental Considerations • Risk to dental professional—hepatitis B, C and other types can be transmitted to the dentist by blood contaminated needles or instrument stick from an infected patient in acute phase of disease. • Clotting factors assessment—if surgery is necessary, obtain preoperative prothrombin time and bleeding time, as in liver diseases deficiency of clotting factor may be present. • Universal infection precaution—dental personnel may act as a source of infection to patient. Dentists who are carriers of HBV and who do not practice universal infection control precautions can transmit the infection to patient. At the same time it is required to avoid infection from patient to be transmitted to dental personnel. • Strict aseptic procedure—strict aseptic procedure—use of masks, gloves for all persons is a must. • Minimize aerosol production—minimize aerosol production by using a slow speed handpiece and using air syringe.
Inflammatory Bowel Disease Chronic infectious diseases of small intestine and large bowel are of interest for dentist because of the oral manifestations that have been reported. In some of the cases it can be initial finding.
Fig. 33-8: Linear ulceration in buccal vestibule with diffuse nodular swelling (Courtesy Dr Milind Chandurkar).
• Aphthous ulcer like lesion—Lesions resembling aphthous ulcer may occur. • Orofacial granulomatosis—an oral granulomatous lesion occurs as nodular mass in mucobuccal fold. • Cobblestone appearance—it shows cobblestone pattern of swelling on buccal mucosa. • Linear ulceration—there is linear hyperplastic fold with ulceration (Fig. 33-8). • Swollen lip—it appears swollen and indurated.
Diagnosis Types • Ulcerative colitis—it is an inflammatory disease that is confined to the mucosa and submucosa of colon. • Crohn’s disease—it is an inflammatory disease involving the entire wall of a portion of small gut.
• Clinical diagnosis—linear ulceration with granulomatous lesion with gastrointestinal symptoms may give clue to diagnosis. • Laboratory diagnosis—biopsy shows non-necrotizing granulomatous inflammation.
Clinical Features
Management
• Age—it is seen in teenagers as compared to adults. • Symptoms—upper and lower abdominal pain, usually cramping in nature along with fever and episodes of bloody diarrhea. Weight loss and malnutrition may occur in these patients. • Anorectal fistulae—anorectal fistulae develop, as well as segmental narrowing of the intestinal lumen and rectal bleeding. • Erythema nodosum—in some cases, there is presence of erythema nodosum of skin.
• Sulfa drugs—patient can respond to sulfasalazine. The metabolites of which are concentrated in the intestinal tissue. • Corticosteroids—corticosteroids such as prednisolone can be use in combination with immunosuppressive drug azathioprine. Therapy is being used in increasing frequency in inflammatory bowel disease. • Management of oral lesion—oral lesion are treated by topical and intralesional corticosteroids. Persistent lesions are treated with thalidomide.
Oral Manifestations
Dental Considerations
• Site—the most frequently affected areas are the buccal mucosa, vestibule and lip.
• Precaution—it may necessitate alteration of dental therapy or special precautions on the part of dentist.
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• Corticosteroids therapy—patients on corticosteroid therapy may develop both, hyperglycemia and osteoporosis, both of which have adverse effect on contemplated dental therapy.
Gastroesophageal Reflux Disease
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Gastroesophageal reflux disease is a common condition. Regurgitation of gastric contents will reduce the pH of the oral cavity below 5.5. This acidic pH of oral cavity begins to dissolve enamel of teeth. It is most commonly seen on the palatal surfaces. Erosion of the enamel exposes the underlying dentin, which is a softer, opaque material. The extent of erosion depends on the frequency and the quantity of exposure along with the duration of disease. Newly exposed dentin is smooth and shiny, while dentin from previous exposures may be stained. Erosion differs from dental caries in that it is a hard, dished-out area where enamel has dissolved and the underlying dentin is exposed. On the other hand, caries reveals soft, discolored dentin and results from the bacterial breakdown of sugars on the surface of the teeth. The prevalence of caries is not increased in persons with GERD, possibly because the acidic environment interferes with the formation of the dental biofilm. Good dental care and control of acid helps decrease the prevalence of erosion. However, once the erosion occurs, it is irreversible and can only be treated with surgical restorative procedures. Therefore, early recognition and patient education is the most effective treat.
Causes • Hemolysis—there is increased destruction of red blood cells with excessive pigment production. • Gilbert’s syndrome—it is a common form of congenital hyperbilirubinemia. • Transport disease—inability of the liver to transport bilirubin into the bile. • Others—jaundice can occur due to primary biliary cirrhosis, cystic fibrosis and traumatic biliary strictures.
Clinical Features • Urine—increased urobilinogen excretion causes the urine to turn dark. • Anemia—pallor occurs due to anemia and thus can be noticed on nails. • Splenomegaly—it occurs due to excessive reticuloendothelial activity. • Others—pruritus, abdominal pain and pale stools can also occur in jaundice. • Icterus—yellowish discoloration of sclera of eye is also present. This yellow discoloration is caused by hypercarotenemia (Fig. 33-9).
Oral Manifestations • Icterus of oral mucosa—it can be seen on palate and in the sublingual area. • Spontaneous bleeding—in cases of severe jaundice patient may present with spontaneous bleeding in the oral cavity or severe bleeding following oral surgical or periodontal operation.
Jaundice It is a symptom rather than a disease, resulting from excess of bilirubin in circulation. Jaundice can be recognized by color of skin, oral mucous membrane and sclera of the eyes. There is yellowish discoloration of skin, muscle membrane and sclera of eyes due to increased level of bilirubin and deposition of bile pigment tissues. Jaundice appears when serum concentration exceeds 2 to 3 mg /dl.
Diagnosis • Clinical diagnosis—icterus and yellow discoloration of skin can easily be noted • Laboratory diagnosis—serum bilirubin level is increased
Types • Hemolytic jaundice—results from an excessive hemolysis or destruction of erythrocytes produced by an inherited abnormality in the cells, some acute diseases and certain drugs or poisonous agent or acquired immune disease. • Obstructive jaundice—caused by gallstone and external pressure on biliary passage, associated with infection or neoplastic lesions. • Hepatocellular jaundice—it can be caused by diseases such as hepatitis and alcoholic and postnecrotic cirrhosis.
Fig. 33.9: Icterus seen in eyes of patient who is suffering from jaundice. Note also yellowish discoloration of facial skin (Courtesy Dr Milind Chandurkar).
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Specific System Disorders 803 Management
Clinical Features
• Consult the physician—if dentist discoveres the jaundice patient should be send to physician for further treatment and consultation.
• Site—it usually affects lower one third of esophagus, stomach and the duodenum in increasing order of frequency. • Symptoms—the most common symptom is epigastric pain, usually occurring either just before eating or 1-3 hours after eating. The pain is burning in nature and associated with nausea and vomiting. It is characteristically relieved by food. If ulceration is large enough to erode an artery, bleeding may be a primary symptom. • Coffee ground vomitus—it is manifested by black tarry stools or more rarely by vomiting of blood. The vomitus appears like ‘coffee ground because of blood reaction with acid.
Diseases of Esophagus • Plummer-Vinson syndrome—It is characterized by an esophageal web with resulting dysphagia, particularly in the upper segment of esophagus, as well as by atrophic changes in the mucous membrane of mouth and by a hypochromic microcytic anemia. • Dysphagia—it is difficulty in swallowing which may result from mechanical obstruction in the esophagus or from disorders of the nervous system that prevent the coordinated reflex contraction of the appropriate muscles. • Esophageal ulcer—it can be associated with tetracycline therapy. It occurs more often after dry swallow of tablet or capsule, especially at bedtime. The patient complaints of severe retrosternal burning pain. • Dental consideration—due to unique position in treating in the oral cavity, dentist may be the first to detect this condition and should promptly refer it to physician for early diagnosis and prompt treatment. Special precautions should be taken while treating these diseases, to avoid aspirations secondary to dental procedures. Patients who have been prescribed tetracycline should be warned to swallow the capsule or tablet with adequate amount of liquid.
Peptic Ulceration Ulceration of the mucosa of gastrointestinal tract caused by the action of protein-digesting pepsin on mucosa is one of the most common disease affecting GIT and one of the most common disease to afflict man.
Oral Manifestations • Site—vascular formation is more commonly seen at the inner surface of the labial commissure and is more common in males than females. • Vascular malformation—it is rarely manifested in the oral cavity but in certain cases, vascular formations of lip are also found in peptic ulcer. The vascular formations are of three types: • Microcherry—it is small, sharply circumscribed, red dot type of lesion. • Glomeruli—a conglomeration of tortuous, thin walled vessels 1-2 mm or more in size. • Venous lakes—dilated submucosal vein resembling a miniature varix. • Complication—massive bleeding, obstruction, perforation and intractability to medical treatment.
Diagnosis • Clinical diagnosis—coffee ground vomitus with vascular malformation of lip may give clue to diagnosis.
Management Predisposing Factors • Acid production—the normal stimuli for acid secretion include the thought, sight, smell or taste of food, which is mediated by the anterior hypothalamus, acts by vagal stimulation directly on the mucosa of stomach to cause acid production. • Hypoglycemia and mental stress—hypoglycemia and mental stress also act by the same mechanism to increase stomach acid production. • Gastrin production—presence of food in the antrum of stomach wall, by the mechanism of distention, cause increased production of the hormone gastrin, which acts directly on the acid producing cells of stomach.
• Sedatives—it is given to reduce mental stress, when it is the etiological factors. • Antacids—it is given to neutralize the excess acid present in stomach. When antacids are given they usually are prescribed 1-3 hours after meals and at bedtime. Most antacids are combination of calcium carbonates, magnesium hydroxide and aluminum hydroxide. • Anticholinergic drugs—it is given to decrease production of acids by the gastric mucosa. • H 2 histamine-receptor blocker—such as cimetidine, famotidine, nizatidine or ranitidine. It blocks the action of histamine on the gastric parietal cells, thus reducing food stimulated acid secretion.
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• Sucralfate—it act by covering and protecting the ulcer, thus promoting the healing. • Omeprazole—it suppress gastric acid secretion by inhibiting an enzyme system at the secretory surface of the gastric parietal cells.
Variation of Frey’s Syndrome
Dental Considerations
Etiology
• Drugs used—the dentist should avoid administration of drugs that exacerbate ulceration, the most common of which is aspirin or one of its related compound. Patients who are given oral penicillin should be given penicillin V, instead of penicillin G, because of resistance of the former to gastric acid. Patient with anticholinergic drugs often present with dry mouth, which may present problems because of increase in the viscosity of mucus and discomfort in wearing complete dentures. There is also increased incidence of cervical caries. Many antacids contain calcium, magnesium and aluminum salts that bind both, erythromycin and tetracycline. These antacids may decrease the absorption of antibiotics by as much as 75 to 85%, if administered within 1 hour of such antacid therapy. • Sedation before treatment—a patient who reacts in a particular stressful way to dental procedure should be sedated before dental treatment.
Neuromuscular Disorders Auriculotemporal Syndrome It is also called as Frey’s syndrome or gustatory sweating. It is characterized by flushing and sweating of facial skin along the region of distribution of auriculotemporal nerve. It is an unusual phenomenon which arises as a result of damage to the auriculotemporal nerve.
• Chorda tympani syndrome—it occur when there is injury to the submandibular gland. • Gustatory lacrimation syndrome—this occur when there is injury to facial nerve proximal to geniculate ganglion.
• Surgical operation—it follows surgical operations such as removal of a parotid tumor or ramus of mandible. It may follow superficial parotidectomy. • Parotitis—parotitis of some type may damage the auriculotemporal nerve. • Congenital—it may be due to birth trauma. • Drainage of abscess—it may caused by inadvertent incision for drainage of parotid abscess. • Transaxonal excitation—some cases of gustatory sweating appear due to transaxonal excitation, rather than actual anatomic misdirection of fibers. • Radical neck dissection—some cases may develop after radical neck dissection.
Clinical Features • Age and sex—there is no age and sex predilection. • Symptoms—the patient exhibits preauricular flushing and sweating of the involved side of face, following ingestion of food or visual stimulation by food. Patient may sometimes feel pain while eating. The severity of sweating is increased by tart food. Profuse sweating may be evoked by parenteral administration of pilocarpine or eliminated by the administration of atropine. Local skin temperature can increase up to 2 °C. • Crocodile tears—in it patient exhibits profuse lacrimation when food is eaten particularly hot and spicy food. • Cutaneous hyperesthesia—presence of cutaneous hyperaesthesia in front and above the ear, the area supplied by the auriculotemporal nerve.
Diagnosis
Pathogenesis • Auriculotemporal nerve—it gives sensory supply to the preauricular and temporal region, carries parasympathetic fibers to parotid gland. • Scar formation—after damage to nerve scar formation occur around the nerve. • Re-established innervations—the fibers regenerate, become misdirected and become connected with sympathetic nerve fibers of sweat gland and blood vessels of the facial skin. • Sweating and vasodilation—parasympathetic fibers would therefore induce salivation; inadvertently stimulate the preauricular-dermal sweat gland and arterioles, causing vasodilation.
• Minor starch iodine test—this test is done for the diagnosis. The test is as follows: • Coating with 1% iodine—preauricular area is coated with 1% iodine. • Application of starch—area is dried after application of iodine. After drying starch is applied on the skin. • Sweating stimulant—patient is given chocolate to induce sweating. • Positive minor test—bluish black discoloration is seen in area of sweating.
Management • Nerve dissection—intracranial division of auriculo— temporal nerve has been reported to be successful.
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Specific System Disorders 805 • Inserting physical barrier—to prevent re-innervations of the sweat gland, many clinicians prefer to insert a physical barrier at the time of surgery. Materials used are porcine dermal collagen, autogenous tissue like fascia lata, temporalis muscle. • Pharmacological agents—pharmacological agents used are atropine, scopolamine, and glucopyrrolate. It can be used topical or in injection form. Most commonly given injection is 1% glucopyrrolate lotion or cream. • Botulinum toxin—this is the recent advance in the management of Frey’s syndrome. BTX is the neurotoxin that blocks the release of acetylcholine by irreversible binding to presynaptic cholinergic autonomic nerve terminals. • Antimuscarinic agent—systemic antimuscarinic agent oxybutynin chloride can be useful in treatment of Frey’s syndrome. • Diluted formalin soaks—the use of local skin application of diluted formalin soaks is well documented. It prevents hyperhydrosis. It act by blocking the effect of acetylcholine on sweat receptor, thereby inhibiting sweating locally. It should be applied before function to prevent embarrassing symptoms.
Bell’s Palsy It is also called as 7th nerve paralysis or idiopathic facial paralysis.
Pathogenesis • Normal course—the cortical tract communicating with the motor nucleus ambiguous of facial nerve crosses over to get innervated into the lower face musculature. Upper face fibers are ipsilateral proximal to the nucleus. • Lower face palsy—a cortical lesion will cause contralateral lower face palsy. • Total hemifacial palsy—lesions of brainstem, main trunk or peripheral fibers will result in total hemifacial paralysis.
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nerve, its compression in the bony canal and finally, paralysis. Familial—familial and hereditary occurrence is also reported in cases of Bell’s palsy. Facial canal and middle ear neoplasm—these are usually associated with sensorineural hearing loss where 7th nerve palsy is a feature. Tumors—tumors of cranial base, parapharyngeal space and infratemporal fossa often cause 7th nerve palsy. Other causes—other causes like multiple sclerosis, atmospheric pressure change, and pregnancy can be triggering factors of facial paralysis.
Clinical Features • Age and sex—women are more commonly affected than men and usually, it occurs in the middle age group. It arises more frequently in spring and fall, than at any other time of the year. • Onset—it begins abruptly as paralysis of the facial musculature, usually unilaterally. • Prodromal symptoms—in some cases, it is preceded by pain on the side of the face which is ultimately involved, particularly within the ear, temple, and mastoid area or at the angle of the jaw. • Symptoms—speech and eating is difficult and occasionally, taste sensation on the anterior portion of tongue is lost or altered. Food is retained in the upper and lower buccal and labial folds due to weakness of buccinator. • Eye—on the affected side, eye cannot be closed and wrinkles are absent on that side. There is watering of eye, which leads to infection. • Facial features—when the patient smiles, the paralysis becomes obvious since the corner of the mouth does not rise nor does the skin of the forehead wrinkles or the eyebrows raise (Fig. 33-10).
Etiology • Cold—it usually occurs after exposure to cold. But many workers believe that it is a chance finding. • Trauma—it may be a causative factor as Bell’s palsy occurs after extraction of teeth and after injection of local anesthesia. Extraction and injection may cause damage to the nerve and subsequent paralysis. • Surgical procedure—surgical procedures such as removal of parotid gland tumor in which the facial nerve is sectioned can also cause facial paralysis. • Ischemia—it may caused by ischemia of the nerve near the stylomastoid foramen, resulting in edema of the
Fig. 33-10: 7th nerve paralysis showing paralysis on left side of patient (Courtesy Dr Datarkar).
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• Mask like face—the patient has a typical mask-like or expressionless appearance. • Drooling of salvia—the muscular paralysis manifests itself by dropping of the corner of mouth, from which saliva may dribble. • Syndrome associated—it is associated with MelkerssonRosenthal syndrome.
Diagnosis • Clinical diagnosis—slurred speech, mask like face, drooling of salvia can diagnose this condition.
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Management • Vasodilator—the use of vasodilator drug like histamine has been proved beneficial in some cases. • Surgical decompression and anastamosis of nerve—surgical anastamosis of nerves has been carried out, especially with facial and hypoglossal nerve; thus can restore partial function. • Nicotinic acid—administration of physiologic flushing dose of nicotinic acid. • Other—systemic steroids or ACTH injection have been successful in treating Bell’s palsy.
• Steppage gait or stork-leg appearance—patient notices atrophy of foot, leg and hand muscles ultimately occurs with the appearance of a typical foot-drop, steppage gait and stork-legs. Progressive bulbar palsy • Age and sex—it generally occurs in the children and young adults. There is no gender predilection. • Symptoms—It is characterized by difficulty in swallowing and phonation, hoarseness, facial weakness and weakness of mastication. Chewing is difficult as facial muscles becomes weakened. • Signs—atrophy of facial, masseter, temporal muscles and tongue, with fasciculation of the face and tongue. There is also impairment of palate and vocal cords.
• Degeneration of motor neuron cells—the motor system disease results from degeneration of the motor neuron cells of cranial nerves, anterior horn of spinal cord and pyramidal tract. • Genetic—it is transmitted as autosomal recessive disorders.
Amyotrophic lateral sclerosis • Age and sex—it generally occurs between the ages of 40 and 50 years and affects males more frequently. • Precipitating factors—precipitating factors include fatigue, alcohol intoxication and trauma. Infections like syphilis, influenza, typhus and epidemic encephalitis can also lead to amyotrophic lateral sclerosis. • Symptoms—the initial symptoms consist of weakness and spasticity of limbs, difficulty in swallowing and talking with indistinct speech and hoarseness. • Signs—atrophy, flaccidity, symmetric weakness, slowness of movements, and impairment or loss of palatal movements may also occur. • Fasciculation—there is small, synchronous, subcutaneous muscle contraction of the shoulders and thighs. • Tongue—in earlier stages, the tongue is slightly weakened, leaving articulation relatively unaffected. In the middle stages, a gradual and generalized weakening of tongue occurs, accompanied by spasticity which results in reduced rate, range and force of articulatory tongue movements. In the later stages, there is virtually unintelligible articulation.
Types
Diagnosis
• Progressive muscular atrophy—it is seen in childhood. • Progressive bulbar palsy—it is seen in children and young adults. • Amyotrophic lateral sclerosis (Lou Gehrig disease)—it is seen in middle age.
• Clinical diagnosis—dysphagia, steppage gait, stork-leg appearance, tongue weakness and fasciculation are diagnostic point of motor neuron disease.
Motor System Disease Motor system disease is neurodegenerative disorder which is characterized by progressive weakness and wasting of muscles.
Etiopathogenesis
Clinical Features Progressive muscular atrophy • Age and sex—it usually occurs in childhood. It shows a strong hereditary pattern, affects males more frequently than females. • Symptoms—the initial symptoms usually consist of difficulty in walking with leg pain and paresthesia.
Management • Antiglutamate agents—antiglutamate agent riluzole shows some improvement in this disease. As such there is no specific treatment for this disease and it is usually fatal.
Multiple Sclerosis It is also called as disseminated sclerosis. This disease affects central nervous system. It is autoimmune disease.
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Specific System Disorders 807 Etiology
Diagnosis
• Allergic—the lesions are allergic hypersensitivity manifestations of the nervous tissue due to antigenantibody reactions. • Altered coagulation of blood—the lesions are due to scattered venous thromboses in the nervous system associated with altered coagulation of blood. • Transitory local vasoconstriction—the lesions are due to repeated, transitory localized vasoconstriction in various portions of the nervous system, precipitated by emotional disturbances or fatigue.
• Clinical diagnosis—bilateral trigeminal neuralgia with speech difficulty and vision problems will diagnose this condition.
Management • Drug treatment—beta interferon, mitoxantrone, and glatiramer can be effective in this patient. Medication to reduce muscle fatigue can also be used. • Physical and occupational therapy—this can be use to patient up to certain extent.
Clinical Features • Age and sex—it occurs chiefly in younger age group with an onset of symptoms between the ages of 20 and 40 years. There is slight female predilection with familial occurrences. • Symptoms—fatigability, weakness and stiffness of the extremities with ataxia or gait difficulty, involving one or both legs. Superficial or deep paresthesia. Personality and mood deviation towards friendliness and cheerfulness. • Signs—variety of ocular disturbances including visual impairment as a manifestation of retrobulbar neuritis, nystagmus and diplopia. • Staccato speech—staccato (a series of short, detached sound or words) type of speech. • Charcot’s triad—it consist of intentional tremors, nystagmus, dysarthria and scanning speech.
Oral Manifestations • Jaw weakness—facial and jaw weakness occur in some patients. • Reduced mouth opening—this may occur due to stiffness and weakness of muscle (Fig. 33-11). • Trigeminal neuralgia—this occurs in multiple sclerosis patients and it usually bilateral. • Facial palsy—this can also be present in the multiple sclerosis.
Cerebral Palsy The term cerebral palsy refers to a group of disorders with motor manifestations due to nonprogressive brain damage, occurring before or after birth.
Causes • Anoxia and ischemia—anoxia and ischemia during labor can cause cerebral palsy. • Congenital infection—congenital infection like toxoplasmosis, rubella, cytomegalovirus disease, herpes simplex, syphilis and influenza can also cause cerebral palsy.
Clinical Features • Forms—cerebral palsy can be manifested in spastic, dyskinetic, ataxic or a combination, affecting one or four limbs. • Spastic form—legs are commonly involved. Speaking problems with dysarthria, chewing and swallowing difficulty. Sometime, there are seizures associated with mental retardation. • Dyskinetic form—it is characterized by athetotic purposeless movement, involving both agonist and antagonist muscles, which is increased by voluntary activity. Head movement and facial grimacing are characteristic. • Lead pipe type movement—this occur due to excessive muscle tone.
Oral Manifestations
Fig. 33-11: Multiple sclerosis patient showing reduce mouth opening due to stiffness of facial muscle.
• Sialorrhea—drooling of saliva, this can lead to both functional and esthetic inconvenience. • Enamel hypoplasia—an increased incidence of enamel defects. • Malocclusion—this is present due to abnormal muscle behavior. Upper teeth are inclined. • Maxilla—maxillary arch is tapered and ovoid in shape with high arch palate.
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Diagnosis • Clinical diagnosis—lead pipe type of movement with hemiplegia will lead to the diagnosis. There is also delay in development of motor skill.
Management
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• Physiotherapy should be instituted as early as possible, in order to prevent contractures. • Orthopedic surgery can be helpful in some cases. • Drugs therapy—in case of seizures, drugs therapy like dantrolene sodium diazepam or L-dopa may be used. • Anti-cholinergic drugs—for drooling of saliva, anticholinergic drugs such as benzhexol, atropine and scopolamine are used.
Epilepsy It is a disorder, which results due to a sudden discharge by cerebral neurons, resulting in convulsive movements. It can cause sensory and motor abnormalities as well as loss of consciousness. Convulsions can also be seen with high grade fever, brain tumor, head injury, hypoglycemia, hypocalcemia, and drug toxicity.
Types • Grand mal—it is most common type of seizure which can occur alone or with other types of seizure. • Petit mal—it is the second most common type and it occur without aura and with little or no clonic or tonic movements. • Psychomotor—the seizures are preceded by an aura, which is often a hallucination or a felling of déjà vu. • Jacksonian—in it, attack begins in one part and spreads gradually. • Simple partial seizure—it originates from one localized area of the brain and does not feature loss of consciousness. • Complex partial seizure—it is same as psychomotor, with impairment of consciousness. • Status epilepticus—it is the period of recurrent seizure attacks, without recovery between each attack.
Clinical Features • Grand mal—it begins in childhood. There is warning followed by loss of consciousness. • Aura phase—a grand mal seizure begins with aura in which patient experiences epigastric discomfort, an emotion or hallucination of hearing, vision or smell. • Tonic phase—the aura is followed, in seconds to minute, by unconsciousness, cry, and tonic muscle spasms. There is also breathlessness due to spasm of respiratory muscles and the patient becomes cyanotic.
• Clonic phase—the tonic phase is followed by clonic phase composed of convulsive jerky movements, incontinence and tongue biting. Jaw is clamped shut and there is foaming at the mouth. Patient may injure itself, if he is near hard or sharp object. • Postictal state—a postictal state is characterized by headache, confusion, lethargy, occasional temporary neurological deficit and deep sleep. • Petit mal—they are present exclusively in children and frequently disappear during second decades of life. The patient looses his consciousness and appears to stare into the space. He will continue his normal activity immediately after the seizure. • Psychomotor—during the seizure, the patients exhibit purposeless movements and bizarre behavior. Patient may wander about aimlessly, may get undressed or exhibit violent behavior during the seizure. • Jacksonian—the seizure begins with clonic movement of a distal portion of extremities or the face. The convulsive movement spread up to the affect limb, becomes generalized and causing loss of consciousness.
Diagnosis • Clinical diagnosis—tonic muscle spasm, convulsive jerky movement with headache and confusion will diagnose this condition.
Management • Immediate care of seizures—you should move person away from danger like fire, water, machinery and furniture. After convulsion ceases it turns into recovery position, i.e. semiprone position. Do not insert anything in the mouth as tongue biting occurs at the start of seizure, so it cannot be prevented. If convulsion continues for more than 5 minutes or recur without person regains coconscious, summon urgent medical attention. Give intravenous anticonvulsants, i.e. diazepam, if convulsion continues or repeated. Airway should be kept patent during the epileptic fits. • Anticonvulsive drug therapy—the drug of choice for grand mal, psychomotor and Jacksonian seizure is phenytoin (Dilantin), often in combination with phenobarbital. Patient resistant to it are given primidone. Drug of choice for petit mal is ethosuximide because of few side effects associated with it. Other drugs used are trimethadione, paramethadione and acetazolamide.
Dental Considerations • Gingival enlargement—patients taking anticonvulsant drug such as phenytoin, develop gingival hyperplasia which may exacerbate due to local inflammatory factors. You should also look for level of drug in the gingival tissues and the effect of drug on gingival mast cells.
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Specific System Disorders 809 • Side effects of phenytoin—other side effects of phenytoin are megaloblastic anemia, lymphadenopathy, connective tissue and bone changes. Phenytoin blocks the effect of parathyroid hormone on bone, resulting in bone and root changes. • Drug interference—aspirin, azole and metronidazole can interfere with phenytoin. So this drug is contraindicated in epilepsy.
Parkinson’s Disease It is a major cause of chronic disability in patients over 50 years of age.
Causes • Depletion of neurotransmitter—it is caused by depletion of neurotransmitters, dopamine and norepinephrine in the basal ganglion. • Other disease—some are caused by encephalitis, trauma, carbon monoxide intoxication, atherosclerosis, metal poisoning and brain tumor.
Clinical Features • Triad—the triad is rigidity, tremor and bradykinesia (slowness in the initiation of movements). • Onset—the onset is insidious. Mild stiffness of muscle of the extremities and tremor of hand are early signs. • Pill-rolling movement—the typical hand tremors are called as pill-rolling movements and are caused by movement of thumb and fingers rubbing against one another. • Gait—walking becomes more difficult and patients develop a slow shuffling gait in a stooped position because of the inability to stand straight. • Speech—speech becomes slow owing to lack of muscle control (dysarthria) and as the disease progresses there is a decrease in all voluntary movements and increase in tremor.
Oral Manifestations • Appearance of face—rigidity of facial muscle is common. The loss of flexibility gives the patient an expressionless or masklike face. • Drooling—the muscle rigidity also causes difficulty in swallowing, resulting in drooling. • Tremors—tremor of tongue and mandible are also common, making speech and eating difficult for the patient and dental procedures difficult for the dentist. • Complication of Levodopa therapy—due to Levodopa therapy, patient exhibits purposeless chewing, grinding and sucking movements that are quite bizarre. The patient may thrust or shake his tongue and chew or suck vigorously when there is nothing in mouth.
Diagnosis • Clinical diagnosis—triad of tremor, rigidity and bradykinesia can be seen.
Management • Levodopa—levodopa can cause dramatic reversal of symptoms of Parkinson’s disease. • Anticholinergic drugs—mild form of Parkinson’s disease can be managed by anticholinergic drugs such as trihexyphenidyl, like benzotropine or ethopropazine. • Propranolol—propranolol an adrenergic antagonist may be used to reduce tremors. • Bromcriptine—bromcriptine is one of the newer drugs which are an agonist at the dopamine receptors.
Dental Considerations • Pretreatment sedation—anxiety will increase both, tremor and degree of muscle rigidity. Pretreatment sedation with diazepam is often recommended, as it will reduce anxiety. • Precaution while changing posture—when the dental treatment has finished, the patient should be warned to take care while changing from a supine to standing position, since levodopa has a significant orthostatic hypotensive effect.
Orofacial Dyskinesia It is caused by extrapyramidal disorders, complication of phenothiazine therapy and dentures in gross malocclusion. It is more commonly occurs above 60 years. It is characterized by severe involuntary, dystonic movements of the facial, oral and cervical musculature. Irregular and involuntary movements such as lip-smacking and lip-licking, protrusion of lips -as in pouting, protrusion of tongue and mandible with uncoordinated movements are mostly observed. Correction of the denture occlusion may be effective therapy. Anti-Parkinsonism drugs therapy can be effective in some of the cases.
Granulomatous Disorders Wegener’s Granulomatosis It is a disease of unknown etiology which basically involves the vascular, renal and respiratory systems. It is a granulomatous involvement of blood vessels resulting in necrosis of tissue. It is generally thought that the disease is aberrant hypersensitivity reaction to an unknown antigen.
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Types (Clinical) • Generalized or classic Wegener’s granulomatosis—it involve upper respiratory tract, pulmonary and renal lesions. • Localized or limited Wegener’s granulomatosis—it affects oral and nasal cavity and the lungs. • Superficial Wegener’s granulomatosis—it exhibits lesion of skin and mucosa.
Clinical Features
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• Age and sex—it usually occurs in 4th or 5th decade of life, with slight predilection for males. • Symptoms—the most common symptom of Wegner’s granulomatosis is nasal stuffiness with chronic discharge, which is sometimes bloody. Patient soon develops cough, hemoptysis, fever and joint pains. There is also presence of rhinitis, sinusitis and otitis or ocular symptoms. There are also non-specific symptoms of malaise, arthralgia and weight loss. • Signs—hemorrhagic or vesicular skin lesions are also commonly present. • Renal symptoms—glomerulonephritis, which develops ultimately to uremia and terminal renal failure. • Prognosis—the disease is usually fatal, with mean survival time of 5 months. Death occurs due to involvement of kidney.
Oral Manifestations • Onset—the disease usually starts with tumor like vegetations in mouth and nose (Fig. 33-12). Then inflammatory process starts in the interdental papilla, spreading rapidly in to the periodontium. • Ulceration—ulceration can occur on any surface. Ulceration is usually perforating in nature.
• Strawberry gingivitis—involvement of gingiva is the most common manifestation; which is characterized by ulceration, friable granular lesions or simple enlargement of gingiva. Inflamed, hyperplastic appearing and hemorrhagic gingiva may be found. Strawberry gingivitis is the term used for this type of gingiva. • Palate—oral lesions typically include ulceration of the palate by extension of nose lesions and destruction of nasal septum. This will lead to perforation of palate. • Teeth—there may be loosening of teeth with in some cases spontaneous exfoliation. After extraction of teeth patient is usually noticed poor healing. • Other features—cranial nerve palsies, jaw claudication, labial mucosal nodule, oroantral fistulae, and parotid swelling.
Radiological Features • Alveolar bone—there are often signs of alveolar bone loss.
Diagnosis • Clinical diagnosis—typical strawberry gingivitis with necrotic ulceration in the oral cavity. • Laboratory diagnosis—cytoplasmic localization is present with Wegener’s granulomatosis. Histopathologically chronic inflammatory cells and multinucleated giant cells are found.
Differential Diagnosis Agranulocytosis, leukemia, lymphoma—diagnosis by blood picture, possibly histology.
Management • Cotrimoxazole—it is combination of trimethoprim and sulfamethoxazole. It has proved to be effective as an adjuvant or sole therapy in both localized and generalized forms. • Corticosteroids—regimen of cyclophosphamide 12 mg/ kg body weight/day with prednisolone 1 mg/kg body weight have been utilized to obtain complete remission. • Others—other treatment modalities includes cyclosporine, intravenous pooled immunoglobulin, and local irradiation.
Sarcoidosis
Fig. 33-12: Vegetative growth with ulceration in the palate in case of Wegener’s granulomatosis (Courtesy Dr Parate).
It is also called as Boeck’s sarcoid, Besnier-Boeck-Schaumann disease. It is a disease of unknown etiology. It is a multisystem granulomatous disease. It is characterized by depression of delayed type of hypersensitivity, suggesting an impaired cell-mediated immunity and raised or abnormal serum immunoglobulin, suggesting lymphoproliferation.
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Specific System Disorders 811 Clinical Features • Age, sex and race distribution—it commonly affects young adults with female predilection. It shows more prevalence in blacks. • Site—lesions are most common in lungs, skin, lymph nodes, salivary glands, spleen and bones. • Symptoms—mild malaise, fever, weight loss, fatigue and cough can be the chief features of the disease. • Signs—there is presence of bilateral hilar lymphadenopathy, and pulmonary infiltration. • Lupus pernio—these are the cutaneous lesions which appear as multiple, raised red violaceous patches. It occurs in group, grows slowly and does not ulcerate or crust. • Erythema nodosum—it is nonspecific tender erythematous nodule seen on lower leg. • Eye lesion—it includes anterior uveitis. In case of involvement of lacrimal gland patient may suffer from keratoconjunctivitis sicca. • Lofgren’s syndrome—it consist of erythema nodosum, bilateral hilar lymphadenopathy and arthralgia.
• Stage 3—no enlargement of the lymph nodes, but extended and sometimes patchy or striped changes in both lung fields. The patches may be confluent and bullae may be formed.
Diagnosis • Clinical diagnosis—salivary gland involvement with lymph nodes involvement with non-specific ulcer in the oral cavity, aids in clinical diagnosis. • Kveim-Siltzbach test—is an intracutaneous test for the diagnosis of sarcoidosis—Kveim-Siltzbach test is positive in some cases. In this test, intradermal injection of a saline suspension of known human sarcoid tissue used as an antigen is given to a patient suspected to have sarcoidosis. One month after the injection, any palpable nodule is excised and examined histologically for evidence of a sarcoid reaction, or epithelial tubercle. • Laboratory diagnosis—there is increased serum angiotensin converting level. Histopathologically asteroid bodies and Schumann’s bodies are found.
Oral Manifestations
Management
• Site—it is rare in oral cavity, but cases are reported on salivary gland, lip, palate and buccal mucosa. • Salivary gland involvement—it will lead to enlargement of salivary gland. This enlargement will lead to xerostomia patient. Due to xerostomia there is increased incidence of dental caries and ulceration of buccal mucosa. • Lip—it appears as small papular nodules or plaques or resembles herpetic lesions or fever blisters. • Palate and buccal mucosa—on the palate and buccal mucosa, it is described as bleb like, containing a clear yellowish fluid or as solid nodules. • Heerfordt’s syndrome—it consists of parotid enlargement, anterior uveitis, facial paralysis and fever.
• Corticosteroid—asymptomatic patient requires no treatment as the lesion may resolve in 2 years of duration. In patient with symptoms corticosteroids can be given. • Refractory (does not respond to treatment) sarcoidosis—in this case methotrexate, azathioprine, chlorambucil and cyclophosphamide is used.
Radiological Features
Etiology
• Jaw bone—there is ill-defined radiolucencies which eroded the cortex. Expansion is absent in this case. • Chest radiograph—radiological changes in lungs are of paramount importance. Based on chest radiograph, four stages of sarcoidosis can be distinguish: • Stage 0—characterized by a normal radiograph of the thorax. • Stage 1—bilateral enlargement of the hilar nodes, without pathologic changes in the lung fields. It represents an early stage of the disease. • Stage 2—bilateral enlargement of the hilar lymph nodes with pathologic changes in the lung fields around the hili.
• Immune mechanism—Lethal granuloma is due to a dysfunction of the immune mechanism normally responsible for granuloma formation. • Hypersensitive response—Nowadays, it represents a fulminant hypersensitivity response to an unidentified antigen. • Vascular allergy—vascular allergy like arthus phenomenon or periarteritis nodosa.
Midline Lethal Granuloma It is also called as malignant granuloma, midline lethal granulomatous ulceration and midline nonhealing granuloma. It is described as idiopathic progressive destruction of nose, palate, face and pharynx. Midline lethal granuloma is also associated with T cell lympho-proliferative disorders.
Clinical Features • Age—it is more commonly seen in adults. • Site—commonly involved sites are nose, palate, face and pharynx.
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• Onset—it begins as superficial ulceration of the palate or nasal septum, often preceded by a feeling of stuffiness in the nose. This may persist for a month or two to several years. Pain may be present. • Progress—eventually ulceration spreads from the palate to the inside of the nose and then to the outside. • Signs—the palatal, nasal and malar bones may become involved, undergo necrosis and eventually sequestrate. Destruction is a prominent feature and loss of entire palate is common (Fig. 33-13). The patient may exhibit purulent discharge from the eyes and nose; perforating sinus tracts may develop and soft tissues of face may slough away leaving a direct opening into the nasopharynx and oral cavity. • Prognosis—the patient ultimately dies of exhaustion or of hemorrhage if a large blood vessel is eroded. Death can also occur due to localized destruction of tissue in the midline of face.
Management • Corticosteroids—corticosteroid therapy has proven beneficial in some cases. • Radiation therapy—radiation therapy of 5000 rad appears to be a treatment modality, in which remission of over 15 years is reported.
Chronic Granulomatous Disease It is an uncommon hereditary disease with X-linked mode of transmission. It is characterized by severe recurrent infections as a result of defect of intracellular leukocytes enzymatic function, with decreased oxidative metabolism, in which there is failure to destroy certain catalase-positive microorganisms, including staphylococci.
Clinical Features • Age and sex—majority of the patient are males, but females are also commonly affected. It is commonly found in children and infants. • Site—there is widespread infection from infancy; usually affecting lymph nodes, lung, liver, spleen, bone and skin. • Skin lesion—skin lesions occur on face, leading to tissue necrosis and granuloma formation. • Signs—abscess, septicemia, pneumonia, pericarditis, meningitis and osteomyelitis are common features.
Oral Manifestations
Fig. 33-13: Destruction of palate seen in midline (Courtesy Dr Chole).
• Appearance—ganulomatous lesions of the oral and oropharyngeal mucosa usually present as sessile, lobulated, moderately firm and relatively nontender nodules and papules with normal coloration and with little or no surrounding inflammatory mucosal erythema. • Ulcerative lesion—with time, some of the granulomas may ulcerate centrally and present as a deep, painless ulcer with a nonerythematous rolled border, reminiscent of squamous cell carcinoma. • Other features—there is diffuse stomatitis, and benign migratory glossitis is also present.
Diagnosis • Clinical diagnose—destructive lesion in the midline of palate will diagnose this condition. • Laboratory diagnosis—biopsy shows extensive necrosis with infiltration of some inflammatory cells and formation of occasional new capillaries.
Diagnosis
Differential Diagnosis
Management
• Wegener’s granulomatous—in it there is presence of lung and renal diseases. • Noma—in midline, lethal granuloma location is typical.
• Conservative surgical excision—localized lesions without systemic connection can be treated by conservative surgical removal and plastic surgical reconstruction.
• Clinical diagnosis—granulomatous sessile lesion will give clue to diagnosis. • Laboratory diagnosis—it is established by neutrophils function test.
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Specific System Disorders 813 • Medication—intralesional and systemic corticosteroids, low-dose radiotherapy, methotrexate, dapsone, salazosulfapyridine (sulfasalazine), hydroxychloroquine sulfate, among others. No therapy has proven to be universally effective in orofacial granulomatosis without systemic involvement.
Collagen Disorders Scleroderma It is also called as systemic sclerosis, or Hidebound disease. It is rare collagen disorder, which is characterized by hardening and tightening of the skin that can manifest as either localized or systemic form. It is a disease which involves connective tissue, blood vessels and lead to fibrosis. It is also called as progressive systemic sclerosis. Name is derived from sclero—hard derma—skin.
Types • Systemic or progressive systemic sclerosis—it is diffuse and involves both skin and internal organ. • Localized form—it involve the underlying muscle and bone along with skin and subcutaneous tissue. It is of two types: • Morphea—it is circumscribed form and is characterized by local changes limited to skin • Linear—it affects face, scalp and frontoparietal region.
Etiology • An endocrine dysfunction—in some cases of endocrine dysfunction mainly thyroid and parathyroid disturbances can cause scleroderma. • Vascular disease—basically an endarteritis obliterans, resulting in decreased vascular supply. • Nervous disorder—since skin lesion often follows the distribution of nerves, nervous disorder may be causative factor. • Toxic or infectious agents—shock or pneumonia, influenza, diphtheria and exanthematous disease. • Allergic reaction—an antigen-antibody type of reaction is observed in scleroderma. • Environmental factors—such as exposure to silica dust, vinyl chloride, benzene and tryptophan.
Clinical Features Progressive systemic sclerosis • Age and sex—it generally begins in childhood or young adult and greatest incidence is between 30 and 50 years of age. Females are more commonly affected with a ratio of 3:1. • Site—it usually begins on face, hand or trunk.
• Symptoms—there is development of indurated edema of skin, neuralgia and paresthesia. • Signs—Initial sign of PSS is frequently Raynaud’s phenomenon, a paroxysm vasospasm of finger. In several months the edema is replaced by tightening and hardening of the skin, which results in difficulty in movements of the affected parts. • Involvement of internal organs—hyperpigmentation, telangiectases and subcutaneous calcification may occur, leading to deformity and severe cosmetic problems along with involvement of internal organs. • Acro-steolysis—resorption of terminal phalanges is also occur in scleroderma. Finger may also become clawlike. • Skin involvement—skin area has thickened, hidebound cavity with lack of mobility of skin, limited mouth opening and renal involvement. • Syndrome associated—it can be associated with progressive hemifacial atrophy (Parry-Romberg syndrome). Localized form (circumscribed or morphea) • Site—it usually occurs on the sides of the chest and thighs. They may be present for several months to many years. • Onset and progress—it begins with violaceous patches on the skin. These lesions enlarge; become indurated and eventually loose hair and ability to sweat. • Hidebound character—due to thickening patient assumes hidebound (constricted) character. • Signs—progressively, these lesions turn into hypo or hyperpigmented areas depressed below the level of the skin. They may become stiff and hard. Affected skin appears rigid, inelastic, atrophic and shiny. Localized form (linear) • Appearance—a linear form of disease develops as a thin band of sclerosis that may run the entire length of extremities involving underlying muscle, bones and joints. • En coup de sabre—a band made up of furrow with an elevated ridge on one side is often termed as ‘ coup de sabre’ since it resembles the mark produced by the blow of saber (curved sword).
Oral Manifestations • Site—the tongue, soft palate, lips and larynx are commonly involved. • Appearance—these are characterized by mild edema, which is followed by atrophy and induration of mucosal and muscular tissue. • Mask like facies—involvement of facial skin results in characteristic smooth, taut and masklike facies. • Mouse facies—nasal alae may become atrophied resulting in pinched appearance to the nose resulting in mouse species.
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• Lips—the lips become thin, rigid and partially fixed, producing microstomia. • Microstomia—the oral aperture narrows considerably. Skin folds are lost around the mouth. • Tobacco pouch mouth or purse string appearance—it can be seen periorally where furrow rows radiate from the atrophic vermilion borders, creating the so-called tobacco pouch mouth or purse string appearance. • Tongue—tongue can become hard and rigid, losing its mobility and papillary pattern, making speaking and swallowing difficult. The color of tongue changes to a livid appearance. In the end stages, the tongue lays as a stiff, reduced body in the floor of mouth. • Lingual frenum—the lingual frenum, which usually reflects the first oral change, shortens, becomes tendinous and finally disappears. • Neuropathy—resorption of mandible may lead to pressure of the inferior alveolar nerve. This will results in neuropathy. • Dysphasia—involvement of esophagus causes dysphagia. • Temporomandibular joint—involvement of soft tissues around the TMJ leads to restricted movement of mandible, causing a pseudoankylosis. • Mandible—when the facial tissues and muscles of mastication are involved the pressure exerted will cause resorption of mandible at the attachment of masseter muscle. • Salivary hypofunction—in some cases salivary hypofunction can also be present. • Gingiva—gingival hyperplasia may result from calcium channel blocker.
Radiographic Features • Periodontal ligament—extreme widening of the periodontal ligament, two to four times the normal thickness, which is more prominent around posterior teeth with intact lamina dura. The periodontal changes are the direct result of changes within the membrane due to the underlying disease. • Margins—borders of the lesions are smooth and sharply defined. • Bone resorption—bone resorption occur usually at the angle of mandible. It is bilateral and symmetrical. • Condylar involvement—partial or complete resorption of condyle and coronoid process of the mandible, as a result of abnormal muscle pull or pressure from soft tissues is reported.
• Radiological features—periodontal ligament widening with resorption of bone at angle of mandible. • Laboratory diagnosis—anticentromere antibodies or antiScl 70 are detected.
Management • D-penicillamine—a drug has shown promise in the management by decreasing both, the skin thickening and organ involvement by interference with crosslinking of collagen and immunosuppression. • Extracorporeal photochemotherapy—it is beneficial in skin lesion. • Other therapy—other therapy like angiotensin converting enzyme inhibitor and calcium channel blocking agents may control hypertension in the patient. • Dental management—the mouth opening may be increased by use of stretching exercises. Effective treatment of it is to use an increasing number of tongue blades between posterior teeth. If this is insufficient, bilateral removal of commissure may be necessary. Patient with extensive resorption of the angle of mandible is at risk of fracture and should therefore avoid trauma.
Kawasaki Disease Kawasaki disease, or mucocutaneous lymph node syndrome, is a vasculitis that affects medium and large arteries with a corresponding cutaneous lymph node syndrome.
Clinical Features • Age—it most commonly occurs in children between 3 months and 12 years of age. • Symptoms—patients present acutely with edema, erythema of the hands and feet, fever and rash. The associated temperature must exceed 38.5°C (101.3°F) for 5 days to meet diagnostic criteria. • Signs—bilateral congestion of ocular conjunctiva, indurative edema, erythema of palms, soles and membranous desquamation of fingers and toes. There is also polymorphous exanthema of torso without vesicles or crusts. • Lymphadenopathy—acute nonpurulent swelling of cervical lymph nodes. • Cardiac sequelae—cardiac sequelae to the vasculitis may result in aneurysm and myocardial infarction. Myocarditis commonly occurs within a week after the fever. Within 2-3 weeks, the previously edematous palms and soles peel and slough.
Diagnosis • Clinical diagnosis—claw like finger, ulceration in finger, Raynaud’s phenomenon, shiny skin, tobacco pouch mouth are typical features of this disease.
Oral Manifestations • Strawberry tongue—strawberry like reddening and swelling of tongue papillae and diffuse reddening of
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Specific System Disorders 815 oral and pharyngeal mucosa, sometimes with gingival ulceration. • Lip—the labia are cracked, cherry red, swollen, and hemorrhagic. The last of these may be due to the longstanding high-grade fever. • Facial palsy—it is also some time seen in Kawasaki disease.
Diagnosis • Clinical diagnosis—for diagnosis, 4 of the 5 following criteria must also be met: (1) peripheral extremity edema, erythema, or desquamation; (2) polymorphous exanthem; (3) bilateral conjunctival injection; (4) erythema and strawberry tongue in the oral cavity; and (5) acute cervical adenopathy. • Laboratory diagnosis—there is proteinuria, leukocytosis, increased sedimentation rate and positive C-reactive protein.
Fig. 33-14: Superficial red macule seen over the skin in case of Pityriasis rosea ( Courtesy Dr Pincha).
Oral Manifestations
Skin Disorders
• Incidence—the oral lesion occurs either concomitantly with, or subsequent to the skin manifestations. • Site—it can occur on buccal mucosa, although tongue and palatal lesions have been reported. • Appearance—oral lesion appears as erythematous macule, with or without central area of grayish desquamation. • Size and margins—the lesion may be single or multiple, irregular in shape, occasionally showing raised borders and vary in size from few mm to 1-2 cm in diameter.
Pityriasis Rosea
Diagnosis
It is an acute skin eruption of unknown etiology.
• Clinical diagnosis—herald spot on the skin will give clue to diagnosis. • Laboratory diagnosis—biopsy shows acanthosis and focal parakeratosis with microvesiculation or simply sprinkling of leukocytes within the epithelium.
Management • Intravenous gammaglobulin—it is the most effective treatment in case of Kawasaki’s disease. • Other drugs—aspirin or systemic steroids can also be given in some cases.
Clinical Features • Age and sex—it is more common in spring and autumn and it involves young adults chiefly, with no sex predilection. • Symptoms—the lesion often manifests mild headache and low grade fever and cervical lymphadenopathy. • Primary lesions—the generalized outbreak is frequently preceded by the appearance of a ‘primary lesion’ or ‘herald spot’ seven to ten days previously. • Appearance—it is characterized by the appearance of superficial, light red macules or papules, generalized over most of the skin surface (Fig. 33-14). • Size—the spot is bright-red and larger (3 to 4 cm in diameter) than the multiple eruptions which follow its appearance. • Shape—the individual exanthematous lesion is commonly ovoid, with long axis parallel to the natural lines of cleavage of skin and are covered by a thin silvery scales.
Management It requires no treatment since the disease is self limiting and generally undergoes rapid spontaneous regression.
Incontinentia Pigmenti It is also called as Bloch-Sulzberger syndrome. It is transmitted as sex-linked dominant trait.
Clinical Features • Age and sex—it appears shortly after birth and exclusively seen in females. • Appearance—it is characterized by the appearance of erythematous and vesiculobullous lesions on the trunk and extremities which frequently disappear and
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reappear. Then, they are gradually replaced by white keratotic, lichenoid, papillary or verrucous lesions, which then persist for some months. • Infant lesion—some of the lesions in infants are brownish gray macules in a streaked, patchy distribution over the trunk and extremities, occurring subsequent to the verrucous keratotic lesions. • Melanin pigmentation—there is heavy melanin pigmentation of epithelium, dropping down into cluster of chromatophores in the upper dermis (incontinence), which gives the disease its name. • Associated defect—other defects can be seen like cataract, optic atrophy, strabismus, retrolental fibroplasia, central nervous system involvement and lesions of skeletal system.
Clinical Staging • Vesicular stage—vesiculobullous lesion seen in trunk and limbs. Resolution within 4 months. • Verrucous stage—verrucous cutaneous plaques develop. Resolution by 6 months. • Hyperpigmentation stage—brown skin lesion with swirling (twisting) pattern. • Atrophy and depigmentation stage—atrophy and depigmentation of skin can occur (Fig. 33-15).
Oral Manifestations • Site—both the deciduous and permanent dentitions may be affected. • Teeth—there is delayed tooth eruption, peg and cone shaped crowns, congenitally missing teeth, malformed teeth and additional cusps.
Diagnosis • Clinical diagnosis—depigmentated or vesicular lesion on trunk with cone shaped crown may suspect this disease. • Laboratory diagnosis—biopsy shows intraepithelial clefts filled with eosinophils. It may show melanin containing macrophages.
Management Dental management—dental defects can be corrected with the assistance of orthodontics and prosthetic dentistry.
Acanthosis Nigricans It is acquired dermatological disorders characterized by velvety brownish discoloration of the skin.
Types • Benign—it may be present at birth or occur later in childhood; appears to be genetic in origin inherited as a dominant characteristic. • Malignant—it is associated with internal malignancy like adenocarcinoma of stomach and occurs in older age group. • Pseudoacanthosis nigricans—it is most common and is associated with endocrinopathy.
Clinical Features • Site—the most common areas involved are axilla, palms and soles and face and neck. • Appearance—skin lesions are symmetric with mild hyperpigmentation and mild papillary hypertrophy of only small patchy areas. In some cases, it is heavily pigmented, aggressively verrucous lesion involving much of the skin. • Symptoms—the verrucous lesions are often pigmented and generalized pruritis is also a common finding.
Oral Manifestations
Fig. 33-15: Depigmentated lesion seen on leg of patient in Incontinentia pigmenti (Courtesy Dr Pincha).
• Site—the tongue and lips are most commonly involved, followed by buccal mucosa. • Incidence—oral manifestations are most common with malignant form. • Tongue—there is hypertrophy of the filiform papillae producing a shaggy, papillomatous surface on the dorsal tongue. • Lips—the lips may be enlarged and covered by papillomatous growths, particularly at the angle of mouth. • Buccal mucosa—the buccal mucosa may show a velvety white appearance with occasional papillary lesion.
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Specific System Disorders 817 • Gingival hyperplasia—gingival hyperplasia may also occur. Interdental gingiva may become so hyperplastic that it interferes with eating as it covers the teeth.
Diagnosis • Clinical diagnosis—brownish alteration of skin velvety white appearance of buccal mucosa may be diagnostic features of scleroderma. • Laboratory diagnosis—there is marked acanthosis, coupled with peculiar parakeratosis.
• Temporomandibular joint—hypermobility of temporomandibular joint resulting in repeated dislocations of the jaw have been reported. • Teeth—there may be lack of normal scalloping of the dentinoenamel junction, formation of irregular dentin and increased tendency to form pulp stones with hypoplastic changes in enamel.
Diagnosis
Management
• Clinical diagnosis—hyperelasticity, hyperextensibility of joint and Gorlin’s sign can give clue to diagnosis. • Laboratory diagnosis—clotting time is normal, but capillary fragility test is usually positive.
Keratolytic lesion—this may improve appearance of benign form.
Management
Ehlers-Danlos Syndrome
Not specific—there is no specific treatment for this disease, but surgical procedures should be carried out carefully as healing problems can exist.
It is also called as cutis hyperelastica and it is a group of hereditary disorders of connective tissue. There is production of abnormal collagen, resulting in selective defect in collagen synthesis.
Tuberous Sclerosis It is also called as Epiloia-Bourneville syndrome. It is inherited as autosomal dominant trait.
Clinical Features
Clinical Features
• Hyperelasticity—there is hyperelasticity of skin, hyperextensibility of the joints and fragility of skin and blood vessels, resulting in excessive bruising as well as defective healing of skin wounds. • Rupture of large arteries—rupture of large arteries as well as of intestine often occurs, producing a life threatening situation. • Rubber man—in some patients, skin extensibility is pronounced, so that he can stretch the skin significantly. It is called as ‘rubber man’. • Signs—hypertelorism, a wide nasal bridge, epicanthic folds, protruding ears and frontal bossing are often present. • Subcutaneous nodules—freely movable subcutaneous nodules are frequently found, which represent fibrosed lobules of fat. • Papyraceous scarring—the scarring of skin following wound healing in these patients is unusual, as the scars tend to spread rather than contract in time. It resembles crumpled cigarette paper.
• Facial angiofibroma—it is also called as adenoma sebaceum. These are smooth surface papules (Fig. 3316) which occur on nasolabial fold. Some lesions are also found under margins of nails. • Shagreen patches—these are seen on skin and they resemble sharkskin-derived shagreen cloth. • Ash-leaf spots—it appear on cutaneous surface. • CNS features—it includes seizure, mental retardation. Potato like growth (tuber) can be seen at autopsy in CNS. • Cardiac rhabdomyoma—it is tumor of heart. Myocardial function may hamper due to this tumor.
Oral Manifestations • Oral mucosa—oral mucosa is of normal color but is excessively fragile and bruises easily. • Gingiva—the gingival tissue appears fragile and bleeds after toothbrushing. • Gorlin sign—it is positive in this patient. Patient can touch its nose with the tip of tongue.
Fig. 33-16: Multiple papular facial lesions seen on face in case of tuberous sclerosis (Courtesy Dr Pincha).
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• Angiomyolipoma—it can also occur in this syndrome and it is vascular smooth muscle adipose tissue tumor.
Oral Manifestations • Enamel defect—there is developmental pitting defect on facial aspect of permanent dentition. • Fibrous papule—it can also be present in this syndrome. These are most commonly occur in anterior gingival mucosa. In some cases diffuse gingival enlargement can also occur.
Diagnosis
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• Clinical diagnosis—presence of facial angiofibroma, shagreen patch, mental retardation, and cardiac angiolipoma may diagnosis this disease. Gingival fibroma and enamel pit can also occur. • Laboratory diagnosis—biopsy shows nonspecific fibrous hyperplasia in gingival fibroma.
Management • Anticonvulsant agents—these are given to manage seizure. • Maintenance of oral hygiene—as phenytoin is given in these cases, maintenance of oral hygiene is very important.
Seborrheic Keratosis It is skin lesion which is characterized by benign proliferation of epidermal basal cells.
Management • Cryotherapy—cryotherapy with liquid nitrogen is used to remove the lesion.
Sebaceous Hyperplasia It is localized proliferation of sebaceous gland of skin.
Clinical Features • Age—it is common in older age group and seen in fourth decade of life. • Site—it is seen most commonly on facial skin in the region of cheeks and forehead. • Symptoms—it is usually painless. • Signs—it is soft, nontender with yellow and white discoloration. There is small central depression which represents area where duct of sebaceous gland terminated. • Compression test—after compression of lesion sebum (thick yellow product) is expressed from sebaceous gland.
Diagnosis • Clinical diagnosis—compression test showing sebum from the lesion. • Laboratory diagnosis—biopsy shows collection of enlarged sebaceous gland around the centrally located sebaceous ducts.
Management
Clinical Features • Age—it is common in older age group and seen in fourth decade of life. • Site—it is seen on face, trunk, and extremities. • Appearance—these are multiple, small tan to brown macule which enlarge gradually. They appear as stuck onto the skin. • Surface—surface of lesion is fissured, pitted and verrucous. • Size—size is less than 2 cm in diameter. • Dermatosis papulosa nigra—it is seen in black people and is characterized by multiple, small dark brown papule scattered in zygomatic and periorbital region. • Leser-Trelat sign—sudden appearance of seborrheic keratosis with pruritis has been associated with internal malignancy. This is called as Laser-Trelat sign.
Diagnosis • Clinical diagnosis—small brown papular lesion seen on face and trunk will diagnose this condition. • Laboratory diagnosis—there is exophytic proliferation of basilar epithelial cells with surface keratinization, acanthosis and papillomatosis.
• Excisional biopsy—this is done to differentiate it with basal cell carcinoma.
Actinic Lentigo Lesion which occurs due to ultraviolet light damage to skin. It is also called as lentigo solaris, solar lentigo, age spot, liver spot and senile lentigo.
Clinical Features • Age—it is common in older age group, in the age group of 40 to 70 years. • Site—it is common on dorsal surface of hand, face and arms. Commonly seen in white people. • Appearance—it is multiple with individual lesion appear as uniformly pigmented brown to tan macule with well demarcated and irregular border. • Size—size is less than 5 mm.
Diagnosis • Clinical diagnosis—brown to tan pigmented macule on face may give clue to diagnosis
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Specific System Disorders 819 • Laboratory diagnosis—elongated and club-shaped rete pegs are present.
Management • Topical retinoic acid—this can reduce the color intensity of lesion. • Laser—Q shaped ruby laser can be use for the treatment of this lesion.
Melasma It is symmetric hyperpigmentation of sun exposed skin, face and neck. This is usually associated with pregnancy so it is also called as mask of pregnancy.
Clinical Features • Age—it is seen in adult women. • Site—it is seen in midface, forehead, upper lip, and chin. • Appearance—it is bilateral, light to dark brown cutaneous macule. Pigmentation may darken with time. • Size—size range from few millimeter to 2 cm in diameter.
Diagnosis • Clinical diagnosis—skin cancer in young individual will give strong clue to diagnosis of Xeroderma pigmentosum. • Laboratory diagnosis—biopsy shows features of cutaneous malignancies.
Management • Topical chemotherapeutic agents—topical chemotherapeutic agent’s 5-fluorouracil is used to treat actinic keratosis. • Genetic counseling—it should be done before marriage. • Prevention—patient is ask to avoid sun exposure, wear protective clothing
Muscle Disorders Muscular Dystrophy It is genetically determined disease characterized by degeneration of muscle leading to progressive weakness.
Diagnosis
Types
• Clinical diagnosis—bilateral symmetric pigmentation in pregnancy patient will diagnose this condition • Laboratory diagnosis—there is increase melanin deposition in epidermis.
• Three percent hydroquinone and tretinoin—it is effective in many cases.
• Severe generalized familial muscular dystrophy—it is described as a rapidly progressive muscle disease, usually beginning in early childhood and presenting a strong familial transmission. • Mild restricted muscular dystrophy—it is a slowly progressive proximal myopathy which primarily involves the muscles of shoulder and face and has a weak familial incidence. It is transmitted as an autosomal dominant trait.
Xeroderma Pigmentosum
Clinical Features
It is genodermatoses in which multiple cutaneous malignancies develop. It is inherited as autosomal recessive trait and caused by defect in the excision repair mechanism of DNA.
• Age and sex—it predominately affects males. It begins in childhood, usually before the age of 6 years and rarely after 15 years. • Symptoms—the earliest symptom is inability to walk or run due to which, the children fall readily and is associated with muscular enlargement and weakness. In case of mild restricted dystrophy, patient is unable to raise arms above the head and inability to close eyes. • Waddling gait—the muscular enlargement ultimately proceeds to atrophy and the limbs appear flaccid. It is the atrophy which is responsible for the postural and ambulatory defects, such as waddling gait. • Signs—scapular muscles become atrophic and weak with subsequent alteration in the posture. • Cardiac abnormalities—cardiac abnormalities including cardiomegaly and tachycardia are often present and many patients die of sudden cardiac failure.
Management
Clinical Features • Age—it occurs in early age group. • Symptoms—there is increased tendency to sunburn. Patient also notices freckled pigmentation and patchy depigmentation of skin. Patient also notices neurological manifestation like below normal intelligence. • Actinic keratosis—it is evident in early age group. These lesions will change into basal cell carcinoma or squamous cell carcinoma. • Oral features—squamous cell carcinoma develops on lower lip and tongue.
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Oral Manifestations • Location—the muscles of mastication, facial ocular, laryngeal and the pharyngeal muscles are usually involved, only in the late course of disease. • Teeth—due to lack of muscle tension, teeth cannot be kept properly aligned in the arch. • Tapir-lips—the lips develop a characteristic looseness and protrusion, which have been described as ‘tapirlips’. The patient is unable to whistle or smile. • Open bite and diastema—there may be severe open bite and development of diastema. • Temporomandibular joint—locking and clicking of the jaw.
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Diagnosis • Clinical diagnosis—there is muscular weakness, waddling gait, tapir-lip will give clue to diagnosis. • Laboratory diagnosis—there is gradual disappearance of muscle fibers, as the disease progresses no fibers may be recognized. Serum creatinine phosphokinase levels are elevated in all males.
• Myopathic facies and swan neck—the masseteric atrophy produces narrowing of the lower half of the face which, with ptosis and generalized weakness of the facial musculature gives the patient a characteristic ‘myopathic facies’ and ‘swan neck’. • Percussion contraction—electrical and physical stimulation of a muscle produces the characteristic prolonged contraction or ‘percussion contraction’. • Dysphagia—pharyngeal and laryngeal myotonia also exhibit weakness manifested by a weak, monotonous nasal type of voice and subsequent dysphagia. • TMJ—recurrent dislocations of the jaw is also reported in this disease. • Eye—blinking with strong closure of the eyes will sometimes produce a prolonged contraction of the lids. • Other—other features are testicular atrophy, cataract, hypothyroidism with cold extremities, slow pulse, loss of hair and functional cardiac changes.
Diagnosis
Myotonias are the disorders characterized by abnormally slow relaxation after muscle contraction.
• Clinical diagnosis—swan neck, muscular weakness, myopathic facies and atrophy of muscles of mastication. • Laboratory diagnosis—there is enlargement of scattered muscle fibers and the presence of centrally placed muscle nuclei in long rows. True hypertrophy in some fibers, is found, as well as in isolated fibers which show extreme degenerative changes including nuclear proliferation, intense basophilic cytoplasmic staining and phagocytosis.
Types
Management
• Dystrophic myotonica—it is also called as myotonic dystrophy or dystrophic myotonica. It is inherited as an autosomal dominant trait. • Myotonica congenita (Thomsen’s disease)—it is transmitted as an autosomal dominant trait with incomplete penetrance in some families. It is generalized myotonia without weakness. • Myotonia congenita (Becker type)—it appears late in childhood and characterized by muscle hypertrophy.
There is no specific treatment for this disease.
Management There is no treatment for this disease. Physical therapy may help prolong the use of specific muscle group.
Myotonias
Hemifacial Spasm It is a disease characterized by a repeated, rapid, painless, irregular, nonrhythmic, uncontrollable, unilateral contraction of the facial muscles. It may occur due to compression of the facial nerve, in the facial canal, adjacent to the stylomastoid foramen.
Clinical Features
Clinical Features • Location—atrophy of the muscles is seen usually in the hands and forearms. It can be seen in muscles of face, jaws, neck and levator of eyelids. • Symptoms—there is associated weakness of the muscles. Muscular contraction induces a severe, painless muscular spasm, and an actually delay in relaxation. • Facial muscle—alteration in the facial muscles, which consist of ptosis of the eyelids and atrophy of the masseter and sternocleidomastoid muscles.
• Location—it usually begins in the periorbital muscles, but soon spreads to the entire half of the face. • Precipitating factors—these spasms are often triggered by fatigue, tension or facial activity and are of brief duration, usually lasting for only a few seconds. • Symptoms—it is first manifested as a brief transitory twitching, but may progress to sustain a spasm. • Signs—in cases of long standing hemifacial spasms, mild facial contracture may occur with lid closure and lip pursing.
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Specific System Disorders 821 Diagnosis • Clinical diagnosis—muscular spasms which is triggered by fatigue and twitching.
Management • Decompression of the nerve—decompression of the nerve in its canal has offered relief in some cases. Prognosis is good, remission and recurrence may occur over a period of years.
Paramyotonia It is a nonprogressive myotonia, inherited as an autosomal dominant characteristic that is not associated with muscular wasting. Characteristically, the cramping attacks are precipitated on exposure to cold.
Clinical Features • Symptoms—it is manifested by cramping, stiffness and weakness of the muscles of the face and neck, fingers and hands, upon exposure to cold. Muscles cramping may disappear within an hour; the weakness may persist for several days. • Mask-like appearance—the eyelids are closed and the face assumes a mask-like appearance. • Tongue—the tongue may exhibit a similar cramping after drinking cold liquids and the speech becomes blurred. In many cases, myotonia of the tongue may be induced by percussion.
Diagnosis • Clinical diagnosis—masklike appearance seen in face. Muscle cramping will disappear within hour after exposure to cold.
Management There is no specific treatment for it, but the prognosis is excellent with frequent improvement during adult life.
Myasthenia Gravis It is an autoimmune chronic disease characterized by progressive weakness of the skeletal muscles, particularly those innervated by the cranial nerves. It is characterized by easy fatigability of the striated muscles secondary to disorders at the neuromuscular junction. It affects acetylcholine receptors of muscle fibers resulting in fatigability of skeletal muscle.
Etiology • Defective neuromuscular transmission—there is a defect in the neuromuscular transmission, which occurs due to
coating of acetylcholine receptors by circulating antibodies. This will result in the fault acetylcholine mechanism. • Hyperplasia of thymus—it may occur in the endocrine system due to thymus hyperplasia or tumors of the thymus. • Other factors—it may be related to pregnancy, menstruation and hyperthyroidism.
Clinical Features • Age and sex—it occurs in adults in the middle age group with a predilection for women. • Symptoms—there is rapidly developing weakness in voluntary muscles, following even minute activities. Patient may suffer from diplopia (double vision) and ptosis (drooling eyelids) and extraocular muscular paresis (an inability to focus the eyes) and dysarthria (slurring of word). • Sorrowful appearance of face—there is dropping of the face, leads to sorrowful appearance of the patient. • Signs—the neck muscles may be so weak that the head can not be held up without support. • Progress—patients become exhausted, looses weight becomes further weakened and may eventually become bedridden. Death frequently occurs from respiratory failure.
Oral Manifestations • Symptoms—the patient’s chief complains may be difficulty in mastication, deglutition and dropping of the jaw. Speech is often slow and slurred and disturbance in taste sensation occurs. Dysphagia and regurgitation of food are common. • Tongue—there may be weakness of the tongue and palatal muscles. Protrusive movements of the tongue may become weak leading, at times to posterior collapse of the organ with airway obstruction.
Diagnosis • Clinical diagnosis—ptosis, diplopia, dysphagia, sorrowful appearance of face. • Laboratory diagnosis—elevated serum AChr (acetylcholine) level. Biopsy shows focal collection of small lymphocytes or lymphorrhages around small blood vessels in the interstitial tissue of the affected muscles.
Management • Anticholinesterases—pyridostigmine, edrophonium, and neostigmine, administered intra-muscularly improve the strength of the affected muscles few minutes. • Corticosteroids—these can be use in combination with cholinesterase inhibitors.
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• Thymectomy—this is done in condition when myasthenia gravis is associated with thymoma. • Plasmapheresis has been temporary valued in patient with severe exacerbation.
• Lips—telangiectatic lesions of vermilion border of lips and cheeks may also occur. • Teeth—there is purplish black intrinsic staining of teeth.
Radiographic Features Dermatomyositis It is also called as ‘polymyositis’. It is an acute or a chronic disease of unknown etiology and is characterized by gradual onset with vague and indefinite prodromata, followed by edema, dermatitis, myositis and sometimes neuritis and mucositis.
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Clinical Features • Age and sex—it may occur in patients of any age ranging from very young children to elderly, but majority occurs in the 5th decade of life. There is no sex predilection. • Onset—it begins with erythematous skin eruptions, edema, tenderness, swelling and weakness of the proximal muscles of limbs. Fever may be associated with it. • Progress—the weakness of muscle is progressive and characteristically spreads to face, neck, larynx, pharynx and heart. • Skin—the skin becomes the seat of violaceous erythema and edema with a predilection for the eyelids, malar area and dorsa of hands. The typical skin lesions include heliotrope (liac-colored) changes around the face and fingers. • Signs—the edema which gives the skin a puffy consistency including the face, leaves a reticulated telangiectatic erythema when it subsides. • Calcinosis cutis—the skin lesions frequently calcify and form calcium carbonate nodules with a foreign body reaction which is known as calcinosis cutis. • Calcinosis universalis—the term calcinosis universalis is applied when these calcified masses are found generalized throughout the soft tissues. • Prognosis—muscle involvement may become severe enough to confine the patient to bed or cause death owing to failure of respiratory muscle.
Oral Manifestations • Diffuse stomatitis and pharyngitis—the oral lesions consist of diffuse stomatitis and pharyngitis and are extremely common. • Symptoms—involvement of the muscles of jaw, tongue and pharynx may pose problems in eating and phonation. • Oral mucosa—the oral mucosa may show dark red or bluish erythema. • Tongue—in the early stages, tongue is swollen and later becomes harder and gradually it becomes atrophic. The tongue may become rigid owing to severe calcinosis.
• Pulp calcification—there is severe calcification and obliteration of pulp chambers of deciduous and permanent teeth.
Diagnosis • Clinical diagnosis—heliotrope lesion with dark red oral mucosa, calcinosis cutis will give clue to the diagnosis. • Radiological diagnosis—pulp calcification and obliteration is present. • Laboratory diagnosis—the muscle fibers in dermatomyositis exhibit widespread degeneration and hyalinization. Many fibers show vacuolization, granulation and fragmentation with phagocytosis of disintegrating fibers. There is also mild anemia or leukocytosis. In addition, creatinuria is a constant finding as well as elevated levels of serum transaminase and aldolase.
Management • Corticosteroids—corticosteroid should be given but its effectiveness is doubted.
Immunological Disorders Primary Immune Deficiency These are hereditary abnormalities characterized by an inborn defect of the immune system. These diseases may involve the B-cell system, T-cell system or a defect in both.
Types • Sex linked agammaglobulinemia—- it is caused by a defect in B-cell function with the T-cell function remaining intact. Due to this, these patients slack the ability to synthesize all classes of antibodies including the secretory immunoglobulin, making them more susceptible to bacterial infection. The symptoms begin at 6 months of age. • Primary adult immunoglobulin deficiency—it is characterized by an abnormality of the B-cell or humoral antibody system that does not become clinically apparent until adulthood. Usually one or two Ig classes are deficient. The selective deficiency accounts for the relatively asymptomatic nature of the disease throughout childhood. • Thymic hypoplasia—it consists of DiGeorge’s syndrome and Nezelof’s syndrome. These patients have normal
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Specific System Disorders 823 levels a serum immunoglobulin but lack cell mediated immunity. It consists of both, abnormalities of thymus and parathyroid glands. The lack of parathyroid hormone will lead to hypocalcemia and tetany; lack of thymus function causes absent T-lymphocyte response. • Secondary combined immunodeficiency—it can be inherited as either sex-linked or an autosomal recessive trait. In these diseases, there is both T-cell as well as B-cell deficiency. The patients have low peripheral lymphocytes count severe deficiency of immunoglobulin and complete lack of cellular immunity. • Immunodeficiency with ataxia talangiectasia—it is inherited as an autosomal recessive trait. There is combined T-cell and B-cell deficiency. Progressive neurologic disease form severe degenerative changes on the cerebellum, leading to cerebellar ataxia. It becomes apparent when the child begins to walk.
Clinical Features • Sex-linked agammaglobulinemia—patients experience severe recurrent bacterial infections of lungs, meninges, skin and sinuses. There is hypoplasia of lymph nodes, adenoid and tonsils. There is increased incidence of rheumatoid arthritis, dermatomyositis, lymphoma and leukemia. • Primary adult’s immunoglobulin deficiency—the most common symptoms include recurrent gram-positive bacterial infections of upper and lower respiratory tracts. • Thymic hypoplasia—there is increased susceptibility to infections with virus and fungi. Infection with Candida albicans is especially prominent. • Severe combine immunodeficiency—symptoms begin in first few week of life and include bacterial, viral and fungal infections. Localized and systemic candidiasis is common. The patient dies of overwhelming infections during the first year of life, unless a histocompatible relative is found for a bone marrow transplant. • Immunodeficiency with ataxia telangiectasia—telangiectasia of the skin and eyes becomes apparent at about 3 years of age. The lesion becomes more extensive with age and mainly occurs on conjunctiva, ears and malar eminences. These are also associated with Gonadal dysgenesis and increased incidence of malignancies of lymphoreticular system.
Oral Manifestations • Infection—in T-cell deficiency, there may be chronic oral candidiasis and herpes simplex infection. In B-cell deficiency, there are recurrent bacterial infections and chronic maxillary sinusitis.
• Congenital defects—congenital defects like cleft palate, micrognathia, bifid uvula and short philtrum of upper lip. • Oral ulcerations—occasionally, oral ulceration is seen in these patients but it is not the diagnostic of these disorders.
Diagnosis • Clinical diagnosis—increase susceptibility to infection and severe recurrent infection will suspect immune deficiency.
Management • Control of local infection—minimize the chances of local infection or septicemia and oral candidiasis, treated with antifungal therapy, prior to dental treatment. • Concentrated human gamma globulin—patient with symptomatic B-cell abnormalities are usually given continuous therapy with concentrated human gamma globulin. When oral surgery is necessary, an extra dose of gamma globulin should be administrated the day before surgery. • Blood replacement therapy—patients with B cell deficiency resulting in the absence of particular immunoglobulin may experience severe transfusion reaction when receiving blood from a patient who has normal immunoglobulin levels. The immunoglobulin acts as a foreign protein and causes an allergic response. For these reasons, patient with selective IgA deficiency must be given IgA depleted blood in blood replacement therapy.
Miscellaneous Conditions Drug Allergy Allergy or hypersensitivity is an unwanted response of the body to the complete dose of drug.
Mechanism • Formation of antibody—a patient previously exposed to a drug or other antigen has antibody, primarily IgE, fixed to basophils and mast cells. • Releasing of active mediators—when the antigen in the form of a drug, food or airborne substance is reintroduced into the body it will react with the fixed antibody, bind complement and open the mast cells releasing active mediators such as histamine and slow reactive substance of anaphylaxis. • Vasodilation and increases capillary permeability—these substances cause vasodilation and increased capillary
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permeability resulting in fluid and leukocytes leaving the blood vessels and accumulating in the tissue forming areas of edema. • Constriction of bronchial smooth muscle—constriction of bronchial smooth muscle also may result, when IgE is bound in the pulmonary region.
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Clinical Features
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Localized anaphylaxis • Urticaria—when it involves the superficial blood vessels, urticaria (hives). It begins with pruritus in the area of release of histamine and other active substances. • Skin—wheals (welts) then appear on the skin as an area of localized edema on an erythematous base. • Edema—there is also macular papular or nodular rash with edema of skin and subcutaneous tissue. Angioneurotic edema • Causes—it can be caused by contact with an allergen or can be idiopathic. A recurrent form is inherited as an autosomal dominant trait. There is deficiency of an alpha-2 globulin, which normally acts as an inhibitor of the first component of complement and kallikrein. • Locations—Angioneurotic edema of lips, tongue, eyelids, larynx and bronchi may occur. • Appearance—in angioneurotic edema, when deeper blood vessels in the subcutaneous tissue are affected, a large diffuse area of subcutaneous swelling is produced under the normal overlying skin. • Respiration—it is temporarily disfiguring, but not serious, unless the posterior portion of the tongue or larynx compromise respiration. Serum sickness • Causes—it frequently occurs after administration of foreign serum, which before antibiotics, was given for the treatment of infectious disease. It occurs from tetanus antitoxin, rabies antiserum and drugs that combine with body proteins to form allergens. • Mechanism—in it, antibodies form immune complexes in blood vessels with administrated antigens. The complexes fix complement, which attract the leukocytes to the area causing direct tissue injury. • Symptoms—major symptoms consist of fever, swelling, lymphadenopathy, joint and muscle pain and rash. • Signs—less common manifestation include peripheral neuritis, kidney disease and myocardial ischemia. Generalized anaphylaxis • Mechanism—it is an allergic emergency with no time to call consultants. It is reaction of IgE antibodies with an allergen, causing the release of histamine, bradykinin and SRS-A (slow reacting substance of anaphylaxis). These chemical mediators cause contraction of smooth
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muscles of the respiratory and intestinal tracts as well as increase vascular permeability. Precipitating factors—the risk of anaphylaxis is increased if the drugs are given parenterally, family history of allergy, history of asthma and administration of high risk allergens such as penicillin. Onset—anaphylactic reaction may occur within seconds of drug administration or occur 30 to 40 minutes later. The generalized reaction occurs in four systems cardiovascular, intestinal, respiratory and skin. Skin—the first sign occurs on skin and it includes urticaria, angioedema, erythema and pruritus. Pulmonary symptoms—pulmonary symptoms include dyspnea, wheezing and asthma. Gastrointestinal tract—gastrointestinal tract symptoms like vomiting, cramps and diarrhea occur. Cardiovascular system—if these are untreated, symptoms of hypotension appear that result from the loss of intravascular fluid. If left untreated, this leads to shock. Prognosis—the patients with generalized anaphylactic reaction may die from respiratory failure, hypotensive shock or laryngeal edema.
Management • Cutaneous rashes—oral administration or injection of chlorpheniramine, intramuscularly. • Angioneurotic edema—the patient’s respiratory distress should be treated immediately with 0.5 ml epinephrine, 1:1000 subcutaneously or 0.2 ml injected slowly intravenously. When immediate danger is passed, then 50 mg of diphenhydramine hydrochloride should be given 4 times daily, until the swelling is diminished. • Severe symptoms—injection hydrocortisone sodium succinate or injection epinephrine. • Serum sickness—It is self-limiting with spontaneous recovery within 1 to 3 weeks. Other treatment is symptomatic with aspirin, for arthralgia and antihistamines, for skin rashes. • Anaphylactic reaction with sudden cardiovascular and respiratory collapse can be treated by following method:• Make the patient to lie down in supine position. • Patent airway is to be maintained. • Administer 100% O2. • Injection epinephrine 1.1000 IM. It should be given if the blood pressure falls below 60 mm of Hg. • For bronchospasm, slowly inject aminophylline 250 mg IV over a period of 10 minutes. Too rapid administration can lead to fatal cardiac arrhythmias. • Start IV infusion stat. • Monitor pulse, blood pressure and respiration. • Hydrocortisone 100 mg IV.
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Specific System Disorders 825 • Antihistaminic should be given. • Refer to physician and arrange for hospitalization.
Syncope It is also called as ‘simple faint’, ‘swoon’, ‘psychogenic syncope’, and ‘vasodepressor syncope’. It is a transient loss of consciousness due to cerebral anoxia.
Causes • Young and poor health person—it is commonly seen in younger individuals and people having poor health. • Precipitating factors—the other factors are anxiety, fear, and sight of blood, pain, exhaustion, fasting and hot environment. These emotional stresses induce release of increased amount of catecholamine. • Cerebral anoxia—the chief cause is cerebral anoxia or anemia. A blood loss of one liter will cause fainting.
Clinical Features • Presyncope—victim falls gently to the floor, regains consciousness almost immediately or within a short period of time, appears to recover completely. • Early signs and symptoms—the patient complains for warmth in the neck and face. He bathes in beads of cold sweat. He also complains of nausea and feeling vague. Blood pressure at this time is at baseline or slightly lower than baseline. There is also rapid heart rate. Face is pale or has ashen gray skin tone. • Late signs and symptoms—as the process continues papillary dilation, yawning, hyperpnea, coldness in hand and feet, hypotension, bradycardia, visual disturbances, dizziness and loss of consciousness occur. • Syncope—with loss of consciousness, breathing may become irregular, jerky and gasping. The pupils of eye dilate and patient has deathlike appearance. Convulsive movements or muscular twitching of hands, legs or facial muscle. Blood pressure is low and pulse rate is also decrease. • Post syncope—with proper positioning, recovery usually appears rapidly. Patient exhibits pallor, nausea, weakness and sweating, which may persist for few minutes to few hours.
Fig. 33-17: Supine position to be maintained in the syncope.
• Loosening of tight clothing and belt—tight clothing and belt should be loosened. • Maintenance of patent airway—a patent airway should be maintained. Inhalation of aromatic spirit or application of cold sponge to the face helps in securing reflex stimulation. • Oxygen administration—if cyanosis is developing, 100% oxygen is administered and vital signs are recorded. • Ammonia ampule—an ammonia ampule is crushed and held under the patient’s nose for speed recovery. • After recovery—after complete recovery, patient should be slowly brought to semi-reclining, rather than sitting, position. • Prevention—it is usually advisable to treat patients in supine or semi-reclining position. The role of premedication before surgery should be considered. Patient who is fasting is more prone to vasovagal attack.
Shock If the primary shock or syncope is not tackled and allowed to persist, the secondary or true shock appears. Shock can be hemorrhagic, hypovolemic, septic, anaphylactic shock.
Clinical Features Management • Supine position—when there are signs of fainting he/ she should be made to lie down in supine position with legs raised to improve venous return to the heart (Fig. 33-17). In case of patient being on the dental chair the back of the chair should be immediately lowered so that the head of the patient is at a lower level than the feet.
• Symptoms—the patient is unconscious with ashen gray face and cold clammy skin. • Signs—mucous membrane is pale, whereas lips, nails, fingertips and lobules of ear are grayish blue. Pulse is weak and thready. • Face—face is expressionless with sunken eyes. • Pupil—pupils are dilated, but react feebly to light.
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Management
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• Establishing the cause—establish the cause of shock like loss of blood, extremely painful stimulus, emotional reasons, toxemia or anaphylaxis and the treatment should be given. • Patient position—put the patient in position with head at lower level than feet. • Maintenance of body heat—maintain the body heat by covering the patient with blanket and keeping a hot water bottle between the thighs. • Airway management—check the patency of airway and control the loss of blood by pressure packs, ligation of vessels or crushing of bone. • Restoration of body fluids—restore the lost body fluids; Ringer’s lactate solution should be used to maintain the intravenous line and to restore the volume loss. If hemoglobin is fallen due to toxemia, packed cells are given. • Oxygen—administer 100% of oxygen to the patient for adequate oxygenation of the body tissue. • Monitoring of vital signs—the blood pressure, pulse rate and respiration rate should be constantly monitored to assess signs. • Steroids injection—injection hydrocortisone sodium hemisuccinate 100 mg, dissolved in 5 ml of sterile water is given. • Mephentermine injection—injection mephentermine is given for hypotension. • Injection atropine—if pulse is weak injection atropine is diluted with 5 ml of distilled water and is injected slowly till the radial pulse becomes palpable. • Antibiotics—broad spectrum antibiotics through IV route are given. • Adrenaline—one ampule of 1:1000 dilution of adrenaline in 10 ml of sterile water is given intravenously. • Painkiller—a potent painkiller like narcotic analgesic to gain relief from pain.
Suggested Reading 1. Academy report. Periodontal management of patients with cardiovascular disease. J Periodontal 2002;73:954-68. 2. Alexandridis C, White SC. Periodontal ligament changes in patients with progressive systemic sclerosis. Oral Surg 1984; 58:113-8. 3. Allen CM, et al. Wegener’s granulomatosis: report of three cases with oral lesions. J Oral Maxillofac Surg 1991;49:294-8. 4. Auluck A, Pai K. Progressive hemifacial atrophy with morphea of cheek. JIAOMR 2006;18(3):172-5. 5. Bader JD, Bonito AJ, Shugars DA. A systemic review of cardiovascular effects of epinephrine on hypertensive dental patient. Oral Surg, Oral Med, Oral Pathol, Oral Radiol 2002; 93:647-53. 6. Bali RK, Chhabra N, Zarina. Frey’s syndrome as a sequelae of superficial parotidectomy” JIAOMR 2006;18(3):181-3. 7. Bartlett DW, Evans DF, Anggiansah A, Smith BG. A study of the association between gastro-oesophageal reflux and palatal dental erosion. Br Dent J 1996 Aug 24;181(4):125-31.
8. Batal G, Chou LL, Cottrell DA. Sarcoidosis medical and dental implication. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1999;88:386-90. 9. Blanchaert RH Jr. Ischemic heart disease. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod. 1999;87(3):281-3. 10. Blinder D, Yahatom R, Taicher S. Oral Manifestation of sarcoidosis. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod: 1997;83:45861. 11. Campbell RL, Langston WG, Ross GA. A comparison of cardiac rate pressure products and pressure rate quotient with Holter monitoring in patient with hypertension and cardiovascular disease. A follow up report. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod. 1997;84(2):125-8. 12. Carmona IT, Dios PD, Scully C. An update on the controversies in bacterial endocarditis in oral region. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 2002;93:660-70. 13. Challacombe SJ. Orofacial granulomatosis and oral Crohn’s disease are they specific disease and do they predict systemic Crohn’s disease? Oral dis 1997;3:127-9. 14. Chemaly D, Lefrancosis A, Perusse R. Oral and maxillofacial manifestation of multiple sclerosis. J Can Dent Asso 2000;66 (11):600-605. 15. Chuang TY, Stitle L, Brashear R, Lewis C. Hepatitis C virus and lichen planus. A case-control study of 340 patients. J Am Acad Dermatol 1999 Nov; 41(5 Pt 1):787-9. 16. Cohen RE, et al. Gingival manifestations of Wegener’s granulomatosis. J Periodont 1990;61:705-9. 17. Dajani S, Taubert KA, et al. Prevention of bacterial endocarditis. Recommendation of American Heart association. JADA 1997; 128(8):1142-251. 18. Daley TD. Intraoral sebaceous hyperplasia. Diagnostic criteria. Oral Surg, Oral Med, Oral Pathol 1993;75:343-7. 19. Damm DD, Tomich CE, et al. Intraosseous fibrous lesion of the jaws, a manifestation of tuberous sclerosis. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1999;87:334-40. 20. De Rossi SS, Glick M. Dental consideration for the patient with renal disease receiving hemodialysis. JADA 127;211-29. 21. Demas PN, McClain JR. Hepatitis implication for dental care. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1999;88:2-4. 22. Demir Y, Karaslan T, et al. Linear scleroderma ‘en coup de sabre’ of the cheek. J Oral Maxillofac Surg 2003;61:1091-4. 23. Dent CD, Hunter WE, Svirsky JA. Sebaceous gland hyperplasia. Case report and literature review. J Oral Maxillofac Surg 1995; 53:936-8. 24. Doyle IL, et al. Eosinophilic ulcer. J Maxillofac Surg 1989;47: 349-52. 25. Droblik C, Laskawi R. Frey syndrome: treatment with Botulinum toxin. Acta Otolaryngol 1995;1115-59. 26. Dunlap CL, Friesen CA, Shultz R. Chronic stomatitis. An early sign of Crohn’s disease. JADA 1997;128:347-8. 27. Elzay RP. Traumatic ulcerative granuloma with stromal eosinophilia. Oral Surg, Oral Med, Oral Path 1993;72(5):59-61. 28. Eufinger H, Machtens E, Akuamoa-Boateng E. Oral manifestation of Wegener’s granulomatosis. Review of literature and report of a case. Int J Oral Maxillofac Surg 1992;21:50-3. 29. Eversole LR, Jacobsen PL, Stone CE. Oral and gingival changes in systemic sclerosis (scleroderma). J Periodontal 1984;55:175-8. 30. Fishoff DK, Sirosis D. Painful trigeminal neuropathy caused by severe mandibular resorption and nerve compression in a patient with systemic sclerosis, case report and literature review. Oral Surg, Oral Med, Oral Pathol, Oral Radiol 2000;90:456-9. 31. Fiske J, Boyle C. Epilepsy and oral care. Dent update 2002;29: 1807. 32. Fridrich KL, Fridrich HH, et al. Dental implication in Ehlers-Danlos syndrome. A case report. Oral Surg, Oral Med, Oral Pathol 1990;69:431-5. 33. Gaulard P, Henni T, et al. Lethal midline granuloma (polymorphic reticulosis) and lymphomatoid granulomatosis. Evidence of monoclonal T cell lymphoproliferative disorders. Cancer 1988; 62:705-10.
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Specific System Disorders 827 34. Gavalda C, Bagan JV, et al. Renal hemodialysis patient. Oral, salivary and periodontal finding in 105 adults cases. Oral Disease 1999;5:299-302. 35. Ghandour K, Issa M. Oral Crohn’s disease with late intestinal disease. Oral Surg Oral Med Oral Pathol 1991;72:565-7. 36. Gibson J, Wray D, Bagg J. Oral staphylococcal mucositis. A new clinical entity in orofacial granulomatosis and Crohn’s disease. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000; 89(2): 171-6. 37. Giler JP, Vinciguera M, Heler A, et al. Treatment of gingival Crohn’s disease with laser therapy. N Y State Dent J 1997;5:32-5. 38. Glick M. New guideline for prevention, detection, evaluation and treatment of high blood pressure. JADA 1998;129:1588-94 39. Gonzales TS, Coleman GC: Periodontal manifestations of collagen vascular disorders. Periodontol 2000 1999; 21: 94-105. 40. Haers PE, Sailer HF. Mandibular resorption due to systemic sclerosis. Case report of surgical correction of secondary open bite deformity. Int J Oral Maxillofac Surg 1995;24:261-7. 41. Halme L, Meurman JH, Laine P, et al: Oral findings in patients with active or inactive Crohn’s disease. Oral Surg Oral Med Oral Pathol 1993 Aug; 76(2): 175-81. 42. Handlers JP: Oral manifestations of gastrointestinal disease. J Calif Dent Assoc 1999 Apr;27(4):311-7. 43. Herman W, Konzelman J, Prisant M. New national guidelines on hypertension. JADA 2004135;576-84. 44. Herman WW, Konzelman JL. Angina an update for dentistry. JADA 1996;127:98-104. 45. Hildebran J, Plezia RA, Rao SB. Sarcoidosis report of two cases with oral involvement: Oral Surg, Oral Med, Oral Pathol 1990;69:217-22. 46. Jowett NI, Cabot LB. Patient with cardiac diseases. Consideration for dental practitioner. Br Dent J 2000;189:297-302. 47. Kerr AR. Update of renal disease for dental practitioner. Oral Surg 2001;92:9-16. 48. Knight JM, Hayduk MJ, Summerlin DJ, Mirowski GW. “Strawberry” gingival hyperplasia. A pathognomonic mucocutaneous finding in Wegener granulomatosis. Arch Dermatol 2000 Feb;136(2):171-3. 49. Lapointe HJ, Armstrong JE, Larocque B. A clinical decision making framework for the medically compromised patient. Ischemic heart disease and chronic obstructive pulmonary disease. J Can Dent Asso 1997;63:510-12, 515-6. 50. Laskawi R, Ellies M, et al. Gustatory sweating: clinical implication and etiologic aspect. J Oral Maxillofac Surg 1999;57:642-9. 51. Lilly J, Juhlin T, et al. Wegener’s granulomatosis presenting as oral lesion. A case report. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1998;85:153-7. 52. Little JW. The impact on dentistry of recent advances in the management of hypertension. Oral Surg, Oral Med, Oral Pathol, Oral Radiol 2000;90:591-9. 53. Lodi G, Carroozzo M, et al. Hepatitis C virus associated oral lichen planus. J Oral Pathol Med. 2000;29:39-42. 54. Lygidakis NA, Lindenhum RH. Oral fibromatosis in tuberous sclerosis. Oral Surg, Oral Med, Oral Pathol 1989;68:725-8. 55. Malins TJ, Wilson A, Ward-Booth RP. Recurrent buccal space abscesses. A complication of Crohn’s disease. Oral Surg, Oral Med, Oral Pathol 1991 Jul;72(1):19-21. 56. Marmary Y, Glaiss R, Pisanty S. Scleroderma. Oral Manifestation Oral Surg, Oral Med, Oral Pathol 1981;52:32-7. 57. Mathew T, Casamassimo PS, et al. Effect of dental treatment on the lung function of children with asthma. JADA 1998;129:1120-8. 58. Milam PE, Griffin TJ, Shapiro RD. Dentofacial deformity associated with Incontinentia pigmenti. Report of cases. Oral Surg, Oral Med, Oral Pathol 1990;70:420-4. 59. Moskowitz L. Cardiac disease and hypertension. Consideration for office treatment. Dent Clin North Am. 1999;43(3):495-512. 60. Mostofi RS, Hayden NP, Soltani K. Oral malignant acanthosis nigricans. Oral Surg, Oral Med, Oral Pathol 1983;56:372-4. 61. Muzyka RC, Glick M. The hypertensive dental patient. JADA 1997;128:1109-20. 62. Nagata Y, Kanekura T, Kawabata H, et al. A case of sarcoidosis involving the tongue. J Dermatol 1999 Oct;26(10):666-70.
63. Nagy G, Kovacs J, Zeger M, Czirjak L. Analysis of the oral manifestations for systemic sclerosis. Oral Surg, Oral Med, Oral Pathol 1994;77:141-6. 64. Napier SS, Allen JA, Irwin CR, McCluskey DR. Strawberry gums: a clinicopathological manifestation diagnostic of Wegener’s granulomatosis? J Clin Pathol 1993 Aug;46(8):709-12. 65. Napier SS, et al. Strawberry gums–A case of Wegener’s granulomatosis. Br Dent J 1993 Nov 6 175(9):327-9. 66. Naylor GD, Fredericks MR. Pharmacological consideration in the dental management of the patient with disorders of the renal system. Dent Clinic North Am. 1996;40:665-83. 67. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology (2nd edn), Saunders Elsevier, 2004 . 68. Oliver AJ, et al. Monosodium glutamate-related orofacial granulomatosis: review and case report. Oral Surg, Oral Med, Oral Pathol 1991;71:560-4. 69. Parson E, et al. Wegener’s granulomatosis-A distinct gingival lesion. J Clin Periodont 1992;19:64-6. 70. Patten SF, Tomecki KJ. Wegener’s granulomatosis. cutaneous and oral mucosal disease. J Am Acad Dermatol 1993;28(5 Pt 1): 710-8. 71. Patton LL, Valdez IH. Xeroderma pigmentosum. Review and report of case. Oral Surg, Oral Med, Oral Pathol 1991;71:297-300. 72. Plauth M, Jenss H, Meyle J. Oral manifestations of Crohn’s disease. An analysis of 79 cases. J Clin Gastroenterol 1991 Feb; 13(1): 29-37. 73. Ramirez-Amador V, Esquivel-Pedraza L, et al. Oral manifestation as a hallmark of malignant acanthosis nigricans. J Oral Pathol Med 1999;28:278-81. 74. Ramsey MJ, Der Simonian R, et al. Corticosteroid treatment for idiopathic facial nerve paralysis. A meta analysis. Laryngoscope 2000;110:335-41. 75. Rubin MM, San Filtppo RJ. Resorption of mandibular angle in progressive systemic sclerosis. J Oral Maxillofac Surg 1992;50: 75-7. 76. Sasakura Y, Kumasaka S, et al. Myasthenia gravis associated with reduced masticatory function. Int J Oral Maxillofac Surg. 2000; 29:381-3. 77. Schwartz RA. Acanthosis nigricans. J Am Acad Dermatol 1994 Jul;31(1):1-19;quiz 20-2. 78. Scully C, Cawson RA. Medical problems in dentistry. 5th edn Churchill Livingstone. An imprint of Elsevier:2005. 79. Scully C, Shotts R. The mouth in neurological disorders. Practitioner 2001;245:539-49. 80. Sedano HO, Gorlin RJ. Acanthosis nigricans. Oral Surg, Oral Med, Oral Pathol 1987;63(4):462-7. 81. Sklavolinm A, Laskaris G. Eosinophilic ulcer of the oral mucosa. Oral Surg, Oral Med, Oral Path 1984;58:431-6. 82. Smith A, Speculand B. Amyloidosis with oral involvement. Br J Oral Maxillofac Surg 1985 Dec; 23(6): 435-44. 83. Spratt H, Boomer S, et al. Cyclosporine associated gingival overgrowth in renal transplant patient. Br Dent J 1997;183:89-94. 84. Thomas D, Rapley J, et al. Tuberous sclerosis with gingival overgrowth. J Periodontal 1992;63:713-7. 85. Thomson PJ, Langton SG. Persistent haemorrhage following dental extractions in patients with liver disease. Two cautionary tales. Br Dent J 1996 Feb 24;180(4):141-4. 86. Tokata Y, Tateishi A, et al. Hepatitis G virus infection in high risk subgroup of hospitalized dental patient. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1999;87(4):442-5. 87. Tyldesley WR. Mouth lesions as markers of gastrointestinal disease. Practitioner 1983;227:587-90. 88. Tyler MT, Ficarra G, Silverman S Jr, et al. Malignant acanthosis nigricans with florid papillary oral lesions. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1996 ;81(4):445-9. 89. Vogt J, Matheson J. Incontinentia pigmenti (Bloch-Sulzberger syndrome). A case report. Oral Surg, Oral Med, Oral Pathol 1991; 71:454-56. 90. Wysocki G, Brooke R. Oral manifestations of chronic granulomatous disease. Oral Surg, Oral Med, Oral Pathol 1978; 46:815-9.
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Diseases of Bone Manifested in Jaw
Introduction
Second Classification
Bone is a dense calcified tissue which is specifically affected by a variety of disease that often causes it to react in a dynamic fashion. These diseases of bone may arise at any age; some are congenital and present at birth, while other develop in early childhood or in young adulthood.
Fibro-osseous Lesions In it, normal bone is replaced by benign fibrous tissue showing varying amounts of mineralization. The subject of benign fibro-osseous enlargement of the jaws has many facets, the most sinister of which is the possibility that a healthy good looking person may take on a monstrous appearance.
Second classification given in 1993 by Waldron reclassified these lesions as follows: • Fibrous dysplasia • Reactive (dysplastic) lesions arising in the tooth bearing area— These are presumably of periodontal ligament origin. Depending on their reference they are divided into three types although they seem to represent the same pathologic process: • Periapical cemental dysplasia • Focal cemento-osseous dysplasia • Florid cemento-osseous dysplasia • Fibro-osseous neoplasms—These are widely designated as cementifying fibroma, ossifying fibroma, or cementoossifying fibroma.
Classification
Fibro-osseous Lesions of Medullary Bone Origin
First Classification
Fibrous Dysplasia
• Fibro-osseous lesions of medullary bone origin • Fibrous dysplasia • Fibro-osteoma • Cherubism • Juvenile ossifying fibroma • Giant cell tumor • Jaw lesions in hyperparathyroidism • Paget’s disease • Fibro-osseous lesions of periodontal origin • Periapical cemental dysplasia • Florid osseous dysplasia • Cemento-ossifying fibroma • Cementifying fibroma • Ossifying fibroma
It arises from the bone forming mesenchyme in the spongiosa and develops by proliferation of fibrous tissue. Lichtenstein in 1938 coined the term ‘fibrous dysplasia’. It is also called as ‘fibrocystic disease’, ‘osteitis fibrosa localisata’, ‘focal osteitis fibrosa’ and ‘fibro-osteodystrophy’. There is no general agreement as to the etiology of lesion. It appears to have no familial, hereditary or congenital basis.
Etiopathogenesis • Developmental—Jaffe and Lichtenstein considered it as a developmental anomaly caused by aberrant activity in the bone forming mesenchymal tissue. Most theories
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Diseases of Bone Manifested in Jaw 829 favor a developmental anomaly because the disease begins in early life and is active during the growth period. • Endocrine disturbances—Sternberg and Joseph considered complex endocrine disturbances with local tissue susceptibility as the cause. • Genetic—fibrous dysplasia results from postzygotic mutation in GNAS I (guanine nucleotide binding protein) gene. If mutation occurs in early embryonic period, the polyostotic type of fibrous dysplasia will occur. If mutation occurs during postnatal life, monostotic type of fibrous dysplasia occurs.
Classification First classification • Monostotic fibrous dysplasia—in it, only one bone is involved. • Polyostotic fibrous dysplasia—in it, more than one bone is involved • Jaffe type—fibrous dysplasia involving variable number of bone, accompanied by pigmented lesions of the skin or ‘Café-au-Lait’ spots. • Albright’s syndrome—a severe form of fibrous dysplasia involving nearly all the bones in the body, accompanied by pigmented lesions of the skin plus endocrine disturbances of various types.
Polyostotic fibrous dysplasia (Jaffe’s type) • Sex—polyostotic fibrous dysplasia involves multiple bones, with female to male ratio of 3:1. • Sites—the most common site for these are the back, buttocks, thighs, shoulders, chest, neck and face in the mentioned order. • Skin lesions—the skin lesions consist of irregularly pigmented, light brown melanotic spots, described as ‘cafe-au-lait spot’. • Symptoms—recurrent bone pain is the most common presenting skeletal symptom. • Skeletal lesions—skeletal lesions may be unilateral in distribution or may involve nearly all bones of the body. Skeletal lesions become static with the cessation of growth but proliferation may continue, particularly in the polyostotic form. • Complication—spontaneous fracture is a common complication. • Signs—in rare cases, continuous and inexorable extension result in great deformity and blindness.
Second according to Stewart • Monostotic—indicates involvement of a single bone. • Monomelic—it refers to the involvement of one extremity and is rarely found. • Polyostotic—many bones involved. • Albright’s syndrome Subclinical fibrous dysplasia Many a times, an unsuspected lesion of fibrous dysplasia comes to light accidentally on routine radiographic examination, without any clinical evidence of the suspected disease. Such examples are termed as subclinical fibrous dysplasia.
Clinical Features Monostotic fibrous dysplasia • Age and sex—fibrous dysplasia discovered in young patients, usually in children younger than 10 years affecting both the sexes equally. • Sites—monostotic fibrous dysplasia involves only one bone and presents no extra-skeletal effects, other than occasional pigmented skin lesions. Most frequent sites are ribs, femur, maxilla and mandible. • Appearance—swelling is seen on affected site (Fig. 34-1).
Fig. 34-1: Monostotic fibrous dysplasia showing swelling on face (Courtesy Dr Parate).
McCune-Albright’s syndrome • Sex—Albright’s syndrome is exclusively found in females. • Features—Albright’s syndrome, in addition show, endocrinal disturbances like precocious puberty, goiter, hyperthyroidism, hyperparathyroidism, Cushing’s syndrome and acromegaly. • Café au lait spot—these are coffee with milk color spot. There is irregular flat area of increased skin pigmentation. • Symptoms—vaginal bleeding has been noted. • Signs—secondary sexual characteristics such as pubic and axillary hair and development of breasts are evident by the age of 5 years. It may result in crippling deformities or fracture
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• Precocious puberty—it is rare in boys and is manifested as gynecomastia. • Sites—long bones are frequently affected. • Prognosis—generally, the active period ceases in adult life. If growth continues the rate of activity is markedly reduced. However, calcification of the fibrous tissue may continue for years. Occasionally, the lesions may remain inactive for several years. For some unknown reasons they may renew the activity.
Oral Manifestations
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Monostotic • Sites—maxilla (Fig. 34-2) is more commonly affected than mandible, with most changes occurring in the posterior region. Most common area involved is premolar-molar area.
• Symptoms—swelling is usually painless but patients may feel discomfort in some cases and while others complain of frank pain. • Cortical plates—enlarging deformities of alveolar process mainly buccal and labial cortical plates. • Mandible—in mandible, it causes protuberant excrescence of the inferior border of mandible. • Teeth—the teeth present in the affected area are either malaligned (Fig. 34-4) and tipped or displaced. Dental anomalies such as supernumerary teeth have been reported in connection with the monostotic fibrous dysplasia. The most commonly affected site is maxillary midline and mandibular premolar region. These supernumerary teeth often remain impacted and may affect the eruption of normal teeth.
Fig. 34-2: Swelling seen on right side in maxillary region in case of fibrous dysplasia.
• Appearance—there may be unilateral facial swelling, which is slow growing with intact overlying mucosa (Fig. 34-3).
Fig. 34-3: Unilateral swelling seen on right side with intact overlying mucosa (Courtesy Dr Bande).
Fig. 34-4: Malalignment of teeth seen in upper arch on right side due to fibrous dysplasia (Courtesy Dr Ashok L).
Craniofacial fibrous dysplasia • Sites—if fibrous dysplasia extends to involve the maxillary sinus, the zygomatic process, floor of orbit and sometimes, it extends toward the base of the skull, known as craniofacial fibrous dysplasia. • Symptoms—it results in severe malocclusion and marked facial deformity. Craniofacial lesions may lead to anosmia (loss of sense of smell), deafness and blindness. • Signs—there may be proptosis of the affected eye. Polyostotic • Appearance—expansion and deformities of jaws. Asymmetry of facial bones. There is ballooning of jaws, so there is gross enlargement and deformity. • Teeth—the eruption pattern of teeth is disturbed because of loss of support of the developing teeth. • Pigmentation—in some cases, intraoral pigmentation can be seen.
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Diseases of Bone Manifested in Jaw 831 Radiographic Features Lesions showing predominance of fibrous tissue • Early—radiolucent with ill defined borders. The bonydefect may be often unilocular but occasionally bony septa may be apparent creating an impression of multilocular cavity. • Margins—margins may be well defined with a tendency to blend imperceptibly with surrounding normal bone. • Granular appearance—surrounding the margins of the radiolucent area, there may be wider band of increased density, but granular in appearance (Fig. 34-5). • Lamina dura—when the lesion involves the apices of teeth there is loss of lamina dura or if retained, it has less density than normal. • Teeth—resorption of roots and destruction of developing teeth. • Jaws—when the lesion comes to the surface, there may be expansion of the jaws.
4 Fig. 34-6: Mixed type lesion seen in fibrous dysplasia,
Fig. 34-5: Granular type appearance seen in fibrous dysplasia patient.
Lesions showing mixed radiolucent and radiopaque appearance • Appearance—radiographic appearance of lesions with heterogeneous distribution of fibrous and osseous tissue shows a mixed radiolucent and radiopaque appearance, depending on the maturity of the lesions (Fig. 34-6). • Granular appearance—the new bone takes the form of very small opacities of poor density. When they become larger they appear as granular. • Maxillary lesion—it may spread to involve the adjacent bone such as zygoma, sphenoid, occiput and base of skull.
Mature radiopaque lesions where bone is predominant • Stippled • Orange peel—the radiograph shows bone of increased density. The normal structure of bone is replaced by a stippled appearance which resembles the ring of orange which is called as called as ‘orange peel’. • Teeth—tilting and bodily displacement of teeth in the affected area. • Maxillary sinus—it may obliterate the maxillary sinus. • Thumb print appearance—when mandible is affected, the vertical depth of mandible is increased. The inferior border of mandible appears as a ribbon like cortex. In some cases, the localized area over the cortex is lost and instead, there is a smooth curved downward projection of the inferior margins of the bone. The appearance resembles a ‘thumb print’ (Fig. 34-7), as if the bone had been soft and pressed upon by the thumb. • Expansion—bony expansion usually extends to the buccal and distal aspect. • Smoky mottled appearance—as the lesions mature, dysplastic bony trabeculae increase in size and number and appear like smoky mottled radiopacities. • Granular appearance • Ground glass appearance—another characteristic appearance of fibrous dysplasia is ground glass appearance, also termed as granular. Apart from the appearance everything else is similar as in stippled type. It may demonstrate areas of whorled amorphous partially calcified materials that are well circumscribed.
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Fig. 34-7: Thumb print appearance seen in fibrous dysplasia.
• Dense structureless, homogeneous—in this, the lesion shows a dense structure less, homogeneous appearance (Fig. 34-8). Any part of the joint may be affected. The commonest site is the base of the skull with involvement of the maxilla and nasal bones. Encroachment or obliteration of the antrum and spread into the adjacent bone including the base of skull take place. • CT features—CT is useful to evaluate the extent of facial lesions; especially orbital involvement. The CT characteristics of the fibrous dysplasia include expansion of the involved bones in a heterogeneous pattern with scattered or confluent islands of bone formation (Fig. 34-9). CT attenuation (density) values can reach 34 to 513 Hounsfield units or more particularly in dense lesions. The variation in the values reflects the complex, and often non-uniform, distribution of primitive bony trabeculae.
Fig. 34-8: Homogeneous pattern of fibrous dysplasia seen on computed tomography (Courtesy Dr Iswar).
Fig. 34-9: Confluent pattern seen on CT scan on right side in case of fibrous dysplasia.
Obisesan et al classified the lesions of fibrous dysplasia radiographically into 6 types. • ‘Peau d’ orange’ or orange peel—in this type, there are alternating areas of granular density and lucency giving a radiographic appearance resembling the ring of orange. • Whorled plaque like type—in this type, the matrix of the well circumscribed lesion is composed of plaques of amorphous material of intermediate radiodensity, which on close examination are seen to be arranged in whorled onion peel appearance. • Diffuse sclerotic type—the lesions of this show as homogeneous dense area, which gradually merges with the normal bone. • Cyst like type—in this type, the lesions are radiolucent. It is unilocular or multilocular, more often multilocular with well defined margins. • Pagetoid type—in this type of lesions, the affected area of bone markedly expands and shows alternating areas of radiopacities and lucency, as those seen in Paget’s disease of bone. • Chalky type—it manifests itself as a well circumscribed lesion consisting of an amorphous dense radiopaque material. Craniofacial fibrous dysplasia • Density—radiograph reveals the presence of a marked density which encroaches to a variable degree upon the orbit and antral cavity. • Granular type—changes in the base of the skull is of granular type and structureless, so that affected portion of the bone is thickened and of greater density.
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Diseases of Bone Manifested in Jaw 833 • Frontal bone—the frontal bone is also thickened with homogeneous or variegated type of density. • Nasal septum—the nasal septum is grossly thickened, dense and curved, so that it represents the gross caricature of the letter S.
Diagnosis • Clinical diagnosis—painless swelling seen in the maxillary region with intact mucosa. Café au lait spots are seen. • Radiological features—ground glass appearance, granular appearance is seen. • Laboratory diagnosis—when the polyostotic lesions are numerous and active, the serum alkaline phosphatase levels may be elevated in 50% of the cases. Biopsy shows bone made up of proliferating fibroblast in a compact stroma of interlacing collagen fibers. Irregular trabeculae of bone are scattered throughout the lesion, with no definite pattern of arrangement. Some of these trabeculae are C-shaped and described as Chinese character shaped.
Differential Diagnosis Lesions are likely to be confused in the osteolytic stage of fibrous dysplasia • Central giant cell granuloma—it has got faint wispy trabeculae coursing through it whereas internal calcifications may occur in fibrous dysplasia and appear to be stippled and granular appearance. • Traumatic bone cyst—there is no cortical bulging and displacement of teeth. • Dental cyst—it has a thin, well defined cortex which is smooth, while in fibrous dysplasia, cortex tends to be wider and more granular in appearance. • Aneurysmal bone cyst—there is hemorrhagic aspirate. • Chronic osteitis—it is always associated with the roots of pulp less teeth. • Chronic osteomyelitis—it manifests itself in older age group (30-80 years) as compared to fibrous dysplasia (10-20 years). In addition, patients with osteomyelitis will give a history of trauma, fracture or any debilitating systemic disease. • Peripheral and central squamous cell carcinoma—it also occurs in older age group and shows a predilection for mandible. Fibrous dysplasia grows by slow expansion whereas central and peripheral squamous carcinoma spreads rapidly. • Metastatic tumor—seen in older age groups and shows a predilection for premolar-molar region of mandible. • Reticular cell sarcoma and Ewing’s sarcoma are rarely seen in maxilla.
The mottle type of fibrous dysplasia • Lymphoma of bone—is rare and is poorly defined. The radiographic pattern is irregular and bizarre. In fibrous dysplasia smooth, well contoured external bony borders are always maintained. • Chondrosarcoma—is an uncommon malignant tumor of the jaws which is often painful and affects a much older age group than fibrous dysplasia. • Osteoblastic metastatic carcinoma—seldom shows a monotonous pattern as in fibrous dysplasia. A history of either symptoms or treatment for a primary tumor elsewhere will be elicited during history taking. Osteoblastic metastatic carcinoma is found in older age group. • Osteosarcoma—its appearance is disorderly with sunburst pattern, codmans triangle and asymmetrical band like widening of the periodontal ligament. • Paget’s disease—classically, Paget’s disease simultaneously affects several bone of the skeleton. It is a disease of the later age group; the serum alkaline phosphatase level is elevated in Paget’s disease whereas in fibrous dysplasia, it is within normal limit. Rare in adolescents and young adults. Bilateral involvement. • Cementifying and ossifying fibroma—it exhibits a similar mottled appearance to that seen in fibrous dysplasia. The following differences are recognized. • Shape—cementifying and ossifying fibroma as predominantly rounded while those of fibrous dysplasia are more rectangular. • Jaw expansion—jaw expansion caused by cementifying and ossifying fibroma is usually nodular or dome shaped whereas in fibrous dysplasia it is usually the elongated fusiform type. • Margins of fibrous dysplasia are indistinct, blending imperceptibly with normal bone while in cementifying and ossifying fibroma, the margins are sharply defined. • Predominance in jaws—approximately 70% of cementifying and ossifying fibroma occur in mandible while fibrous dysplasia shows a slight predilection for maxilla. • Predominant age—the age range for cementifying and ossifying fibroma is from 7-58 years. The majority of active cases of fibrous dysplasia are found in patients under the age of 20 years. • Chronic osteomyelitis—in it, radiolucent–radiopaque appearance can mimic the mottled appearance of fibrous dysplasia. Generally, when purulent discharge is present, the diagnosis is of chronic osteomyelitis. Mature phase • Paget’s disease and giant cell lesion of hyperparathyroidism— a solitary painless fusiform enlargement, which is firm smooth, covered by normal mucosa and has a
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radiopaque ground glass appearance, occur in the jaw bones of relatively young person is almost certainly fibrous dysplasia. Paget’s disease and giant cell lesions of hyperthyroidism can produce ground glass appearance but the overall effect is rarefaction and not radiopacities.
Management • Surgical—surgical removal of the lesion should be carried out. • Osseous contouring—it is necessary for correcting the deformity for esthetics or pre-esthetic purposes.
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Juvenile Ossifying Fibroma It is also called as ‘young ossifying fibroma’, ‘juvenile aggressive ossifying fibroma’, and trabecular desmoosteoblastoma’. This name has been given as this occurs in younger age group.
Classification Slootweg and colleagues have separated the lesions into two distinct groups: • Juvenile ossifying fibroma WHO type—it occurs predominantly in the maxilla and mandible. Here, the designation of juvenile ossifying fibroma should be restricted exclusively to those lesions whose histomorphology is consistent with that described in the 1992 WHO monograph on jaw lesions. This trabecular variant has strands of immature cellular osteoid within the lesion and usually occurs in childhood with a slight maxillary predilection. • Juvenile ossifying fibroma with psammoma like ossicles—it occurs in the paranasal sinuses and extragnathic bones. The psammomatoid variant has small spherical ossicles surrounded by osteoid rims within the lesion. It occurs over a wider age range than the trabecular variant and usually affects the orbit or paranasal sinuses.
Fig. 34-10: Swelling seen in maxillary region due to ossifying fibroma.
Radiographic Features • Internal structure—it may appear as unilocular or multilocular lesion. • Appearance—it may be radiolucent or show mixed appearance containing radiopaque foci (Fig. 34-11). • Margin—it has got distinct radiopaque border.
Clinical Features • Age—it is seen under the age of 15 years. • Site—no site predilection and with equal frequency in both the jaws. Although there is report that this is more commonly found in maxillary region. • Symptoms—the presenting clinical symptom is of swelling (Fig. 34-10). • Effect on surrounding structure—neoplasm can impinge on neighboring structure. Due to impingement, patient may noticed nasal obstruction, exophthalmos and proptosis. In some cases, permanent blindness may occur. • Intracranial extension—in some cases, meningitis may arise due to intracranial extension.
Fig. 34-11: Juvenile ossifying fibroma showing mixed radiopaque radiolucent lesion (Courtesy Dr Bande).
Diagnosis • Clinical diagnosis—it is not possible to make clinical diagnosis. • Radiological diagnosis—mixed lesion in young patient will give clue to the diagnosis. • Laboratory diagnosis—biopsy shows non-encapsulated lesion. There are also myxomatous foci, nuclear crowding, and multinucleated osteoclasts.
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Diseases of Bone Manifested in Jaw 835 Differential Diagnosis
Clinical Features
• Ossifying fibroma—juvenile ossifying fibroma occurs at a far lower mean age (8.5 years) than ossifying fibroma (26.4 years). Ossifying fibroma contains lamellar bone and cementicles as well as smoothly contoured cells, poor curvilinear trabeculae, features that are absent in juvenile ossifying fibroma.
• Age and sex—early childhood between the ages of 2 to 4 years males are affected about twice as frequently as females. • Sites—it shows predilection for angle of mandible bilaterally and occasionally posterior maxilla. • Appearance—in the rapidly increasing stage, the child assumes a chubby, cherubic facial appearance (Fig. 34-12), especially if combined with involvement of the orbital floor with upward displacement of the globe and exposure of the scleral rims. This appearance results due to bilateral involvement of posterior mandible.
Management • Excision—complete local excision of tumor is the treatment of choice.
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Cherubism It is also known as ‘familial fibrous dysplasia of the jaws’, ‘disseminated juvenile fibrous dysplasia’, ‘familial multilocular cystic disease of the jaws’ and ‘Hereditary fibrous dysplasia of the jaws’. Above terms of cherubism are related to fibrous dysplasia but there is no similarity between fibrous dysplasia and cherubism so, this term should be avoided. The clinical entity was first described by Jones in 1933 who coined the term ‘Cherubism’ reflecting the characteristic of chubby facial appearance similar to plump cheeked little angle (cherubs) seen in Renaissance painting. It is autosomal dominant inherited fibro-osseous disease that affects only the jaws causing bony expansion.
Classification It depends on the severity and location of the lesion and the extent to which jaws are affected. • Grade I—the fibro-osseous expansion tends to be bilateral and symmetrical. It is primarily in the ramus of the mandible. • Grade II—in more severe cases, the ramus and the body of the mandible are involved resulting in congenital absence of the third and occasionally the second mandibular molar teeth. In this group, the tuberosity region of the maxillae is also affected. • Grade III—in these cases, the lesions affect the mandible and maxilla entirely and may result in considerable facial deformities.
Fig. 34-12: Cherubic appearance of the child in cherubism.
• Symptoms—the patient may have difficulty in speech, deglutition, mastication, respiration and limited jaw movement. • Signs—swelling is firm and hard on palpation (Fig. 34-13). Overlying mucosa is intact and non-painful.
Etiology • Developmental defect—anomalous development of dental structures with disturbance in the development of bone forming mesenchyme may lead to this condition. • Hormonal—cherubism can be present in latent hyperparathyroidism and hormone dependent benign neoplasm. • Other—other factors which are responsible for cherubism are trauma and an aberration in ossification.
Fig. 34-13: Firm swelling seen in the jaw of patient of cherubism.
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• Jaws—bilateral enlargement of mandible in this condition produces full, round lower face. Bilateral enlargement of maxilla gradually follows. • Eye raised to heaven—pulling or stretching of skin of the cheek, depresses the lower eyelid, exposing a thin line of sclera and resulting in the so called “eyes raised to heaven” look. • Orbital floor—tumor encroachment on the orbital floor often causes partial obliteration of the palatal vault with resulting ‘V’ shaped cleft. • Alveolar process—the alveolar process are so wide, as to occupy almost the whole of the roof of the mouth; the actual palate being reduced to a narrow fissure between the two approximating alveolar process. • Lymph nodes—there may be enlargement of submandibular lymph nodes. • Progress—there is rapid increase in size up to 7-8 years of age, after which the lesions become static or progress very slowly until puberty. After puberty the maxillary lesions tend to regress. The mandibular lesions progress slowly up to the age of 20 years and then regress; the facial appearance almost returns to normal in the 4th and 5th decades of life. • Teeth—the fibrous replacement of bone displaces the deciduous dentition. The primary teeth may be irregularly spaced and some may be absent. There is premature loss of primary teeth. The developing permanent teeth are affected, giving rise to displaced unerupted or absent teeth along with malocclusion.
Radiographic Features • Radiodensity—cyst like radiolucency of mandible, bilaterally symmetrical which is up to several centimeters in diameter. • Progress—initiation of bone destruction near the angle of the mandible with later expansion of lesions posteriorly into ramus and anteriorly into the mandibular body. • Appearance—it appears as a classic multilocular cavity due to internal radiopaque septa, which tends to coalesce as they enlarge. On posteroanterior views, teeth are seen to be hanging in air. • Margins—they are well defined, well corticated and smooth around most of the radiolucency. • Effect on surrounding structure—there is also expansion of buccal and lingual cortical plates (Fig. 34-14). In mandible, the inferior alveolar canal may be displaced and the lesion may occupy alveolar process, the angle and the ramus. The thin cortex may eventually disappear. Maxillary lesions enlarge at the expense of maxillary sinus. • Effect on teeth—displacement of numerous teeth but prior to enamel calcification. Erupted deciduous teeth in the
area of bone involvement shed prematurely. Few posterior teeth may be missing due to early developing expanding masses which destroy the buds and incipient follicle.
Fig. 34-14: CT scan of patient of cherubism showing bilateral swelling in mandibular posterior region (Courtesy Dr Iswar).
Diagnosis • Clinical diagnosis—typical cherubic appearance of child with bilateral swelling in the jaw • Radiological diagnosis—cyst like radiolucency present bilateral in the mandible • Laboratory diagnosis—in active cases, serum alkaline levels may be raised. Biopsy shows large multinucleated giant cell in a loose delicate fibrillar connective tissue stroma.
Differential Diagnosis • Fibrous dysplasia—cherubism is bilateral. • Giant cell granuloma- it occurs frequently in the anterior segment of mandible in contrast to cherubic lesions, which are seen in the posterior part of mandible. • ABC—the lesions of ABC are tender, whereas cherubic lesions are painless. • Central hemangioma—there is localized gingival bleeding and pumping tooth syndrome. • Giant cell lesions of hyperthyroidism—are not bilateral and they can be differentiated on abnormal blood chemistry levels. • Metastatic tumors—it is seen in older age group as compared to cherubism and also there will be signs and symptoms or history of primary tumor elsewhere in the body. • Ameloblastoma—it is seen unilaterally and frequently in an older age group than that of cherubism • Odontogenic myxoma—history of missing tooth, as it is of developmental origin.
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Diseases of Bone Manifested in Jaw 837 • Nevoid basal cell carcinoma—no facial swelling is seen in cherubism. There are characteristic cutaneous abnormalities or rib anomalies seen on chest radiograph. • Multiple dentigerous cyst—impacted teeth present.
• Signs—palpation may elicit tenderness. Growth is slow. • Teeth—teeth in the area may become mobile but maintain their vitality, until they are exfoliated. • Prognosis—recurrence rate of 12% for lesions under 2 cm and 37% recurrence for lesions over 2cm in size.
Management • Surgical contouring—surgical procedures should be delayed, as long as possible, as the cystic lesion defect usually becomes static and regresses during adulthood. Occasionally, surgical contouring of the lesions is necessary to improve esthetics and in case of active growth. • Homogeneous bone grafts—in cases of extensive involvement, homogeneous bone grafts can be given to prevent pathological fractures of mandible. • Orthodontic care—orthodontic care may be required to ensure proper alignment of the teeth. • Calcitonin—this therapy is under trial nowadays, awaiting results of some study.
Central Giant Cell Granuloma
Radiographic Features • Radiodensity—solitary unilocular (Fig. 34-15) or multilocular radiolucency.
4 Fig. 34-15: Unilocular radiolucency seen in mandibular anterior region.
It is a non-neoplastic bone disease reactive to some unknown stimulus. It was first described in the jaws by Waren 1837. It has been called as osteoclastoma, myeloid sarcoma, chronic hemorrhagic osteomyelitis and giant cell reparative granuloma initially. But nowadays the term reparative is dropped and it is called as giant cell granuloma only.
Types • Non-aggressive—it exhibits slow growing benign behavior. • Aggressive—it shows typical features of rapidly growing, destructive lesion.
• Location—it may occupy whole of the mandibular body and may extend past the midline to the opposite side (Fig. 34-16). • Appearance—as it grows, it causes bossing of buccal cortex i.e. uneven, variable bulging or undulation of the cortical contour. • Margins—borders may be smooth, undulating, moderately well defined and moderately well corticated. • Honeycomb appearance—it shows bony trabeculation within their contour and tends to be mildly wavy on close inspection. It may have wispy delicate quality. Sometimes, they may have honeycomb appearance.
Clinical Features • Age—lesion of adolescent and young adult with 60% cases in younger than 20 years and 74% cases in younger than 30 years. • Sites—mandible is twice as frequently involved than maxilla, with anterior half showing greatest incidence with fairly high percentage crossing the symphysis. The commonest site being the anterior and bicuspid region in mandible and the canine fossa and ethmoid region in maxilla. • Symptoms—the earliest sign of the lesion may be expansion of bone with premature loosening and shedding of deciduous teeth. There is jaw swelling associated with facial asymmetry. Usually painless, but local discomfort may be noted.
Fig. 34-16: Radiolucency seen in mandible crossing the midline.
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• Effect on surrounding structures—when they involve maxillary bone, they may erode or expand bone. Displacement of adjacent teeth, tooth buds and resorption may occur.
Diagnosis
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• Clinical diagnosis—expansive swelling in the anterior region of mandible may suspect central giant cell granuloma. • Radiological diagnosis—radiolucency crossing the midline is typical of central giant cell granuloma (Fig. 34-17). • Laboratory diagnosis—biopsy shows loose fibrillar connective tissue stroma with many interspersed proliferating fibroblast and small capillaries. Multinucleated giant cells are prominent.
Fig. 34-17: CT scan of central giant cell granuloma showing destructive lesion in mandibular anterior region
Differential Diagnosis • Ameloblastoma—it is uncommon in a younger age range, which is most susceptible to giant cell granuloma. Seen in posterior mandible in contrast to giant cell granuloma which occurs anterior to the first molar. Ameloblastoma demonstrates internal, hard curved arch like septa whereas giant cell granuloma has lighter wispy septa. Ameloblastoma is usually multiloculated. • Aneurysmal bone cyst—it does not occur in anterior segment of mandible. Aspiration produces blood. • Odontogenic myxoma—multiloculated and typical honeycomb appearance. Missing or impacted tooth is usually a finding. • Giant cell tumor—it is described in Table 34.1 • Traumatic bone cyst—no bodily movement of teeth is present. No expansion of overlying bone cortex. • Fluid filled odontogenic cyst—internal septa are not present. No bony spicules protrude from radiographic margins. Regular smooth bony expansion of cortical plates while scalloped, undulating bulging of cortex. • Brown tumors of hyperthyroidism—serum calcium levels are elevated. • Cherubism—it is bilateral in the posterior part of mandible and there is history of familial involvement. It does not cross the midline. • Metastatic tumors—it is seen in older age groups and also predominant lesions are multilocular with history and symptoms of primary tumor in addition to local lesions. • Central hemangioma—it shows localized bleeding around the necks of teeth and also the pumping tooth syndrome. • Post extraction socket, surgical defect and residual cyst—it can mimic unilocular appearance of central giant cell granuloma. Patients with surgical defect will give a history of previous surgery and history of extraction in residual cyst and post extraction socket.
Table 34.1: Difference between giant cell tumor and giant cell granuloma
Giant cell tumor
Central giant cell granuloma
It is more common in 3rd and 4th decades and unusual in patient below 20 years of age common in males
It occurs mainly in children and young adults often in females
Common in long bone like femur, tibia and rare in jaw
Most common in mandible, appearing anterior to 1st molar tooth bearing area
Microscopically tumor giant cell contains more nuclei and has larger dimension
It contains fewer nuclei and smaller dimension
Even distribution of giant cells throughout the tumor, in every field
In it giant cells are unevenly distributed
It is not preceded by trauma
It is preceded by trauma
New bone formation is absent
Foci of osteoid and new bone are frequently present
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Diseases of Bone Manifested in Jaw 839 Management • Curettage—thorough curettage of the lesion should be carried out. • Corticosteroids—weekly injection of corticosteroids directly into tumor with triamcinolone acetonide can give dramatic results. This should be given weekly. • Calcitonin—systemic administration of salmon calcitonin can lead to resolution of lesion. It should be given daily for 12 months as intradermal injection or nasal spray. • Interferon alfa—this is also given in some cases of central giant cell granuloma. • Surgical—partial resection should be done in case of aggressive tumor.
Paget’s Disease It is also called as ‘osteitis deformans’. It was discovered in 1877 by Sir James Paget. It fondly refers to as ‘collage of matrix madness’. There is abnormal resorption and apposition of bone in one or more bones. The disease is initiated by an intense wave of osteolytic activity with resorption of normal bone resulting in irregularly shaped resorption cavity followed by vigorous osteoblastic activity forming woven bone after variable period.
Etiology • Inflammatory—initially it is thought to be inflammatory disease, but later on this cause is ruled out. • Circulatory disturbance—the bone in Paget’s disease is excessively vascular and it has been suggested that vessels are similar to arteriovenous aneurysms. • Slow virus theory—slow viruses are those viruses which take a long time for incubation. The possibility of an infective, viral Etiology for Paget’s disease is suggested by ultra-structural demonstration of intra-nuclear inclusions in abnormal osteoclast. • Genetic and environmental factors—genetic and environmental factors appear to be important. It is transmitted as autosomal dominant trait with genetic heterogeneity. • Connective tissue factors—it may be a disorder of connective tissue biosynthesis. • Others—vasculitis, trauma, hormonal imbalance, degenerative neurologic disorders.
Clinical Features • Geographical prevalence—it is seen most frequently in Britain and less frequently in North America and Western Europe. • Age and sex—predominantly in patients over 40 years of age with a slight predilection for men. Male to female ratio is 2:1.
• Sites—it is prone to occur in the axial skeleton especially the skull, femur, sacrum and pelvis. It is usually polyostotic. • Symptoms • Skull enlargement—first complaint is that patient needs to buy a hat of larger size because of skull enlargement. • Pain—bone pain is a consistent symptom and most often directed towards weight bearing areas. The patients may have ill defined neuralgic pain as a result of restriction of foramina and canals, which occurs due to pressure created by mass on structures passing through the foramina. • Deafness—deafness due to involvement of the petrous portion of temporal bone with compression of cochlear nerve in the foramen. • Neurological symptoms—there may be mental disturbance, and dizziness. • Signs—bowing of legs, curvature of spine and enlargement of skull. The involved bones are warm to touch because of increased vascularity and are prone to fracture. • Simian appearance (likes an apes or monkey)—due to grotesque facial appearance along with waddling gait and short stature patient has got simian appearance. • Waddling (short step) gait—broadening and flattening of the chest and spinal curvature. The patient assumes waddling gait. • Complication—skeletal deformities, fracture of limbs, compression of spine, and occurrence of giant cell lesion. Another complication includes renal calculi, salivary calculi and hypercalcemia.
Oral Manifestations • Sites—maxilla is involved three times more commonly than mandible. It is bilaterally symmetrical in the involved jaw. • Symptoms—movement and migration of affected teeth occurs. Due to migration patient may noticed malocclusion. In case of edentulous patient as alveolar ridge becomes enlarged patient complaint of poor fit of denture. • Signs—increase in alveolar width associated with flattening of palate when maxilla is involved (Fig. 34-18). • Appearance—as the disease progresses, the mouth may remain open exposing the teeth as the lips are too small to cover the enlarged jaws. • Extraction sites—extraction sites heal slowly and incidences of osteomyelitis are higher. Extraction may be further complicated by excessive bleeding from highly vascular abnormal bones in the lytic phase of disease. • Complications—osteogenic sarcoma, osteomyelitis, pathological fracture and facial paralysis. Sarcoma is
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Fig. 34-18: Patient of fibrous dysplasia showing increases width of alveolar ridge (Courtesy Dr Bande).
suspected in cases that experience a marked increase in intensity of bone pain or other symptoms and show marked increased in alkaline phosphatase. • Prognosis—it is poor in patients showing development of osteogenic sarcoma in Paget’s disease.
Radiographic Features Early radiolucent stage • Appearance—inferior cortex of mandible may appear osteoporotic and possess a laminated structure. • Trabecular arrangement—bone pattern in which trabeculae though reduced in number, run linearly in the direction of length of bone and have few intersections between them. This appearance is most commonly seen posterior to bicuspid. In the anterior region, the bony trabeculae are coarse and relatively straighter than normal, but they intersect producing bone spaces that are larger than normal. Coarse and sparse trabeculae, sometimes, tend to converge towards the midline of mandible which is highly suggestive of Paget’s disease. In this stage, inferior border of the mandible may appear osteoporotic and have a laminated structure. • Effect on root—root resorption is common. • Osteoporosis circumscripta—in the skull, early lytic lesion may be seen as discrete radiolucent areas termed as osteoporosis circumscripta. The margins are somewhat irregular. There is appearance of denser bone around the radiolucency. • Lincoln’s sign or black beard—this sign is present in bone Scintigraphy. Bone scan may demonstrate marked uptake throughout the entire mandible. This is called as Lincoln’s sign or black beard. Granular or ground glass appearance • Radiopaque patches—there are rounded radiopaque patches of abnormal bone of greater density within the
A dense, more radiopaque stage • Cotton wool appearance—in later stages, rounded radiopaque patches of abnormal bone are often seen giving an impression of cotton wool. As the fully opacified area becomes more numerous and enlarged, they tend to coalesce. The bone is denser and appears whiter on the radiograph. • Enlargement of bone—it enlarges the affected bone and it may be four times than their normal thickness on lateral radiographs. In some cases there is irregular enlargement of alveolar processes which become prominent and bulge. • Prognathism of mandible—due to deposition of bone in mandible, it may appear prognathic. • Effect of maxillary sinus—lesions in maxillary area may encroach the maxillary sinus and obliterate it. • Hypercementosis—it may be produced on one or more teeth (Fig. 34-19). • Ankylosis of teeth—it may obliterate the areas of lamina dura and periodontal ligament space around both, normal and hypercementosed roots resulting in ankylosis of teeth. • Osteogenic sarcoma—development of osteogenic sarcoma may produce frank dissolution or destruction of bone. In it, there is loss of continuity of the margins on the one side of the lesion which is suggestive of the destruction. Also in some cases, soft tissue shadow is seen.
Diagnosis • Clinical diagnosis—in this simian appearance, enlargement of skull, bowing of leg and bone pain may give clue to the diagnosis.
Fig. 34-19: Hypercementosis of teeth in the mandibular teeth (Courtesy Dr Bhaskar Patle).
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Diseases of Bone Manifested in Jaw 841 • Radiological diagnosis—cotton wool appearance, Lincoln sign, and osteoporosis circumscripta are diagnostic features of Paget’s disease. • Laboratory diagnosis—serum alkaline phosphatase level is increased, occasionally, attending the level of 200 or more KA units. Serum calcium and serum phosphorus levels are within normal limits. Urinary hydroxyproline levels increase from normal levels of 440 mg/ 24 hours to 1 gm/24 hours. Histological there is appearance of mosaic bone.
Differential Diagnosis Early stage—radiolucent appearance • Giant cell lesions of hyperparathyroidism—in Paget’s disease, there is an increase in serum alkaline phosphatase only whereas in Giant cell lesions of hyperparathyroidism there is elevation of serum alkaline phosphatase as well as serum calcium levels with decrease in serum phosphate levels. Also in case of hyperparathyroidism, there is overall radiolucency. • Osteoporosis—in early stages, it may be confused with Paget’s disease but if the bony area in question is pathologically enlarged and if straight linear trabeculae are seen in the affected bone parallel to the long axis, osteoporosis is ruled out. Blood chemistry is normal. • Osteomalacia—pseudofractures are common in cases of osteomalacia. Serum calcium and serum phosphorus levels are decreased in osteomalacia whereas in Paget’s disease, they are normal. • Multiple myeloma—it causes painful enlargement of the jaws and shows typical radiolucent punched out lesions on the skull radiograph. Positive test for Bence Jones proteins. Second stage—mixed radiolucent radiopaque appearance • Osteogenic sarcoma—it occurs in a younger age group (10-40) than that of Paget’s disease and it shows a variety of radiographic appearance i.e. sunburst and Codman’s triangle. • Cementifying and ossifying fibroma—it is predominately seen in the younger age group and they show well defined margins in contrast to that of Paget’s disease which is diffuse. • Fibrous dysplasia—age difference, Paget’s disease spreads more diffusely, seen bilaterally, cotton wool appearance. Maxillary sinus is reduced in size in the case of fibrous dysplasia but in the case of Paget’s disease, it fails to reduce the air space. • Osteoblastic metastatic carcinoma—it will give a history of parent tumor or show signs and symptoms of primary tumor. • Ossifying sub-periosteal hematoma—it can be excluded if the patient gives a recent history of trauma and in addition it is seen in patients less than 15 years of age.
• Ossifying post surgical defect—it will give a history of surgery. • Chronic osteomyelitis—it is rare in maxilla. • Chondroma and chondrosarcoma—it produces pain, which is not a feature of Paget’s disease. Advanced stage—purely radiopaque • Florid osseous dysplasia—it is confined to jaw bone and hypercementosis is present. • Osteosclerosis—small and confined to jaw bone. • Tori—same as above. • Osteoma—same as above.
Management • Medical • Calcitonin—a parathyroid hormone antagonist produced by the thyroid gland, suppresses bone resorption and also relieves pain and decrease serum alkaline. • Sodium phosphate—it retards bone resorption. • Bisphosphonates—they have also been used, since they inhibit bone resorption as well as mineralization. Bisphosphonates which are used are etidronate, pamidronate, alendronate, tiludronate or risedronate. • Mithramycin—it is considered as a second line agent due to its toxicity; is cytotoxic to osteoclasts. • Plicamycin—it inhibits osteoclastic activity • Surgery—surgical approach for esthetics correction should be carried out. • Radiation—in some cases radiation therapy can be useful.
Giant Cell Lesions of Hyperparathyroidism It is discussed in the Chapter 36: Endocrine Disorders.
Fibro-osseous Lesions of Periodontal Origin Periapical Cemental Dysplasia It is described in Chapter 14: Odontogenic Tumor of Jaw.
Florid Osseous Dysplasia It is also called as ‘chronic sclerosing osteomyelitis’, ‘sclerosing osteitis’, ‘multiple enostosis’ and ‘sclerotic cemental masses’. It is considered to be a widespread form of periapical dysplasia. It is derived from the cells in or near the periodontal ligament space. Robinson defined it as an abnormal reaction of bone to irritation or stimulation and the term florid osseous dysplasia includes chronic diffuse sclerosing osteomyelitis
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and sclerotic cemental masses. It is inherited as an autosomal dominant trait. In florid osseous dysplasia, the normal bone is replaced by fibrous tissue and mineralized structure like cementum, bone or both.
Clinical Features
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• Age and sex—females are exclusively affected. Most common age is middle age, with a mean age 42 years with predilection for blacks. • Sites—the lesion is restricted to the jaw bone with mandible being most commonly affected. • Symptoms—there is a painless expansion of the alveolar process of mandible. Patients may complain of intermittent poorly localized pain in the affected bone area, with or without an associated bony swelling. • Signs—if the lesion secondarily infected features of osteomyelitis may develop. Mucosal ulceration with fistulous tract may be present. Teeth in the involved bone are vital.
Radiographic Features • Location—lesions of florid osseous dysplasia present bilaterally in both the jaws. Lesions occur above the inferior alveolar nerve canal. It involves all four quadrants. • Radiodensity—it varies from an equal mixture of radiolucent and radiopaque region to almost complete radiopaque. • Size—individual lesions do not exceed 2-3 cm in diameter. The lesions may extend into the mandibular ramus or into the maxillary sinus. • Margins—margins are fairly regular and well defined. Each lesion is surrounded by a radiolucent capsule and a cortical rim. • Radiolucent stage—in this stage, well defined radiolucent area are superimposed over the apical area of adjacent tooth. • Mixed stage—in this stage radiolucent cavity, partially filled with one or more dense radiopaque masses. As lesions mature, the radiopacities increase. This stage also shows target appearance with central calcified masses in the radiolucent lesion. • Radiopaque stage—this shows multiple radiopacity continuous with the surrounding bone, but they were separated from adjacent teeth periodontal ligament space. In this stage cotton wool appearance (lobular or lump shaped and soft radiopaque characters like that of cotton wool) is seen. • Active hypercementosis—hypercementosis of tooth in the affected area is seen. There is an also wide periodontal ligament space.
Differential Diagnosis • Paget’s disease—no radiolucent capsule and increased serum alkaline phosphatase levels. Paget’s disease affects entire mandible while florid osseous dysplasia occur above the inferior alveolar canal. • Chronic sclerosing osteomyelitis—signs of infection is present in osteomyelitis. • Osteopetrosis—profuse thickening of the skull base or calvarium and diffuse bony radiopacities. It will cause enlargement of bone, which is not a feature of florid osseous dysplasia.
Diagnosis • Clinical diagnosis—painless expansion in four quadrant of jaw will give clue to diagnosis. • Radiological diagnosis—radiopaque, mixed lesion in all four quadrants with active hypercementosis will diagnose this condition.
Management • Effective oral hygiene—if teeth present effective oral hygiene should be maintained since with this disease, patients exhibit poor healing and osteomyelitis may develop after tooth loss. • Recontouring—patients with more severe form of the disease has superficial lesions which are located near the crest of alveolar ridge, these may require recontouring to accommodate the denture or to prevent ulceration.
Cemento-ossifying Fibroma This is the terminology used for cementifying fibroma and ossifying fibroma. Cemento-ossifying fibroma is a benign fibro-osseous neoplasm. The description of the ossifying fibroma of the jaws was first given by Montgomery in 1927. It is a benign neoplasm that is osteogenic (non-odontogenic), well defined and rarely encapsulated, consisting of fibrous tissue with variable amounts of mineralized material similar to bone and/ or cementum. Chromosomal abnormalities have been identified in the ossifying fibroma; however, the molecular mechanisms that causes the development of this tumor remain unknown.
Nomenclature The previous nomenclature of ossifying fibroma or cementifying fibroma was based upon the histopathology which displayed predominantly bone like or cementum like tissue, characterized by osteoblasts and cementoblasts respectively. This terminology was first used by Hamner, but is of little practical value because of the range of the behavior of these lesions with identical histopathological appearance. Furthermore many of them contained both bone and cementum like elements. Therefore these lesions
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Diseases of Bone Manifested in Jaw 843 appear to represent points on a spectrum of histological appearances extending from bone to cementum. This indicates that they probably originated from the same progenitor cell, which Waldron suggested is to be found within the periodontium. Taking account of the wide range of histological manifestation, the WHO in 1992 revised its nomenclature to refer to the separate lesions of the cementifying fibroma and ossifying fibroma as a single entity termed ‘cementoossifying fibroma’. Fig. 34-21: Giant ossifying fibroma showing lesion over 80 mm in diameter.
Clinical Features • Age and sex distribution—it predominantly occurs in females in third or fourth decades of life. • Bones affected—it can arise from any part of the facial skeleton and skull with over 70% of cases arising in the head and neck region. Cemento-ossifying fibromas ostensibly do not occur outside the craniofacial complex. Although it has been principally found in the jaws, it has also been reported in the orbitofrontal bone, nasopharynx, paranasal sinuses and skull base. Most lesions arise in the tooth bearing areas of the mandible and maxilla (Fig. 34-20). It mostly occurs in molar and premolar mandibular area above the inferior alveolar canal. In the maxilla, it occurs most often in the canine fossa and zygomatic arch area. • Symptoms—there is occasional facial asymmetry is seen in some of the cases. When in maxilla, symptoms may include nasal stuffiness and epiphora on the affected side. • Signs—there may be associated exophthalmos, with visual disturbances, depending on the extent of compression of its orbital content by the tumor. • Giant ossifying fibroma—large lesions increasing in size to over 80 mm in their greatest diameter have been termed ‘giant ossifying fibroma’(Fig. 34-21). • Teeth—the lesion is slow growing and in some cases, there is displacement of teeth. • Cortex—bony cortex and covering mucosa remain intact.
Fig. 34-20: Cemento-ossifying fibroma involving maxillary lesion (Courtesy Dr Bhaskar Patle).
• Progress—the lesion may be slow growing initially, with a rapid increase in size in a relatively short time. • Maxillary sinus—if sinus is affected it may fill the sinus completely and expands the sinus wall.
Radiographic Features • Periphery—the borders of cemento-ossifying fibroma lesions usually are well defined. A thin radiolucent line, representing a fibrous capsule, may separate it from surrounding bone. Sometimes, the bone next to the lesion develops a sclerotic border. • Internal structure—it is a mixed radiolucent/ radiopaque density with a pattern that depends on the amount and form of the manufactured calcified material. In the early stages solitary cyst-like osteolytic lesions without periosteal reaction are seen. In some instances, the internal structure may appear almost totally radiolucent with just a tint of calcified material. In the type that mainly contains abnormal bone, the pattern may be similar to that seen in fibrous dysplasia, or a wispy (similar to stretched tufts of cotton) or flocculent pattern (similar to large, heavy snowflakes) may be seen (Fig. 34-22). Lesions that produce more cementum like material may contain solid, amorphous radiopacities (cementicles) similar to those seen in cemental dysplasia. • Effect on surrounding structure—cemento-ossifying fibroma can be distinguished from the previously mentioned bone dysplasia by its tumor like behavior. This is reflected in growth of the lesion, which tends to be concentric within medullary part of bone with outward expansion approximately equal in all directions. These neoplasms have propensity for osseous cortical expansion and encroachment on contiguous structures. A significant point is that the outer cortical plate, although displaced and thinned remains intact. In the mandible, bowing or erosion of the inferior cortex is seen. It results in displacement of the inferior alveolar canal. The cemento-ossifying fibroma lesion can grow into and occupy the entire maxillary sinus, expanding its walls outward; however, a bony partition always
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Fig. 34-22: Cemento-ossifying fibroma presenting a flocculent pattern.
exists between the internal aspect of the remaining sinus and the tumor. In the orbit they may displace the globe. Expanding lesion can cause displacement of the teeth. The lamina dura of involved teeth usually is missing and resorption of teeth may occur.
Diagnosis • Clinical diagnosis—not so specific. Facial asymmetry is seen. • Radiological diagnosis—mixed radiopaque radiolucent lesion seen with sclerotic border. Displacement of teeth can also be seen • Laboratory diagnosis—large number of fibroblasts, with flat elongated nuclei is present within the network of interlacing collagen fibers. Chinese letter shaped islands of bone or calcification is also seen.
Differential Diagnosis Early radiolucent stage • Post extraction socket and residual cyst—history of extraction and history of surgery • Primordial cyst—it is always associated with a missing permanent tooth which is not a case with cementifying/ ossifying/cemento-ossifying fibroma. • Ameloblastoma—it occurs in posterior most part of the mandible and is accompanied by paresthesia of the lip. It often shows a multilocular appearance. • Periapical cemental dysplasia—it occurs at the apices of vital teeth. However, they affect an older age group than cementifying/ossifying/cemento-ossifying fibroma and have a predilection for the lower incisor region whereas cementifying/ossifying/cemento-ossifying fibroma often occurs in premolar-molar region.
Mixed radiopaque radiolucent lesion • Calcifying epithelial odontogenic tumor—it occurs in posterior body and ramus of mandible. • Osteoid osteoma—it is more common in males under 30 years of age and is not frequently seen in jaws, whereas, cemento-ossifying fibromas are tumors predominantly of jaws and are common in females in their third or fourth decade of life. It causes pain that predominantly occurs in night time, which is a distinguishing feature as cemento-ossifying fibroma is mostly an asymptomatic lesion. Radiographically, it appears as a well-circumscribed radiolucent area with sclerotic halo in initial lesions. In more mature lesions, the central radiolucency may have a radiopaque foci representing abnormal bone. • Osteoblastoma—it is rare lesion in the head and neck. Histologically, it exhibits bone to stroma ratio of one to one, with frequent fibroblastic atypia and occasional mitotic figures, features which help in differentiation from cemento-ossifying fibroma when radiographic features are confusing. • Osteosarcoma—it should be differentiated on the basis of malignant characteristics of the tumor such as aggressive growth, destruction of cortical bone, invasion into surrounding soft tissues and along the periodontal ligament, whereas, cemento-ossifying fibromas has a benign behavior. • Benign cementoblastoma—it occurs in second and third decades of life in posterior mandibular region. It is characteristically attached to the part of the root with frequent root resorption. Cemento-ossifying fibroma is not attached to the root although it may resorb the roots. Radiographically it is an opaque lesion with a radiolucent halo. Histological study reveals agglomerates of material similar to cementum and connective tissue stroma. Many of the cemental trabeculae are surrounded by cementoblasts. Clinically, it may sometimes manifest as a pain and swelling unlike cemento-ossifying fibroma, which is usually not associated with pain. • Juvenile ossifying fibroma—Contrary to cemento-ossifying fibroma, which occurs mostly in third and fourth decades of life, juvenile ossifying fibroma appears in patients under 15 years of age. Cemento-ossifying fibroma most commonly affects mandible predominantly premolarmolar region, whereas, juvenile ossifying fibroma affects predominantly maxilla. It has a rapid growth that frequently erodes the surrounding bones. Though the radiographic appearance of this entity has similarities to cemento-ossifying fibromas, it shows differences histopathologically. Histological picture is characterized
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Diseases of Bone Manifested in Jaw 845
•
• • •
by a cellular vascular stroma with variable amount of giant cells, scarce collagen and small ossicles surrounded by an osteoid halo. They do not have fibrous capsule. Metastatic osteoblastic carcinoma and chondrosarcoma—illdefined borders with periosteal bone formation. It is rapidly growing, as compared to cementifying/ ossifying/cemento-ossifying fibroma which has well defined margins and separated from normal adjacent bone by a radiolucent fibrous capsule. Periapical cemental dysplasia—as described in differential diagnosis of periapical cemental dysplasia. Paget’s disease—cotton wool appearance and enlargement of affected bone. Fibrous dysplasia—homogeneous radiopaque area with an internal architecture that is evenly granular and obliterates normal bone marrow space. Borders are ill defined and gradually blend into surrounding normal bone. Root resorption is rare. It is more commonly found in mandible, with an equal sex distribution.
Mature stage • Periapical spherical type of hypercementosis—it is attached to a part of root and is separated from the periapical bone by a radiolucent periodontal ligament space which surrounds the entire root. • Condensing osteitis—it can be ruled out because it occurs at the periapex of a non-vital tooth. It does not have a radiolucent rim which is seen in fibro-osseous lesions. • Periapical idiopathic osteosclerosis—it occurs in the periapical region of vital teeth. Cementifying/ossifying/ cemento-ossifying fibroma however is smoothly contoured and almost round and ovoid, whereas periapical idiopathic osteosclerosis is usually quite irregular in shape and also there is absence of a radiolucent rim. • Complex odontoma—density is not uniform and also it seldom occur periapically.
Management • Enucleation—small, clinical encapsulated lesions are treated by conservatively enucleation. • Resection—it is recommended if there is involvement of inferior border, extension into maxillary sinus occurs.
• An excrescent, ulcerated, painful, friable lesion that bleeds when touched could be observed. • Clinically, they usually present as reddish brown, firm, pedunculated or sessile masses at the site of trauma (Fig. 34-23). • The overlying mucosa may be ulcerated and this may draw the patient’s attention to the lesion. If the patient is dentate, the adjacent teeth may be mobile.
4 Fig. 34-23: Peripheral ossifying fibroma (Courtesy Dr Soni).
Radiographic Features • In edentulous patients, there may appear to be some superficial erosion of the underlying bone on radiographs. • Intra-oral films taken with low penetration may show varying amounts of calcification within the lesion.
Diagnosis • Clinical diagnosis—not so specific. • Radiological diagnosis—erosion of underlying bone below the lesion with calcification will give clue to diagnosis.
Other Lesions of Bone
Peripheral Ossifying Fibroma
Osteoporosis
It presents as a tumor like growth of the oral soft tissues and is often associated with sharp teeth, rough restoration, and ill- fitting dentures.
There is reduction in the inorganic constituent of bone. There is abnormal persistence of calcified cartilage. Spongy portion of affected bone ultimately becomes a solid block of calcified cartilage leaving inadequate space for hemopoiesis. It is characterized by low bone mass and microarchitectural bone fragility. It is usually rarefaction of bone resulting from deficiency of bone matrix rather than deficit mineral.
Clinical Features • Even though cemento-ossifying fibroma is considered as an intraosseous lesion, affects the gum and soft tissue have also been described.
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Types • Primary (associated with aging). • Secondary (reduction of histologically normal bone that has been accelerated by abnormal or iatrogenic circumstance such as corticosteroid or heparin therapy or condition such as malnutrition and scurvy.
Mechanism of Bone Loss
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• Imbalance between bone resorption and bone formation—it is caused by imbalance between bone resorption and bone formation with an exaggeration of resorption, reduction in bone formation or combination of both. • Postmenopausal and senile—it occurs due to overall decrease in anabolic hormones (estrogen) in postmenopausal women. There may be lag in formation of bone and since bone resorption is continued, it results in osteoporosis. After the age of 60 years, generalized atrophy of bone occur (senile osteoporosis). Senile osteoporosis is caused by decrease in calcium absorption, vitamin D absorption and metabolism with age, which in turn decreases the anabolic hormones, muscular proteins and flow of blood to bone. By virtue of this condition, bone resorption occurs. Another cause of bone resorption in adults is that, in elderly person altered hormonal function lead to formation of small thrombi which plug small vessels in bone and cause loss of bone vitality and hence resorption. • Cushing’s syndrome—the symptoms are caused by an increased output of glucocorticosteroids, especially cortisol. The excess cortisol acts to produce osteoporosis by two ways: • It contributes to the degradation of proteins and severely limits the formation of bone matrix by reducing the amount that each osteoblast synthesizes. • It promotes the formation of osteoclasts from the osteogenic undifferentiated cells and thus enhances bone resorption. • Drug-induced osteoporosis—prolonged administration of cortisol and cortisone show Cushing’s like syndrome and cause osteoporosis in the same way as that in Cushing’s syndrome. Contraceptive drug can also cause osteoporosis; as after administration of contraceptive drug, there is increase in level of cortisol. Combination of these two compounds leads to production of abnormal megakaryocytes, which in turn leads to formation of abnormal sticky platelets. These sticky platelets fuse to form thrombi which occlude small vessels in the tissue due to which the bone dies and get resorbed. • Malnutrition state—sufficient protein must be absorbed from intestine to supply constant need for matrix formation. Deficiency causes osteoporosis and may result from protein poor diet or from GIT disturbances
such as colitis, regional arteritis. Vitamin C deficiency may weaken sinusoidal vessel walls in medullary bone which tend to dilate and rupture, resulting in pooling of blood and hypoxia, which leads to loss of vitality and removal of bone by physiologic osteoclast. • Stress—there is interaction between the progesterone compounds and increased level of cortisol by stress, leading to formation of multiple small thrombi. The thrombi occlude small vessels of osseous tissue, which results in death and resorption of bone, leading to osteoporosis. • Thyrotoxic osteoporosis—it is usually seen in children with hyperthyroidism. Thyroxin mediates the action of cortisol on bone and an excess of thyroxin results in a more efficient utilization of steroids. Thus there is increased resorption. • Osteoporosis and oral bone loss—a decrease in bone mass from unbalanced system in which there is decreased bone formation or increased bone resorption, is designated as skeletal osteopenia. The designation of osteoporosis being given when the changes in bones are accompanied by pain, deformity or fracture. It is also defined as too little calcified bone and as a condition when the concentration of bone (mineral) lies more than two standard deviation below the corresponding values for the age, when matched with normal value.
Clinical Features • Age—either present at birth (congenital) or developed in early life (infantile). • Fracture—bones are fragile and susceptible to fracture. These fractures typically affect the forearm (Colle’s fracture), spine (vertebral fracture) and hip (femur fracture). • Congenita form inherited as an autosomal recessive disorder is invariably fatal in early life due to massive hemorrhage, anemia and rampant bone infections occurring due to progressive loss of bone marrow and their cellular products. • Percussion—percussion over the affected vertebrae is painful. • Symptoms—osteoporotic patient may notice gradual loss of height due to shortening of trunk. In advanced cases, clinical onset is often characterized by attack of severe pain which is aggravated by movements and occurs after trauma. • Osteomyelitis—it may occur due to relatively avascular and there may be bone pain.
Oral Manifestations • Osteomyelitis—marked predilection for development of osteomyelitis.
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Diseases of Bone Manifested in Jaw 847 • Jaws—fracture of jaws during tooth extraction. • Enamel hypoplasia—enamel hypoplasia. Microscopic dentinal defect. • Teeth—arrested root development, retardation of tooth eruption. Delayed eruption and early loss of teeth missing teeth and malformed teeth. Teeth are poorly calcified and are prone to caries.
Radiographic Features • Appearance—typical wedge appearance of affected vertebrae, on a lateral radiograph. • Internal structure—reduction in number of trabeculae is least evident in the alveolar process. Persistent trabeculae tend to occur along planes of bone stress. Trabeculae may be arranged in a radial manner, with wide spaces in between. • Cortex—reduced density and thinning of cortical boundaries, such as inferior mandibular cortex (Figs 34-24 and 34-25). • Lamina dura—the lamina dura surrounding the teeth may appear thinner than normal • Anatomic shadows such as the nasal fossa and maxillary sinus are less distinct.
Fig. 34-24: Osteoporosis presenting as decrease in density of bone (Courtesy Dr Parate).
Fig. 34-25: Senile osteoporosis showing reduce density of the bone.
Diagnosis • Clinical diagnosis—osteomyelitis of the jaw with fragile bone and fracture of bone will give clue to the diagnosis. • Radiological diagnosis—wedge shaped appearance of the vertebrae with reduce density of bone in the jaw. • Laboratory diagnosis—there is anemia, hepatomegaly, decrease RBC count and increase serum phosphatase levels. Biopsy shows lack of physiologic bone resorption. Osteoblasts are prominent but osteoclasts are seldom found. Trabeculae are in disorder arrangement.
Differential Diagnosis • Infantile cortical hyperostosis—positive history of highly specific soft tissue and bony abnormalities are found. Sites of involvement limited to few bones. New bone is subperiosteal and continuous to inferior border.
Management • Life style changes—good nutrition and regular exercise helps to prevent osteoporosis. Person should be asked to stop smoking and alcohol. • Calcium supplement—they are widely used as an adjunct to other treatment in the prevention and treatment of osteoporosis. Recommended dose is 1000 mg/day. • Anabolic steroids such as stanozolol, vitamin D and vitamin D active metabolites are also used. • Bisphosphonates—new drug for systemic osteophonates are under evaluation and this includes bisphosphonates. These are synthetics analogue of pyrophosphate that absorb on to bone surface and become incorporated into the bone matrix. When the bone contains bisphosphonates is ingested by resorbing osteoclasts, the drug released within cell in high concentration and thus exerts a toxic effect, leading to cell death and inhibits the bone resorption. • Hormone replacement therapy—hormone replacement therapy with estrogen is the treatment of choice of prevention of osteoporosis. Progesterone should be added to estrogen in women with intact uterus, to reduce the risk of endometrial carcinoma. • Alendronate 110 mg daily with calcium supplement is also effective. Etidronate 400 mg daily for 2 weeks followed by 13 weeks calcium supplement is also useful. • Calcitonin injection—injection of calcitonin to reduce bone resorption can be given. But it is rarely used due to side effects as hot flushes and nausea. • Grafting procedures to rebuild the residual ridge and implants to stabilize dentures are being used in advanced cases of bone loss. • Prevention of bone loss—oral bone loss can be prevented by plaque control, removal of local etiologic factors and use of antibiotics in case of early onset periodontitis.
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Infantile Cortical Hyperostosis It is also called as ‘Caffey’s disease’, ‘Caffey-Silverman syndrome’. It was first described in detail in 1945. It is characterized by unusual cortical thickening of certain bones and it occurs in two forms i.e. autosomal dominant form and sporadic form.
Etiology
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• Embryonic osteodysgenesis—it may be an embryonic osteodysgenesis consequent to local defect in blood supply to the area. • Inherited defect—Inherited defects of arterioles supplying the affected part results in hypoxia producing focal necrosis of overlying soft tissue and periosteal proliferation. • Allergy as the basis of disease, edema and inflammation producing periosteal elevation and subsequent deposition of calcium. • Hereditary being an autosomal dominant trait.
Clinical Features • Age and sex—it is equal in males and females, with average onset at 9 weeks of age, with most of the cases arising before 6 months. • Sites—bones commonly affected are mandible, clavicle, scapula, frontal bone and ulna. There is bilateral involvement in every case. Of all these bone clavicle and mandible are the most common sites. • Symptoms—infants will develop fever and become hyperirritable. • Signs—soft tissue swellings have a sudden onset, especially in the facial area and early in disease, they may be warm and tender. Swelling is devoid of clinical signs of inflammation on the overlying skin. Swelling disappears slowly, but may suddenly recur at the same place or new site may be involved. • Others feature—other features are pseudo-paralysis, pleurisy and dysphasia.
Oral Manifestations • Sites—mandible is one of the commonest bones affected in infantile cortical hyperostosis. • Symptoms—patient may have malocclusion and enamel hypoplasia may be present. • Signs—residual asymmetric deformity of mandible, usually in the angle and ramus area.
Radiographic Features • Incidence—only after swelling have subsided and ceased to be tender, many bone changes occur.
• Cortex—thickening of inferior cortex caused by new bone formation deep to the periosteum takes place. • Mandible—overall enlargement of body of mandible with homogeneously increased density throughout. • Laminated appearance—occasionally, the new bone may be laid down in layers giving the inferior cortex a laminated appearance. • Surface—the surface of new bone may be smooth in some cases, while irregular in some cases. • Lamina dura—the lamina dura and cortices of tooth follicle are normal.
Diagnosis • Clinical diagnosis—infant with fever, soft tissue swelling, with swelling in the jaw will give clue to the diagnosis. • Radiological diagnosis—thickening of cortex with laminated appearance. • Laboratory diagnosis—anemia, leukocytosis, elevated erythrocyte sedimentation rate, monocytosis and increased serum alkaline phosphatase levels.
Differential Diagnosis • Callus formation—unilateral or at least asymmetrical, when seen bilaterally. • Osteoma—rarely discovered in a younger age. • Cherubism—multilocular expansile radiolucency with no cortical thickening. • Osteoporosis—in infantile cortical hyperostosis, abnormal bone production is subperiosteal while in osteoporosis, it is cancellous. • Osteomyelitis—osteomyelitis of jaw may be associated with laying down of much subperiosteal new bone. But infantile cortical hyperostosis occurs within 6 months of life, as compared to osteomyelitis which occurs very unusually below 6 months of life. In osteomyelitis, whole of the mandible is not involved. • Periostitis of jaw—it is apparently unilaterally involved and is localized. It is possible to see underlying cause of the condition. Laminated structure in periostitis is visible only at the inferior margins as compared to infantile cortical hyperostosis which is visible all over the bony surface of jaw. • Fibrous dysplasia—Caffey’s disease represent the changes added to be the bone, while fibrous dysplasia is an abnormality within the bone. • Hypovitaminosis A—it produce the condition called as cortical hyperostosis. But it usually affects metacarpal bone and occurs over the age of 1 year, while infantile cortical hyperostosis occurs below 6 months and mandible is commonly affected.
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Diseases of Bone Manifested in Jaw 849 Management
Oral Manifestations
• There is no specific treatment for this disease.
It is also called as ‘Marble bone disease’, ‘Albers-Schonberg disease’, ‘osteosclerosis fragilis generalisata’. It is a rare disorders characterized by an increase in density of bones, which becomes hard and brittle. This is a result of endosteal bone production with a lack of concomitant bone resorption and remodeling. The reason for this is that there is lack of normal osteoclast formation.
• Sites—it is most common in mandible and occasionally, in maxilla. • Osteomyelitis—osteomyelitis of jaws associated with osteopetrosis probably follows the obliteration and fibrosis of marrow is caused by reduced osseous circulation. • Paranasal sinus—paranasal sinus may become readily obliterated. • Teeth—there may be enamel hypoplasia, defective dentin, disturbed tooth development, small pulp and tendency towards caries.
Types
Radiographic Features
• Infantile osteopetrosis or malignant osteopetrosis—it is a malignant childhood condition with a severe form showing severe skeletal and neurological signs. Those affected rarely live beyond the age of 2 years. It is autosomal recessive. • Intermediate osteopetrosis—this is less severe form of osteopetrosis with fracture occurring at the end of first decade. It is autosomal recessive. • Transient osteopetrosis—it shows radiographic evidence of diffuse sclerosis and it resolves without therapy. It is autosomal recessive. • Adult’s osteopetrosis or benign osteopetrosis—it is an autosomal dominant form. The adult form is characterized by predominantly skeletal signs with long having little or no defect.
• Radiodensity—there is diffuse homogeneous sclerotic appearance of all bones, within distinction between the cortex and the marrow. This type of appearance is called as marble bone appearance (Fig. 34-26).
Osteopetrosis
Clinical Features • Age—it can occur in infant and some cases are diagnosed later in life. • Skeletal features—almost every one has a varying degree of poor skeletal development, if the disease appears early in life. Subsequent skeletal deformities occur later due to bending of the long bones and improper healing after pathological fractures. • Symptoms—as a result of continuous bone deposition and lack of bone resorption, the foramina of cranial nerves are constricted, hence there is loss of hearing, disturbed vision, which diminish progressively. • Facial palsy—facial nerve palsy is also seen. • Signs—due to displacement of hematopoietic bone marrow, anemia ensues and the hematopoietic function is assumed by the liver, spleen and the lymph nodes resulting in hyperplasia of lymphoid tissues and hepatosplenomegaly. There is also frontal bossing, obliteration of maxillary sinus and possible hydrocephalus and mental retardation. • Prognosis—prognosis of infantile osteopetrosis is very poor as compared to adult’s osteopetrosis.
Fig. 34-26: Homogeneous sclerotic appearance seen in marble bone disease (Courtesy Dr Ganju).
• Skull changes—the changes in the skull are often striking. The base of skull becomes grossly thickened and of great radiographic density. Loss of normal skull marking and structures. The dipoles are effaced, the head of patient resembles bladder of lard. There is gross thickening and increased opacity of the cranial base, with narrowing of foramina. • Fracture—due to increased calcification there is increased fragility, so fractures are common. • Bones—bones are shorter than normal, heavy, thick and deformed. The ends of long bone spay out.
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• Cortex—the cortices are thickened and differentiation between them and adjacent bone is greatly lessened. • Internal structure—less marked changes may produced are the increase in overall density but trabeculation may be apparent. The trabeculae may get thickened and the marrow spaces are correspondingly small. • Lamina dura—the lamina dura is almost lost in the general density. Some time density is such that the roots are nearly invisible on dental radiographs. • Teeth—the roots of the teeth may be obscured, partially or totally, depending upon the bone density. • Cortex—the medullary cavity is replaced by bone and cortex is thickened.
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Diagnosis • Clinical diagnosis—hearing deformity, fracture of bone with skeletal deformity will give clue to the clinical diagnosis. • Radiological diagnosis—marble bone appearance is seen which is typical of this disease. • Laboratory diagnosis—red blood cell count below 1,000,000 cells per cu mm. Elevated serum acid phosphate levels have been reported in patients with benign dominant osteopetrosis. Biopsy shows prominent osteoblasts, but osteoclasts are seldom found.
Differential Diagnosis • Polyostotic fibrous dysplasia—fibrous dysplasia usually involves a part of bone, rather than the complete bone. Hence, involved bone generally exhibits asymmetric enlargement. • Paget’s disease—it can be differentiated from osteopetrosis by its classic bones. It most often involves the skull, pelvis, vertebrae, femur, maxilla and mandible. Also, serum chemistry measurements show markedly elevated alkaline phosphate levels. • Sclerotic cemental masses—have a stronger predilection for black women over 30 years of age. The most common salient feature of this disease is that only jaws are affected, radiograph of the jaws reveal radiopaque masses frequently rimmed by radiolucent borders. • Infantile cortical hyperostosis—skeletal changes are subperiosteal and not endosteal. Mandible is more commonly involved.
Management • Bone marrow transplantation—this is the treatment of choice in osteopetrosis patient. But to find matched donor is a difficult process. • Interferon gamma 1b—if interferon gamma 1-b is given in combination with calcitrol will reduce the bone mass.
• Other modalities—corticosteroid, parathormone, macrophage colony stimulating factor and erythropoietin can also be given. • Supportive treatment—this is given to combat infection, osteomyelitis. Antibiotics which are given in infection are fluoroquinolones and lincomycin. Hyperbaric oxygen therapy can also be given. • Precaution—avoid major surgery in patients with osteopetrosis. Performing dental extraction osteopetrosis patient has a risk of osteomyelitis and jaw fracture.
Osteogenesis Imperfecta It is also called as ‘brittle bone’, ‘Lobstein disease’. It is a serious disease of unknown etiology. It represents a hereditary autosomal dominant trait.
Pathogenesis There impairment of collagen maturation. Collagen is main part of bone, dentin, sclera, ligament and skin. So collagen impairment will result in change in this structure.
Types • Congenital or Vrolik’s type—it is present at birth. • Tarda or Lobstein’s type—it is recognized later in life. It is also called as osteopsathyrosis.
Clinical Features • Age—many infants with this disease are stillborn or die shortly after birth. • Bone deformity—patient is having bone deformity and hyper extensibility of the joint. There is also bowing of the bone (Figs 34.27A and B). • Fracture of bone—extreme fragility and porosity of bones with an attendant proneness of fracture. Fracture heals readily but new bone is of similar imperfection. It is common for fracture to occur while the infant is walking or crawling. Hyperplastic callus formation, which may mimic osteosarcoma, take place. • Blue sclera—there is occurrence of pale blue sclera which is thin; pigmented choroids show and produce the blue color (Fig. 34-28). • Signs—there is deafness due to osteosclerosis; laxity of ligament and peculiar shape of the skull. There is also abnormal electrical reaction of muscle. Increased tendency for capillary bleeding.
Oral Manifestations • Dentinogenesis imperfecta—most of the times, osteogenesis imperfecta is associated with dentinogenesis imperfecta.
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Diseases of Bone Manifested in Jaw 851
Fig. 34-28: Blue sclera seen in patient of osteogenesis imperfecta.
Clinical Types • Neonatal lethal type—it is characterized by multiple fractures in infants and the child seldom survives. • Severe non-lethal type—disease is not evident until late childhood and patient shows fracture of bone with minimum trauma. Although the fractured bone heals up rapidly, considerable skeletal deformity and dwarfed stature often develop. • Moderate and deforming type—it is associated with dentinogenesis imperfecta and blue sclera. • Mild and non-deformity type—the patients are clinically normal, but they have increased tendency for bone fracture, due to trauma.
A
Radiological Features • Wormian bones—patient may show wormian bone (bones in skull sutures) (Fig. 34-29).
B Figs 34-27A and B: Patient of osteogenesis imperfecta showing bone deformity (Courtesy Dr Lambade).
• Enamel hypoplasia—some times, there is also hypoplasia of teeth. Sometimes there is class I malocclusion and greater incidence of impacted 1st and 2nd molars. • Deciduous teeth—deciduous teeth are poorly calcified and semi-translucent or waxy. Appearance of teeth is faint dirty pink, half normal size, with globular crowns and relatively short roots in proportion to other dimension. • Malocclusion—there is increased prevalence of malocclusion which is caused by maxillary hypoplasia.
Fig. 34-29: Wormian bone seen in osteogenesis imperfecta (Courtesy Dr Lambade).
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• Bone deformity—there is skeletal deformities manifested by bowing of bone and fracture of bone (Fig. 34-30). • Internal structure—the bone is osteoporotic, there is less density and trabeculae are fewer in number. • Appearance—the chin is sharply pointed, as a result of softening of bone, leading to flattening of sides of the mandible.
• Bird facies—arrested development and ensuing hypoplasia of mandible ultimately produce the characteristic bird facies (Fig. 34-31). Mandibular hypoplasia yields a retrognathic appearance.
4 Fig. 34-31: Mandibular retrognathism resulting in characteristic bird face appearance.
Fig. 34-30: Bowing of bone seen in radiograph of patient with osteogenesis imperfecta (Courtesy Dr Lambade).
Diagnosis • Clinical diagnosis—severe bone deformity with blue sclera are diagnostic features of osteogenesis imperfecta. • Radiological diagnosis—multiple wormian bones with osteopenia will diagnose this condition. • Laboratory diagnosis—bone is composed of immature spongy bone. Osteoblastic activity retarded and there is failure of fetal collagen to be transformed into mature collagen.
• Tongue—the retruded mandible results in posterior displacement of the tongue. • Cleft palate formation—abnormal descent of tongue occurs between the palatal shelves resulting in cleft palate (Fig. 34-32).
Management • Management of fracture—management of fracture should be done in patient. • Management of teeth—teeth management should be same as that is carried out in dentinogenesis imperfecta. Fig. 34-32: Cleft palate formation seen in patient with Pierre Robin syndrome.
Pierre Robin Syndrome It is also called as ‘Robin anomalad’. It results arrested development.
Clinical Features • Triad—it is triad of cleft palate, mandibular micrognathia and glossoptosis (causes airway obstruction).
• Respiration—there is respiratory difficulty due to failure of support of tongue musculature because of micrognathia, allowing the tongue to fall down and backwards, partially obstructing the epiglottis. Difficulty in respiration is noted from birth and it can cause asphyxiation.
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Diseases of Bone Manifested in Jaw 853 • Others—there may be congenital heart defects, other skeletal abnormalities and ocular lesions. Mental retardation is also a common finding.
Diagnosis • Clinical diagnosis—triad of cleft palate, micrognathia and glossoptosis will diagnose this condition.
Management • Breathing support—breathing support and feeding assistance are necessary during infancy. • Surgical—surgical closure and orthodontic treatment are indicated.
Marfan’s Syndrome It is also called as ‘Marfan-Achard syndrome’, ‘arachnodactyly’. It is hereditary disease transmitted as autosomal dominant trait. It is basically a disease of connective tissue related to defective organization of collagen which is abnormally soluble.
Clinical Features • Spider finger—excessive length of the tubular bones resulting in disproportionately long, thin extremities, the finger and toes are long, thin and tapering so that the name ‘spider finger’ has been applied. • Shape—the shape of face and skull is characteristically long and narrow. • Joint—hyperextensibility of joint with habitual dislocations, kyphosis or scoliosis and flatfoot. • Bilateral ectopia lentis—it is caused by weakening or rupture of the suspensory ligaments. • Cardiovascular complications—cardiovascular complications like aortic aneurysm and aortic regurgitation, valvular defects and enlargement of the heart are common.
Down’s Syndrome It is also called as ‘Trisomy 21 syndrome’ and ‘mongolism’. It is associated with subnormal mentality in which an extremely wide variety of anomalies and functional disorders may occur. It results from excessive chromosomal material involving all or a portion of chromosome 21. It is cause by advanced maternal age, uterine and placental abnormalities and chromosomal aberration.
Type • Typical type—trisomy–21 with 47 chromosomes (95 percent of cases). • Translocation type—46 chromosomes. • Chromosomal mosaicism.
Clinical Features • Skull—flat face, large anterior fontanelle, open sutures. There is also brachycephalic skull shaped with frontal prominence and occipital flattening (Figs 34-33A and B). • Palpebral fissures—they are almond shaped with superior-lateral or Mongolian obliquity. • Eyes—small slanting eyes with epicanthal folds. Eyes are widely spaced. There is also ocular hypertelorism. • Nose—there is flattened nasal bridge (Fig. 34-33). • Others—sexual underdevelopment, cardiac abnormalities and hypermobility of the joints.
Oral Manifestations • Palate—high arched palatal vault is very prevalent. • Maxilla and mandible—bifid uvula, malocclusion and multiple odontogenic cysts of maxilla and mandible. • Temporomandibular joint—there may be temporomandibular dysarthrosis.
Diagnosis • Clinical diagnosis—spider finger, with high arched palate, hyperextensibility of joints.
Management
A
There is no specific treatment for this syndrome and prognosis is good.
B Figs 34-33A and B: Brachycephalic skull shaped with widely shaped eyes. Nose has flattened bridge.
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Oral Manifestations
Diagnosis
• Tongue—macroglossia with protrusion of tongue (Fig. 34-34), fissured tongue or pebbly tongue from enlargement of papilla. • Others—open mouth, frequent prognathism and high arched palate. • Maxillary sinus—there is hypoplasia or aplasia of maxillary sinus. • Teeth—teeth are malformed, enamel hypoplasia and microdontia. • Malocclusion—it attributable to small maxillary arch relative to the mandibular arch. • Periodontal disease—universal severe destructive periodontal disease that do not appear to be local in origin.
• Clinical diagnosis—wide open eyes with brachcephalic shaped with malocclusion will give clue to the diagnosis. • Radiological diagnosis—it is not specific.
Management There is no specific treatment for this syndrome and many patient died during first year of life.
Achondroplasia It is also called as ‘chondrodystrophia fetalis’. It is a disturbance of endochondral bone formation, which results in a characteristic form of dwarfism. It is a hereditary condition, which is transmitted as an autosomal dominant trait.
Clinical Features • Appearance—patient is quite short, usually less than 14 meters in height and thickened muscular extremities, brachycephalic skull and bowed legs. • Hands—hands are usually small and fingers are stubby. • Skull—the base of the skull is small and constricted as a result of retarded growth of the cartilaginous portions. The calvarium is large and bulges frontally and laterally. • Nose—there is also depression of the bridge of nose. • Lumbar lordosis—lumbar lordosis with prominent buttocks and protruding abdomen is often present. • Joints—joints exhibit limitation of motion. • Others—arms do not hang freely at the sides and the elbows can not be straightened. Fig. 34-34: Malocclusion with macroglossia of tongue (Courtesy Dr Parate).
Radiological Features • Periodontal destruction—periodontal destruction of bone can be observed on the radiograph (Fig. 34-35).
Oral Manifestations • Proganthism—maxilla is often retruded because of restriction of growth at the base of skull which may produce relative mandibular prognathism. • Teeth—congenital missing teeth with disturbances in shape of teeth may also occur.
Radiographic Features • Shorter bone and bone clubbing—long bones are shorter than normal and there is thickening or mild clubbing at the ends. • Epiphysis—epiphysis may close, either early or late. • Narrow foramen magnum—bones at the base of the skull fuse prematurely, producing shortening as well as a narrow foramen magnum.
Diagnosis Fig. 34-35: Periodontal destruction of bone seen in the OPG (Courtesy Dr Parate).
• Clinical diagnosis—short bone, depression of nose, malocclusion of teeth and prognathism will give clue to diagnosis.
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Diseases of Bone Manifested in Jaw 855 • Radiological diagnosis—narrow foramina magnum and short bone • Laboratory diagnosis—there is retardation or even aplasia of zone of provisional calcification of endochondral growth. Cartilage columns lack orderly arrangement, fail to calcify properly and are not resorbed and replaced by bone in the usual fashion.
• Emetics—administer emetics if the patient possesses a gag reflex i.e. if he is not vomiting. • Glucose—glucose, to reverse hyperkalemia and calcium gluconate to maintain sodium and calcium levels must be given. • Sodium bicarbonate—sodium bicarbonate or Ringer lactate must also be given to increase salivary flow, decrease acidosis, to increase pH and to increase excretion of fluoride.
Management There is no specific treatment for this disease.
Skeletal Fluorosis (Fluoride Toxicity) Fluoride toxicity can be manifested in two forms i.e. acute and chronic. It can be cause by mutation and other genetic disorders.
Clinical Features • Symptoms—nausea, vomiting and epigastria distress. Excess salivation, diarrhea and mucus discharge with headache and sweating. There is pain in joints of hand, feet and spine. • Signs—barely detectable pulse, hypotension, cardiac arrhythmias and disturbance in electrolyte balance. There is also stiffness of gait, limitation of movement occurs. • Severe cases—in most severe cases, there is almost crippling of movement and extreme pain because the spine and joints become rigid and virtually, immobilization of the individual occurs. • Complication—respiratory and metabolic acidosis and coma.
Generalized Cortical Hyperostosis It is also called as ‘Von Buchem disease’ and it represents an excessive deposition of endosteal bone throughout the skeleton in a pattern suggestive of a hereditary condition, with an autosomal recessive characteristic.
Clinical Features • Appearance—facial appearance of this patient may be swollen, particularly with widening of the angles of mandible and at the bridge of nose. • Symptoms—in some patients, there is loss of visual activity and loss of facial sensation; some degree of facial paralysis and deafness occurs and all this is due to cranial nerve involvement through closure of foramina. • Alveolar process—intraorally, there is sometimes overgrowth of alveolar process.
Radiological Features • Increase density—a skeletal radiograph reveals increased density of many bones of body. • Skull sclerosis—the skull exhibits diffuse sclerosis which may be present in the jaws.
Radiographic Features
Diagnosis
• Bone density—density of bone is increased. • Thickening of bone—bones of extremities show thickening and osteophytes. • Calcification—calcification occurs in tendons and ligaments.
• Clinical diagnosis—overgrowth of alveolar process, facial paralysis and deafness. • Radiological diagnosis—skull sclerosis, and increases density of bone • Laboratory diagnosis—the bone is normal dense bone, but without evidence of remodeling.
Diagnosis • Clinical diagnosis—excess salivation, headache, sweating and joint pain will give clue to diagnosis. • Radiological diagnosis—calcification and thickening of bone.
Management There is no treatment although patient may live his normal life.
Massive Osteolysis Management • Elimination of fluoride from body—all attempts should be to eliminate the toxic dose of fluoride from the body. • Maintenance of vital signs—support all the vital signs.
It is also called as ‘vanishing bone’, ‘disappearing bone’, ‘phantom bone’, ‘progressive osteolysis’ or ‘Gorham syndrome’. It is characterized by spontaneous, progressive resorption of bone with ultimate total disappearance of bone.
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Pathogenesis In this condition, there is progressive destruction of bone. The bone is replaced by fibro-vascular tissue. It occurs due to proliferative vascular and connective tissue response to unknown mechanism.
Clinical Features
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• Age and sex distribution—it is most common in older children, young and middle age adults. There is no sex predilection. • Sites—the most commonly affected bones are the clavicle, scapula, humerus, ribs, ilium, ischium and sacrum. • Symptoms and progress—the disease may or may not be painful, begins suddenly and advance rapidly, until the involved bone is replaced by a thin layer of fibrous tissue surrounding a cavity.
Oral Manifestations • Site—intraorally mandible is more commonly affected as compared to maxilla. • Symptoms—the patients may present with pain or facial asymmetry. In some cases there is history of gradual progressive recession of the lower jaw. • Pathological fracture—there is pathologic fracture of bone following even minor trauma. • Signs—there may be complete destruction of mandible (Fig. 34-36). Deviation of mandible can also occur in the affected side. Ulceration of the lesion is usually absent.
Fig. 34-37: Vanishing bone disease showing destruction of bone on left side of the mandible (Courtesy Dr Chandrasekhar Kadam).
• Lamina dura—there is absence of lamina dura and thinning of cortical plates.
Diagnosis • Clinical diagnosis—pain, facial asymmetry and pathological fracture without any apparent cause may suspect massive osteolysis • Radiological diagnosis—it will show complete destruction of bone in the jaws • Laboratory diagnosis—biopsy shows vascular proliferation with osteoclastic reaction.
Management
Fig. 34-36: Destruction of mandible seen with no ulceration in buccal mucosa in mandibular posterior region (Courtesy Dr Chandrasekhar Kadam).
• Surgical—it can be managed by intra-periosteal or extraperiosteal resection followed by autogenous grafts. • Radiation therapy—some authors suggest that the role of moderate dose of radiation therapy. It is one of most successful treatment for the massive osteolysis. • Zeledronic acid—it has got anti-angiogenic properties which inhibits osteoclasts can be useful in resorptive process of vanishing bone disease. • Nutritional treatment—vitamin D-50000 units/week, calcium glycerophosphate 6 gm/day and fluoride. • Other treatment—various other treatment modalities like chemotherapy, calcitonin, mithramycin disphosphonates also has been tried but with limited success.
Suggested Reading
Radiological Features • Radiodensity—it has got osteolytic pattern radiologically. • Appearance—radiolucency is present in the mandible showing complete destruction. Margins of the lesion are indistinct (Fig. 34-37).
1. Adoranto MC, Paticoff KA. Intralesional corticosteroid injection for treatment of central giant cell granuloma. JADA 2001;132:18690. 2. Arnott DG. Cherubism: an initial unilateral presentation. Br J Oral Surg 1978-1979;16:38.
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Diseases of Bone Manifested in Jaw 857 3. Baden E, et al. Periapical cemental dysplasia and periodontal disease. A case report with review of literature. J Periodon 1987; 58(3):187. 4. Bakeman RJ, Abdelsayed RA, et al. Osteopetrosis: a review of literature and report of case complicated by osteomyelitis of the mandible. J Oral Maxillofac Surg 1998;56:1209-13. 5. Bhaskar SN, et al. Multiple exostosis: report of cases. J Oral Surg 1968;26:321-6. 6. Cannon JS, Keller EE, Dahlin DC. Gigantiform cementoma. Report of two cases (mother and son). J Oral Surg 1980;38:65-70. 7. Catena DL, et al. Monostotic fibrous dysplasia with dental anomalies. Oral Surg 1971;32:136. 8. Chaudhary AP, et al. Periapical fibrous dysplasia (cementoma) J Oral Surg 1958;16:483. 9. Cohen MM Jr, Howell RE. Etiology of fibrous dysplasia and McCune-Albright syndrome. Int J Oral Maxillofac Surg 1999; 28:366-71. 10. Coleman H, Altini M, Kieser J, Nissenbaum M. Familial florid cemento-osseous dysplasia—a case report and review of the literature. J Dent Assoc S Afr 1996;51:766-70. 11. Cooke BED. Benign fibro-osseous enlargements of the jaws. BDJ 1957;102:1. 12. Desai SS: Down syndrome: a review of literature. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1997;84(3):279-85. 13. Eversole LR, et al. Radiographic characteristics of central ossifying fibroma. Oral Surg 1985;59:522. 14. Eversole LR, Leider AS, Nelson K. Ossifying: a clinicopathologic study of 64 cases. Oral Surg, Oral Med, Oral Pathol 1985;60:50511. 15. Fitzpatrick DN. Fibrous dysplasia and infection of the mandible. Oral Surg 1966;22:209. 16. Fredericksen N, Wesley K, et al. Massive osteolysis of the maxillofacial skeleton—a clinical radiographic histologic and ultra structural study. Oral Surg, Oral Med, Oral Pathol 1983;55:550. 17. Groot RH, van Merkesteyn JP, Bras J. Diffuse sclerosing osteomyelitis and florid osseous dysplasia. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1996;81:333-42. 18. Groot RH, van Merkesteyn JPR, Bras J. Diffuse sclerosing osteo-myelitis and florid osseous dysplasia. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1996;81:333-42. 19. Hall EH, et al. Early aggressive cemento-ossifying fibroma: A diagnostic and treatment dilemma. Oral Surg 1987;63:132. 20. Hamner J F, et al. Benign fibro-osseous jaw lesions of periodontal membrane origin. An analysis of 249 cases. Cancer 1967;22:861. 21. Higuchi Y, Nakamura N, Tashiro H. Clinicopathologic study of cemento-osseous producing cysts of mandible. Oral Surg, Oral Med, Oral Pathol 1988;65:339-42. 22. James WM, et al. Aggressive ossifying fibroma of the maxilla. Review of literature and report of a case. J Oral Surg 1979;37:276. 23. Johnson RP, et al. Polyostotic fibrous dysplasia. J Oral Surg 1967;25: 521. 24. Kaffe I, Ardekian L, et al. Radiological features of central giant cell granuloma of the jaws. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1996;81:720-26. 25. Kawai T, Hiranuma H, et al. Cemento-osseous dysplasia of the jaws in 54 patients: a radiographic study. Oral Surg, Oral Med, Oral Pathol 1997;87:107-14. 26. Keith Fisher. Gorham’s syndrome massive osteolysis a rare case report. J Oral Maxiilofac Surg 1990;48:1222-25. 27. Leslie H, Doku HC, et al. Perspective on massive osteolysis: a report of cases and review of literature. Oral Surg, Oral Med, Oral Pathol 1983;55:331. 28. Loh FC, Yeo JF. Florid cemento-osseous dysplasia in Orientals. Oral Surg, Oral Med, Oral Pathol 1989; 68:748-53. 29. Loh FC, Yeo JF. Florid osseous dysplasia in oriental. Oral Surg, Oral Med, Oral Pathol 1989;68:748-53. 30. Lucas RB. Cherubism. In Pathology of tumors of the oral cavity. Third edition: 1976; Churchill living stone.
31. MacDonald-Jankowski D. Fibrous dysplasia in the jaw of Hong Kong population: a radiographic presentation and systematic review. Dentomaxillofac Radiol 1999;28:195-202. 32. Mailander JC. Black bear sign of monostotic paget disease of the mandible. Clin Nucl Med 1986;11:325-7. 33. Mehta DS, et al. Ossifying fibroma of the mandible: A case report JIDA 1984;36:345. 34. Melrose RJ, Abrams AM, Mills BG. Florid osseous dysplasia. A clinical-pathologic study of thirty-four cases. Oral Surg, Oral Med, Oral Pathol 1976;41:62-82. 35. Melrose RJ, Abrams AM, Mils BG. Florid osseous dysplasia. Oral Surg, Oral Med, Oral Pathol 1976;41:62-82. 36. Melrose RJ, Abrans AM, Mills BG. Florid osseous dysplasia clinical: pathologic study of thirty four cases. Oral Surg, Oral Med, Oral Pathol 1976;41:62-82. 37. Melrose RJ, et al. Florid osseous dysplasia: A clinical pathologic study of 34 cases. Oral Surg 1976;41:62. 38. Meti M, Patil N, Puranik S. Gorham’s massive osteolysis. A rare case report. JIAOMR 2006;18(2).119-23. 39. Miyake M, Nagahata S. Florid cemento-osseous dysplasia. Report of a case. Int J Oral Maxillofac Surg 1999;28:56-7. 40. Morgan GA, Morgan PR. Oral and skull manifestation of Paget’s disease. J Can Dent Assoc 1969;35(4):208-12. 41. Murphy JB, et al. Osteitis deformans: report of a long standing case with extensive oral involvement. Oral Surg 1978;46:765. 42. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology (2nd edn), Saunders Elsevier, 2004. 43. Obisesan A, et al. The radiologic features of fibrous dysplasia of the cranio-facial bones. Oral Surg 1977;44:949. 44. Oikarinen K, Altonen M, Happonen RP. Gigantiform cementoma affecting a Caucasian family. Br J Oral Maxillofac Surg 1991; 29:194-7. 45. Pogrel MA, Regezi JA, et al. Calcitonin treatment for central giant cell granuloma. J Oral Maxillofac Surg 1999;57:848-53. 46. Poon C, Kwan P, Chao S. Giant peripheral ossifying fibroma of the maxilla: Report of a case. J Oral Maxillofac Surg l995;53:695-8. 47. Rafik A, Abdelsayed, et al. Gigantiform Cementoma: clinicopathologic presentation of 3 cases. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 2001;91:438-44. 48. Rodney M, Phillips, et al. Massive osteolysis (phantom bone, disappearing bone). Oral Surg 1972;34(6):887-96. 49. Sarala K, Jayachandran S, et al. Florid cemento-osseous dysplasia. JIAOMR 2006;18(3):176-80. 50. Schamamann, et al. Benign fibro-osseous lesions of the mandible and maxilla. Cancer 1970;26:306. 51. Schneider LC, Mesa ML. Differences between florid osseous dysplasia and chronic diffuse sclerosing osteomyelitis. Oral Surg, Oral Med, Oral Pathol 1990;70:308-12. 52. Schofield IDF. An aggressive fibrous dysplasia. Oral Surg 1974; 38:29. 53. Schwartz S, Tsipouras P. Oral finding in osteogenesis imperfecta. Oral Surg, Oral Med, Oral Pathol 1984;57:161-7. 54. Scully C, Cawson RA. Medical problems in dentistry (5th edn), Churchill Livingstone: an imprint of Elsevier, 2005. 55. Shafer WG, et al. A text book of oral pathology (4th edn), Philadalphia, WB Saunders, 1983. 56. Slootweg PJ, Panders AK, et al. Juvenile ossifying fibroma: an analysis of 33 cases with emphasis on histopathological aspects. J Oral Pathol Med 1994;23:385-8. 57. Smith J, Eveson J. Paget’s disease of bone with particular reference to dentistry. J Oral Pathol 1981;10:233-47. 58. Su L, Weather DR, Waldron CA. Distinguishing feature of focal cemento-osseous dysplasia and cemento-ossifying fibroma: I A pathological spectrum of 316 cases. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1997;84:301-9. 59. Summerlin DJ, Tomich CE. Focal cemento-osseous dysplasia: a clinicopathological study of 221 cases. Oral Surg, Oral Med, Oral Pathol 1994;78:611-20.
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60. Sundharam B, Rajaram P, et al. Report of two patients with paget’s disease-one with typical clinical and radiological manifestation including cardiac involvement and the other subclinical but with radiological changes. JIAOMR 2006;18(4): 228-33. 61. Tillman HH. Paget’s disease of bone: a clinical radiographic and histopathological study of twenty four cases involving the jaws. Oral Surg, Oral Med, Oral Pathol 1962;15:1225-34. 62. Toffanin A, Benetti R, Manconi R. Familial florid cemento-osseous dysplasia: a case report. J Oral Maxillofac Surg 2000;58:144046. 63. Von Wowern N. General and oral aspect of osteoporsis: a review: Clin Oral Invet 2001;5:71-8. 64. Waldron CA, Giansanti JS, Browand BC. Sclerotic cemental masses of the jaws (so-called chronic sclerosing osteomyelitis,
65. 66. 67. 68. 69.
sclerosing osteitis, multiple enostosis, and Gigantiform cementoma). Oral Surg, Oral Med, Oral Pathol 1975;39:590-604. Waldron CA. Fibro-osseous lesion of the jaws. J Oral Maxillofac Surg 1993;51:828-35. Waldron CA. Fibro-osseous lesions of the jaws. J Oral Maxillofac Surg 1985;43:249-62. Wolf J, Heitamen J, Sane J. Florid cemento-osseous dysplasia (gigantiform cementoma) in a Caucasian woman. Br J Oral Maxillofac Surg 1989;27:46-52. Younau F, Eisenbud L, Sciubba JJ. Osteopetrosis: a case report including gross and microscopic finding in the mandible at autopsy. Oral Surg, Oral Med, Oral Pathol 1988;65:214-21. Young SK, Markowitz NR, et al. Familial gigantiform cementoma: Classification and presentation of a large pedigree. Oral Surg, Oral Med, Oral Pathol 1989;68:740-7.
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AIDS
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AIDS
Introduction AIDS is a devastating fatal disease which is in epidemic form throughout the world. It is an incurable viral STD (sexually transmitted disease) which is caused by human immunodeficiency virus (HIV). It stands for:• A—Acquired, i.e. contagious not inherited. • I—Immune, i.e. power to resist disease. • D—Deficiency. • S—Syndrome, i.e. number of signs and complaints indicative of a particular disease. The case of AIDS was detected in June 1981 when five young homosexual men came with the suffering from rare lung infection due to microorganism called Pneumocystis carinii. In India, the first description of AIDS came in Chennai where six women out of 125 who were screened were HIV positive in high risk group of prostitutes. HIV attacks the immune system of the body. Due to that an individual is not able to protect himself from potentially harmful organism. AIDS appears to be endemic in central and equatorial Africa and it may be old disease of Africa that has gone unrecognized. HIV infection has also become the primary emphasis of effort at controlling STDs. Moreover, the knowledge gain about sexual and other behavior associated with transmission of HIV, as well as strategies that have been effective in modifying those behaviors, is transferable to other sexually transmittable and blood-borne infections. These above factors have revolutionized standard approaches to the control of these infections. Oral and perioral lesions are common in patients with human immunodeficiency virus, which are often the presenting feature and may have deterioration of general health and a poor prognosis.
Definition WHO has given the following definition of AIDS.
• One or more opportunistic infections listed in clinical features that are at least moderately indicative of underlying cellular immune deficiency. • Absence of all known underlying causes of cellular immune deficiency (other than HIV infection) and absence of all other causes of reduced resistance reported to be associated with at least one of those opportunistic diseases.
Prevalence It is more common in African country and Western countries particularly in the United States. The largest population of AIDS occurs in homosexuals, intravenous drug users, and heterosexuals with sexual contact with AIDS patient. It can also occur in patients who received transfusion of blood or blood pigments donated by the person with risk factors. About 92% of victims are males, 6.5% females with 1% children. It is common in the age group of 25 to 49 years.
Transmission • Sexual transmission—it is in 90% of cases. It depends upon number of sexual partners, receptive anal intercourse and presence of other STDs. All these are in high risk group. Prostitution is a major heterosexual factor associated with AIDS. Homosexuals have more risk of transmitting HIV than the heterosexual males. • Use of contaminated blood products—intravenous drug users, HIV-contaminated blood transfusion, blood clotting concentrate and organ transplantation. • Perinatal transmission—it occurs in 13% among children born to HIV seropositive mother. • Other nosocomal routes—transmission from patient to patient due to reuse of contaminated and shared needles.
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• Professional hazards—the risk of transmission from HIVinfected patient to health care workers is more than health care workers to patient. • Saliva transmission—HIV has been found to be present in saliva. Saliva reduces the ability of HIV to infect its target cells. So transmission through saliva is rare possibility. But, there are some rare example which documented that HIV is transferred from the saliva of the patient.
History of Nomenclature of Virus
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• T lymphocytes—there is quantitative and qualitative deficiency of T4 helper cells in AIDS patients. This lead to certain investigators to focus their efforts on determining if etiologic agent was a virus that manifested a particular tropism for T4 helper lymphocytes. • HTLV-III virus—Dr Robent C Galleo determined that type C retrovirus was tropic for T4 lymphocytes in adult T-cell leukemia/lymphoma. He named the virus, Human T cell leukemia/lymphoma virus (HTLV–I). So, it is considered to be etiological agent for AIDS. It causes lymphoproliferation in T cell leukemia, whereas AIDS is a disease of lymphodepletion. The answer came in the discovery of type D retrovirus of HTLV family that has been termed as HTLV-III. • LAV virus—on the other hand, virus called lymphadenopathy associated virus (LAV) was isolated from the AIDS patient in Europe. • Cytopathic human T lymphocytotropic virus—HTLV III and LAV are closely related members of same class of virus. Finally it is proved that HTLV and LAV are cytopathic human T–lymphocytotropic viruses that manifested selective infectivity for the helper/inducer subset of T cells that as phenotypically designated reactivity with monoclonal antibody T4 or Leu3. • HIV—in order to avoid different nomenclatures, retrovirus responsible for the AIDS are named ‘Human immunodeficiency virus’ which belong to family of retroviruses.
Characteristic of the HIV Virus HIV virus is lymphotropic virus and its primary target is T4 cell. HIV is a spherically enveloped virus, about 90-120 nm in size which is much smaller than bacteria. The nucleocapsid has an outer icosahedral shell and inner cone-shaped core, enclosing the ribonucleoproteins. The genome is diploid, composed of two identical single stranded, positive sense RNA copies. Inside the envelops, there is a protein core, which contains enzymes reverse
transcriptase, intregrase, protease etc. all essential for viral replication and maturation. When the virus infects a cell, the viral RNA is transcribed by the enzymes, first into single-stranded DNA and then to double-stranded DNA (provirus) which is integrated into the host cell chromosomes. The virus is extremely sensitive to heat, thus boiling and autoclaving are very effective measures of inactivating the virus.
Mechanism of Action • Normal mechanism—pathogenic viruses →identified by macrophage → it activates T lymphocytes →it gets differentiated into effector cell like T helper cell (T4) and T suppresser cell (T8 ) → T 4 cells secrete various lymphokines which induce lymphocyte to be differentiated into plasma cell →it secretes specific antibodies against viral antigen →it destroys the virus. • Mechanism in AIDS • Antigenic stimulation—when the virus enters the blood stream, it evokes antigenic stimulation which activates CD4, T helper lymphocytes and macrophages. • Secretion of TNF and interleukin 6—lymphocytes and macrophages then secrete growth factors, tumor necrosis factor (TNF) and interleukin-6. This results in increase in CD4 cells thereby increasing number of cells vulnerable for HIV virus. • Adherence of virus to CD4 cells—HIV virus then adheres to CD4 surface via interaction between viral gp120 surface glycoprotein and CD4 cell surface membrane receptors. This surface interaction occurs with the help of transmembrane protein (chemokine receptor-5 or CCR-5). • Replication of HIV virus—after this, HIV virus will replicate in CD4 cell which also proliferates by antigenic stimulus. • Incubation period—once the viral genes are integrated into cells of own DNA, they can apparently remain dormant for an indefinite period of time, without causing any effects. This is called as ‘incubation period’ • Fate of CD4—initially CD4 cells reduce the number of HIV virus by cellular and humoral attacks. But as continuous replication of virus occurrs in lymph nodes, it will destroy the lymph nodes. This will lead into unchecked replication of virus which will lead to decrease in CD4 count of the human being. When the number of CD4 count is severely depleted below 200/mm3, the immune system collapses and variety of infections occur. At this stage, the patient is said to have AIDS. • Window period—it is time between entry of virus into the body and the blood test becoming positive. This period
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AIDS is about 1 to 3 month and person is infectious during that period.
Six Groups at Risk of Developing AIDS • • • • •
Homosexuals or bisexuals—71.4% Intravenous drug users—18.4% Hemophilia Recipient of multiple blood transfusion Infant born of parents belonging to first 3 high risk groups • Heterosexual contacts of high risk group.
Classification 1993 Revised Classification System for HIV Infection The Centers for Disease Control and Prevention (CDC) has revised the classification system for HIV infection to emphasize the clinical importance of the CD4+, Tlymphocyte count in the categarization of HIV-related clinical conditions. Consistent with the 1993 revised classification system, CDC has also expanded the AIDS surveillance case definition to include all HIV-infected persons who have less than 200 CD4+, T-lymphocytes/μL, or a CD4+, T-lymphocyte percentage of total lymphocytes of less than 14. This expansion includes the addition of three clinical conditions pulmonary tuberculosis, recurrent pneumonia, and invasive cervical cancer. Measures of CD4+, T-lymphocytes are used to guide clinical and therapeutic management of HIV-infected persons. The revised CDC classification system for HIVinfected adolescents and adults categorizes persons on the basis of clinical conditions associated with HIV infection and CD4+, T- lymphocyte counts. The system is based on three ranges of CD4+, T-lymphocyte counts and three clinical categories. CD4 + T cell categories
A Asymptomatic, acute HIV and PGL
B Symptomatic, not A or C conditions
C AIDS indicator condition
Category I > 500/µL (>28%)
A1
B1
C1
Category 2 : 200 to 499/µL (14-28%)
A2
B2
C2
Category 3 < 200/µL (1 month. • Unexplained persistent fever for >1 month (> 37.6°C intermittent or constant). • Persistent oral candidiasis (thrush). • Oral hairy leukoplakia. • Pulmonary tuberculosis within the last 2 years. • Severe presumed bacterial infections (e.g. pneumonia, empyema, pyomyositis, bone or joint infection, meningitis, bacteremia). • Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis. • Conditions for which confirmatory diagnostic testing is necessary. • Unexplained anemia (hemoglobin 100,000 copies of HIV-RNA/ml) initial viral loads is mostly used in less advanced cases. • The NRTI + NNRTI PI is generally reversed for advanced disease or those with short life expectancy or repeated failures, because of risk of multiclass drug resistance and high toxicity. • Four drug regimens have also been tested, but their superiority is not established.
Suggested Reading
Highly Active Antiretroviral Therapy (HAART) • HAART are combinations involving a protease inhibitor and other antiretroviral drugs—nucleoside reverse transcriptase inhibitors (NRTIs) and Non-nucleoside reverse transcriptase inhibitors (NNRTIs)—which have reduced the incidence of opportunistic infections. • It has extended life substantially and decreased the infective load of HIV and other viruses. • Orofacial disease caused by HIV infection has been significantly reduced by HAART.
Therapeutic Regimen • Treatment should be aggressive (HAART) aiming at suppressing plasma viral load to undetectable levels (20 mg/ day). Short term high dose therapy, alternate day therapy and topical administration produce minimal adrenal side effect and little adrenal suppression. In long therapy where large dosage are employed, alternate day therapy is more effective and tolerable to patient due to less side effect, as there is recovery period between each dose is equally effective. When the drug has to be used in large dosage, short acting synthetic steroids with minimal mineralocorticoid effect is to be selected. The placenta metabolizes hydrocortisone and prednisolone to the less active cortisone and prednisone. Unlike mother the fetus cannot convert cortisone and prednisone to hydrocortisone and prednisolone. By contrast dexamethasone and betamethasone cross the placental barrier to achieve high concentrations in the fetal circulation and can suppress the fetal HPA axis. Therefore in a pregnant woman needing treatment with a glucocorticoid, prednisolone should be used in preference to dexamethasone and betamethasone.
Classification Glucocorticoids • Short acting [biological half life less than 12 hours] • Hydrocortisone (cortisol) • Cortisone • Intermediate acting [biological half life in 12-36 hours] • Prednisolone • Methyl prednisolone • Triamcinolone
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Corticosteroids 1003 • Long acting [biological half life more than 36 hours] • Paramethasone • Dexamethasone • Betamethasone Mineralocorticoids • Deoxycorticosterone acetate (DOCA) • Fludrocortisone • Aldosterone
• Calcium metabolism and bone—glucocorticoids antagonize the action of vitamin D on the gut and reduce absorption of calcium. Given in large doses for prolonged periods, they interfere with the development of cartilage and inhibit linear growth in children. • Electrolyte and water metabolism—it promotes sodium retention and potassium excretion
Anti-inflammatory Action
Glucocorticoids Mechanism of Action Cellular Action • Activation of receptor—corticosteroids penetrate the cells and bind to the specific receptor protein leads to activation of receptor in the cytoplasm of cell called as ‘Human-Glucocorticoid receptor’ resulting from structural changes in the protein. • Specific protein synthesis—this receptor moves to nucleus, interacts with specific site on chromatin and induces transcription of specific mRNA results in specific protein synthesis. This process takes at least 30-60 min. Once appropriate proteins are synthesized, effect persists for long time.
Metabolic Action • Carbohydrate and protein metabolism—they prevent conversion of amino acid into proteins i.e. antianabolic effect. They promote gluconeogenesis of new glucose formation in liver. Glucocorticoids stimulate gluconeogenesis and glycogen synthesis in the fastest state. Glucocorticoids increase the serum glucose level and thus stimulate the insulin release and inhibit the uptake of glucose by muscle cells. • Fat metabolism—act directly- breakdown of Triglycerides to Fatty acids (lipolysis), Indirectly-formation and storage of fats (lipogenesis). It stimulates the hormonesensitive lipase and thus lipolysis. The increased insulin stimulate lipogenesis and inhibit lipolysis leads to net increase in fat deposition and also increases release of fatty acid and glycerol into the circulation. Prolonged administration of glucocorticoids causes a redistribution of fat in the body, with loss from extremities and a deposition in the neck (buffalo hump) and supraclavicular area and face (moon face). Hence, the release of amino acid from muscle catabolism, supply of glucose from gluconeogenesis, inhibition of peripheral glucose uptake, stimulation of lipolysis, all are contribute to maintain adequate supply to brain and body.
Glucocorticoid dramatically inhibits the manifestations of inflammation viz. edema, fibrin deposition, capillary dilatation, migration of leukocytes to the inflamed region and phagocytosis. After glucocorticoid administration, changes are maximal at 6 hours and are dissipated in 24 hours are as follows: • Increases in neutrophils concentration—It is due to increased influx of neutrophils from bone marrow into the blood and decreased migration from blood vessels leading to reduction in the number of cells at the sites of inflammation. • Decrease in lymphocytes concentration—T lymphocytes are decreased more as compared to the B lymphocytes. Decrease in concentration of monocytes, eosinophils, basophils due to their movement from vascular bed to lymphoid tissue. • Inhibition of macrophage migration factor—it inhibits the macrophage-migration inhibition factor, tumor necrosis factor, interleukin (IL-1,IL-2,IL-3,IL-6). • Reduction of prostaglandin—it influences the inflammatory response by reducing the prostaglandin, leukotriene and platelet activating factor results from activation of phospholipase and decrease expression of cyclooxygenase. • Vasoconstriction—it causes vasoconstriction when applied directly to the skin by suppressing the mast cell degranulation. It also decreases the capillary permeability by reducing the amount of histamine released by basophils and mast cells.
Other Effect • Catabolic action—corticoids stimulate protein and RNA synthesis. They have catabolic action on lymphoid, connective tissue, muscle fats and skin. • Hemopoietic action—glucocorticoids increases the hemoglobin and red cell content of the blood, but decreases the blood lymphocytes, eosinophils, monocytes, and basophils due to their redistribution rather than destruction. It causes an increase in polymorphonuclear leukocytes and platelet count in the blood.
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• Immunosuppressive action—glucocorticoids do not significantly decrease the concentration of antibodies in the circulation and thus the individual exhibits normal antibody-antigen response. It prevents manifestations of humoral and cellular hyperimmunity. It inhibits the development of early step of immunity by disturbing the intracellular communication among the leukocytes or function of lymphocytes. It interferes with immune mechanism by influencing the function of macrophage by inhibiting tumor necrosis factor, interleukins. • CNS effect—it maintains level of sensory perception and normal level of excitability of neurons. Pharmacological doses show mild euphoria. Large dosage of glucocorticone may increase intracranial pressure. • Gastrointestinal effect—it increases the basal and nocturnal gastric acid secretion. It also aggravates peptic ulcer. • Anti allergic—thymus derived lymphocytes are susceptible to the actions of corticosteroids so that cell immune responses are modified following their administration. Corticosteroids, thus, in large doses can cause lysis of the T cells, prevent homograft rejection and suppress cell mediated hypersensitivity reaction. • Suppress release of hormone—it suppresses the pituitary release of ACTH, GH, TSH, LH. • Development of fetal lung—important effect on the development of fetal lung like production of pulmonary surface active material which is required for airbreathing is stimulated by glucocorticoids. • DNA synthesis—it inhibits cell division or synthesis of DNA.
Uses • Substitution therapy—it is used as substitution therapy in Addison’s disease and hypopituitarism. • Intensive short term therapy—it can save life and reduce morbidity in certain potentially lethal conditions in which inflammatory or the metabolic response of the body itself threatens life. For example, allergic emergencies such as anaphylactic shock, status asthamaticus, acute necrotizing vasculitis, etc. • Prolonged high dose suppressive therapy—it is indicated in acute rheumatic fever, ulcerative colitis, subacute hepatitis, autoimmune hemolytic anemia, pemphigus, ITP, Hodgkin’s disease, etc. • Low dose chronic palliative therapy—use of small doses of glucocorticoids as an adjunct to some other drugs like salicylates in rheumatic arthritis. Chronic suppression of pituitary ACTH secretion is indicated in congenital, virilizing adrenocortical hyperplasia.
• Topical application—topical application is found invaluable in many dermatological, oral, ocular and external ear conditions. • Diagnostic test—dexamethasone suppression of adrenal function, cortisone test in hypocalcemia and prednisolone test to distinguish intra- and extra-hepatic obstructive jaundice. • Dental use—corticosteroids because of their antiinflammatory action are used in many oral diseases. Corticosteroids are used in the management aphthous stomatitis, pemphigus, erythema multiforme, lichen planus, oral submucus fibrosis, and sinusitis. • Miscellaneous—it is used in a variety of conditions like Bell’s palsy, infective hepatitis, encephalitis.
Precaution • History—before starting the therapy, enquire about history suggestive of peptic ulceration. • Glucose estimation—examine urine periodically for sugar. • Weight and blood pressure record—keep record of weight and blood pressure. • Do not stop abruptly—instruct the patient not to stop the therapy abruptly. • Increase dose—if the patient develops an acute infection or has to undergo therapy, increase the dose of steroids. • Restrict use—glucocorticoids must not be used in the presence of infection unless the latter can be simultaneously treated with antibiotics.
Hydrocortisone (cortisol) It is naturally occurring steroid. It acts rapidly but has short duration of action. • Action—anti-allergy, anti-inflammatory. • Therapeutic uses— • OSMF—hydrocortisone injected intralesionally in the areas of fibrosis in dose of 25- 50 mg/ ml fortnightly. Topically, it is applied intraorally on the oral mucosa can be combined with orabase. Hydrocortisone 25 mg tablets in dose of 100 mg/day can be given systemically helps in relieving burning sensation. Hydrocortisone 25 mg tab. Can be combined with Dexamethasone 90 mg can be given at biweekly interval. It is mainly attributed to fibrinolytic, antiallergic, anti-inflammatory action by decreasing fibroblastic production and deposition of collagen. • Aphthous ulcer—Topical application of steroid with Orabase is effective in case of aphthous ulcer. Presence of saliva may dilute drug and effectiveness. Intralesional injections of hydrocortisone acetate (25 mg/ ml) into the mucosal lesion is given.
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Corticosteroids 1005 • Desquamative gingivitis—topical hydrocortisone cream and ointment (0.25- 0.5%) are applied intraorally to the affected lesion gives better result. • Osteoarthritis—intraarticular injections (25 mg/ ml) are indicated in acute inflammation. Repeated injections may be associated with painless destruction of bone joint. • Addison disease—cortisol is administered 20- 30 mg / day in divided doses usually 20 mg in morning and 10 mg in afternoon as best replacemental therapy. • Congenital adrenal hyperplasia—hydrocortisone is given orally as 0.6 mg/kg dose in 2-4 divided doses. • Lichen planus, pemphigus, and eczematous skin disease— for oral lesions, topical application of creams and oral suspensions, ointment 1 % applied locally twice a day. Severe episodes of pemphigus require systemic steroid administration which may be life saving drug. • Ulcerative colitis, Crohn’s disease—administered orally as a lower dose on alternate day with hydrocortisone 100 mg gives better results. Care should be taken in high doses as it may result in intestinal perforation. • Shock, status asthmatics—100 mg I.V bolus + 100 mg infusion in every 8 hrs may be given. • Trade name—CORTEF, EFCORLIN, WYCORT, ORABASE-HCA. • Preparation—Oral: 5, 10, 20 mg tablets. Topical: 1% eye drop-solution, 0.025 nasal drops and 0.25-2.5% skin creams, ointment. Hydrocortisone acetate—Parenteral: 25, 50 mg/ml suspension for soft tissues intralesional/intraarticular inj. Hydrocortisone sodium phosphate—Parenteral: 50 mg/ml for IV, IM, SC inj. Hydrocortisone sodium succinate—Parenteral: 100, 250, 500, 1000 mg/vial for IV, IM injection.
Cortisone It is next potent drug than hydrocortisone. Nowa days it is used very occasionally. • Action—anti-allergy, anti- inflammatory. • Therapeutic uses— • Oral submucous fibrosis—cortisone can be given orally in dose of 25 mg tablet. Inj.25 mg/ml can be given intramuscularly, gives better results. • Addison disease—Daily dose of 25-40 mg is given as a maintenance dose. • Hodgkin lymphoma—systemic use of cortisone in lower doses can be used. Thrombocytosis /Thrombocytopenia. Drugs can be used systemically. • Trade name—CORLIN, CORTONE • Preparation available—oral: 5, 10, 25 mg tablets. Parenteral: 22, 25 mg/ml of solution.
Prednisolone It is four times more potent than hydrocortisone. It is most selective glucocorticoid. • Action—it is mainly anti-inflammatory but, has little sodium retentive activity. It also used as an anti-allergic and immunosuppressive. • Therapeutic uses— • Rheumatoid arthritis—initial dose of prednisone 10 mg/day is given in divided doses. Initial dose should be small and increases gradually until desired degree of control is achieved. • Collagen disease—collagen diseases like Polyarteritis nodosa, Granulomatous polyarteritis. Prednisone 1 mg/kg daily is given. If favorable results are not achieved, dose is increased in 20 mg daily and then reduced gradually to 5 mg/ week. • Systemic lupus erythematous—prednisone used intramuscularly and intravenously. For oral use, topical application of prednisone 2-3 times daily can be used. • Leukemia—mainly in acute lymphoblastic leukemia, it is used as maintenance dose. It can be used orally for at least 2-3 years. • Erythema multiforme—prednisone gives in dose of 30 mg/day for several days and terminate after symptoms subsides. It is life-saving drug in severe form of erythema multiforme. • Pemphigus—prednisone is used topically mainly for oral lesions. Intralesional injections give better results to subside oral lesions. It is used systemically to bring the disease under control. After that, the dose is reduced. Mainly prednisone with immunosuppressive drugs like cyclosporine is effective in pemphigus. • Bullous pemphigoid—systemic prednisone with immunosuppressive drugs with dapsone is given in lower doses for shorter period of time. • Behçet’s syndrome—systemic prednisone with immunosuppressive drugs is used in life threatening condition. It can be used to reduce ocular, oral, genital manifestation. Intralesional drugs are administered in mucocutaneous lesions. Topical application for oral mucosal lesion which is not controlled by systemic therapy. • Rheumatic arthritis—prednisone dose of 40 mg/day in divided doses is given. • Bronchial asthma—Oral administration of prednisone is also useful. prednisone of 40-60 mg is useful to control status asthmaticus and then withdrawn gradually. Recently, inhaled corticosteroids are found for the treatment of bronchial asthma.
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1006 Textbook of Oral Medicine • Malignancies—prednisone is most commonly used at the dose of 30 mg/ day gives symptomatic relief in advanced malignancies. • Post herpetic neuralgia—prednisone 40-60 mg given orally is used daily for 1-2 weeks. Intramuscular and intravenous injections can be given in a patient with age more than 60 years. Other diseases like amyloidosis, cyclic neutropenia, purpura, urticaria, renal diseases. • Trade name—DELTA-CORTEF,PRELONE,WYSOLONE, METICORTEN. • Preparation available—oral: 5, 10, 20 mg tablets. 15 mg/5 ml syrups. 5 mg/ml suspension as pediatric drops. Parenteral: Injections of 25, 50 mg/ml for soft tissue, intramuscular, intralesional, intravenously.
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It is slightly more potent and more selective than prednisone. • Action—anti-inflammatory, antiallergic, immunosuppressive. • Therapeutic uses—same as that of Prednisolone. Initial effect of methyl prednisolone is for pulse therapy. It is mainly used for rheumatoid arthritis, renal transplantation and ulcerative colitis. • Trade name—MEDROL, DEPOMEDROL. • Preparation available—oral: 2 mg tablets. Parenteral: 20, 40, 80 mg/ml for I.M, I.V, Intralesional, intra-articular.
• Ocular disease—ocular lesions of interstitial keratitis, spring cataract, iritis are treated by topical triamcinolone 0.1% eye drops for every 4 hours in day time. • Osteoarthritis—intraarticular injections are given in the dose of 20 mg/ml. • Purpura—in adults, triamcinolone 40 mg/ml is given intramuscularly until the platelet level rise to normal than tapered until the drug is withdrawn. • Contact cheilitis, exfoliative cheilitis, plasma cell cheilitis, granulomatous cheilitis—triamcinolone is applied topically (0.2%) gives symptomatic relief. Repeated intralesional injections into the lips may give better result in very few weeks. • Benign mucous membrane pemphigoid—topical or intralesional steroids injections are helpful. • Hemangioma—intralesional and intramuscular injections of steroids are administered for better results. Injections are usually given at different intervals. It is commonly combined with immunosuppressive drugs are given in increasing frequency as it may cause hyperglycemia and osteoporosis by using single dose. • Trade name—KENACORT, KENALOG, LEDERCORT, ARISTOCORT, ATOLONE • Preparation available—Oral: 1, 4, 8 mg syrup. Topical: 0.1% eye drops, skin ointment. Parenteral: 3, 10, 40 mg/ ml for I.M, intraarticular, intralesional injections.
Triamcinolone
Dexamethasone
It is slightly more potent than prednisolone but highly selective glucocorticoids. • Action—immunosuppressive, anti-inflammatory, hemopoietic action. • Therapeutic uses— • Lichen planus, oral submucus fibrosis, aphthous ulcer— injections of 0.5 to 1 ml triamcinolone acetonide (1020 mg/ml) directly into the mucosal lesions are usually repeated at different interval. Topical application of triamcinolone 0.1% ointment is applied intraorally 2-3 times a day on mucosal lesion gives relief in several days. But presence of saliva dilutes the drug and thus reduces the effectiveness. • Bronchial asthma—triamcinolone systemic dose of 40 mg given orally. Injections of 40 mg/ml are given IM. • Rheumatoid arthritis—for relief of painful symptoms in the joint. Intraarticular injections of triamcinolone 10 to 40 mg for large joints and 2 to 6 mg/ml for small joints are administered. intralesional injections may be given for mucosal lesions.
It is very potent and highly selective glucocorticosteroids. It is mainly used for adrenal cortical suppression. Dexamethasone has no adverse effect on fluid retention and in hypertension. • Action—immuno-inflammatory, Antiallergic • Therapeutic uses— • Allergic diseases, serum sickness, urticaria, hay fever, contact dermatitis, angio-neurotic edema—dexamethasone 24 mg is administered IV. Topical application by using skin ointments on affected areas 2-4 times a day. • Benign migratory glossitis—used by topical application on affected tongue 4-5 times a day. • Ocular diseases—in case of inflammatory and allergic conditions of eyes, dexamethasone ointments, 1% eyedrops, every 4 hours in day time and at bed time. • Shock, cerebral edema—dexamethasone is mainly used in the dose of 24 mg/ml IV infusion and IM injections because this drug has fluid retention capacity. Topically can also be used. • Trade name—DECADRON, DECADRON-L, WYMESONE.
Methyl Prednisolone
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Corticosteroids 1007 • Preparation available—oral: 0.25, 0.5, 0.75, 1, 2, 4, 6 mg tablets. Topical: 0.1% eye drops, ear drops, skin ointments. Parenteral: 4, 8, 10, 20 mg/ml for IV, IM, intralesional and intra-articular injections. To give IV, only 24 mg/ml suspension is used. And for intraarticular injections, 16 mg/ml suspensions are used.
Betamethasone • Action—this drug has similar action that of dexamethasone. • Therapeutic uses—same as dexamethasone. It is mainly preferred in cerebral edema and shock. • Trade name—Celestone, Betnovate, Betnesol, Betnelan. • Preparation available—oral—oral drops 0.5 mg/ml, tablets 0.5-1 mg. Topical—0.1% eye drops, ointments, 0.05% nasal drops, 0.12% skin creams. Parenteral— 4 mg/ml for IM, IV, intralesional and intraarticular.
Adverse Effects of Glucocorticoids Long terms administration of glucocorticoids can cause adverse effects. These are deposition of fat in cheeks, shoulders, edema and weight gain, osteoporosis, acne, hypertension, striae/Bruises, diabetes, glycosuria, peptic ulcer, growth retardation mainly in children, delayed wound healing and adrenal suppression.
Contraindication • Cushing syndrome (absolute contraindication)—most patients who are given daily doses of 100 mg of hydrocortisone of longer than 2 weeks undergo series of changes termed as cushing syndrome. It is characterized by fat deposition, rounding appearance of faces (moon facies), weight gain, muscle wasting, thinning of the skin with striae and bruising, hyperglycemia, development of osteoporosis, diabetes and impaired wound healing. • Diabetes mellitus—steroid containing fluorine intensifying diabetes more than other and so it should be avoided in diabetes. • Hypertension—it increases intracranial hypertension due to hypokalemia, hypochloremic alkalosis, there is increased in blood pressure. • Pregnancy and lactation—it is best to avoid in 1st trimester of pregnancy due to risk of cleft palate and intrauterine growth retardation in the fetus. • Peptic ulcer—risk of bleeding and silent perforation of ulcers may occur. Dyspeptic symptoms are frequent with high dose therapy. • Osteoporosis—it appears to antagonize the effect of vit.D on calcium absorption and on hemopoietic system, increase in the number of platelets and red blood cells.
• Glaucoma—steroid increases the intraocular pressure. • Heart disease like CHD—sodium retention action of corticosteroid may aggravate the CHF. • Herpes simplex infection—corticosteroid are only palliative, do not remove the cause of inflammation. It favors the spread of infections as the capacity of defensive cells to kill microorganisms is impaired.
Caution Glucocorticoids should be used cautiously in pregnancy, tuberculosis, epilepsy, in debilitating and other patients.
Newer Drugs • Budesonide (TN: Budecort)—preparation available-topical 100,200,400 mcg/puff inhaler. It is used mainly in chronic bronchial asthma. Used inhalation in the dose of 200-1600 mcg/day in adults and 200-800 mcg/day in 2-4 divided doses in children. • Clobetasol (TN Emosone)—preparation available-topical 0.05% ointments, lotion, gel. It is used in dermal infections by topical application on skin 2-4 times a day. • Fluocinolone (TN: Flucort 0.05%) • Fluticasone (Flixotide 25, 50 mcg/puff inhalers)—it is new inhaled steroid with high inflammatory activity and negligible systemic absorption. It is used as aerosol 2 times a day for prophylaxis of asthma. • Halocinonide (TN: Clobederm-H 0.025 to 0.1%) • Mometasone (TN: ELOCON 0.1%)—they are newer drugs used mainly for dermal infections twice a day on affected skin.
Mineralocorticoids Important mineralocorticoids are aldosterone, fludrocortisone, desoxycortisterone.
Mechanism of Action Mineralocorticoids have main effect on electrolyte (sodium, potassium) and fluid balance. They have sodium retaining and potassium depleting action. Hence, it influences the salt and fluid water equilibrium in the body. Mineralocorticoids act by binding to the receptors present in the cytoplasm of principal cells forming drug-receptor complex which activate the series of events similar to described for glucocorticoids. It increases reabsorption of sodium and secretion of potassium by electrolyte and water metabolism. Single dose of aldosterone produces sodium retention and increased urinary loss of potassium. As a result of
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aldosterone deficiency the renal tubules are unable to conserve sodium.
• Systemic hypotension • Weight gain.
Desoxycortisone Acetate (DOCA)
Contraindication
It has mainly mineralocorticoid activity. It serves as precursor of Aldosterone. • Action—sodium and potassium balance retaining action. • Therapeutic use— • Hypoaldosteronism—it is given systemically by intramuscular injection at weekly interval in dose of 20 mg/ml. • Severe postural hypotension—as this drug has sodium retaining action, it cures the manifestations in short period of time by using sublingual administration of DOCA in the dose of 2-5 mg/day. • Addison disease—2-5 mg sublingually, 10-20 mg intramuscularly once or twice a week is quite effective in Addison’s disease. It can be given as replacemental therapy. • Trade name—Percorten • Preparation available—Oral: 2-5 mg sublingually. Parenteral: 5, 10, 20 mg/ml IM.
• • • •
Fludrocortisone It is more potent mineralocorticoid having some glucocorticoids action. • Action—sodium retention action. Anti-inflammatory action only at high doses. • Therapeutic uses— • Addison’s disease—0.1mg tablets are used as initial doses; gradually dose is reduced to 0.1 to 0.2 mg daily as maintenance dose. It is used to replace the Aldosterone. • Autonomic neuropathy—fludrocortisone is drug of choice for autonomic neuropathy. It is used to achieve vasoconstrictor tone. It is used in the dose of 0.5 to 1 mg/day. • Hypotension—as the drug has sodium retention capacity. It is used mainly in hypotension. • Congenital adrenal hypoplasia: Tablets of 0.1 mg/day is used because in such patients, salt resting is comparatively more. • Trade name—Florinef • Preparation available—Oral: 0.1 mg tablets.
Adverse Effect • • • •
Edema Hypokalemia Progressive rise in blood pressure Fluid and electrolyte balance disturbance
Hypertension Systemic heart diseases Osteoporosis Cushing syndrome.
Dental Consideration • Physician consultation—it is preferable to consult patient physician before carrying out any dental treatment in patient on steroid therapy to determine any alteration required in the dose before dental treatment. • Osteoporotic changes—patient receiving long term steroid therapy results in adrenal suppression causes osteoporotic changes in jaw bone and degenerative changes in periodontium. So; dentist should look for such symptoms. • Stressful condition—patient may show hypotension, vomiting, glucose intolerance, arthralgia in stressful conditions. In such conditions, majors should be taken to support blood pressure, fluid volume and to maintain normal electrolyte balance. • Minimum stress dental treatment—dental treatment should be carried out with minimum stress. Minor dental procedure like minor restoration, minor biopsy, denture orthodontic adjustment, scaling and prophylaxis may not required any alteration in the dose of corticosteroids. • Doubling the dose—for moderate stressful dental procedure in suppressed patients, normal dose should be doubled 8 hours before the procedure like 3rd molar impaction, vertical extraction, incision and drainage of dental infection. The dose should be tapered back to normal during post operative period after the cessation of pain, fever and other symptoms of stress. • Major dental surgery—for major dental surgery under general anesthesia, due to facial trauma, severe oral infection and Orthognathic surgery, parental administration of corticoids 100 mg cortisol intramuscularly 8 hours before the procedure followed by intravenous infusion of hydrocortisone ( 300 mg cortisol) during procedure is given.
Suggested Reading 1. Barar FSK. Essential of pharmacotherapeutics (3rd edn), S Chand and Company Ltd, 2000. 2. Chaudheri. Quintessence of medical pharmacology (3rd edn), Central publisher, 2005.
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Corticosteroids 1009 Summary chart
Drugs
Trade name
Route
Dose
Indications
Contra-indications
Adverse effects
Hydrocortisone
Wycort (2.5%) ointment Orabase HCA (0.5%) Locoid cream (0.001%) Cortef (5 mg tablet ) Aeroseb HC (0.5%) Efcorlin
Topical Topical Topical Oral Inhalation
3-4 times 3-4 times 3-4 times 100 mg 6 hourly 1-2 ml per day
Lichen planus Erythema multiforme, Pemphigus, recurrent aphthae, desquamative gingivitis, oral submucous fibrosis, Asthma, Osteoarthritis, Addison’s disease
Viral infection HSV I and II Diabetes mellitus. TB, Osteoporosis, pregnancy and not to be given IV/IM
Cutaneous atrophy. Susceptibility to infection, delayed healing, glaucoma
Prednisolone
Predicort Prid Wysolone,Deltacortef, meticorten, prelone
Oral
5-60 mg/day in divided doses
Lichen planus, Erythema multiforme, serum sickness, Pemphigus, thrombocytopenia, Behçet’s syndrome, post herpetic neuralgia, malignancies.
Hypersensitivity, Viral infection, Diabetes mellitus, TB, peptic ulcer
Hyperglycemia, muscular weakness, psychosis, HPA axis suppression
Triamcinolone
Kenolog cream (0.1%)
Topical
Kenolog spray (0.2%) Kenacort (1,4,8 mg) Tac-3 suspension (3 mg /ml) Aristcort suspension (25 gm/ml) Ledercort (4 mg) Ledercort ointment 0.1% Pericort-4
3-4 times daily Inhalation 40-100 mg day Oral 4-2 mg /day Intralesional 02-03 ml/day Intralesional 02-03 ml/day
Lichen planus, Viral infection, Erythema multiforme, TB, not to be recurrent aphthae, given IV/IM desquamative gingivitis, oral submucous fibrosis, Asthma, contact cheilitis, hemangioma.
Cutaneous atrophy, Susceptibility to infection, delayed healing, Muscular weakness and psychosis
Lichen planus Viral infection Erythema multiforme, Live viral recurrent aphthae, immunization desquamative gingivitis, oral submucous fibrosis, Asthma, Mucous membrane pemphigoid
Secondary infection, Delayed healing, Cutaneous atrophy
Betamethasone Diprovate cream (0.05%) Valisone cream (0.1%) Betnovate cream (0.12%) Diprosone (0.1%)
Topical Topical Topical Inhalation
3-4 3-4 3-4 3-4
Fluocinolone
Topical Topical
3-4 times daily Lichen planus, 3-4 times daily recurrent aphthae,
Flucort (0.025%) oint Cuti cream (0.025%)
times times times times
3. Craig CR, Stitizel RE. Moderate pharmacology with clinical application (5th edn), Little Brown and company, 1997. 4. Gomes MW. Synopsis of medical pharmacology (1st edn), National Series, 2002. 5. Hardman, Limbird, Gilman. Goodman and Gillman: the pharmacological basis of therapeutics (10th edn), McGraw Hill, 2001. 6. Mycek MJ, Harvey R, Champe P. Lippincott illustrated review: pharmacology, (2nd edn), Lippincott Williams and Wilkins publisher.
daily daily daily daily
Viral infection
Secondary infection Delayed healing, Cutaneous atrophy
7. Salil and Bhattacharya, Sen A, Ray A. Pharmacology (2nd edn), Elsevier, 2003. 8. Seth. Textbook of Pharmacology (2nd edn), Elsevier, 1999. 9. Sharma HL, Sharma KK, Gupta DK. Textbook of dental pharmacology (1st edn), Paras Publisher, 2008. 10. Tripathi KD. Essential of Pharmacology for Dentistry (1st edn), Jaypee Brothers Medical Publishers, 2005. 11. Yagiela, Neidle, Dowd. Pharmacology and thereaputics for dentistry (1st edn), Mosby Harcourt India, 2001.
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Desensitizing Agents, Gum Paints and Mouthwashes
Dentinal Hypersensitivity Introduction It is certain that the teeth of man have been hurting for many thousands of years. Pain has been so closely associated with dentistry that the word “pain” and “dentistry’ ’have almost become inseparable and one of the most important objective of dentistry has been the control and elimination of the pain. Clinical experience suggests that dentin hypersensitivity is a relatively common cause of pain associated with the teeth. Despite this, the condition has been justifiably described as “an enigma” being frequently encountered but ill understood. Even the suitability of the term “dentin hypersensitivity” may be questioned. Such symptoms as sharp, painful, responses of short duration are associated with many conditions in which dentin is exposed including the dental caries. Furthermore, there is no evidence to indicate that “hypersensitive” dentin differs in any way from normal dentin (or that specific pulpal changes occur). The term “dentin sensitivity” may be more appropriate. The international association for the study of pain (IASP) termed hypersensitivity as “allodynia” which is pain resulting from a non-noxious stimuli to normal skin and hence, it can be appropriate to call dentinal hypersensitivity as “allodontia”.
• Age group—dentinal hypersensitivity has been shown to peak in 20 to 30 year olds and then rise again when in their 50’s. The condition generally involves the facial surfaces of teeth near the cervical aspect and is very common in premolars and canines. • More common in periodontal patient—72-98% of the periodontal patients suffer from dentin sensitivity due to loss of attachment and exposure of root surface. Patients undergoing periodontal treatment are particularly susceptible to this condition because of the recession following periodontal surgery or loss of cementum following non-surgical periodontal therapy. • More common in females—females are more commonly affected than males as females because of esthetic reasons, females tend to brush their teeth more vigorously than males. • More common on facial surface—the condition generally involves the facial surfaces of teeth near the cervical aspect and is very common in premolars, canines and second premolars. • More common on left side—left side of the arch is more commonly affected than the right side of arch (Righthanded tooth brushers tend to use more force on left buccal surfaces).
Definition Prevalence of Dentinal Hypersensitivity • Incidence—the prevalence of dentinal hypersensitivity has been reported over the years in a variety of ways: Cross Sectional Surveys have shown dentinal hypersensitivity to be ranging anywhere in between 8%57% of adult dentate population and up to 30% of adults at some time during their lifetime. It is claimed that 14.3% of all dental patients have some degree of dentin hypersensitivity.
Short, sharp pain arising from exposed dentin in response to thermal, evaporative, tactile, osmotic or chemical stimuli which cannot be ascribed to any other form of dental defect or pathology. Common terminologies used for hypersensitivity are dentin sensitivity, dentin hypersensitivity, dentinal hypersensitivity, cervical hypersensitivity/sensitivity, root hypersensitivity/ sensitivity, and cemental hypersensitivity/ sensitivity.
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Desensitizing Agents, Gum Paints and Mouthwashes 1011 Mechanism of Dentin Sensitivity The dental pulp is richly innervated by variety of nerve fibers. (Only a few of the 1000 to 2000 nerves found in each tooth reach dentin). Pulp is richly innervated by both myelinated (A fibers -25%) and unmyelinated (C fibers 75%)—both are responsible for sensitivity of dentin. According to conduction velocity, the nerve units are classified into: • A fibers—they are having conduction velocity of more than 2 m/sec. A fiber responsible for dentin hypersensitivity. They induce sharp pain in teeth. • C fibers—they are having conduction velocity of less than 2 m/sec. C fibers activated only when stimulus reaches the pulp proper (intense heating). It may play a role in mediation of dull radiating pain associated with pulpal inflammation.
Causes and Clinical Features of Dentin Hypersensitivity • Causes—dentin exposure due to loss of enamel from the crown of the tooth or denudation of the root surface by loss of cementum and overlying periodontal tissues. Factors responsible for it are enamel loss, occlusal wear (attrition), tooth brushing (abrasion), dietary erosion, parafunctional habit, loss of cementum, denudation of root surface (gingival recession), chronic periodontal disease, following periodontal surgery, tooth abnormally positioned in arch, root preparation, leaching margins of restorations. Improper oral hygiene technique and dental caries. • Symptoms – • The chief symptom is a sharp, sudden pain of short duration, although some patients complain of dull, lingering sensitiveness. • Sensitivity to cold, but pain may also be elicited by the use of toothpick and or brushing. • In some cases, hot liquids and sweet or sour foods may evoke a response. Although most teeth are sensitive to more than one stimulus, not all hypersensitive teeth respond to the stimulus.
Theories of Dentinal Hypersensitivity Transducer Theory According to this theory the “synaptic like” relationship exists between the terminal nerve endings and the odontoblastic process. But if true synapse were present between these two elements to facilitate the transmission of dentinal sensation then neural transmitting substance such as acetylcholine would be expected in this area of the odontoblastic process
and the predentin. There is no direct evidence for the presence of acetylcholine activity in the neural transmission in the pulp.
Modulation Theory On any irritating stimulus to the dentin, the odontoblasts may become injured and subsequently release a variety of neurotransmitting agents as well as vasoactive and pain producing amines and proteins. These substances may modulate associated nerve fiber action potentials by increasing neuronal cramp levels through cell membrane adenylate cyclase receptors.
Odontoblastic Transduction Theory Odontoblasts are neural crest in origin. This theory assumed that odontoblasts extend till the periphery of the dentinal tubules and the stimuli excites the odontoblastic process. The membrane of odontoblasts may come in close apposition with that of nerve endings in the pulp or in the dentinal tubule. These odontoblasts transmit the excitation to these nerve endings but odontoblastic process extends only part way through dentin and odontoblast membrane potential is too low to permit transduction.
Gate Control Theory and Vibration According to this theory, the medullated nerves, i.e. A-delta fibers, can accommodate the vibrations without getting excited but unmyelinated nerve fibers, i.e. C-fibers, cannot accommodate such vibrations and get stimulated unproportionately leading to sensitivity.
Hydrodynamic Theory It is the most widely accepted theory till date. In 1966, Branstromm provided the scientific explanation for hydrodynamic theory. Most dentinal stimuli cause pain by generating action potentials in intradental nerves through a hydrodynamic mechanism. Application of any stimuli to dentin increases the rate of fluid flow in dentinal tubules (Fig. 46-4). The fluid flow in turn excites nerve terminals at the inner ends of the tubules or in the outer layer of the pulp. (Exceptions to this are electric current and intense cold, which can stimulate pulpal nerves directly). Treatment of dentin hypersensitivity aims to interrupt this sequence of event by: • Creation of tubular plug—providing a chemical ion that can react with and precipitate one of the components of the protoplasmic fluid and thus create a tubular plug. • Sealing of dentinal tubules—sealing or physically occluding the outer end of dentinal tubules.
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1012 Textbook of Oral Medicine
Fig. 46-1: Excitation of sensory nerve ending of dentin can cause the dentinal hypersensitivity.
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Fig. 46-4: Increase fluid flow in dentinal tubules.
• • • • • •
The number and location of sensitive teeth The area of tooth from which the sensitivity originates The intensity of pain The trigger of stimulus which initiates sensitivity The frequency and duration of each episode Recent restorative, periodontal and hygiene treatment change in diet or oral hygiene aids or home bleaching.
Fig. 46-2: Heat—slow inward movement of dentinal fluid.
Differential Diagnosis of Dentinal Hypersensitivity • • • • • •
Fig. 46-3: Dehydration, cold and hypertonic solutions—outward movement of dentinal fluid.
The displacement occurs in either on outer or inward direction (Figs 46-1 to 46-3) and their mechanical disturbance activates the nerve endings present in the dentin or pulp.
Question to be asked for Diagnosis of Hypersensitivity • History and nature of pain
• • • • • •
Abscessed or non-vital tooth Cracked tooth syndrome Dental caries Diet sensitivity Genetic sensitivity Restorative sensitivity (Open or defective margins of restoration, fractured restorations) Bruxism Medication sensitivity Bleaching sensitivity Barodontalgia Gingival and periodontal pain Non-oral cause of dental pain like neurological causes, sinus pathology and psychogenic causes and atypical facial pain.
Clinical Examination for Diagnosis of Dentinal Hypersensitivity • • • •
Tactile examination Air flow from air-water syringe Percussion Biting pressure
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Desensitizing Agents, Gum Paints and Mouthwashes 1013 • • • •
Duration of pain after stimulus Radiography Gingival recession, loss of attachment, enamel loss Cracked cusps, fractured or leaking restoration, occlusal interface, hyperfunction.
Methods of Measuring Tooth Hypersensitivity To measure the sensitivity of tooth, following methods can be used. These are mechanical, chemical, electrical, evaporative, thermal, osmotic, verbal rating scale and visual analog scale.
Mechanical (Tactile Stimuli) • Instrument—it is done by explorer or probe. Constant pressure by probe (yeaple), mechanical stimulator and scaling procedure. • Identification of area of sensitive dentin—all clinicians use a dental explorer to identify regions of sensitive dentin. To understand how movement of an explorer across dentin can cause a hydrodynamic stimulus, one must consider the following. • Applying the force—although the use of a gentle force of 5 to 10 gm on the explorer seems as though it would be a trival stimulus, that force is localized on the tip of explorer which is about 500 µm2. This is sufficient to overcome the elastic limit of dentin, leading not only to compression of dentin and smear layer creation under the explorer tip but also to permanent (yet microscopic) deformation of dentin (scratch development). You should lightly pass a sharp dental explorer over sensitive area of a tooth and grade the response of patient on scale • Results—results of sensitivity test is as follows: • 0—no pain is felt • 1—slight pain or discomfort • 2—severe pain • 3—severe pain that lasts • A yeaple probe—it is a compact handpiece that contains an explorer line in an adjustable electromagnetic field. The force should be applied to the same area at 90° to the surface in a static inwardly directed manner. The patient is asked to response whether there is pain or no pain at each test. The instrument is adjusted in 5-10 gm increments from 10-70 gm. Each increasing force compress more and more dentin. People who are more sensitive tend to react with pain at lower forces than people who are not sensitive or those who are desensitized. • Chemical—it is done by hypertonic solutions like NaCl, Glucose, sucrose, CaCl2
Electrical Stimuli • Instrument—it includes electric pulp tester and dental pulp stethoscope. Pain response can be obtained from non-sensitive as well as from sensitive teeth. • Mechanism—dentinal fluid movement is not necessary for transmission of electrical stimulus, rather the presence of lower resistance organic material in cementum, enamel or dentin. Sensitive teeth show lower pain thresholds than healthy teeth. • Technique—electrode or probe should apply the electrical stimulus to tooth. Power source is required to vary the electrical stimulus and means of completing the electrical circuit. • Reference electrode—reference electrode, a saliva ejector connecting the patient to a pulp stimulating instrument— pulp stethoscope. • Current applied—electrical stimulus consisting of a direct current pulsed voltage between 0 and 150 or 0 and 300 volts. • Placing of probe tip—place the probe tip on the tooth surface, depress on/off switch. Rotate the ramp adjustment dial. Intensity of electrical stimulus rises from 0 to 25 rms volts and above patient feels the prepain (signals the operator to remove the probe that activates the recorder). • Evaporative stimuli—it includes cold air blast, air thermal system, air jet stimulator, temtronic device (microprocessor temp. Air delivery system)
Thermal Stimuli It is electronic threshold measurement device, cold water testing and heat. • Why cold stimuli is used—because patient are generally more sensitive to cold than to hot stimuli, the use of cold water (10, 15, 20, 25, 30°C) as a simple, quantitative stimulus is gaining in popularity. • Mechanism—thermal stimuli are effective of differences in thermal conductivity and coefficient of expansion or contraction of fluids and their container, enamel and dentin. Thus application of cold causes more rapid volumetric contraction of dentinal fluid that occurs in the dentin. This mismatch of volumetric changes produces negative intrapulpal and intradental pressures that displace mechanoreceptors and cause pain. Heating has the opposite effect but the same result, pain clinically, cold stimuli are more useful than hot stimuli for testing dentinal sensitivity. Patients tolerate cold stimuli better than hot stimuli, and there is danger of causing pulpal damage. • Isolation of tooth—in using cold water, each tooth is isolated with a rubber dam and water at a known temperature.
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1014 Textbook of Oral Medicine • Flowing of water—water is slowly flowed on the exposed dentin surface for a maximum for 3 seconds from a disposable plastic syringe. • Reaction of patient—the patient is forced to decide if that temperature causes pain or not and then the next lower temperature. It is tried until the patient responds unequivocally. • Air burst method—another method which can be used is directing a burst of air (room temperature) from a dental syringe onto the tooth to be tested. Room temperature is cooler than the tooth and cooling by this method can be easily detected as pain if the teeth are sensitive or parallel. 1 second blast from the air syringe, temperature between 65 and 70oC and pressure of 60 psi at right angle to the tooth near CEJ or exposed root surface is used.
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Osmotic It is subjective pain to a sweet stimulus. • Solution used—fresh saturated solution of sucrose; allowing it to reach room temperature. • Application—a cotton applicator saturated with the solution applied to the root surface, allowed to remain for 10 seconds. • Results— no pain—0 and pain –1.
Verbal Rating Scale (VRS) It presents a restrictive choice of words that may not represent the pain experience with significant precision for all patients (Huskinson 1974). Keel [1948] described a four point scale grading pain as slight, moderate, severe and agonizing. More recently, modification of this type of pain scale has been reported and are as follows: • Hansen 1992—simple binary pain scale- pain before the treatment/no pain after the treatment. • Gilliam and Newman 1993—it is as follows • 0 = no discomfort • 1 = mild discomfort • 2 = marked discomfort • 3 = marked discomfort that lasted 10 sec. • Gedalia et al 1987 • 1 = no pain • 2 = discomfort only • 3 = pain • 4 = severe pain • 5 = unbearable pain • Thrash et al 1992— • 0 = no significant discomfort • 1 = discomfort, but no severe pain • 2 = severe pain during application of stimulus • 3 = severe pain during application and continuing after application of stimulus.
• Schiff et al 1998 (Schiff’s cold air score) • 0 = tooth/ subject does not responds to air stimulus • 1 = tooth/ subject responds to air stimulus but does not request discontinuation of air • 2 = tooth/ subject responds to air stimulus and requests for discontinuation of air stimulus or moves away from stimulus. • 3 = tooth/ subject responds to air stimulus considers stimulus to be painful and requests for discontinuation of stimulus.
Visual Analog Scale (VAS) A Visual Analogue Scale (VAS) is a measurement instrument that tries to measure a characteristic or attitude that is believed to range across a continuum of values from none to an extreme amount of pain.
Method Ask the patient to indicate on the line where the pain is in relation to the two extremes. Ask the patient to mark on the line the point that they feel represents their perception of their current state (Fig. 46-5). The VAS score is determined by measuring in millimeters from the left hand end of the line to the point that the patient marks. When the VAS is properly explained to subjects, they can easily understand its use and successfully use it to indicate their level of pain response to hypersensitive stimuli. • Comparison between VAS and VRS—the VAS should be the more appropriate device than the VRS for measuring levels of sensitivity, pain during subject assessment and for measuring tactile and thermal stimuli of hypersensitivity. For those unable to read or to understand the linear visual analogue scale, picture of faces showing increasing distress can be used (Fig. 46-5). • Advantage of VAS—VAS is found to be reproducible therefore a very high correlation between successive measurements of pain severity has been noted.
Fig. 46-5: Visual rating scale is used to determine current state.
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Desensitizing Agents, Gum Paints and Mouthwashes 1015 • Disadvantage—disadvantage of visual analog scale is that patient tends to spread their responses over the entire scale regardless of the magnitude of the actual sensation.
Treatment of Hypersensitive Dentin Treating dentinal hypersensitivity can be challenging for the dental professional because of the difficulty related to measuring the pain response since the response varies from patient to patient. In addition if the dentin exposure is due to personal habits, it may be difficult for patients to change their behavior(s). If the diagnosis confirms dentinal hypersensitivity in the absence of underlying diseases or structural problems, then the following steps can be initiated: • Remove the risk factors by educating the patient about dietary acids and other oral care habits; • Recommend different toothbrushing methods, if appropriate; • Initiate treatment by recommending a desensitizing agent for home use; or • Applying topical desensitizing agents professionally. Grossmann’s ideal requisites for a desensitizing agent. • Non irritant—it should be non-irritant to the pulp. • Painless—it should be relatively painless on applications • Easy application—application of desensitizing agent should be easy. • Action—action should be rapid. • Long term effect—effect of desensitizing agent should be lone term. • No staining—no staining of tooth should not occur. • Consistency—desensitizing agent should be consistent in effectiveness.
Traditional Treatment of Dentinal Hypersensitivity Home care with dentifrices • Potassium nitrate dentifrices—Thermoseal, Thermoseal RA, Thermokind-f, Sensicure k, Sensodent-k, Sensodentkf, Promise, S • Senquel-f, Nitra, Denquel, Sensodyne. • Potassium oxalate dentifrice—Protect. • Sodium fluoride dentifrices—Thermodent, Thermoseal, Colgate, Thermodent, Proevident. • Sodium citrate dentifrices—Protect • Sodium monofluorophosphate dentifrices—Colgate, Thermokind-f, Senquel-f, Sensicure ,Nitra, Sensicure k, Aquafresh, Pepsodent, Sensodent-k, Sensodent-r. • Stannous fluoride dentifrice—Colgate gel, Colgate flourigard, Cibacca fluoride • Calcium chloride—Forhan’s • Calcium carbonate—Colgate, Meswak, Neem active tooth paste
• Strontium chloride—Thermoseal, Sensodyne, Thermodent, Senolin, Stolin, Sensicure • Triclosan—Thermokind-f, Sensicure, Pepsodent, Colgate, Senquel-f • Zinc sulfate—Sensicure, Sensicure k, Sensodent-r In-Office treatment (professional application in dental office) • Physical agents—composites, resins, varnishes, sealants, soft tissue grafts, GIC (glass inomer cement), and laser sealing off tubules. • Chemical agents—corticosteroids, silver nitrate, zinc chloride, strontium chloride, formaldehyde, calcium hydroxide, potassium nitrate, potassium oxalate, fluorides, sodium citrate, sodium monofluorophosphate.
Mechanism of Action of Desensitizing Agents Most of the therapies proposed till date for treatment rely on one of the two major suppressive mechanisms, i.e., sealing off the dentinal tubules or dampening neural impulses (potassium nitrate). Sealing off or the reduction in the diameter of the tubule so as to limit the displacement/ flow of fluid in the dentinal tubules can be achieved by • Formation of smear layer—it is produced by burnishing the exposed root surface. (orange woodstick or toothpick—partially occlude to dentinal tubule) • Formation of insoluble precipitates—topical application will form insoluble precipitates within tubules. for example• Oxalate—oxalate from potassium oxalate reacts with the ionized calcium in the dentinal tubule and forms insoluble calcium oxalate crystals. The crystals block the dentinal tubules and prevent fluid flow through the tubule. • Silver nitrate—silver nitrate precipitates protein constituents of odontoblastic processes, thereby partially blocking the dentinal tubules. • Sodium fluoride—sodium fluoride reacts with calcium and phosphate ions and forms calcium fluoride crystals thus blocking the dentinal tubule • Stannous fluoride—stannous fluoride forms dense layer of tin and fluoride containing tubular particles thus effectively blocking the dentinal tubules. • Fluoride iontophoresis—iontophoresis act by influencing ionic motion by electric currents which may enhance ion uptake by the dentinal tubules and aid in achieving desensitization. The process of influencing ionic motion by electric currents is known as electrophoresis, cataphoresis, or iontophoresis. The objective of fluoride iontophoresis is to drive fluoride ions more deeply into the dentinal tubule that cannot be achieved with topical application of fluoride alone.
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1016 Textbook of Oral Medicine
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• Impregnation of tubules with resins—sealing off the tubules with plastic resins: glass ionomer cement. • Sealing by dentin bonding agents—sealing off the dentinal tubule by dentin bonding agents. They seal the dentinal tubules and thus prevent pain producing stimuli from reaching the pulp. Procedure is as follows: • Clean the sensitive dentin—each for 5 sec—wash and dry for 15-20 sec • A drop of enamel bond applied to dentin • Gluma—dentin bonding agent—5% glutaraldehyde primer and 35% hema (hydroxyl ethyl methacrylate). • Immediate and strong attachment to dentin • Prevent bacterial overgrowth in tooth/restoration interface—beneficial effect in inhibiting plaque accumulation on sensitive root surface • Surgical root coverage procedures—various procedures are used to cover the denuded areas of teeth such as free gingival graft, connective tissue graft, laterally positioned flap, coronally positioned flap, subepithelial connective tissue graft and guided tissue regeneration. • Laser sealing off tubules—helium-neon (HeNe) and Nd:YAG lasers are found to be effective in the treatment of dentinal hypersensitivity without detrimental pulpal effects. The lasers used for the treatment of dentin hypersensitivity can be divided in two groups. • Low output power lasers: helium-neon (HeNe) and gallium/aluminium/arsenide (Ga-Al-As) lasers. • Middle output power lasers- Nd: YAG (1064 nm) and CO2 lasers (10,600 nm) at different wavelengths and exposure time are used to block the dentinal tubules effectively.
Instructions to be given to Patients while Prescribing Desensitizing Agent • Hypersensitivity appears as a result of exposure of dentin, which is inevitable if calculus and plaque and their products are to be removed. • Hypersensitivity slowly disappears over a few weeks. • Plaque control is important for the reduction of hypersensitivity. Patient is instructed about proper tooth brushing technique as improper tooth brushing is one of the etiologic factors in dentin hypersensitivity. • Desensitizing agents do not produce immediate relief. They must be used for several days to weeks (2-6 week) to produce results.
Prevention of Dentin Hypersensitivity Suggestions for Patients • Avoid gingival recession due to poor plaque removal by practicing good oral hygiene technique.
• Avoid using large amounts of dentifrice or reapplying additional dentifrice during brushing. • Avoid hard bristled tooth brushes. • Avoid over brushing with excessive pressure for prolonged periods of time. • Avoid excessive flossing or incorrect use of other interproximal cleaning devices. • Avoid picking at the gum or using tooth picks inappropriately.
Suggestions for Professionals • Avoid over instrumentation of the root surfaces during calculus removal and scaling and root planing as it may cause • Avoid over polishing the exposed roots during stain removal. • Avoid violating the biologic width when placing crown margins causing subsequent recession. • Avoid burning the gingival tissue during in-office tooth whitening or bleaching procedures.
Summary and Conclusion (Table 46-1) Dentinal hypersensitivity is one of the most painful and least predictably treated chronic conditions in dentistry. In clinical practice, the professional approach to dentin hypersensitivity has been heavily treatment-based with little regard for control of the etiological agent and predisposing factors, which creates the problem. This is not surprising since the dentist and the sufferer are virtually bombarded with a vast array of products formulated to treat dentin hypersensitivity. Patients treated for dentin hypersensitivity should be counseled about dietary acids and the importance of proper effective oral hygiene. Over-the-counter dentifrices will continue to have an important role in treating dentin hypersensitivity. Potassium nitrate, potassium oxalate, iontophoresis with 2% sodium fluoride is proven to be effective with varying degree of success in reducing the dentin hypersensitivity. In the future, dental lasers are expected to have an important role in treating hypersensitivity.
Mouthwashes (Table 46-2) Mouthwashes are usually aqueous solutions in concentrated form of a substance with deodorant, antiseptic, local analgesic and astringent properties. Mouthwashes comprise a large group of liquid compound used as oral rinse for cosmetic or therapeutic purpose.
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Desensitizing Agents, Gum Paints and Mouthwashes 1017 Table 46-1: Desensitizing agents
Desensitizing agents
Trade name of toothpaste
Mechanism of action
Strontium chloride
Thermoseal Eanisam Desent Senolin Toss
Bicolloidal binding and blocking of micro-tubular fibrillae on the exposed dentin. Strontium ions stimulate secondary dentin formation Modification of transmission of impulses and stimulation for re-calcification
Potassium nitrate
Senquel Sensodent K
Oxidizing effect or blocking of dentinal tubules
Formalin
Sensoform Dentoform
Protein precipitation
Strontium chloride and formaldehyde
Stolin
Same as strontium chloride and formalin
Potassium nitrate 5% sodium monofluorophosphates 0.7% available fluoride
Senquel-F
Table 46-2: Mouthwashes
Drug
Trade name
0.2 % chlorhexidine gluconate
Clohex, hexidine, rexidin
0.12% chlorhexidine and 2% sodium benzoate
A.M-P.M.
1% Povidone iodine, essential oils
Betadine, alphadine, povidax, povidone
0.15% benzydamine hydrochloride
Tantum oral rinse
1.02% chloroxylenol and 0.12% menthol
Dettolin
Chamomilla extract in alcohol (42.8%), mentha oil (18.5 mg) anise oil (7 mg) and alcohol (0.1ml)
Kamillosan-N
Thymol (0.06%), eucalyptol (0.9%), benzoic acid (0.15%), menthol (0.04%)
Listerine
Indications for Antiplaque Mouthwash • Replacement for mechanical tooth brushing—antiplaque mouthwash is used to replace mechanical tooth brushing when this is not possible acute oral mucosal and gingival infections, after periodontal or oral surgery, during the healing period, after cosmetic jaw surgery, in case of patient using intermaxillary fixation, and for mentally and physically handicapped patients. • Adjunct use—as an adjunct to normal mechanical brushing in situations where this may be compromised by discomfort or inadequacies. • After scaling when there is cervical hypersensitivity due to exposed root surfaces, prescribe mouthwashes for about 4 weeks. Measures to treat hypersensitivity should also be instituted simultaneously. • Following subgingival scaling and root planning when the gingiva may be sore for a few days, use of a mouthwash is recommended for about 3 days.
• Cleaning of mouth—vigorous mouthwashing does help in keeping the mouth clean by moving the food debris, mucus and even bacteria. • Decrease bacterial population—it is also used to decrease bacterial population, to provide topical anesthesia. • Reduction of oral acidity—it also reduces oral acidity and inactivates odor producing salivary or bacterial enzymes. • Refresh the mouth—the patient may use mouthwashes to debride the oral cavity after tooth brushing and to refresh the mouth or as an attempt to correct halitosis. From simple breath fresheners to products that can really influence oral health, a variety of mouthwashes are available in the market. • Resolution of chronic gingivitis—Antiplaque or antimicrobial mouthwash is used to inhibit bacterial plaque formation and prevent or resolve chronic gingivitis. They can affect only supragingival plaque. So they have no role in the treatment of existing periodontal disease, since
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1018 Textbook of Oral Medicine they cannot either reach the subgingival environment or penetrate thick layers of established plaque. In these situations, they are used after supra- and subgingival scaling has been done, rendering the tooth surfaces clean, in order to maintain this situation for a short period when the soreness of the gingiva may prevent effective mechanical plaque control. • Indication for fluoride containing mouth rinse—it is used to prevent dental decay. They may be recommended for children having orthodontic treatment, children with high caries risk, dry mouth and after radiation therapy.
Types of Antiplaque Mouthwashes
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• Mouthwashes containing essential oils—essential oils derived by distillation from plants, have a characteristic odor and taste and should not be used in a concentration greater than 0.2%. The most commonly used essential oils are eucalyptus oil, methylsalicylates, orange oil, peppermint oil and spearmint oil. Listerine, one of the oldest mouthwashes available, is an essential oil/ phenolic mouthwash. It has been shown to have moderate plaque inhibitory effect and some antigingivitis effect. Its lack of profound plaque inhibitory effect is because it has poor oral retention. Ethyl alcohol is used to enhance the solubility of organic compounds in water and should not exceed a concentration of 10% because of possible local irritation. • Phenol and its derivative—they are also used for their antibacterial and anodyne effects in mouthwash preparations. Their value is limited by their toxicity, objectionable taste, sensitization properties, high cost and decreased activity in the presence of organic matter. Commonly used phenol derivatives are hexylresorcinol and thymol. • Mouthwash containing oxygenating agents—oxygenating agents like Hydrogen peroxide, buffered Sodium peroxyborate and peroxy carbonate in mouthwashes have a beneficial effect on acute ulcerative gingivitis, probably by inhibiting anaerobic bacteria. Mechanism by which they inhibit anaerobic bacteria is that they release molecular oxygen which can destroy anaerobic bacteria. • Mouthwash containing bisguanide antiseptic—bisguanide antiseptics, like Chlorhexidine, Alexidine and octenidine possess antiplaque activity. These are cationic agents with fungicidal activity and bactericidal action against gram positive and gram negative organisms. Bisguanide antiseptics are able to kill a wide range of microorganisms by damaging the cell wall. • Mouthwash containing triclosan—triclosan, a trichloro-2’hydroxy diphenyl ether, is a non-ionic antiseptic. It has a moderate antiseptic effect when used as a mouthwash
in combination with zinc. It has been shown to reduce histamine induced dermal inflammation and reduces the severity and healing period of aphthous ulcers. • Colgate total plax mouthwash—colgate Total Plax mouthwash has Triclosan and Sodium fluoride as its components. Triclosan has little or no substantivity, but is oral retention can be increased by its combination with copolymers of methoxy ethylene and maleic acid. • Povidone iodine—povidone iodine appears to have no significant plaque inhibitory activity when used as 1% mouthwash and the absorption of significant levels of iodine through the oral mucosal may make this compound for prolonged use in the oral cavity. It could cause problem of iodine sensitivity in sensitized individuals. Piodin (Glaxo Wellcome), povidine Gargle (Stadmed) are povidone iodine mouthwashes available in the market. • Mouthwash containing sanguinarine—it is a component of an alkaloid extract obtained from the dried rhizome of the bloodroot plant, sanguinaria Canadensis. Recently, it is incorporated with zinc chloride in dentifrices and in mouthwashes as an antiplaque and anti-gingivitis agent. The antibacterial activity is due to its ability to inhibit sulfhydryl dependent enzymes.
Alcohol Content of Mouthwashes Most mouthwashes contain pharmaceutical grade alcohol, as a preservative and as a semi- active ingredient. Significant amounts of alcohol contained in many mouthwashes can lead to certain disadvantages. Care should be taken that they are not accidentally swallowed, especially by children, to avoid toxicity. Small children should not be advised mouthwashes, because they are not able to spit out properly. Moreover, most children have good gingival health. Because of known links between alcohol consumption plus tobacco smoking and oral and pharyngeal cancer, it has been suggested that the frequent use of alcohol containing mouthwashes might increase the incidence of this form of cancer. Lastly, alcohol containing mouthwashes have been shown to reduce the hardness of composite and hybrid resin restorations
Chlorhexidine Mouthwash Chlorhexidine molecule gets adsorbed onto the oral surfaces and gets released at bactericidal level over prolonged periods. Due to this process, Chlorhexidine has antiplaque properties unsurpassed by other agents. The antibacterial action of Chlorhexidine is due to an increases in cellular membrane permeability followed by coagulation of the cytoplasmic macromolecules. It is effective in vitro
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Desensitizing Agents, Gum Paints and Mouthwashes 1019 against Gram +ve and Gram –ve bacteria including aerobes and anaerobes and yeast and fungi. The substantivity (the ability of drugs to adsorb onto and bind to soft and hard tissues) of Chlorhexidine was first described in the 1970s. Due to this property, Chlorhexidine can maintain effective concentration for prolonged periods of time. Different brands of Chlorhexidine are available in the market, e.g., Rexidin (Warren), Clohex (Group) and A.M.-P.M (Elder).
Structure Chlorhexidine is a chlorophenyl bisguanide that has been used as an acetate and more commonly as a gluconate salt. It is N, N-bis (4-chlorophenyl)-3, 12-dimino-2, 4, 11, 13tetra-azotetradecanedimidamide di–D-gluconate.
Mechanisms of Action • Absorption onto oral surface—chlorhexidine molecule gets adsorbed onto the oral surfaces and is released at bactericidal levels over prolonged periods. Due to this process, chlorhexidine has antiplaque properties unsurpassed by other agents. • Antibacterial action—this action of chlorhexidine is due to increase in cellular membrane permeability followed by coagulation of the cytoplasmic macromolecules. It is effective in vitro against gram +ve and gram –ve bacteria including aerobes and anaerobes and yeast and fungi. The positively charged chlorhexidine binds to negatively charged microbial cell surface. It is followed by disorganization of cytoplasmic membrane. Low concentration allows cytoplasmic constituent to leak out and high concentration coagulates them. • Blocking of acidic groups—these groups on the salivary glycoprotein reduce the protein absorption to tooth surfaces.
• Cell wall penetration—in high concentration, chlorhexidine penetrates cell wall and causes precipitation of the cytoplasm.
Indications • Periodontal disease—it is used in all forms of periodontal diseases. • Subgingival irrigation—it is also used for sub-gingival irrigation of periodontal pockets. • Aphthous ulcer—it also reduces the severity and duration of aphthous ulceration. • Substitution of mechanical plaque control—where mechanical plaque control is not useful. • Denture stomatitis—denture stomatitis has been treated by soaking dentures in 0.2% chlorhexidine overnight for 5 months combined with daily use of amphotericin B lozenges for 14 days.
Side Effects of Chlorhexidine • Unpleasant taste—it has an unpleasant taste and it alters taste sensation. Interference with taste sensation is caused by denaturation of surface proteins on the taste buds. • Stains—it produces brown stains on teeth, which is very difficult to remove. This can also affect the mucous membranes and tongue and may be related to the precipitation of chromogenic dietary factors onto the teeth and mucous membranes. Due to this reason, it is important to advise patients using chlorhexidine mouthwash to avoid the intake of tea, coffee and red wine during the duration of its use. Remember to severely restrict its use in patients with visible anterior composite and glass ionomer restorations since they also get stained. • Calculus formation—chlorhexidine encourages supragingival calculus formation. It may be due to rise in pH
Table 46-3: Gum paints
Drugs
Trade name
2% zinc sulfate
Gingisol
Tannic acid (66.27%), glycerin, thymol (0.033%), potassium iodide (0.05%), menthol (0.05%) and iodine (0.03%)
Sensoform
Choline salicylate (8.7%), cetalkonium chloride (0.01%) and ethyl alcohol (39%)
Gelora
Choline salicylate (9%) and benzalkonium chloride (0.02%)
Zytee
Iodine (1gm), potassium iodide (2gm), alum (1.5gm), tannic acid (0.5gm), thymol (0.25mg), camphor (0.2mg) and menthol
Toss gum paint
Choline salicylate (8.7%), lignocaine hydrochloride (2%) and benzalkonium chloride solution (0.01%)
Dentogel Dologel
Tannic acid (2%), zinc chloride (1%) and cetrimide (0.1%)
Stolin
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1020 Textbook of Oral Medicine as a result of absorption of cationic agents and marked impact on bacterial integrity. • Soreness of oral mucosa—desquamation and soreness of the oral mucosa can occur. It is due to precipitation of mucin layer, by reducing its lubricating effect. • Transient parotitis—transient parotitis has also reported. • Altered taste sensation—chlorhexidine mouthwash may alters taste sensation.
Gum Paints (Table 46-3)
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Gum paint is just a stronger solution of a drug, which is used as mouthwash. They are used for topical application. They develop a strong concentration of the drug against inflamed tissue. They are combination of antiseptics and tanning agents. They are used for local application to the gums during severe bacterial infection and their inflammatory conditions. To apply it you have to dry the area and apply using cotton or index finger and it is not to be swallowed. When applied they provide a cooling, soothing, astringent effect and they have germicidal, fungicidal, anesthetics and healing properties. It is used in the treatment of stomatitis, inflamed/bleeding/spongy and painful gum conditions. It reduces sensitivity and increase gingival resistance against infection.
Suggested Reading 1. Anderson DJ. The sensitivity of human dentin. J Dent Res 37;699. 2. Brannstoon M. The hydrodynamic theory of dentinal pain, sensation in preparations, caries and the dentinal crack syndrome. J Endo 1986;12:453-57. 3. Branstorm, Linden and Astrom. The hydrodynamics of dentin and pulp fluid. Caries Research 1967;1:310. 4. Colour Atlas of Dental Medicine—Klaus M. Reteitschak Herbert F. Wolf. 5. Curro F. Tooth hypersensitivity in spectrum of pain. Dent Clin Nortn An 1990;34. 6. Dowel P, Addy M. Dentise Hypersensitivity. A review. J Clin Periodontal 1983;10(4):341-50,351-63. 7. Everett FG, Hall Phatok NM. Treatment of hypersensitive dentin. J Oral the Pharmacol 1966;2:300. 8. Grossman L. A systematic method for treatment of hypersensitive dentin. JADA 1935;22:592. 9. http://ergonomicbasics/ss/painscale.htm 10. Manning M.W. New approach to desensitization of cervical dentin. Dent survey 1961;37:731. 11. Pashley D. Dentist permeability, dentin sensitively and treatment through tubule declosion. J Endod 1986;12:465-74. 12. Pashley D. Mechanisms of dentin sensitivity. Dent Clin North Am 1990;34:449-73. 13. Rosenthal M. Historic review of the Management of tooth hypersensitivity. Dent Clin North An 1990;34:403-27. 14. Yvichi Kinera, Petra Wildes—Inith, 2000 Journal of Clins Periodontology 27(10):715-721 Role of interhypersensitivity by lasers—a review.
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Drugs used in Pregnancy 1021
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Drugs used in Pregnancy
Introduction Administration of drugs to pregnant patient is of significant concern. Two main concerns must be addressed when considering whether to give a drug to pregnant women. The first is that the drug may be teratogenic and the second is that drug can affect near term fetus. One must always be aware of the teratogenic, toxic or otherwise harmful effects of the drug on the developing fetus. The physiologic changes during pregnancy and the consequent alteration in the pharmacokinetics lead to changes in drug absorption, distribution, metabolism and excretion. As a general rule, it is best that no drug should be given during pregnancy, especially during the first trimester as it is period of organogenesis. Fortunately, most of drugs commonly used in dentistry are not contraindicated during pregnancy. Tetracycline and streptomycin are notably exceptions. The fetus may metabolize a particular drug via a different pathway from that of mother or its metabolic product may bound more avidly in fetal thus leading to accumulation of drug or its metabolites in fetus. Also since body systems of fetus are not fully developed, the fetus cannot process medicine like mother’s system so same drug can cause harm to fetus.
Pregnancy Trimesters Pregnancy involves three trimesters each 3 months long. • First trimester—in this trimester, different body organs in the fetus are forming. It is most critical time for teratogenicity. Dental prophylaxis with detailed instructions and a visual examination of the oral cavity without X-rays should be performed if the patient is pregnant. Elective dental treatment should be avoided
in the morning as women may feel nauseated in the morning. • Second trimester—it is an excellent time for the patient to undergo dental prophylaxis if needed. The patient’s periodontal status should be carefully evaluated during this period. • Third trimester—the women begin to feel uncomfortable and it is difficult for her to lie in prone position for long period time. Drugs that may affect the newborn should not be given during this trimester. Positioning of patient on dental chair can cause hypotension due to compression of gravid uterus on the inferior vena cava, resulting in syncope. Stress can precipitate premature labor. Due to hormonal changes, gingival tissue shows exaggerated response to local irritants.
Pharmacokinetics in Pregnancy • Drug absorption—high circulating levels of progesterone slow the gastric emptying as well as gut motility resulting in slower drug absorption. Parenteral drug administration is preferred in order to obtain a quick response. Drug compliance may be poor because of nausea and fear of adverse effect. • Drug metabolism—hepatic drug metabolizing enzymes are induced during pregnancy probably by high concentration of circulating progesterone. This can lead to more rapid metabolic degradation especially of highly lipid soluble drugs. However, this is of little clinical consequence. • Drug excretion—during pregnancy the renal plasma flow increases by 100% and glomerular filtration rate by 70%. Hence, drugs which depend for their elimination mainly on kidney are eliminated more rapidly than in non-pregnant stage, e.g. ampicillin, gentamicin and cephalosporin.
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1022 Textbook of Oral Medicine Recommended Drugs to be used in Pregnancy
Type
Drugs
1st Trimester
2nd and 3rd Trimester
Comment
Local anesthetics
Lidocaine
Yes
Yes
First choice anesthetics, fetal bradycardia near term
Mepivacaine
Yes
Yes
Fetal bradycardia near term
Bupivacaine
No
No
Embryocidal in rabbits and high lipid solubility
Benzocaine
Yes
Yes
Fetal bradycardia near term
Vasoconstrictors
Epinephrine
Yes
Yes
It can produce hypoxia (use cardiac dose)
Analgesics
Paracetamol
Yes
Yes
Teratogenic at over dose level
Codeine
Limited dose
Limited dose
Respiratory distress near term high dose contraindicated
Aspirin
No
No
Bleeding, prolonged parturition, premature closure of paten ductus arteriosus
Ibuprofen
Yes (cautiously) No
Same as aspirin
Penicillin
Yes
Yes
Safe
Erythromycin
Yes
Yes
Safe except estolate form
Antibiotics
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Antifungal
Sedative
Tetracycline
No
No
Stains teeth, affects bone
Clindamycin
No
No
Only if alternative dose not exist
Cephalosporin
Yes
Yes
Safe only if use as indicated
Metronidazole
No
No
Carcinogenic and mutagenic in animals
Clotrimazole
No
Yes with caution Poorly absorbed following topical or intravaginal application, abnormal liver function test in adults can occur.
Ketoconazole
No
No
Embryotoxic in rat
Nystatin
Yes
Yes
Safe
Benzodiazepines
No
No
Cleft lip, neural tube defect
N2O with 50% O2
No
Possible with adequate O2
Ensure adequate oxygen intake, female operators avoid chronic exposure
Use of dental drugs by nursing mother
Types
Drugs
Acceptable
Watch infant for symptoms of
Local anesthetics
Amides
Yes
Central nervous system changes
Vasoconstrictors
Epinephrine
Yes
Hyperactivity or irritability
Analgesics
Aspirin
Yes with caution Avoid feeding for 1 hour after dose, occasional low dose pose no hazard, chronic high dose may pose problems
NSAID
Yes with caution Use ibuprofen (concentration in milk is low) avoid long acting NSAIDs
Acetaminophen
Yes
Present in milk in small amount (peak 1-2 hours)
Opioids
Yes
Small doses no problems and in larger doses sedation, poor feeding and constipation
Penicillin
Yes
Allergic symptoms, diarrhea
Erythromycin
Yes
Present in milk, diarrhea
Cephalosporin
Yes
Allergic symptoms, diarrhea
Tetracycline
No
Tooth staining
Clindamycin
Yes/no
Diarrhea, pseudomembranous colitis
Metronidazole
No
Carcinogenic in animal
Nystatin
Yes
Not absorbed into systemic circulation from mouth or gastrointestinal tract
Clotrimazole
Yes
Excreted in milk, use nystatin first
Ketoconazole
No
Express and discard milk
Antiviral
Acyclovir
Yes
Concentrated in milk
Antianxiety
Nitrous oxide
Yes
Excreted through mother’s lung
Benzodiazepines
No
Sedation, infants metabolize oxidized agent more slowly
Antibiotics
Antifungal
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Drugs used in Pregnancy 1023 • Increase total blood volume—there is increased total blood volume, because of increased fluid retention. This leads to change in cardiac output, blood pressure and glomerular filtration rate. This results in change in volume of distribution of drug, change in metabolism, change in absorption, change in excretion of drug, change in protein binding of drugs and passage of drug through placenta. • Teratogenicity—it refers to capacity of a drug to cause fetal abnormalities when administered to pregnant mother. Drug can affect fetus at three stages, i.e. stage of fertilization and implantation, stage of organogenesis and stage of growth and development Drugs
Abnormalities
Thalidomide
Phocomelia
Anticancer drug
Multiple defect, Fetal death
Tetracycline
Discolored and deformed tooth, Retarded bone growth.
Phenytoin
Craniofacial and limb defect, cleft lip, cleft palate
Phenobarbitone
Various malformations
Carbamazepine
CNS defect
Retinoids
Various abnormalities
Alcohol
Fetal alcohol embryopathy
•
•
• •
•
•
premature labor or neonatal toxicity. The adverse effect of drugs on the fetus is dependant on the drug and the phase of pregnancy in which the drug is administrated. Preventive dental prophylaxis—preventive dental prophylaxis should be undertaken at the beginning of the 2nd and 3rd trimester. Radiographs—radiographs are contraindicated in all but emergency situation, when taken lead shielding is mandatory. Reduce chair time—prolonged chair time must be avoided to prevent supine hypotension. Position—sitting up position is best for patient since low head position may cause pressure on vena cava and aorta in 2nd trimester Fainting—in case of fainting, place patient on left side with legs and head elevated. Oxygen and lime juice with glucose could be given and vital sign monitored. Serious complication—more serious complication such as seizures and active vaginal bleeding or severe cramping require emergency care in hospital.
Guidelines for Prescribed Drugs in Pregnancy
Dental Management of Pregnant Patient • Elective treatment—it can be postponed easily for the pregnant patient after parturition. However, emergency care should be taken into consideration. The best method of treatment is to eliminate source of pain. Thus for removal of caries, an infected pulp or tooth, surgical procedure should be done under small doses of local anesthetics to minimize use of systemic drugs. Dental procedures are best performed in 2nd trimester for benefit of fetus and optimal comfort of pregnant women. • 1st trimester—it is roughly 12–13 weeks. In this first 12 days from conception to implantation known as ‘preimplantation period’, exposure to harmful drugs can kill the embryo. From the 13th day, there is period of organogenesis and so the fetus is susceptible to insult and injury resulting in malformation. • 2nd and 3rd trimester—after completion of organogenesis, there is considerable growth and development of existing structures like teeth, bones, CNS, endocrine, genitals and immune system. Malformation is less in II and III trimester but drug like streptomycin can still be harmful causing retardation of physical and mental growth,
• Don’t use drug unless it is absolute necessary—use drug in pregnant patient only when it is absolutely necessary. • Ruling out possibility of pregnancy—rule out possibility of pregnancy in every female of reproductive age group and restrict drug usage. • Risk and benefit ratio—prioritize drug usage in the situation and avoid drug usage if the non-usage can do i.e. risk Vs benefit ratio should be calculated. • Lower doses—use lower than usual doses of drug if necessary for short term.
Consideration in Lactation Almost all drugs are excreted into the breast milk to some extent. An infant normally ingests approximately 1% of the total material dose of a drug. Dental practitioner must remember that drugs should be selected which have short half-life, sustained release formulation should be avoided, drugs should be taken immediately after nursing.
Suggested Reading 1. Barar FSK. Essential of pharmacotherapeutics (3rd edn), S Chand and Company Ltd, 2000. 2. Chaudheri. Quintessence of medical pharmacology (3rd edn), Central publisher, 2005.
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1024 Textbook of Oral Medicine 3. Craig CR, Stitizel RE. Moderate pharmacology with clinical application (5th edn), Little Brown and company, 1997. 4. Gomes MW. Synopsis of medical pharmacology (1st edn), National Series, 2002. 5. Hardman, Limbird, Gilman. Goodman and Gillman: the pharmacological basis of therapeutics (10th edn), McGraw Hill, 2001. 6. Mycek MJ, Harvey R, Champe P. Lippincott illustrated review: pharmacology, (2nd edn), Lippincott Williams and Wilkins publisher.
7. Salil and Bhattacharya, Sen A, Ray A. Pharmacology (2nd edn), Elsevier, 2003. 8. Seth. Textbook of Pharmacology (2nd edn), Elsevier, 1999. 9. Sharma HL, Sharma KK, Gupta DK. Textbook of dental pharmacology (1st edn), Paras Publisher, 2008. 10. Tripathi KD. Essential of Pharmacology for Dentistry (1st edn), Jaypee Brothers Medical Publishers, 2005. 11. Yagiela, Neidle, Dowd. Pharmacology and thereaputics for dentistry (1st edn), Mosby Harcourt India, 2001.
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Emergency Drugs used in Dentistry 1025
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Emergency Drugs used in Dentistry
Introduction Though rare, life-threatening medical emergencies can and do occur in the dental environment whose incidence is largely unknown. All health care providers, dentists must be prepared to recognize and properly manage patients of medical emergencies in the dental office. In all cases of emergencies, the best and foremost method of managing medical emergencies is by preventing them from occurring. With this in mind, it is essential to take a comprehensive medical history from any patient who is about to receive dental care. The following section reviews the more common emergency drugs that the dental team may have to administer in general dental practice.
Emergency Management First and foremost in emergency management is the ability to effectively provide basic life support, or BLS (includes cardio-pulmonary resuscitation), when appropriate. It is recommended that all dental health care professionals receive regular training in BLS for health care providers, because these skills are maintained only through repetition. For certain individuals, like those who practice in the remote areas where medical services (routine or emergency) are not readily available, additional training in advanced cardiac life support, pediatric advanced life support, or both may be warranted. Didactic and hands-on training in the prevention, recognition and management of common emergencies also is recommended. Examples of common emergencies include seizures, cardiovascular and respiratory distress, altered consciousness, chest pain and drug related emergencies. Advanced cardiac life support training involves the following:
• Adjuncts for airway control and ventilation (including intubation) • Patient monitoring and dysrhythmia recognition. • Defibrillation and synchronized cardioversion. • Cardiovascular pharmacology. • Acid-base balance maintenance. • Venipuncture. • Resuscitation of infants, including the newborn. In addition, all dental offices should maintain at least the basic recommended emergency equipment and drugs. The content and design of these kits should be based upon each practitioner’s training and individual requirements. Proprietary emergency drug kits are available, but none of these kits is compatible with the needs of all practitioners. It does recommend that dentists, after considering their specific training and special needs, design their own individualized emergency kits if proprietary kits do not meet their needs.
Types of Emergency Drugs Drugs that should be promptly available to the dentist can be divided into two categories. • Essential emergency drugs—the first category represents those which may be considered essential. (oxygen, epinephrine, nitroglycerine, salbutamol, antihistamines, aspirin). • Additional emergency drugs—the second category contains drugs which are also very helpful and should be considered as part of the emergency kit. These supplementary drugs. (glucagon, ephedrine, atropine, corticosteroids, morphine/nitrous oxide, nalaxone, lorazepam, midazolam, flumazenil).
Emergency Drug Kit The dental office emergency kit should be as simple as possible. The emergency drug kit describes in the following
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1026 Textbook of Oral Medicine section is a simple organised collection drugs and equipments that has been found to be highly effective in managing those life-threatening situations requiring the administration of drugs. However in most emergency situations, drugs are not necessary for the proper management of the patients. First and foremost in the management of these situations will be the steps of basic life support. In the light of the confusion it seems clear that there is an urgent need to try to rationalise the content of the emergency drugs box and to provide clear, standardised guidance on which emergency drugs they should stock and be able to use. The following section reviews the more common emergency drugs that the dental team may have to administer in general dental practice.
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Adrenaline • Indication—it is the drug of choice for the management of the acute allergic reactions especially in the respiratory and cardiovascular manifestations of allergic reaction. • Anaphylactic shock—an allergic (type 1 hypersensitivity) reaction may be precipitated by any material or drug to which the patient has been sensitized. Lifethreatening events include cardiovascular collapse (90%), bronchospasm (30%), angioedema (25%), and pulmonary edema (49%). Severity varies, and onset of anaphylaxis may be delayed for up to 6 hours or be biphasic, reoccurring in 5% of patients after clinical recovery. In addition to adrenaline, high flow oxygen should be administered to all patients in anaphylactic shock. Second-line drugs, used to prevent relapse, are chlorpheniramine and hydrocortisone. • Acute asthmatic attack—adrenaline is also used in acute asthmatic attacks. • Cardiac arrest—adrenaline is used highly advanced cardiac life support protocols. • Mode of Action • Contraction of vascular smooth muscle—adrenaline is a sympathomimetic amine that activates both alpha and beta adrenoceptors. Contraction of vascular smooth muscle (alpha-mediated). An increased blood pressure helps to maintain cerebral and coronary perfusion. • Increase cardiac output—increased force and rate of cardiac contraction (Beta1-mediated). This action increases cardiac output, which helps to maintain the blood pressure. However, this may be damaging as it increases myocardial oxygen requirements and may precipitate ischemia. • Relaxation of bronchial muscle—relaxation of bronchial smooth muscle (Beta2-mediated). Increasing the caliber of the airway in acute anaphylaxis helps to
re-establish airflow restricted by bronchospasm and edema. • Inhibition of histamine release—inhibition of histamine release by mast cells (Beta2-effect). Histamine is an important early mediator, responsible for some of the hemodynamic changes encountered in anaphylactic reactions. • Undesirable action—undesirable action includes its tendency to predispose the heart to dysrhythmia and its relatively short duration of action. • Administration—adrenaline may be given intramuscularly, subcutaneously or intravenously. • Dose—adrenaline is available in two concentrations: 1:1000 (reserved for intramuscular and subcutaneous use) and 1:10 000 (for intravenous administration). It is available in ampoules or pre filled. The following table outlines the recommended volume of 1:1000 adrenalines that should be administered according to age during anaphylactic reactions. Age
Volume of 1:1000 adrenaline (ml)
Dose (µg)
2
0.2
200
3-4
0.3
300
5
0.4
400
6-12
0.5
500
Adult
0.5-1.0
500-1000
• Side effects, contraindication and precaution—supraventricular and ventricular tachydysrhythmia may develop. Should be used with caution in pregnant women because it may decrease placental blood flow and may induce premature labor.
Chlorpheniramine • Action—it is an antihistaminic drug alternative drug is diphenhydramine. Antihistamines are useful in the treatment of the delayed allergic response and in the definitive management of acute allergic reaction. Antihistamines act as a competitive antagonist of histamine. They do not prevent the release of histamine from the cell in response to injury, drugs, or antigens but do prevent access of histamine to its receptor site in the cell and thereby block the response of the effectors cell to the histamine. They are also the potent local anesthetics, diphenhydramine and triphelennamine being particularly potent in this regard. Potential side effect of most antihistamines is a degree of cortical depression which causes sedation. Therefore, Chlorpheniramine is preferred over diphenhydramine as it is has less sedative effect.
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Emergency Drugs used in Dentistry 1027 • Indication—delayed allergy, definitive management of acute allergy, as local anesthesia in patients having history of allergy to local anesthetics. • Side effects, contraindication, precaution—side effects include central nervous system depression, decreased blood pressure, it causes thickening of bronchial secretions therefore contraindicated in management of acute asthmatic attacks. • Dose—the drug may be given orally, intramuscularly, subcutaneously or intravenously. For the management of allergic reactions localized to the skin, a dose of 4 mg in adults may be administered orally every 4 to 6 hrly, to a maximum of 24 mg/day.
•
Oxygen • Indications—it is the most important drug in the entire emergency kit. Oxygen is indicated in all medical emergencies except hyperventilation. Oxygenation prevents hypoxia that may be damaging to vital organs such as the brain and heart. • Administration—ensuring Airway Patency before oxygen is delivered, it is essential to ensure that the airway is patent. Foreign bodies, blood, vomit, and soft tissues may occlude the air space. The airway may be reestablished by using the head tilt and chin lift or jaw thrust techniques. Airway adjuncts such as oropharyngeal (Guedel) airways may be used in the unconscious patient to hold the tongue in an anterior position away from the posterior pharyngeal wall. These airways are contraindicated in conscious or semiconscious patients where protective reflexes are active. • Oxygenation—if the patient is breathing spontaneously, a facemask with an attached oxygen supply, running at a flow rate between 4 and 6 /min, may be used to deliver oxygen and help prevent hypoxia. Positive pressure ventilatory support may be provided in respiratory arrest. • Dose—during cardiorespiratory arrest, the chest compression to ventilation ratio for adults 15:2 if one resuscitator is present and 5:1 if two are present.
Nitrates and Nitrites (Glyceryl Trinitrate or Nitroglycerine and Amyl nitrite) • Indication—nitroglycerine and amyl nitrite was the first member of this group to be used as coronary vasodilators more than 100 years ago. These vasodilators primarily used in immediate management of chest pain usually caused by angina or myocardial infarction. Glyceryl trinitrate (GTN) is used for the prophylaxis and relief of angina. Angina, defined as discomfort due to myocardial
•
•
•
ischemia, occurs whenever there is an imbalance between myocardial oxygen supply and demand. Atherosclerotic narrowing of the coronary lumen results in insufficient oxygenated blood being delivered to the myocardium during periods of increased activity. Mode of action—the principle site of action of GTN is smooth muscle. Within the smooth muscle cell, GTN is converted to nitric oxide which activates the enzyme soluble guanylate cyclase (SGC). Activation of SGC results in increased cyclic guanosine monophosphate (cGMP) production, which leads to relaxation of thesmooth muscle cell. As the vascular smooth muscle is relaxed and resting blood pressure is lowered, myocardial oxygen requirement is reduced leads to the relief of angina. GTN improves the myocardial oxygen supply: demand ratio by reducing cardiac workload and increasing the blood supply to the myocardium. Side effect, contraindication and precaution—the chief disturbances occur due to sudden hypotension. Headaches, postural hypotension, and flushing of face, tachycardia, thready pulse and fainting and complete nitrate syncope might occur. Tolerance is developed rapidly. Methemoglobinemia because of its mild hypotensive action, nitroglycerine is contraindicated in hypotensive patients. Because nitroglycerine is a unstable drug in tablet form, it must be replaced, usually within 3 weeks of its initial use. Administration—Sublingual tablets (300 micrograms). Uptake is delayed because of the initial time taken for the tablet to dissolve. Spray (400 micrograms metered dose). This is preferable to tablets as the solution is rapidly absorbed, no special storage is required. Dose—if a patient known to suffer from angina experiences chest pain, they should be placed upright to facilitate respiratory movements. In adults, a dose of 0.3 to 1 mg should produce symptomatic relief within 3 minutes. The effective duration of action is only 20 or 30 minutes; thus, dosing may have to be repeated. Oxygen should also be administered to all patients experiencing acute chest pain. If symptoms are not relieved within 10 minutes, myocardial infarction should be suspected.
Nitrous Oxide • Indications—nitrous oxide may be used for its analgesic properties in the initial management of myocardial infarction (MI). The pain experienced during an MI is often more severe and of longer duration than that in angina. It may lead to further deterioration of cardiac function as it increases sympathetic output, which will elevate the oxygen demands of an already starved myocardium.
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1028 Textbook of Oral Medicine • Mode of action—many theories of the mechanism of action of general anesthetic agents such as nitrous oxide have been proposed. It is thought that these agents alter, either directly or indirectly, the function of the membrane proteins involved in the conduction of nervous impulses. • Administration and dose—a combination of 50% nitrous oxide and 50% oxygen is used to produce analgesia without loss of consciousness.
Anticonvulsant (Diazepam, Midazolam)
5
• Indication—convulsion may occur in the dental office under several circumstances like overdose or toxicity to the local anesthetics, epileptic seizures, and febrile convulsions. Therefore anticonvulsant drug should be kept in the emergency kit. Seizure disorder is characterized by a stimulation of the central nervous and cardiopulmonary and cardiovascular system, followed by a period of depression of these same systems. as the degree of post-seizure depression is accentuated and its duration is prolonged because of the pharmacological action of the barbiturate. The benzodiazepines, unlike barbiturates, will usually terminate seizure activity without the pronounced depression of the respiratory and cardiovascular system. It is also used in termination of prolonged seizures caused by status epilepticus, local anesthetic toxicity, in hyperventilation and in thyroid storm for sedation. • Side effect, contraindication and precaution—the major side effect of benzodiazepines is respiratory depression and arrest; however, with proper titration during administration, this is unlikely to occur. • Dose—midazolam in 5 mg/ml in 1, 2, 5, and 10 ml vials, diazepam 5 mg/ml in 2 ml ampules.
Methoxamine/Phenylephrine • Action—this one more vasopressor drug is included in the emergency drugs kit because of various shortcomings of adrenaline. Adrenaline is primarily used in the management of the acute allergic reactions and in cases of clinically mild to moderate hypotention. In addition to an increase in blood pressure, adrenaline cause an increase in workload of the heart through its effect on heart rate and cardiac contraction; it also increases the irritability of the myocardium by sensitizing it to dysrhythmias. For this reason, it seems desirable to utilize a vasopressor that will produce to utilize a vasopressor which produce a moderate increase in blood pressure without unduly stimulating the myocardium. Methoxamine and phenylephrine elevates blood pressure through peripheral vasoconstriction. • Indication—in management of hypotension, in which the status of heart is unknown and the intent is to raise the
blood pressure without cardiac stimulation. Possible uses are in syncopal reaction, drug overdose reaction, postseizure states, acute adrenal insufficiency and allergy. • Side effect, contraindication, precaution—vasopressors are contraindicated in patients with high blood pressure or ventricular tachycardia, and such drugs are to be used with extreme caution in patients with hyperthyroidism, bradycardia, partial heart block, myocardial disease, or severe atherosclerosis. • Availability—methoxamine 10 mg/ml or phenylephrine 10 mg/ml.
Antihypoglycemic (50% Dextrose or Glucagon) Glucagon • Indication—glucagon is a pancreatic hormone that stimulates hepatic glycogenolysis and gluconeogenesis. Glucagon may be given to the unconscious hypoglycemic patient when intravenous access cannot be secured for the administration of glucose. In conscious patients, a sweet drink is sufficient to elevate plasma glucose levels. Oral glucose must not be given to unconscious patients because of the risk of pulmonary aspiration. Hypoglycemia, defined as a blood glucose concentration of less than 2.5 mmol/l, most commonly occurs in insulin-dependent diabetes. Hypoglycemia may result if a patient takes an insulin overdose, patient takes the correct dose but with no food or patient exercises or undergoes a stressful situation. • Mode of action—glucagon increases plasma glucose by stimulating glycogenolysis and gluconeogenesis in the liver. An additional action is inhibition of glycogen synthesis and glucose oxidation. In adipose and hepatic tissues, glucagon causes lipolysis, resulting in the production of fatty acids which further increase gluconeogenesis. • Administration and dose—in adults, 1 mg (0.5 mg in children up to 12 years) may be given intramuscularly into the deltoid or gluteal areas.
Glucose/Dextrose 50% • Indications—glucose may be administered to the conscious or unconscious hypoglycemic patient. • Administration—glucose may be given orally or intravenously. Intravenous administration is the most rapid and effective method of elevating plasma glucose levels.
Salbutamol /Albuterol /Metaproterenol • Indication—asthmatic patients and patients with allergic reactions manifested primarily by respiratory difficulty
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Emergency Drugs used in Dentistry 1029 will require the use of bronchodilator drugs. These are ß β2 adrenergic agonists have specific bronchial smooth muscle relaxing properties with little or no stimulatory effect on cardiovascular or gastrointestinal system. Salbutamol, a potent bronchodilator, is used in the management of acute asthma. Allergic reactions with bronchospasm. • Mode of action—salbutamol is a selective Beta2-agonist which relaxes bronchial smooth muscle. • Administration—to minimize the chance of adverse effects and to produce the most rapid onset of action, salbutamol is administered by inhalation (nebulizer)
Hydrocortisone/Dexamethasone • Action—hydrocortisone, an endogenous adrenal hormone, possesses predominantly glucocorticoids activity and is essential for human survival. Administration of steroids for therapeutic purposes has a negative feedback effect on the hypothalamus and anterior pituitary gland, which eventually leads to atrophy of the adrenal cortex and resultant inability to secrete hydrocortisone in response to stress (acute adrenal insufficiency). Under these circumstances, a patient may collapse due to hypoglycemia and hypotension if a stressful situation, such as dental treatment, is encountered. • Indication—therefore, exogenous hydrocortisone should be administered preoperatively to susceptible patients to restore the normal physiological response to stress. If acute adrenal insufficiency does occur, prompt administration of hydrocortisone and immediate hospitalization is recommended ( Dexamethasone and methylprednisolone are contraindicated in acute adrenal insufficiency). Corticosteroids will be administered in the management of an acute allergic reaction, after the acute phase has been brought under control. The primary value of the corticosteroid is in the prevention of recurrent episodes of anaphylaxis. • Administration and dose—hydrocortisone may be administered by the oral, intramuscular or intravenous routes. The dose varies according to the age and situation (25 to 200 mg). • Side effect, contraindication, precaution—except in life threatening emergencies steroid is contraindicated in presence of pre-existing infection, peptic ulcer, and diabetes mellitus.
node, atropine may provoke tachycardia. Atropine will be of benefit in situations in which the patient has an overload of parasympathetic activity on the heart. Extremely fearful patients are likely candidates for this purpose. When stimulated, the vagus nerve acts to decrease SA node activity, thereby slowing the heart rate, when the heart rate become overly slow, cerebral blood flow is decreased and clonical signs and symptoms of cerebral ischemia are noted. By blocking this effect atropine acts to maintain adequate cardiac output and cerebral circulation. • Indication—bradycardia and hemodynamicaly significant bradydysrhythmia. • Side effect, contraindication and precaution—large dose of atropine may produce clinical signs of overdose, including hot dry skin, headache; blurred nearsightedness; dry mouth and throat; disorientation and hallucinations; atropine is contraindicated in glaucoma or prostrate hypertrophy. • Dose—atropine available in 0.5 mg/ml in 1 ml vial.
Respiratory Stimulant Aromatic Ammonia • Action—aromatic ammonia is a strong respiratory stimulant. It is available in silver gray vaporole, which is crushed and placed under the breathing victim’s nose until respiratory stimulation is affected. Aromatic ammonia has a noxious odour and irritates the mucous membrane of the upper respiratory tract, stimulate the respiratory and vasomotor center of the medulla. This action is in turn increases respiration and blood pressure • Indication—vasodepressor syncope, respiratory depression not induced by opioid analgesics. • Side effect, contraindication and precaution—used with caution in patients with chronic obstructive pulmonary disease or asthma. Its irritating effects on the mucous membrane of the upper respiratory tract may precipitate bronchospasm. • Dose—silver gray vaporole containing 0.3 ml of aromatic ammonia.
Drugs for Advanced Cardiovascular Life Support These drugs should be included only by those doctors who have completed the course in advanced cardiovascular life support. Essential ACLS drugs include epinephrine, oxygen, lidocaine, atropine, dopamine, morphine sulphate and verapamil. Most of the drugs are already discussed.
Atropine • Action—it is a parasympathetic blocking agent, it is recommended for the management of symptomatic bradycardia. By enhancing discharge from the sinoatrial
Lidocaine • Indication—lidocaine (xylocaine) is considered the primary antidysrhythmic drug in ACLS. It is used
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1030 Textbook of Oral Medicine extensively in the management of cardiac dysrhythmias, especially those of ventricular origin that develop after acute myocardial infarction. Lidocaine used in premature ventricular contractions occurring more than six times per minute, sustained ventricular tachycardia and in ventricular fibrillation that is refractory to electrical defibrillation. • Side effects—excessive dose of lidocaine produce myocardial, circulatory, and CNS depression
Dopamine/Dobutamine
5
• Action—dopamine is a chemical precursor of norepinephrine. In large doses it stimulates both α and β adrenergic receptors at lower dose it dilates renal, mesenteric, and cerebral arteries. Dopamine also stimulates the release of norepinephrine; it is indicated for administration in hemodynamically significant hypotension in the absence of hypovolemia. Dobutamine is synthetic sympathomimetic amine that exerts significant ionotropic effects by stimulating β1 and α adrenergic receptors in the myocardium. Its β stimulating action generally overweighs it is α stimulating action, usually results in a mild vasodilatation. • Indication—the primary therapeutic indication for dopamine is to treat hemodynamically significant hypotension in the absence of hypovolemia. • Side effect—dopamine may induce or exacerbate supraventricular or ventricular dysrhythmia. It also may imbalance the supply and demand of O2 to myocardium, inducing or exacerbating myocardial ischemia. Nausea and vomiting frequently are noted with dopamine administration. It is available in 200 mg, 400 mg, 800 mg in 5 ml ampoules.
Morphine Sulphate/Meperidine • Indication—analgesics are used in emergency situations in which acute pain or anxiety is present. Pain or anxiety increases the myocardial workload which increases the O2 requirement of the myocardium which may worse the condition. Two such circumstances include acute myocardial infarction and congestive cardiac failure. It is use in acute myocardial infarction, congestive cardiac failure, intense, prolonged pain or anxiety. • Side effect—opioid agonists are potent central nervous and respiratory system depressants. Monitoring of the vital signs is mandatory whenever these drugs were used. Use of opioid agonists are contraindicated in victims of injury and multiple trauma: and should be used with caution in patients with compromised respiratory function. • Dose—morphine is available as 8,10, and 15 mg/ml and meperidine comes in 50 and 100 mg/ml doses.
Verapamil • Action—it is a calcium channel blocker drug. Verapamil is extremely effective in management of supraventricular tachycardia. It slows conduction through the atrioventricular node, reducing ventricular response to atrial flutter and fibrillation. • Indication—in emergency cardiac care verapamil is primarily used in treatment of paroxysmal supraventricular tachycardia. • Side effect and contraindication—a transient decrease in arterial pressure may be noted because of peripheral vasodilatation. Verapamil is not recommended in ventricular tachycardia; it may induce severe hypotension and predisposed the patient to ventricular fibrillation. It is available for injection as 2.5 mg/ml in 2 ml and 4 ml ampules.
Antidotal Drugs In order to manage the emergency situations like overdose or toxicity reactions caused by various drugs used primarily for sedation or general anesthesia four categories of antidotal drugs are used it includes the following; • Opioid antagonists, e.g. Naloxone or nalbuphine. • Benzodiazepine antagonist, eg. Flumazenil. • Antiemergence delirium drug, e.g. Physostigmine, • Vasodilator, e.g. Procaine.
Naloxone/Nalbuphine • Action and indication—the most significant side effect of opioid agonist is there ability to produce respiratory depression by diminishing the responsiveness of the brains respiratory center to the arterial carbon dioxide. Naloxone is the only opioid antagonist free of any agonistic properties. It also reverse the other properties of the opioid-like analgesia and sedation. Naloxone may be administered endotracheally in situations where IV access is not available. Improved respiratory function is noted within 2 minutes. Nalbuphine, having opioid agonist-antagonist properties, is used successfully to reverse respiratory depression induced by opioid agonists. And because of its own analgesia-inducing properties it does not entirely remove postsurgical analgesia or sedation. • Side effect and contraindication—naloxone’s effect lasts only 30 minutes, respiratory depression may recur if previously given opioid is of long duration. The IM administration of second dose of the naloxone is recommended, its onset is slower but for longer duration than that of IV dose. This minimizes the recurrence of respiratory depression. Naloxone must be administered with extreme care to persons with known or suspected
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Emergency Drugs used in Dentistry 1031 physical dependence on opioid. Naloxone’s complete reversal of agonist effect of opioid may produce severe withdrawal symptoms. • Dose—it is available in 0.4 mg/ml in 1 ml ampoule or 10 ml vial for adults and 0.2 mg/ml in 2 ml ampoules for pediatric administration.
Flumazenil • Action—benzodiazepines are supposed to be most safe drug for anxiety control and sedation. Some side effects like emergence delirium, excessive duration of sedation, and possibly significant respiratory depression do occur. Presence of antagonist for benzodizepines adds safety to the IV sedation. Flumazenil produce rapid reversal of sedation and to improve the patient’s ability to comprehend and obey commands. The duration of antrograde amnesia associate with midazolam was also reduced with use of flumazenil. Flumazenil also decrease the recovery time from midazolam sedation, increase alertness, and provide decrease amnesic effect in geriatric patients. Reversal with flumazenil is not effective following the oral administration of benzodizepines. • Indication—it is used for reversal of clinical action of parenterally administered benzodiazepines. • Side effect—flumazenil may produce rebound anxiety state in some patients.
Physostigmine • Action—several drugs that are primarily used to induce sedation have the ability to produce emergence delirium also called as anticholinergic syndrome. In this phenomenon the patient appears to lose contact with reality. There may be increase muscular movement, and patient makes unintelligible sounds. Physostigmine a reversible cholinesterase with the ability to cross the blood-brain barrier has become a drug of choice in the management of emergence delirium. • Indication—for reversal of emergence delirium. • Side effect, contraindication and precaution—side effects include increase salivation, possible emesis, and involuntary urination and defecation. If administered rapidly physostigmine can produce bradycardia and hypersalivation. Atropine should always available whenever physostigmine is administered because it is antidote to physostigmine. Physostigmine should not be given in patients with asthma, diabetes, cardiovascular disease, or mechanical obstruction of gastrointestinal or genitourinary tract.
Procaine • Action—whenever there is IM or IV administration of the drug is present, a local anesthetic with significant
vasodilating property is recommended in the emergency kit. Indications for the administration of the procaine are extravascular injection of an irritating chemicals and intra-arterial administration of the drugs. In both cases there is problem of localized tissue irritation and compromised circulation in a local area. Procaine possesses excellent vasodilating properties along with its anesthetic actions, which make it an ideal drug in these situations. • Indication—management of vasospasm and compromised circulation following intra-arterial injection of the drug. And in Management of extravascular injection of irritating drugs or chemicals. • Side effect—allergy to the ester type local anesthetics is not uncommon. Sensitivity test is recommended before administration.
Emergency Equipment Along with the emergency drugs the emergency equipments are equally important. Personnel who are expected to use these equipments must be well trained in its proper use. • IV set/cannula/scalp vein set • Oxygen cylinder • O2 delivery system • AMBU bag • Syringe and needles • Tourniquets • Macgill’s forceps • Suction and suction tips • Oropharyngeal airways • Endotracheal tubes • Laryngoscope
Maintenance of Emergency Kit • Freely available—it should be freely available. • Constant place—the place for keeping the emergency kit should be constant and should not be changed. • Sign board—location of the kit should be highlighted by the placard or sign board. • Orientation of working staff—all the working staff should be oriented towards it. • Periodic checking—it should be periodically checked for the working condition of the equipments, shortfall in the drugs, expiry date of the drugs, and prompt rectification should be made. • List of drug—a list of contents of emergency drug kit drugs along with their expiry date, should be paste on the cover of the kit for the convenience of periodic inspection. • Replacement of drugs after used—whenever the drugs are used they should be immediately replaced.
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1032 Textbook of Oral Medicine Emergency kit for dental office
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Group
Drug
Use
Concentration
Dose
Route
Anti-allergy
Epinephrine
Anaphylaxis Acute asthma
1:1000
0.3 mg
Subcutaneously
Opioid antagonist
Naloxone
Opioid overdose
0.4 mg/ml
0.4-2 mg
IV or Subcutaneously
Antihistamine
Benadryl
Allergic reaction
10 mg/ml
50 mg
IM, IV
Anticonvulsant
Diazepam
Prolonged seizure
_____
5-10 mg
IM,IV
Oxygen
Oxygen
Respiratory distress
100% inhalation
___
____
Vasodilator
Nitroglycerine
Acute angina pectoris
0.4 mg/spray
0.4 mg
Sublingually
Stimulant
Aromatic ammonia
Syncope
Inhalant
0.3 ml
Inhalation
Anti-hypoglycemic agent
Glucose
Hypoglycemia
Few teaspoonfuls
___
Orally
Analgesic
Morphine
Myocardial infract
10 mg/ml
10 mg
Orally
Suggested Reading 1. Barar FSK. Essential of pharmacotherapeutics (3rd edn), S chand and Company Ltd, 2000. 2. Chaudheri. Quintessence of medical pharmacology (3rd edn), Central Publisher, 2005. 3. Craig CR, Stitizel RE. Moderate pharmacology with clinical application (5th edn), Little Brown and company, 1997. 4. Gomes MW. Synopsis of medical pharmacology (1st edn), National Series, 2002. 5. Hardman, Limbird, Gilman. Goodman and Gillman: the pharmacological basis of therapeutics (10th edn), McGraw Hill, 2001.
6. Mycek MJ, Harvey R, Champe P. Lippincott illustrated review: pharmacology, (2nd edn), Lippincott Williams and Wilkins publisher. 7. Salil and Bhattacharya, Sen A, Ray A. Pharmacology (2nd edn), Elsevier, 2003. 8. Seth. Textbook of Pharmacology (2nd edn), Elsevier, 1999. 9. Sharma HL, Sharma KK, Gupta DK. Textbook of dental pharmacology (1st edn), Paras Publisher, 2008. 10. Tripathi KD. Essential of Pharmacology for Dentistry (1st edn), Jaypee Brothers Medical Publishers, 2005. 11. Yagiela, Neidle, Dowd. Pharmacology and thereaputics for dentistry (1st edn), Mosby Harcourt India, 2001.
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Professional Hazards of Dentistry 1035
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Professional Hazards of Dentistry
Introduction Medical faculty ensures service to humanity, personal job satisfaction and fulfilment of professional requirements but, it also has certain shortcomings and discrepancies. Dentistry, being an important branch of medical sciences is no exception to this.
Classification • Professional hazards to dentist from the patients. • Hazards to the dentist from his working conditions, methodology of practice and materials used. • Hazards to the dentist from law, i.e. ‘consumer protection act (CPA)’.
Professional Hazards to the Dentist from the Patients Dentistry has an environment, which is at least, dangerous and at worst, lethal. Most often patients suffer from one or the other diseases and due to mass awareness of the importance of these diseases, the problems arise. They are further aggravated by the fact that our profession deals with patient’s saliva, blood and mucus which have potential pathogenic microorganisms and are on a constant look out for a portal of entry. Hepatitis B and AIDS are the most threatening and contagious in almost all cases of infections can be transmitted percutaneously or nonpercutaneously and as dental treatment involves use of small sharp instruments; opportunity always exists for inadvertent percutaneous wounds to operator or the dental staff and thus inevitable spread of infection. Other infectious microorganisms like viruses, bacteria and fungi can also be transmitted in the dental office and
may either cause a relatively innocuous infection (common cold) or lead to temporary or even long-term debilitation or even death. Viruses are often shed asymptomatically in saliva or other secretions and cause infection to dentist, i.e. herpes simplex virus infecting eyes, hands, fingers. Health care providers can also be a victim of measles, chickenpox, infectious mononucleosis, cytomegalovirus infection, herpes zoster or mumps. Possibly, dentist gain an infection from patient in contagious stage of syphilis or tuberculous carrier, which is definitely a matter of concern.
Preventive Approach General • Proper medical history—medical history should be taken thoroughly and should be upto date. • Cleaning instrument—clean the instruments before sterilization, to remove all visible foreign deposits. • Sterilization methods—sterilization methods should be effective against all known pathogens and/or use of autoclave for various instruments. Working surfaces and dental units should be cleaned with chemical disinfectants such as 70% isopropyl alcohol, sodium hypochlorite solution and/or glutaraldehyde. • Disposable items—disposables items like suction tips, impression trays, beakers, needles, towels, masks, and caps should be used. • Aspiration and ventilation—use of high speed aspirators which exhaust externally and proper ventilation will definitely reduce the risk of cross-infection from the aerosols that are formed during certain dental procedures. • Management of sharp items—sharp items like needles, scalpels and local anesthetic cartridges should be placed in a soft container. Collection and incineration of surgical waste should be arranged.
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1036 Textbook of Oral Medicine • Training—all dental staff should understand the policies for prevention of cross-infection and implement them. Review all the procedures from time to time to ensure that they are being carried out correctly. Personal protection • Gloving—use of operating gloves and washing hands in between patients with appropriate chemicals are some of the important protective measure. • Dental dam—uses of dental dam provide an excellent barrier from microbial contamination from primary source, i.e. the patient’s mouth. • Management of cuts and wounds—cuts and wounds should be covered with waterproof dressings, at all times, even if gloves are worn. • Vaccinations—boosting immune defense of the operator by appropriate vaccinations is compulsory. • Face masks and protective eyeglasses—well fitting face masks and protective eyeglasses should be used during high speed cavity preparations or while using ultrasonic scalers and undertaking surgical procedures.
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Professional Hazards to the Dentist from his Working Conditions, Methodology of Practice and Materials Used Psychological Stress and Fatigue • Causes—psychological climate in a dentist’s office is as equally important as is technical expertise. Dentistry has a reputation of being a stressful occupation. Worrying about how others expect you to act, counteracting depression, pressure of keeping time schedules, dealing with anxious and uncooperative patient, law suit threat are all common sources of stress. • Burnout syndrome—we all appear to be prime candidates for the ‘burnout syndrome’ a syndrome of emotional exhaustion and cynicism frequently seen amongst professionals involved in direct communication with patients. • Prevention—you should cope up with and/or resolve the origin of cause and develop a pattern of healthy living.
Musculoskeletal Complaints • Causes—we all are guilty of adopting bizarre positions while treating our patients and even though such technique cause minimal patient discomfort, we as dentist, are in turn rewarded with muscle fatigue, lower back aches, shoulder problems, etc. • Prevention—reduction of physical stress to the body by adopting a correct posture is important in everyday practice. Low seated, closely supported dentistry with
certain physiotherapeutic exercises provide a new ray of hope.
Cardiovascular Complaints • Causes—it includes varicose veins, high blood pressure and occurs due to erect posture adopted during long standing operating procedures. • Prevention—proper positioning of doctor should be maintained.
Radiation Hazards • Cause—they are responsible for causing changes in blood, skin problems, tumor development, shortening of life span and mutations. • Prevention—use of lead partitions, lead aprons and cubicalization of patients in protective cabins of lead glass. Regular check-up of machines for radiation leakage. Periodic health checks-up of the operator.
Sound Hazards • Causes—air driven, high speed handpieces operating from 3900 to 12,500 Hz and electric engines are main contributing factors towards sound pollution. Hearing loss, acoustic stress and impaired power of concentration first affect the individual who are regularly exposed to frequencies above 3000 Hz. • Prevention—personal evaluation by routine otologic and audiometric examination. Noise attenuation by repair and replacement of defective items, especially high speed drills. Treatment rooms should be made acoustically satisfactory. Personal protection by using ear plugs and muffs which reduce high intensity sounds by 30 to 35 dB.
Light Hazards • Causes—dull light or too much bright light can be hazardous. Ultraviolet radiation used to polymerize sealant and composite restorations can be hazardous and may cause skin cancer and chromosomal changes. • Prevention—protective eye glasses for clinician, auxiliaries and patient with regular ophthalmic consultation is a must.
Hazards due to Materials Used • Mercurial hazards—it can be absorbed through skin and gastrointestinal tract but more commonly, poisoning results from absorption of vapors via lung. It is discuss in detail in chapter of pigmentation. Prevention should be done as follows • Education—health education regarding hazards due to mercury toxicity.
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Professional Hazards of Dentistry 1037
•
•
• • •
• Structural design—well-ventilated operatory and a proper structural design. • Floor covering—floor covering of nonporous polyvinyl chloride. • Avoid room heaters—avoiding room heaters and sterilization equipments in working areas, to minimize evaporation of mercury. • Proper storage—proper storage in sealed plastic containers. • Nontouch technique—use of nontouch technique during preparation of mercury. • Cleaning—immediate cleaning of mercuric spills and use of water sprays or suction, to prevent release of mercury dust. • Periodic health surveillance—periodic health surveillance by measuring mercury vapor levels. H2O2 30%—accidental fall of such chemical can cause itching, bleaching and considerable burning of the affected part. Nitrous oxide—if used in high concentrations during anesthetic administration, it may cause increased absorption and thereby liver and kidney damage with neuralgic disease and congenital abnormalities. Volatile oils—oil of clove and eucalyptus oil used in dentistry can cause mild burns. TCA and phenol—their overzealous use can injure both, the patient and the doctor. Root canal sealers—they have one or more contact allergens and thus cause hypersensitivity and dermatological problems.
Consumer Protection Act (CPA/COPRA) Surgeons are, at times, the privileged targets of school of law. Intentional damage to the patients and his minors definitely reaps a liability suit to the dentist but in many cases, the innocent surgeons are clutched by these laws thereby damaging the personal and professional ethics.
Introduction In recent period, the CPA has created a great stir amongst the medical profession on the ground that it would be extremely damaging to the profession and the public service. It was brought into existence in 1986 during which medical service was not included. In April 1995, the national commission, on appeal from Kerala state commission decided that medical service should be covered under CPA. Consumers section 2(d) of CPA defines consumer is a person who buys goods for a consideration which has been
paid or promised or partly paid and partly promised under any system of different payment. He is the one who hires or awaits of any service or services including any beneficiary. It includes user or beneficiary of goods or service, other than the person who actually buys goods or hires/awaits service where such use is made with the approval of the purchasers. According to section 2 (o) of the act service means service or any description which is made available to potential users, but does not include the rendering of any service free of charge or under the contract of personal service.
Purpose of Act CPA 1986 is not a substitute for the existing civil remedies. The redressal machinery set up under the CPA 1986 is an additional facility as stated under section (3) of the act itself. This section says that the act shall be in addition and not in derogation of provision of any other law for the time being in force. The CPA was brought into existence for the protection of interest of the consumer and for the settlement of consumer disputes with limited time frame and with fewer expenses. This enables consumer to make a complaint to a redressal forum in respect of defective service, if the service has been paid for. It provides for establishment of consumer councils and other authorities for the settlement of consumer disputes and for matter connected therefore. The district, state and national commission empowered as ‘quasi-judicial bodies’ has been established which looks into complaints of consumers where deficiency of service have come to the notice. These quasi-judicial bodies observe the principle of natural justice and are empowered to give relief of specific nature and award, wherever appropriate, compensation to consumer.
Advantages • Free—administration of justice under the CPA is totally free. Consumer court do not levy court fee in respect of legal proceedings. • Speedy justice—consumer courts are expected to deliver speedy justice. • Own lawyer—you can be your own lawyer before consumer courts, though appointment of lawyer is not prohibited. Consumer court does not encourage appearance of lawyer and extensive long-winded arguments. • Procedural simplicity—procedural simplicity and amicable atmosphere prevailing in consumer courts is more encouraging to an ordinary litigant as compared to lengthy and procedure oriented civil court proceedings.
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1038 Textbook of Oral Medicine Machinery
6
• District level—district consumer dispute redressal forum to be chaired by district judge and two other members, one of whom should be a man of good reputation and other should be a lady social worker. At district level, claim for compensation towards damages was fixed to a maximum of one lac at the starting which has been enhanced subsequently to rupees of five lacs in 1993. • State commission—it is for cases where compensation is claimed for more than rupee five lacs but less than twenty lacs. The complaint should be lodged before the state consumer dispute redressal commission which is chaired by high court judge and two other members as selected in case of district redressal forum. In this forum, an appeal against orders passed by district forum can be made. • National commission—it is for cases where compensation claimed for is more than twenty lacs. The complaint has to be lodged before the national body, i.e. national consumer redressal forum. This body is constituted by a judge of Supreme Court selected by Union Government to act as a president of forum with four other members including a lady member. It has been empowered to consider appeals arising from orders passed by any state commission. It is the apex body of redressal forum and has a revisional power.
Procedure • Filing of complaint—complaint is filed by consumer or any voluntary consumer organization registered under Society Registration Act, 1860 or under Company Act, 1056. • What complaint means—complaint means any allegation in writing made by complainant in regard to one or more of the following: • That he has suffered loss or damage as a result of any unfaired practices adapted by any doctor. • The service mentioned in complaint suffers from deficiency in any respect. • Timing of complaint—as provided under section 24(A) of CPA the complaint has to be filed within two years from the date on which cause of action arises. The complaint has to be filed in any redressal forum subject to its jurisdiction. • Contain of complaint—a complaint should contain • Name and description and address of complainant. • Name and description and address of opposite party. • The fact relating to complaint and when, where it arose. • Document if any in support of allegation containing the complaint.
• The relief which the complainant is seeking. • The complaint should be signed by complainant or his authorized agents. • Period for giving reply—after receiving the complaint copy of complainant, it has to be sent to opposite party directing him to give his version case within a period of 30 days which may be extended to 45 days. • Chance for appeal—appeal against order of district forum lies to state forum which in turn lies to national commission. • Timing of appeal—appeal has to be filled within 30 days of verdict. No fees have been prescribed for filling the appeal. Appeal has to be accompanied by certified true copy of order of district forum and reasons for filing appeal should be specified.
Medical Service and CPA • Charged service—in the act itself, there is no mention of medical service but a supreme court judgment by a bench comprising of three judges have held that doctors and hospitals who render service as medical practitioners are accountable for any act of medical negligence and ruled that they can be sued for compensation under the CPA provided the service has not been rendered free. Service rendered to a patient by registered medical practitioner, except where doctor renders service free of charge to every patient or under a contract of personal service by a way of consultation and treatment, both medical and surgical would fall within the ambit of services. • Free service will not come under CPA—services rendered free of charge by RMP attached to a hospital or nursing home or a medical officers employed in a hospital or a nursing home, where such services are rendered free of charge to everybody, would not be the service as defined in the act. • NGO service will not come under CPA—srvices rendered at non governmental hospital or nursing home where no charge, whatsoever is made from any persons awaiting the service and all patients (rich and poor) are given free service is outside the expression ‘service’. • Paid NGO service—services rendered at a nongovernmental hospital or nursing homes; where charges are required to be paid by persons, who are in position to pay and rendered free of charge for patients who can not pay fall within ambit of expression ‘service’, irrespective of the fact that the services are rendered free of charge to persons who are not in position to pay. • Free government service—services rendered at the government hospital health center or dispensary where no charge whatsoever is made from any persons awaiting the service and all patients are given free of
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Professional Hazards of Dentistry 1039 service is outside of preview of the act. The payment of token amount of registration purpose only at hospital or nursing would not alter the position. • Paid government service—service rendered at the government hospital health center or dispensary, where service are rendered on payment of charge and also render free of charge to other persons awaiting such service, would fall of the fact that service is rendered free of charge to person who do not pay for such service.
Ill Effects of CPA • Doctor patient relationship—it is contention in medical profession in general that the act itself during formulation, did not mean to include the services of a doctor rendered to his patients as doctor patient relationship is something more than consumer trade relationship. This act will totally disturb the doctor patient relationship which is considered to be noble.
• Extreme laboratory investigation—it will lead to undesirable tendency in doctors, particularly in general practitioner and new graduates, to be more invasive of their responsibilities towards the patients and refer more number of patients or cases to specialists and to advise extensive laboratory investigations which will make their position comparatively safe; without the improvement of clinical mind and experience; thereby making the treatment of general population to be costlier even up to the extent of being beyond the reach of many. • More patient treatment charge—doctors will develop a tendency to assure himself free from dangers of paying compensation by sticking to different professional indemnity insurance firms which are bound to crop-up to make a good business by taking advantage of this system. As a consequence of all this, patients will be charged more than what they are presently charged.
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1040 Textbook of Oral Medicine
50
Forensic Dentistry
Introduction
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Forensic odontology is the subject concerned with the application of medical and paramedical science knowledge to certain branches of law, both civil and criminal. The medicolegal information obtained from the examination of teeth and jaws falls in the preview of forensic odontology. Upon exposure to physical injury and putrefaction, the human dentition, the enamel of which is the hardest substance in the body outlasts all other tissues. The material used in restoration is also extremely resistant to destruction by chemical and physical elements. The fundamental principles of dental identification are those of comparison (when antemortem records of the proposed deceased are available) and exclusion (when antemortem records of other persons are available). In the absence of the antemortem records attempt to elicit dental information is made by interrogating the relatives and friends of the deceased, which may frequently prove unreliable. Forensic odontology may be defined as the application of dental science to the administration of the law and the furtherance of justice.
Scope of Forensic Odontology • Record preparation—the correct handling and examination and the proper preparation and presentation of dental evidence in both civil and criminal legal procedures. • Identification—personal identification, either individually or in context of mass disasters. • Age assessment—to calculate the age of patient. • Bite mark investigation—investigation of criminal cases where bite marks are involved and the interpretation of bite marks.
• Human abuse—recognition of domestic, and child abuse. • Lip print—comparison and identification of lip print. • Legal aspect—legal aspect of dental traumatology.
Record Management • Content—the dental record is a legal document of dentist which contains information about subjective and objective finding of the patient. It also includes pathological report, radiographs, and clinical photographs of the patient. • Treatment plan—treatment plan which is given to the patient should be updated in the record. All the letter of reference, letter of consent, insurance and financial statement should be store in the record of the patient. • Progress note—the progress note of the patient should contain information about the restorative and therapeutic procedure which are carried out on to the patient. • Record of telephonic conversation—summaries of the telephonic conversation with the patient, consultant, insurance company representative and legal authorities should be maintained in the record. • Signing of record—record should be signed by the personnel. Any change made in the record should not erased but a line should be crossed on it, so that it is readable. This will help to remove any fraud intention to alter record. • Electronic maintenance of dental record—it is common nowadays that dental record to be maintained electronically. Nowadays some software programs are developed to maintain patient dental information. This is advantageous as it can be easily networked and transferred. • Storage of record—record should be kept minimum of 7 to 10 years. In the case pediatric patient record should be maintain until the patient reaches the age to maturity.
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Forensic Dentistry 1041
Identification Forensic odontology is concerned with the identification of both living and deceased person.
Role of Teeth in Establishing the Identity Dental Comparison Dental comparison affords a potentially straightforward and simple means of establishing identity. The method of dental identification depends upon: • Resistance of dental tissue—the relative resistance of the mineralized dental tissues and dental restoration to changes resulting from decomposition or harsh environment extremes such as conditions of temperature and violent physical forces. • Individual characteristic of dentition—the unique individual characteristic of the dentition and dental restoration. • Antemortem record—the availability of documentation of the antemortem status of the dentition in the form of dental treatment records and diagnostic radiographs. Each individual has 32 teeth with 5 surfaces each with their own character of size, shape, position and spacing with the result that no 2 sets of teeth are alike (Fig. 50-1). Teeth extracted after death leave a completely different socket from those removed during life. When the tooth is removed or dental work of any sort is carried out the teeth pattern is changed and its record may exist with the dentist. In natural decomposition teeth are practically indestructible. They are not easily destroyed by fire. Being sheltered in the oral cavity they are generally not damaged. Teeth as well as dentures made of acrylic resin are generally resistant to the action of corrosive acids. The identification from data of authenticated teeth depends entirely upon the accuracy and completeness of authenticated records made during life. The record should include: • Number of teeth—the number and situation of teeth present and number and situation of teeth lost. • Arrangement—arrangement, irregularities, erosion, caries, fillings, bridge crown work and dentures. • Shape of arch—exact shape of edentulous arch should be noted down. • Identifying features—some of the common identifying features of teeth pertain to faulty development, faulty alignment, presence of stains, localized wear on certain teeth and missing teeth. • Faulty development—teeth may be undersized, oversized, notched or present some other irregularity as a result of faulty development and malformation. Hutchinson’s teeth constitute a classical example of
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malformation of the incisor in congenital syphilis. These changes are most conspicuous in central incisors which are usually small, widely spaced, notched and less broad at the cutting edge than at the gum margin giving them the appearance of tip of screw driver. Faulty alignment—the defect in the alignment may be in the space between teeth, e.g. widely spaced teeth or overriding teeth. Between the teeth of the upper and lower jaw when there is protrusion of upper incisors resulting in overlap of lateral incisors the bite pattern is known as overbite and the reverse pattern is known as crossbite. Stains—Pan (betel leaf, tobacco) chewing habit stains the teeth with dark brown or black deposits. Yellowish or dark brown stain on the back of incisor teeth is common in cigarette smokers. Chalky white or yellowish brown areas of discoloration are found in fluorosis. Metal poisoning may cause pigmentation of gums and thereby suggest a cause of death. Copper causes green and mercury and lead a blue black line on the gums. Gum hyperplasia induced by phenytoin may aid in identification and suggest epileptic seizure as a cause of death. Localized wear on certain teeth—A pipe smoker may have localized wear on teeth either on incisors or at angle of mouth due to position of pipe. Notched incisors from holding thread, pins, nail, between teeth on day to day basis may suggest the occupation of tailor or hairdresser or cobbler. Missing teeth—The missing tooth may have been lost antemortem or postmortem. Ante mortem loss of teeth due to trauma at or near the time of death if frequently associated with fracture of thin bony plate surrounding the alveolus. In loose tooth which has fallen out it is not so. Extraction or tooth loss in living person is followed by bleeding from its socket which stops in about 24 hrs or sometimes 2 to 3 days when the clot forms in the raw socket. By about 14 days, the clot is obliterated by fibrous tissue and the alveolar rim is smoothened by resorption of bone. By about 5 to 6 months, gradual new bone formation fills the socket but its outline is still visible on X-ray examination. By about 6 months to 1 year remodeling of new bone completely obliterates the socket leaving a slight depression and the socket outline is not visible on X ray examination. In recently recovered remains postmortem tooth loss discloses a clean socket devoid of blood clot. In skeleton in which postmortem loss of teeth is common, the bony rim of alveolus is sharp and feathered.
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1042 Textbook of Oral Medicine Procedure in Dental Identification
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• Area covered—it should include not only the oral cavity of the victim but when applicable, the surrounding scène as well, especially in case of conflagration or injuries when only the remnants of the dental arches may remain scattered and rubble and debris. Dental examination in mass disaster victims often by necessity must be accomplished under accident site and/or temporary mortuary. • Recovery of dental structure—the task of dental identification begins at the site of discovery of the body. When the gross postmortem changes affecting the teeth have occurred, such as charring, disintegration and fragmentation in fires and high impact accident, meticulous care in their recovery and conveyance to the mortuary are of utmost importance. Displaced teeth in decomposed bodies or skeletal remains should be saved, labeled and later secured to the intraoral position using adhesive cement (Fig. 50-1). Most open alveoli are the result of postmortem tooth loss. In recently recovered remains postmortem tooth loss disclose a clean socket devoid of blood clots.
Fig. 50-1: Human dentition consist of 32 teeth with 5 surfaces.
• Instrument—instruments used for dental examination include explorer, mirror, tissue forceps, heavy duty autopsy scalpel, handle and blades, tissue clamps, irrigating syringe, rubber autopsy gloves, polythene specimen bags, gauze sponges (for tooth cleansing) and a source of illumination (flash light or battery operated head lamps); and dental examination form should be used. • Reconstruction and examination—examination should be performed by two persons thoroughly familiar with dental terminology, one actually performing the examination and one recording the data. The recorder should view the actual teeth in order to record the basic morphological pattern of the restoration or cavities. In
some cases, it is necessary to remove the jaw from the body for more detailed examination and future reference. • Transcription of dental records—the point to be considered while charting are missing teeth, unerupted teeth, supernumerary teeth, restoration, prosthesis, dentures, decayed, broken teeth, mal position, overlapping, crowding and spacing, peculiar shape of teeth. • Identification of edentulous bodies—frequently dentures are present in the mouth of unknown bodies or may be found elsewhere. If the denture can be identified and it can be shown to fit the mouth of the deceased, a reliable identification can be made. The most reliable means of identification of denture is for them to be permanently marked with the name of the patient or some code during manufacture.
Problems in Identification Condition of material recovered • It depends upon the circumstances surrounding the death and the care exists in its collection and transport. • Incineration produces damage to teeth ranging from mild scorching of the surface to severe charring of the enamel and dentine with crumbling of the crown. • Sustained very high temperature will result in calcinations of the teeth with considerable overall shrinkage. • Burnt teeth are usually very fragile and suffer separation of the enamel and often gross disintegration of the crowns. • In high impact accidents such as aircraft and high speed road crashes much mechanical damage can occur and teeth and jaws may fracture and disintegrate. • Failure to recover significant material may result in failure to identify a body. Errors in examination—errors can easily be made in the examination and recording of the postmortem dental material. Inadequate antemortem data—errors in charting teeth treated and insufficient descriptive details about the treatment provided are common. Other difficulty arises when a dentist has retired and destroyed his records.
Technique for Identification in Mass Disaster These include X-ray, UV light, postmortem serology and DNA profiling.
X-ray All bodies which are found under suspicious circumstances and which are rendered unrecognizable due to prolonged immersion in water, burning by fire and acid or by any other destructive means such as explosion should
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Forensic Dentistry 1043 be routinely X-rayed. A dental radiograph when available constitutes one of the most valuable pieces of evidence for identification purpose. Panoramic X-ray technique provides excellent pictorial dental record (Fig. 50-2).
Fig. 50-2: Panoramic radiograph provides excellent record.
The CAPMI (computer-assisted postmortem identification) system compares dental record of victims of mass disaster and enables rapid identification of air crash, flood and explosion victims. Radiography can provide information in relation to age, sex, race, and occupation, diagnosis of certain conditions and identification and cause of death. Age—Age can be established by radiography of bones and teeth (for root calcification). Calcification of costal cartilage and osteoarthritic changes in large joints and the spine also help. Sex and race—may be deduced by radiography in some cases. Occupation—this can sometimes be deduced from X-ray. The whole range of pulmonary occupational diseases such as silicosis, asbestosis may show specific radiographic findings. The radial artery in laborer’s using pneumatic drill may show calcification; coal carriers and professional wrestlers are liable to calcified lesions of the ligamentum nuchae. Football players may show calcified hematoma of the thigh muscle. Identification—it is possible by comparison of postmortem and antemortem X-ray (Fig. 50-3). Cause of death—fracture of bones seen on X-ray may indicate their antemortem origin and these include depressed fracture of skull, fracture of hyoid, fracture dislocation of cervical vertebrae, severe injury to bones by cutting instrument or fracture of several ribs which are incompatible with life. Foreign bodies in the upper respiratory tract provide valuable clue. Evidence of poisoning by heavy metals and signs of diseases such as malignant growth may be apparent.
Fig. 50-3: Intraoral periapical radiograph will help to identify the victim on the basis of radiopaque filling.
UV Rays An ultraviolet lamp can be used to locate and define tattoo marks and scars on burned and decomposed remains, and to segregate bones in cases of mix-up. When examined by UV light washed blood stains are readily seen and seminal stains give a bluish white fluorescence.
Postmortem Serology A known postmortem grouping of an individual serves to narrow the range of possible identities. Even in putrefied bodies, blood group antigen may be detectable for serological studies. The bone marrow in skeletal remains may still retain serologically detectable antigens.
DNA Profiling This is useful if suitable tissue (blood, semen stored in bank) is available. If such tissue is available a DNA profiling or autopsy derived tissue should be compared by single probe analysis with that of parent, children, sibling and if be necessary other relatives. This is now used worldwide in aircraft and other major accidents. The techniques which are used for DNA profiling are Restriction fragment length polymorphism (RFLP) and polymerase chain reaction (PCR). RFLP results in splitting source DNA into thousand of fragment. PCR can do evaluation of denture DNA or minute quantity of DNA.
Age Assessment Chronological age assessment may be an important factor in establishing the identity of the living or deceased person.
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1044 Textbook of Oral Medicine It is also important in legal proceedings when specific charge for particular offence may depend on whether the alleged offender is a juvenile. Visual observation—stage of eruption of the teeth and evidence of changes due to function such as attrition can give an approximate estimate of age. Radiography—it can provide a great detail, the gross stage of dental development of the dentition. Histological—it requires preparation of the tissue for detailed microscopic examination, which can determine more accurately the stage of development of the dentition. Physical and chemical analysis—it is done to determine alterations in ion levels with age have been proposed.
Bite Marks
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One of the two major interests of the forensic odontologist is one that has direct relevance to the pathologist, in that it concerns the interpretation of trauma to the body surface. Dental evidence is used to identify the perpetrators of a crime who happened to have left their teeth marks in some substances left at the scene. Generally, it is easier to exclude a certain person than to identify one conclusively from the bite mark.
Definition A bite mark is a patterned injury produced by teeth on animate or inanimate objects, is caused by small enamel defects on the incisal edge of incisor teeth creating individual characteristics during biting procedures. It can be: • Tooth mark—mark left by a tooth (human or non-human). • Arch mark—mark produced by four or five adjacent teeth in the same arch (Fig. 50-4).
Fig. 50-4: Bite marks on inmate subject presented as arch.
Causes • Child abuse—it can be found anywhere on the body, favorite sites being the arms, hands, shoulders, cheeks, buttocks and trunk. Most of the time it is inflicted by the mother. • Sexual assaults—it usually occurs in cases of rape. Most common site of it is breast and nipples but neck, shoulders, thighs, abdomen, pubis and even vulva may be attacked. • It may also be inflicted on police officers when attempting to arrest resisting offenders. • Sports—bites can occur in sporting events especially football and some forms of wrestling. In this, it can occur anywhere but hands, fingers, nose, forearms, ears and even lips may be target. • Self inflicted—falls onto the face or a fit may cause the tongue and lips to be badly bitten. Some persons deliberately bite themselves, sometime to fabricate injuries for a variety of motives ranging from gain to psychiatric disorders.
Importance of Bite Marks It can permit precise identification because the alignment of teeth is peculiar to each individual (Fig. 50-5). The mark may be on the article of food found at the scene of crime or on human being to realize that a bite on human flesh can have marks not necessarily due to break in the continuity of the skin but due to a small subdermal or thin deep hemorrhage.
Fig. 50-5: Bite mark is represented distorted image of human dentition.
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Forensic Dentistry 1045 Bite marks are always contaminated by saliva and therefore contain amylase, ptyalin and blood group which can be determined by the cast of suspect of mouth is made and transparency of his bite compared to that of the unknown bite. It should be remembered that bite marks on skin are modified by its elasticity when the teeth are withdrawn.
biting edges and where there is greater penetration the record is of the labial aspect of the teeth.
Method of Preservation of Bite Marks
Bite Marks in Human Skin
The doctor should be asked how the bite mark may be best preserved. When the substance is plastic such as butter, cheese, lard, or chocolate, it should be stored in a refrigerator to prevent melting or gradual flowing. It should not be deep frozen as this may cause brittleness and cracking. Fruits should be preserved in Campden solution, a metabisulphite fluid used for fruit bottling. If it is not there then 5% acetic acid in 40% aqueous formaldehyde solution can be used. Whatever preservation is recommended, the object should be adequately photographed with film plane at right angles to the bite and a scale placed in the focal plane. Death freezes a bite mark but a subdermal hemorrhage in living person disappears within 20 minutes hence it is important to take an immediate photograph of the bite mark.
Human tissue has been described as one of the least dependable substances for the registration of bite marks as the bite marks in the tissue is affected by several variables.
Classification of Bite Marks
Sex—females tend to bruise easier than males. Once produced a bite mark will be evident for a longer period of time on females as compared to males. In human bite mark can be sexual (Fig. 50-6) or assault (Fig. 50-7) type.
• Non- human (animals) • Human • In foodstuffs (in a part eaten foodstuff abandoned by offenders at the scene of crime). • On non-biological object (on pencils, pipe stems and detonators). • In human skin • Non-criminal (erotic bite) • Criminal—it can be offensive (upon victim by assailant) and defensive (upon assailant by victim).
Time and temperature—bite mark in foodstuff may produce the exact mesial-distal dimension of the teeth provided the record is taken immediately after the bite was made. Dimensional and color changes are expected to occur in the foodstuffs due to effect of temperature.
Status of the Tissue Site—type of tissue/condition of skin. For example loose skin or excessive subcutaneous fat commonly demonstrated easy and extensive brushing leading to a poor bite mark definition. Areas of fibrous tissue or high muscle content tend to bruise less easily and thus are more likely to demonstrate a bite mark. Age—infants and elderly individual tend to bruise more easily than other age groups marking the detection of bite marks more difficult.
Bite Marks on Foodstuff Foodstuff bite marks can be classified into 3 types: • Type I—bites that are found in material such as chocolate, which fracture readily with limited depth of tooth penetration. • Type II—bites formed in foods where teeth obtain a good grip and then bitten piece is removed by fracturing it from main material, e.g. apples. • Type III—bites in which teeth bite right through the bitten material, e.g. cheese. These bit exhibit extensive scrape marks and may give an indication of the relative position of upper and lower incisor teeth in centric occlusion. Depth of penetration of the teeth—where there is only minimum penetration of teeth into the food, the record is of
Fig. 50-6: Sexual bite mark.
The Influencing Factor Bite mark can be influenced by time elapsed between the actual biting and when the impression is made. Depression of the skin as occurs in most bite marks will recover within
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1046 Textbook of Oral Medicine
Fig. 50-7: Assault bite mark.
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10-20 minutes after the bite, although discoloration and swelling may be present 24-72 hours on a living object. The force exerted—the skin appearance of bite mark may vary from bruising, abrasion, and indentation to actual lacerations. The number of teeth—in general the more teeth marks present in the bite marks, the better is the likehood of identification utilizing that bite mark. The type of teeth—in many cases the bite mark is seen to be comprised of the upper anterior teeth. The investigator should take note of the width of teeth. The reaction of the surrounding tissue—bite marks made hours or days before the event will show inflammatory changes and signs of healing microscopically.
Types of Bite Mark • • • • •
Definite bite mark Amorous bite mark Moderately aggressive bite mark Aggressive bite mark Very aggressive bite mark
The Nature of Bite Marks Though called bite marks, but sometimes it may not be from actual teeth. The lips can transiently mark the skin, if forcibly nipped, especially on children. Suction can produce a crop of punctate hemorrhages, either small petechiae or larger ecchymoses merging into a confluent central bruise.
It is caused by front teeth from canine to canine with a gap at either side representing the separation of upper and lower jaw. A human bite is near circular or a shallow oval. A deep parabolic arch or ‘U-shaped’ can only be animal in origin. The teeth may cause clear, separate marks or they may run into each other to form a continuous or intermittently broken line. As the time progresses original teeth marks spread out and blur. Teeth marks may be abrasion, bruises or laceration or a combination of any two of three. The clarity of bite marks depends on a number of factors: • If the contour of the part bitten is irregular or markedly curved, then only part of dental arch is in contact with the tissues. • If the bite is forcible, then extensive subcutaneous bruising may spread and blur the outline. • If the bite is inflicted many days before, then healing of abrasion and lacerations and absorption of bruising will leave progressively less detail. • When the teeth are forcibly applied the typical appearance is of two ‘bows’ with their concavities facing each other and a gap at each end. • Love bites—they are caused by firm application of the lips, which form an airtight seal against the skin, and then sucking action reduces the air pressure over the center. This causes shower petechial hemorrhage to appear from rupture of small venules in the superficial layer of the subcutaneous tissue. If forcible the petechiae are confluent and a frank bruise or even hematoma develops.
Investigations of a Bite Mark Firstly the bite mark should be carefully and fully photographed. The photograph should be taken from different angles, but especially from directly perpendicular viewpoint, with the plane of film at right angle to that of the lesions. An accurate scale should always be held near the lesion, as close as possible. The lesion should almost fill the camera frame in some shots to capture as much detail as possible. When photography is completed, swabs of the bite should be taken to try to recover saliva. Plane cottonwool swab are gently rubbed onto the bite. They should be then deep frozen unless send straight to the serology laboratory. After this, impression of the bite can be taken (Figs 50-8 and 50-9). It is done by laying a plastic substance over the bite mark, which then hardens, so as to produce negative cast of the lesion (Fig. 50-10). It is usually made with a rubber- or silicone-based medium containing catalytic hardeners. Less satisfactory substances are water based pastes, such as plaster of Paris, which are put on wet and allowed to dry before removal. But they have a disadvantage
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Forensic Dentistry 1047 of potential damage to the actual bite. After autopsy, it is also possible for the whole area of the skin carrying the bite to be removed and preserved in formalin for future examination.
Matching the Bite Mark with the Suspect Dentition (Figs 50-11 to 50-14) The teeth of those who are either suspected by the police or who had access to the victims should be examined. In most jurisdictions, it is vital that fully informed consent should be obtained from the persons beforehand. Any refusal must be a bar to any further action. When children are concerned, usually in the setting of child abuse, the consent of fully informed parents or guardian must be Fig. 50-8: Sample bite taken on apple
6 Fig. 50-11: Bite mark of suspect is taken.
Fig. 50-9: Impression is taken of the bite and cast is made.
Fig. 50-10: Study case is made.
Fig. 50-12: Positive replica of bite mark is made.
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1048 Textbook of Oral Medicine
Fig. 50-13: Cast of suspect is made.
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• Graze—abrasion caused by friction between skin and hard surface. • Scratch—it is caused by pointed ends of nails, pins, needles, etc. It is localized linear abrasion. • Imprint abrasion or pattern abrasion—it gives the pattern of object on the skin. For example teeth bite. • Bruise or contusion—subdermal-extravasation of blood from rupture of subcutaneous vessels and capillaries of skin and organs. • Laceration—wound must be produced with a blunt object that penetrates the skin to subcutaneous tissue. • Incised wound—must be cause by sharp edged object like knife. In incised wound length is more as compared to width and depth. • Stab wound—it is caused by pointed end of sharp edged or blunt object. Depth is more as compared to width and length. Contusion and abrasion are described in two dimensions, i.e. length and width. Laceration, incised wound and stab wound described in three dimensions.
Medicolegal Aspects of Dentistry The Dentist Act 1948 The act was passed to regulate the profession of dentistry in general and to constitute the Dental Council of India and for a register called ‘Indian Dentist Register’. It also provides for the constitution and composition of the State Dental Council and for State Register of Dentists.
Duties of Dental Council of India Fig. 50-14: Cast is matched with previous mark.
obtained. Then dentition is examined for number of teeth, missing teeth, complete or partial denture, occlusion, broken teeth, irregular teeth and abnormalities of the teeth. Photographs of dentition of the patient can be taken. After that impression of bite of suspect should be taken. Tracing can be made from the positive cast of a bite impression, inking the cutting edge of front teeth and transferring these to transparent sheets, which can then be laid over the photograph to determine correspondence.
Classification of Skin Wounds Abrasion—it is superficial type of injury only skin part is involved, i.e. both epidermis and dermis. It heals without the scar formation. It is of following types:
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To maintain the dental register. To regulate dental education. To recognize the foreign dental qualification. Appeal against indisciplinary action. To give warning notices to dentist for his/her misconducts.
Duties of State Dental Council • To maintain dentist register. • To take disciplinary control. • To give warning notice to dentist for his/her misconduct.
Hippocrates Oath: The Declaration of Geneva • I solemnly pledge myself to consecrate my life to the service of humanity. • I will give my teacher, the respect and gratitude which are their due.
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Forensic Dentistry 1049 • I will practice my profession with conscience and dignity. • I will respect the secrets which are confided in me. • The health of my patient will be my first consideration. • I will maintain by all the means in my power, the honors and the noble tradition of the medical profession. • My colleagues will be my brothers. • I will not permit consideration of religion, nationality, race, party, politics or social standings to intervene between duties to my patient. • I will maintain utmost respect for human life from the time of conception, even under threat; I will not use my medical knowledge contrary to laws of humanity.
Rights and Privileges Enjoyed by Registered Dental Practitioner • Right to choose the patients. • Right to use title and description of the qualification which is actually possessed. • Right for appointment in public and local hospital. • Right to prescribe and/ or dispense medicine to his patients. • Right to realize fee and other expenses. • Right to issue medical certificates and medicolegal reports regarding dental problems. • Right to evidence in a court of law as an expert witness. • Right to exemption from serving as a juror at an inquest.
Duties of Dental Practitioners • Duty to exercise a reasonable degree of skill and knowledge. • Duties with regard to attendance and examination. • Duty to furnish proper and suitable medicines. • Duty to give instructions. • Duty to control and warn. • Duty towards children and adults incapable of taking care of themselves. • Duty to inform patient of risks. • Duty to notify certain diseases. • Duties with regards to operation. • Duties under Geneva conventions. • Duties with regard to consultation. • Duty in connection with X-ray examination. • Professional secrecy.
• Withholding from health authorities information of notifiable disease. • Performing or enabling an unqualified person to perform an abortion or any illegal operation for which there is no indication. • Violating the provisions of the Drug Act. • Selling scheduled poisons to the public under cover of his qualifications. • Using of touts and agents for procuring patients. • Disclosing the secret of a patient. • Association with manufacturing firms. • Advertising. • Professional association with bodies or societies of unqualified persons formed for the purpose of turning unqualified practitioner. • Running an open shop for sales or medicines for dispensing prescription of other doctor or for sale of medical and surgical appliances. • Refusal to give professional service on religious grounds. • Drunk or disorderly so as to interfere with proper skilled practice or medicine.
Precautions Against Negligence • • • • • • • •
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Professional Misconducts
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• Adultery. • Improper conduct or association with patient or member of patient’s family. • Conviction by court of law. • Issuing false certificates.
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Obtain informed consent of the patient. Establish good rapport with the patient. Keep full, accurate and legible medical records. Employ ordinary skill and care at all time. Confirm diagnosis by laboratory tests. Take skiagrams in bone or joint injuries or when diagnosis is doubtful. Immunization should be done whenever necessary particularly for tetanus. Sensitivity tests should be carried out before injecting preparations which are likely to cause anaphylactic shock. Seek consultation where appropriate. In suspected cases of cancer all laboratory investigations should be done without delay to establish early diagnosis. Do not criticize or condemn the professional ability of another doctor especially in the presence of the patients. Do not make statements admitting fault on your part. Avoid firm overconfident prognosis and promising too much to patients. Never guarantee a cure. Inform the patient of any intended absence from practice or recommended or make avail of a qualified substitute. Transfer the patients if facilities are inadequate to handle his problems. The drug should be identified before being injected. Obtain consent for an operation or giving anesthesia. No experimental procedures should be adopted without the consent of the patient.
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1050 Textbook of Oral Medicine • No procedures should be undertaken beyond one’s skill. • Keep yourself informed of technical advances and use standard procedures of treatment. • Frequently check the condition of equipments and use safety installations. • Proper instructions should be given to patient and proper postoperative care should be given. • The patient must not be abandoned. • No female patient is examined unless a third person is present. • Do not order a prescription over the telephone. • Anesthesia should be given by qualified medical professional only. • Do exercise care in the selection of assistants and allotting duties to them.
Penal Provisions Applicable to Medical Practice
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• S.176 IPC—omission to give notice or information to public servant by person legally bound to give it. • S. 177 IPC—furnishing false information. • S.191 IPC—giving false evidence. • S.192 IPC—fabricating false evidence. • S.193 IPC—punishment for false evidence. • S.197 IPC—issuing or signing false certificate. • S.201 IPC—causing disappearance of evidence of offence, or giving false information to screen offender. • S.203 IPC—giving false information respecting an offence committed. • S.204 IPC—destruction of document (or electronic records) to prevent its production as evidence. • S.39 cr. P.C—every person aware of the commission of
the intention of any other persons to commit any offence punishable under IPC, shall forth give information to the nearest magistrate or police effective of such commission or intention. • 304 (A) IPC—causing death of the patient due to rash or negligent act. • 320 IPC—grievous hurt—the following kind of hurt only designated as ‘grievous’ hurt. • First—emasculation • Second—permanent privation (loss) of the sight of either eye. • Third—permanent privation of hearing of either ears. • Fourth—privation of any member or joint. • Fifth—destruction or permanent impairing of the powers of any member or joints. • Sixth—permanent disfigurement of head or face. • Seventh—fracture or dislocation of bone or tooth. • Eighth—any hurt which endangers the life or which causes sufferer to be during space of 20 days in severe bodily pain, or unable to follow his ordinary pursuits.
Suggested Reading 1. Barsley RE. Forensic and Legal Issue in Oral Diagnosis. Dent Clinic of North Am 1993;37:143-44. 2. Jakush J. Forensic Dentistry. JADA 1989;119:355-68. 3. Standish SM, Stimson PG. Forensic Dentistry Legal Obligation and methods of identification for the practitioner: Dent Clin of North Am 1977;21:1-196. 4. Neville, Damm, Allen, Bouquot. Oral and Maxillofacial Pathology (2nd edn), 2004; Saunders Elsevier.
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Controversial Diseases and Terminologies
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1051
Controversial Diseases and Terminologies
Introduction As there is changing era with more advance diagnostic technology coming up, nomenclature of some of the diseases should be revived and changed. In dentistry, there are many disease names which are nowadays either discarded or had been given new names. But, as it is being said difficulty lies not in new ideas but escaping old one, we many times not accept the newer terms and stick to older ones. This chapter will give emphasis on some of older terminologies and why it should not be used. Some of the diseases in this chapter are described in detail. The reason for this is that in many parts of the world these terminologies are still used. But as a practice, we should start using new terminologies to avoid confusion in mind of budding dental professionals.
• Appearance—it appears as slowly enlarging erythematous patches. • Skin—there is a red and slightly scaly area on the skin, which eventually enlarges and turns into white or yellowish lesion. • Signs—when these scales are removed, it produces a granular surface without bleeding.
Why Discarded Bowen’s disease nowadays synonymous with carcinoma in situ. Histologically, Bowen’s disease is characterized by disorganized growth, presence of large hyperchromatic nuclei and multinucleated cells which are the same features that are seen in carcinoma in situ.
Leontiasis Ossea
Bowen’s Disease It is localized ‘intraepidermoid carcinoma’ that may progress to invasive carcinoma over many years, which is characterized by progressive scaly or crusted plaque-like lesion.
The word ‘leontiasis’ has been used to describe the leonine appearance of some patients with facial leprosy. Virchow added the word ‘ossea’ to describe leonine appearance in bilateral bone disease of the face and thus, the term leontiasis ossea came into being.
Etiology • Sun exposure—this is thought to be causative factor for the Bowen’s disease. • Arsenic ingestion—accidental ingestion of arsenic can lead to this disease.
Clinical Features • Age and sex distribution—it is common in older age group with more predilections for males. • Location—it occurs on male and female genital mucosa and in oral mucosa as erythroplakia, leukoplakia or erythematous lesion.
Etiology • Bone disease—most cases of leonine face are result of bone disease from two conditions i.e. fibrous dysplasia and Paget’s disease. • Metaphysial dysplasia—bilateral and symmetrical involvement of the face and jaws may be seen in some cases of metaphysial dysplasia and in diphysial dysplasia. • Periostitis of jaw bone—some cases of leonine ossea are due to periostitis of the jaw bones or it may be due to osteitis fibrosa.
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1052 Textbook of Oral Medicine Clinical Types • Early childhood type—starts early in life and quickly extends until skeletal growth ends, when the lesion ceases to grow but does not regress. • Young adult type—second group starts in early years and while it progresses slowly or quickly, it does not cease with the end of somatic growth but continues its activity and may produce gross and terrible consequences. • Adult type—the third type starts in early adulthood or even near the middle life and progresses slowly and inexorably.
Clinical Features
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• Appearance—there is bilateral enlargement of the facial bones, sometimes producing the leonine appearance. • Site—a classical case is one in which there is enlargement of maxilla, mandible, and malar bones and in some cases, changes in the frontal as well as ethmoid, sphenoid and temporal bones. In some cases, there is partial deformity of the face, either unilateral or bilateral, but without leonine appearance. • Orbit—the orbital cavity is reduced in size and the eye is protruded. Blindness follows compression of the optic nerve or the eyeball and difficulty in breathing is the result of narrowing of the nasal passage.
• Marrow spaces—in some cases the trabeculae are thickened and dense, with narrowing of the marrow spaces.
Why Discarded Nowadays this term is never used as it requires a lot of imagination to see lion in it.
Previous or Former Cyst Nowadays some of the names which are used to describe earlier are not in use or they are no longer suitable. It includes primordial cyst which is seen to be odontogenic keratocyst, globulomaxillary cyst which nowadays seems to be odontogenic origin as entrapment theory is not accepted. Globulomaxillary cyst is said to be radicular, lateral periodontal cyst or OKC. Other cysts which now said to be not in existence are median mandibular cyst and median palatal cyst which are variants of nasopalatine duct cyst.
Primordial Cyst It is one of the less common types of odontogenic cysts.
Origin
Radiographic Features • Radiodensity—the affected bones vary in size and density. • Appearance—there may be symmetrical thickening and increased density of the bones without any leonine faces. • Mandibular lesions—there is tendency of mandible to present a characteristic appearance. The inferior margins of the bone, deep to bicuspid and molar region projects downward, perhaps very markedly, while the incisor area is either unchanged or only slightly deeper than normal. • W appearance—the effect of altered configuration of the mandible is that it represents a rough caricature of the letter W. • Cumulus cloud—the surface of the bony projection from the inferior aspect of the mandible may present irregular appearance resembling the cumulus cloud. • Nose—the nasal bone is often thickened and nasal septum may or may not be involved. • Frontal bone—in some cases there is marked prominence of frontal bone over the orbits. • Face—there is gross deformity of the face, with large mass of bone projecting from the mandible on one side and another, from the opposite paranasal region. • Skull—the base of the skull tends to be either granular in structure or homogeneous and structureless, but very dense.
• Stellate reticulum—it originates when cystic changes take place in the stellate reticulum of the tooth germ before any calcified enamel or dentin has been formed. So, it is found in place of a tooth rather than directly associated with it. • Supernumerary tooth—it may originate from the enamel organ of supernumerary tooth or from the remnants of dental lamina.
Clinical Features • Occurrence—less common and account for only 5% to 6% of cysts of the odontogenic variety. • Age and sex—it is found in children and young adult between 10 and 30 years of age, although it may persist in older age group and occurs with equal frequency in both the sexes. • Site—it can arise in any portion of the jaw, but most often seen in the ascending ramus of the mandible and in third molar area. It is occasionally associated with an over-retained erupted deciduous tooth. • Symptoms—it has a tendency to painlessly enlarge and slowly replace large portions of cancellous bone before expansion of the cortical plate by way of which it reveals its presence. Pain which is associated with a large cyst
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Controversial Diseases and Terminologies is caused by infection that may follow the perforation of the expanded cortical plate. • Aspiration—when aspirated, they yield a thick granular yellowish material.
Radiographic Features • Radiodensity—cyst-like radiolucency that is well defined and have hyperostotic borders. • Internal structure—it may be unilocular or have a scalloped outline that gives it a multilocular appearance (Fig. 51-1). • Teeth—it produces deflection of adjacent tooth root, but seldom cause any root resorption. The involved tooth is missing because of failure of the tooth to develop. • Those in maxilla are smaller than their mandibular counterparts.
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which occurs at the junction of globular portion of the medial nasal process and maxillary process. Previously existence of globulomaxillary cyst was disputed by Christ who said that development of anterior maxilla occurs by merging of growth center and not by fusion of facial processes so no entrapment occurs because it cannot exist. Recent embryonic studies have demonstrated that Christ’s view of facial development is incorrect. Fusion of facial process does occur and epithelium is entrapped in areas that will later lie between the maxillary lateral incisors and canines. In conclusion, recent evidence favors the re-introduction of the globulomaxillary cyst as a specific pathologic entity with varying histologic features. • Odontogenic origin—recent theory suggests most of cyst originating in globulomaxillary area are of odontogenic origin. This is reason nowadays, it is assumed as variant of lateral periodontal cyst, radicular cyst or OKC.
Clinical Features
Fig. 51-1: Primordial cyst showing radiolucency in lower anterior region with missing central incisor.
Why Discarded Nowadays this term is not used and this cyst is thought to be odontogenic keratocyst.
• Location—it is present between maxillary lateral incisor and canine. • Symptoms—it is asymptomatic and is discovered during routine radiographical examination. If cyst becomes infected, patient may complain of local discomfort or pain in that area. • Teeth—as it enlarges, it expands the buccal cortical plate between maxillary lateral incisors and canines. This will diverge the roots of two teeth and their crown resulting in moving contact point incisally. Adjacent teeth are usually vital. • Signs—mucosa over the expanding cortex remains normal in color. If cortical plate is eroded then fluctuant swelling develops. Palpation will produce crepitus. If it becomes secondarily infected, the expansion will mimic lateral periodontal abscess. Aspiration of the swelling is productive of typical amber colored cystic fluid.
Radiographic Features
Globulomaxillary Cyst It is also called ‘intra-alveolar cyst’. It occurs in globulomaxillary area. There is evidence that the cyst acutely forms in the bone suture between the premaxilla and maxilla, the incisive suture, so that location may be different. Due to this Ferenczy has suggested the term ‘premaxilla-maxillary cyst’.
Pathogenesis • Fissural cyst—it was considered to be an inclusion or developmental cyst that arises from entrapped nonodontogenic epithelium in globulomaxillary suture
• Pear-shaped radiolucency—it appears as pear-shaped (Fig. 51-2) or tear-shaped radiolucency between roots of maxillary lateral incisors and canines. Small end of the pear is directed toward the crest of alveolar ridge. The upper border may invaginate the floor of the nasal fossa or the antrum. • Size—is variable and may reach the maximum level of diameter of 3-4 cm. • Teeth—it may cause divergence of the roots adjacent teeth (Fig. 51-3). Displacement of the teeth is common. In some cases root resorption is also seen. The rotation and separation of the lateral incisor and canine roots will usually be apparent on the radiograph.
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1054 Textbook of Oral Medicine • Traumatic bone cyst—it appears as round shaped with moderately defined outline. Needle aspiration is nonproductive. • Adenomatoid odontogenic tumor—radiolucency is associated with unerupted teeth. In mature stage, it appears as radiolucent with radiopaque foci. • Surgical defect—patients give history of surgery. • Odontogenic myxoma—in myxoma, mandible is more commonly affected. It shows a typical honeycomb pattern. • Anatomical variation—in some cases, prominent incisive fossa can get confused with globulomaxillary cyst. But location of incisive fossa is in anterior region between central incisors. Fig. 51-2: Pear-shaped radiolucency of globulomaxillary cyst seen between lateral incisor and canine. Note there is also root resorption of teeth.
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Why Discarded and Updated Term As the study by embryologist shows that there is no process or bony primordia are separated by epithelium. So there is no chance of entrapment of epithelium in this location so use of term globulomaxillary cyst is discarded. Nowadays any cyst in that location will be either radicular cyst from nonvital lateral incisor, or odontogenic keratocyst or adenomatoid odontogenic cyst.
Median Mandibular Cyst The median mandibular developmental cyst is an extremely rare lesion occurring in the midline of the mandible. It is of questionable existence.
Origin Fig. 51-3: Crop OPG showing radiolucency in lateral and canine region causing the divergence of teeth (Courtesy Dr Ashok L).
• Lamina dura—lamina dura of the adjacent teeth are usually intact.
Differential Diagnosis • Lateral periodontal cyst—radiographically, it appears as a dome-shaped radiolucency more commonly seen in mandibular lateral incisor and first premolar region occurring in an older age group. • Lateral dentigerous cyst—it is commonly associated with impacted teeth. The radiolucency is associated with the crown (attached to the neck of the tooth). • Primordial cyst—it is more common in mandibular posterior region. • Giant cell granuloma—it is more common in anterior region. Usually, it appears as a mandibular multilocular radiolucency.
• Fissural cyst—some authors consider it as a true developmental cyst originating from proliferation of epithelial remnants entrapped in the median mandibular fissure during fusion of bilateral mandibular arches. But, as mandible is single bilobed proliferation of mesenchyma with central isthmus, there is no fusion of epithelium line process occurs, so entrapment of epithelium will not occur. So this theory is not possible for the development of median mandibular cyst. • Odontogenic origin—nowadays, it appears that this entity, is a variant of lateral periodontal cyst or odontogenic keratocyst.
Clinical Features • Site—it has got predilection for the inferior part of the mandible, in the central incisor region. • Symptoms—most are clinically asymptomatic and are discovered only during routine radiographic examination.
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Controversial Diseases and Terminologies • Signs—they seldom produce obvious expansion of the cortical plate of bone. • Teeth—associated teeth react normally to pulp vitality test.
Radiographic Features • Appearance—it is unilocular, well-circumscribed radiolucency, although it appears multilocular. • Shape—the image is well defined, round or ovoid radiolucency that may be regular or irregular in shape. • Lamina dura—the lamina dura around the lower incisor teeth is intact. • Teeth—as it expands, it diverges the roots of the mandibular incisors.
Why Discarded This cyst is discarded as there is no possibility to have epithelial entrapment during embryonic fusion in mandible.
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Differential Diagnosis • Radicular cyst—vitality test and periapical radiographs demonstrate intact lamina dura and normal periodontal ligament space in median palatine cyst. • Palatal space abscess—soft, fluctuant swelling and yield pus on aspiration and non-vital teeth found adjacent to it which give rise to infection. • Incisive canal cyst—it occurs in canal above palatine papillae while midpalatine cyst occurs in midline of palate posterior to palate. • Retention phenomenon—seen laterally and not in midline. Aspiration would not yield amber colored fluid but viscous clear sticky liquid. • Malignant and benign tumors of salivary gland—laterally and not in midline.
Why Discarded This cyst is nowadays thought to be posterior extension of nasopalatine cyst.
Median Palatine Cyst
Adenomatoid Odontogenic Tumor
It is rare fissural cyst that developed due to entrapment of epithelium in line of fusion of lateral palatal shelves of maxilla. It is very difficult to distinguish from the nasopalatine cyst. Nowadays it is known as posterior extension of incisive canal cyst.
It is also called ‘Adenoameloblastoma’ or ‘ameloblastic adenomatoid tumor’. It is tumor of odontogenic epithelium with a duct-like structure and varying degrees of inductive changes in the connective tissue. The tumor may be partly cystic and in some cases the solid lesion may be present only as masses in the wall of a large cyst. A well-circumscribed lesion derived from odontogenic epithelium that usually occurs around the crowns of unerupted anterior teeth of young patients and consists of epithelium in sworls and ductal patterns interspersed with spherical calcifications.
Clinical Features • Site—it is very rare and develops in the midline of the hard palate posterior to pre-maxilla. • Symptoms—patient notices the swelling in the midline of palate posterior to palatine papilla. It is usually asymptomatic but some patients may complain of pain. • Signs—it is fluctuant and non-tender. Overlying mucosa is normal. Corticated plate may be perforated as the cyst grows. Expansion is rare in this cyst. • Teeth—maxillary teeth are vital and aspiration produces amber colored fluid. • If floor of nasal fossa is eroded, cyst may be superiorly displaced.
Radiographic Features • Site—radiolucent lesion is behind the incisive canal in premolarmolar area. • Margins—well-defined borders which are hyperostotic. • Appearance—nasal septum image crosses the septum and appears on occlusal radiographs. • Teeth—in some cases, divergence of teeth may occur.
Origin • Dental epithelium—the close resemblance of the columnar cells to ameloblasts and the frequent association of the tumor with unerupted teeth indicate its origin from dental epithelium.
Types • Peripheral adenomatoid odontogenic tumor • Central adenomatoid odontogenic tumor • Follicular type—it is associated with embedded tooth • Extrafollicular type—it is not associated with embedded tooth.
Clinical Features • Incidence—it represents 3% of odontogenic tumors and is a developmental outgrowth of odontogenic tissue.
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Fig. 51-4: Swelling seen in anterior maxillary region due to adenomatoid odontogenic tumor or cyst.
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• Age and sex distribution—it is found in individuals ranging from 5 to 50 years with 70% occurrence in 2nd decade with an average age of 16 years. Females are affected more than males in a ratio of 2:1. • Site—it occurs more commonly in the maxilla than in the mandible, usually in the anterior region and especially in the cuspid area (Fig. 51-4). It is commonly associated with an unerupted tooth. • Symptoms—commonly presented as an area of swelling over an unerupted tooth which is asymptomatic. Sometimes, it may expand cortical bone but is not invasive. • Signs—it is frequently associated with an unerupted tooth in which the epithelial proliferation is confined within a connective tissue capsule that is attached to the tooth in a manner similar to the attachment of a dentigerous cyst. When the tumor occurs independently of unerupted teeth, it is often encapsulated. The tumor causes expansion of bone and fluctuation may be elicited. • Progress—it is slow growing and is a gradually increasing painless swelling leading to asymmetry, frequently associated with missing teeth. • Extraosseous tumor—very uncommonly, it develops extraosseously usually in the gingiva.
Fig. 51-5: Radiolucency showing calcification in it may be due to AOT or AOC.
• Target appearance—there is a radiolucent circumferential halo which envelops a dense, central and round radiodense mass. • Effect on surrounding structure—separation of roots or displacement of a adjacent tooth occurs frequently. There is also cortical expansion and root resorption. The lesion may inhibit the eruption of involved tooth (Fig. 51-6).
Radiographic Features • Radiodensity—well-demarcated mixed radiolucent or opaque lesion. • Site—tumor surrounds the entire tooth, most often canine in the maxilla. Radiolucency usually extends apically beyond the cementoenamel junction. • Margin—it may or may not be well circumscribed. Borders are sclerotic. • Internal structure—unilocular radiolucency but may contain faint to dense radiopaque foci which may be seen peripherally as the lesion matures (Fig. 51-5). Dense cluster of radiopacities appear as ‘small pebbles’.
Fig. 51-6: CT scan of AOT or AOC showing lesion with impacted tooth in maxilla ( Courtesy Dr Iswar).
Differential Diagnosis • Dentigerous cyst—it is seen in 2nd to 4th decade as compared to adenomatoid odontogenic tumor which is seen in young age. It is seen in posterior region as
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Controversial Diseases and Terminologies
• • •
•
•
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compared to adenomatoid odontogenic tumor which is seen in anterior region. Adenomatoid odontogenic tumor has tendency to surround more than just crown of the unerupted tooth. Ameloblastoma—it is more common in older age and posterior region. It is multilocular. Ameloblastic fibroma—it is seen in premolar-molar region and is multilocular. Ameloblastic fibro-odontoma—it is multilocular and radiopacities of enamel and dentin are seen inside the radiolucency as compared to adenomatoid odontogenic tumor where snowflakes are seen at the periphery. Calcifying odontogenic cyst—it occurs in older age as compared to adenomatoid odontogenic tumor and mandibular premolar area is mostly affected. Odontogenic fibroma or myxoma—tennis racket pattern is seen.
Why Discarded and Updated Term Today we call this tumor as an adenomatoid odontogenic cyst. The reason for this is that after close inspection of the cyst’s it seems proliferation which fills the lumen emerges from the epithelial lining. The calcification present in this cyst is identified as dentinoid material which derived from root sheath epithelium to induce root dentin. So due to all these factors more appropriate term for adenomatoid odontogenic tumor will be adenomatoid odontogenic cyst.
Cementoma It is a true neoplasm of functional cementoblasts, which forms large masses of cementum or cementum-like tissue on the tooth root.
Clinical Features • Age and sex—it occurs most frequently under the age of 25 years and with no significant sex predilection. • Site—mandible is affected three times more frequently than the maxilla. Mandibular first molar is the most frequently affected tooth (Fig. 51-7); other involved teeth are the mandibular second and third molars. • Symptoms—associated tooth is vital unless coincidentally involved. In some cases, pain may be there. • Sign—lesion is slow growing and may cause expansion of cortical plates of bone. Periapical cementomas are multiple.
Fig. 51-7: Cementoma presenting as radiopaque structure in relation with lower left first molar.
Why Discarded and Updated Term Nowadays this disease is recognized as periapical cementoosseous dysplasia. This is disorganized product of bone periodontal membrane cementum complex.
True Cementoma Earlier students were told the true cementoma represents benign proliferation of cementoblasts present in roots of premolar and molar teeth.
Why Discarded and Updated Term Nowadays, this disease is recognized as cementoblastoma which is slow growing neoplastic proliferation of cementoblasts.
Gigantiform Cementoma This is rare case of large round radiopaque mass seen in jaws.
Radiographic Features
Why Discarded and Updated Term
• Appearance—there is an area of increased density surrounded by the dark line of the fibrous capsule and with a thin white line of the adjacent cortical layer of the bone.
Nowadays this disease is recognized as ossifying fibroma. The reason for this is that these lesions are usually large ossifying fibroma with mature ossification.
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1058 Textbook of Oral Medicine
Reparative Giant Cell Granuloma It occurs in young persons usually before the age of 20 years. It is most often seen anterior to the first permanent molar. Most of the lesions are single, but more than one lesion can be seen. Spontaneous regression can be seen in reparative granuloma. Size of the lesion varies greatly from a very small localized area of bone destruction, to one involving greater part of the bone. The margins may be poorly defined, so that exact limits of the lesion are unclear and indefinite. There is no cortex at the periphery of the lesion, as seen with the cyst. The outer and inner cortical plate of bone may become involved in the extension of the tumor and become destroyed, but the periosteum usually lays down a bony covering. The jaw is said to be expanded by the tumor. There is undulating or irregular bony covering.
Clinical Features
It is an uncommon hemorrhagic lesion of the bone which is rarely seen in the jaw. It was first described as a clinicopathological entity by Jaffe and Lichtenstein in 1942. It is most often categorized as to be a tumor-like reactive lesion of bone. The name of this entity is misleading, in that, it does not contain vascular aneurysms and it is not a true bony cyst. It represents an exaggerated localized proliferative response of the vascular tissue. It may be similar to peripheral and central giant cell granuloma to which it resembles in some ways including the histological presence of giant cells.
• Age—although it may be seen in adults, it is more commonly seen as abnormalities of older children and adolescents with more than 90% of lesions occurring in individuals younger than the age of 30 years. • Sex—it is more common in females than in males. • Site—it usually involves the mandibular molar region as compared to anterior region. • History—history of traumatic injury and of recent displacement of teeth which remain vital. • Symptoms—aneurysmal cyst of the jaw produces a firm swelling which may be painful and tender on motion. Swelling becomes progressively worse and the rate of development is often described as rapid. Sometimes, patient may complain of difficulty in opening the mouth when there is impingement of the lesion on the capsule of TMJ. • Signs—usually there is tilting or bodily displacement of teeth in the affected areas though it does not devitalize the affected tooth. Excessive bleeding may occur. When the lesion perforates the cortex and is covered by periosteum or only a thin shell of bone, it may exhibit springiness or egg-shell crackling, but it is not pulsatile. Bruit is not heard.
Pathogenesis
Radiographic Features
• Local alteration in hemodynamics—persistent local alteration in hemodynamics leads to increased venous pressure and development of dilated and engorged vessels in transformed bone area. Resorption of bone occurs, to which giant cells are related and this is replaced by connective tissue, osteoid and new bone. • Repair of hematoma of bone—exuberant attempt at repair of hematoma of bone, similar to that of central giant cell granuloma. But, in the case of aneurysmal bone cyst, it is postulated that hematoma maintains a circulating connection with the damaged vessel. This would lead
• Radiodensity—the aneurysmal bone cyst is an expansile osteolytic process within the affected bone and is projected as a definite radiolucency. • Internal structure—invariably, fine septa are seen crossing through the lesion in a random pattern. • Appearance—the term ‘soap bubble’ may be applied to describe an occasional multilocular radiographic appearance. • Margins—are somewhat less regular and distinct than odontogenic cyst but more discrete than a central malignancy.
Why Discarded and Updated Term
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to a slower flow of blood through the lesion and account for a clinical “welling” of blood. This is the only difference between the aneurysmal cyst and the giant cell granuloma that is in later lesion, the blood vessels fail to retain circulating connection with lesion. • Hemodynamic force—Biesecker and his associates have proposed a new hypothesis for etiology and pathogenesis of this lesion that a primary lesion of the bone initiates an arteriovenous fistula and thereby creates, via its hemodynamic forces, a secondary reactive lesion of the bone. Thus occurrence of this cyst is secondary in association with osseous lesions like nonosteogenic fibroma, benign osteoblastoma and hemangioma of bone.
Nowadays, this is called central giant cell tumor. The reason for this is that the process which occurs in this disease is destructive rather than reparative. Second reason is that it is not a granuloma but proliferative reaction.
Aneurysmal Bone Cyst
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Controversial Diseases and Terminologies • Expansion—as the cyst enlarges to more than a few centimeters in anterior-posterior dimension, it also produces expansion of the buccal and lingual cortical plates. • Teeth—simple tilting and bodily displacement of erupted teeth. Some degree of external root resorption may be seen though it will not devitalize the tooth. • Cortex—there is also buccal and lingual expansion of the cortex often marked and described as ballooning or blowing out.
Differential Diagnosis • Ameloblastoma—it is more common in older age group and in the mandibular posterior region. • Giant cell granuloma—more common in the anterior region. • Central hemangioma—it is more common in the mandible and it shows profuse hemorrhage if aspirated. Bruit is heard in such lesion. • Multilocular cyst—it is more common in the mandibular posterior region of jaw and also the borders of the lesion are well defined. • Odontogenic myxoma—it is more frequently associated with congenitally missing or unerupted tooth. It shows a typical honeycomb appearance. • Cherubism—it occurs in a younger age group and it is a bilateral lesion. • Metastatic tumor—it occurs in older age group. • Giant cell lesion of hyperparathyroidism—more common in the older age group. Serum shows high levels of alkaline phosphatase.
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to be occurred due to calcification of stylohyoid ligament. But nowadays it is seen that there is actually ossification of stylohyoid ligament with mature bone. Also, there is evidence that maximum of intervertebral ligament are also ossified.
Hand-Schuller-Christain Disease, Letterer Siwe Disease, Eosinophilic Granuloma and Histiocytosis X It is an inflammatory reticuloendothelioma condition with evidence suggesting that it may be reaction to some type of infection. There is pathological accumulation of histiocytes and eosinophilic leukocytes.
Why Discarded and Updated Term Nowadays dominant histolytic cells identified as antigen processing Langerhans cells. So it is now called Langerhans cell histiocytosis (LCH). All the three diseases are now called separated clinical entity under the heading of Langerhans cell histiocytosis.
Neurilemmoma, Neurinoma and Neuro-lemmoma The above terms are derived from Greek word: neuron meaning nerve and lemma means husk or covering.
Why Discarded and Updated Term Today we call this cyst as central giant cell tumor. The reason for this is that all the central giant tumors have venous pressure bleeding quality. ABC has macroscopic blood-filled spaces rather than microscopic spaces. The term aneurysmal is also false as blood-filled spaces contain fibroblasts rather than endothelium. It also lacks cystic lining so the term aneurysmal bone cyst is discarded.
Why Discarded and Updated Term Today we called this as Schwannoma. The reason for this is that tumor consists of Schwann cells around the nerve and not the nerve fiber or nerve sheath. Also, there is only proliferation of Schwann cells and not the basal lamina or other component of the neurilemma.
Traumatic Bone Cyst
Eagle Syndrome In this syndrome there is neck pain associated with elongated calcified styloid process.
It is empty space seen in the bone and many times it is not related to trauma.
Why Discarded and Updated Term
Why Discarded and Updated Term Today we called this as part of DISH syndrome (diffuse intraosseous skeletal hypertrophy). Initially, it is thought
Today we call this as idiopathic bone cavity. There is no epithelium present in this cavity so use of term traumatic bone cyst should be avoided.
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Suggested Reading 1. Ellis JD, et al. Aneurysmal bone cyst of the maxilla. J Oral Surg 34; 26:1972. 2. Gruskin ES, et al. Aneurysmal bone cysts of the jaws. J Oral Surg 26;523:1968. 3. Oliver LP. Aneurysmal bone cyst-Report of a case. Oral Surg 35;67:1973.
4. Philipsen HP, Reichart PA, et al. Adenomatoid odontogenic tumor: biological profile base on 499 cases. J Oral Pathol Med 1994;23:1-11. 5. Marx RE, Stern DS. Oral and maxillofacial pathology, a rationale for Diagnosis and treatment. Quintessence Publishing Co, Inc 2003. 6. Krandorf MJ, Sweet DE. Aneurysmal bone cyst: concept, controversy, clinical presentation and imaging. AM J Roentgel 195;164:573-80.
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Causes and Classifications
Classifications of Diseases White Lesions Variation in structure and appearance of normal mucosa • Leukoedema • Fordyce’s granules • Linea alba White lesion with definite precancerous potential • • • • • • • • • • • •
Leukoplakia Erythroplakia Tobacco keratosis, actinic keratosis Lesion associated with electrogalvanism Carcinoma in situ Verrucous carcinoma Lichen planus Lichenoid reaction Oral submucus fibrosis Dyskeratosis congenita Lupus erythematosus Acanthosis nigricans
Precancerous lesion • • • • •
Leukoplakia Erythroplakia Palatal lesion associated with reverse smoking Verrucous hyperplasia Carcinoma in situ
Precancerous condition
Traumatic keratosis Focal epithelial hyperplasia Psoriasis Geographic tongue Pachyonychia congenita White sponge nevus Hereditary benign epithelial dysplasia Stomatitis nicotina Hyperkeratosis palmoplantaris with gingival hyperkeratosis Darrier’s disease Intraoral skin grafts Pseudoxanthoma elasticum Hyalinosis cutis et mucosa oris Oral condyloma acuminatum Hairy leukoplakia
Nonkeratotic white lesion • White hairy tongue
Burns –thermal, chemical, electrical Desquamative gingivitis Epidermolysis bullosa Pemphigus Benign mucous membrane pemphigoid (BMMP) Diphtheria Syphilitic mucus patches Acute necrotizing ulcerative gingivitis (ANUG) Koplik’s spot of measles Candidiasis Median rhomboidal glossitis Verruca vulgaris
Precancerous Lesion and Condition
White lesion without precancerous potential • • • • • • • • • • • • • • •
• • • • • • • • • • • •
• • • • •
Oral submucus fibrosis Sideropenic anemia Erosive lichen planus Discoid lupus erythematosus Dyskeratosis congenita
Histological Classification of Cancer and Precancer of the Oral Mucosa—Histological typing of cancer and precancer (WHO 1997) Carcinomas • • • • • • •
Squamous cell carcinoma Verrucous carcinoma Basaloid squamous cell carcinoma Adenoid squamous cell carcinoma Spindle cell carcinoma Adenosquamous carcinoma Undifferentiated carcinoma
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1064 Textbook of Oral Medicine Benign lesions capable of microscopically resembling oral squamous cell carcinoma and oral verrucous carcinoma • • • • • • • • • • •
Papillary hyperplasia Granular cell tumor Discoid lupus erythematosus Median rhomboid glossitis Keratoacanthoma Necrotizing sialometaplasia Juxtaoral organ of Chievitz Chronic hyperplastic candidiasis Verruciform xanthoma Verruca vulgaris Condyloma acuminatum
Precancerous lesions (Clinical Classification) • Leukoplakia • Erythroplakia • Palatal keratosis associated with reverse smoking Precancerous lesions (Histological Classification) • Squamous epithelial dysplasia • Squamous cell carcinoma in situ • Solar keratosis Benign lesions capable of resembling oral precancerous lesions • • • •
White lesions resembling leukoplakia Red lesions resembling erythroplakia Focal epithelial hyperplasia Reactive and regenerative atypia
• • • • • • • •
Hemangioma Sturge-Weber syndrome Rendu-Osler-Weber disease Hereditary hemorrhage telangiectasia Median rhomboidal glossitis Geographic tongue Melkersson-Rosenthal syndrome Crohn’s disease
Purpura Polycythemia Agranulocytosis Polyarteritis nodosa Leukemia
Dermatological
Red Lesion of Oral Mucosa Inflammatory condition Inflammation associated with traumatic injury • Mechanical—cheek biting, ill fitting denture, sharp edge, overhanging restoration and ecchymoses due to trauma. • Chemical—aspirin, formocresol and TCA. • Thermal—hot food, hot beverage and hot instrumentation. • Radiation—mucositis, cheilitis.
Fungal • Atrophic candidiasis • Angular cheilitis • Acute pseudomembranous candidiasis
Congenital-hereditary developmental condition
• • • • •
Sideropenic dysphagia Lichen planus Oral submucus fibrosis Syphilis Discoid lupus erythematosis Xeroderma pigmentosum Epidermolysis bullosa
Infection Bacterial • Scarlet fever (red fever) • Gonococcal stomatitis • Vincent infection or gingivostomatitis • Acute pharyngitis, tonsillitis
Allergic/Immunological • Pyogenic granuloma • Giant cell epulis • Pregnancy tumor • Traumatic hemangioma • Inflammatory fibrous hyperplasia • Desquamative gingivitis
Vascular disease and blood disorder
Precancerous conditions • • • • • • •
Viral • Measles—Koplik’s spot • Lymphnodular pharyngitis • Herpes simplex infection • Herpes zoster • Herpangina • Chickenpox • Hand-foot-mouth disease
• • • • • • • •
Pemphigus Erythema multiforme Stevens Johnson Lichen planus Lichenoid reaction Epidermolysis bullosa Psoriasis Lupus erythematous
Other systemic disease • • • • •
Uremic stomatitis Diabetes stomatitis Scurvy Pernicious anemia Ulcerative stomatitis
Premalignant and malignant lesion • • • • • •
Atrophic leukoplakia Erythroplakia Squamous cell carcinoma Carcinoma in situ Kaposi’s sarcoma Hemangioendothelioma
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Appendix 1: Causes and Classifications 1065 Vesiculobullous Lesions 1st Classification Hereditary • Epidermolysis bullosa • Familial benign chronic pemphigus • Dyskeratosis congenita • Acrodermatitis enteropathica Viral infection • Primary herpetic gingivostomatitis • Secondary herpetic gingivostomatitis • Varicella (chickenpox) • Shingles (herpes zoster) • Measles • Hand-foot-mouth disease • Small pox and cat-scratch disease • Infectious mononucleosis • Herpangina • Acute lymphnodular pharyngitis • AIDS Mucocutaneous diseases • Pemphigus vulgaris • Pemphigus vegetans • Benign mucous membrane pemphigoid • Bullous pemphigoid • Lichen planus • Toxic epidermal necrolysis Miscellaneous • Oral submucus fibrosis • Hyperacidity or gastritis • Constipation and malabsorption syndrome • Impetigo • Oral blood blister • Erythema multiforme 2nd Classifications
• Erythema multiforme • Stevens-Johnson syndrome Cysts of the Oral Cavity Odontogenic Developmental • Primordial cyst • Odontogenic keratocyst • Gingival cyst of infant • Gingival cyst of adult • Lateral periodontal cyst • Dentigerous cyst • Eruption cyst • Calcifying epithelial odontogenic cyst Inflammatory • Radicular cyst • Periodontal cyst • Inflammatory collateral cyst • Paradental cyst Non-odontogenic • • • • • • • • •
Nasopalatine cyst Median palatine cyst Median alveolar cyst Median mandibular cyst Globulomaxillary cyst Nasolabial cyst Nasoalveolar cyst Simple bone cyst Hemorrhagic bone cyst
Cysts Associated with maxillary sinus • Benign mucosal cyst of maxillary antrum • Mucocele–mucus retention cyst • Surgical ciliated cyst
Vesicular lesion Non-febrile lesion • Recurrent herpes labialis • Recurrent herpes stomatitis • Reiter’s syndrome • Contact stomatitis • Impetigo • Dyskeratosis congenita Febrile lesion • Herpetic gingivostomatitis • Herpangina • Hand-foot-mouth disease • Chickenpox • Herpes zoster • Smallpox Bullous lesion • Pemphigus • Familial benign chronic pemphigus • Bullous pemphigoid • Benign mucous membrane pemphigoid • Epidermolysis bullosa • Dermatitis herpetiformis
Soft tissue cysts • • • • • • • •
Dermoid Epidermoid Branchial Thyroglossal Anterior median lingual cyst Oral cyst with gastric epithelium Cystic hygroma Parasitic cyst, hydatid cyst, cysticercosis cellulosae
Cysts of the salivary gland • Mucocele • Ranula Oral Manifestation of AIDS Fungal infection • • • • •
Candidiasis Histoplasmosis Toxoplasmosis Cryptococcosis Geotrichosis
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1066 Textbook of Oral Medicine Malignant odontogenic tumor
• Mucormycosis • Aspergillosis • Actinomycosis
Odontogenic carcinoma • Malignant ameloblastoma • Primary intraosseous carcinoma • Malignant variant of other odontogenic epithelial tumor • Malignant changes in odontogenic cyst
Bacterial • • • • •
HIV gingivitis HIV necrotizing gingivitis HIV periodontitis Sinusitis STD
Odontogenic sarcoma • Ameloblastic fibrosarcoma • Ameloblastic dentinosarcoma
Viral
2nd Classification
• • • • • • •
Benign
Herpes simplex Herpes zoster Hairy leukoplakia Verruca vulgaris Condyloma acuminatum Focal epithelial hyperplasia Cytomegalovirus infection
Epithelial • With inductive changes in the connective tissue • AOT • Ameloblastic fibroma • Dentinoma • Calcifying odontogenic tumor • Odontoameloblastoma • Odontoma • Without inductive changes in connective tissue • Ameloblastoma • CEOT • Epithelial atypia • Ameloblastic changes in odontogenic cyst
Neoplasm • Kaposi’s sarcoma • Squamous cell carcinoma • Non-Hodgkin’s lymphoma Neurological • Trigeminal neuralgia • Facial palsy • AIDS dementia
Mesenchymal • Odontogenic myxoma • Odontogenic fibroma • Cementoma • Periapical cemental dysplasia • Cementifying fibroma • Benign cementoblastoma
Miscellaneous • • • • •
Recurrent aphthous stomatitis Erythema multiforme Lichenoid reaction Progressive necrotizing ulceration Toxic epidermal necrolysis
Malignant
Odontogenic Tumor 1st Classification Benign odontogenic tumor Odontogenic epithelium without odontogenic ectomesenchyme • Ameloblastoma • Squamous odontogenic tumor • Pindborg tumor • Clear cell odontogenic tumor Odontogenic epithelium with odontogenic ectomesenchyme with or without dental hard tissue formation • Ameloblastic fibroma • Ameloblastic fibro-odontoma • Ameloblastic fibrodentinoma • Odontoameloblastoma • Adenomatoid odontogenic tumor • Complex and compound odontome Odontogenic ectomesenchyme with or without included odontogenic epithelium • Odontogenic fibroma • Odontogenic myxoma • Benign cementoblastoma
Epithelial • With inductive changes in connective tissue • Ameloblastic fibrosarcoma • Ameloblastic odontosarcoma • Without inductive changes in connective tissue • Malignant ameloblastoma • Primary intraosseous carcinoma • Malignant changes in odontogenic cyst Benign Tumors of the Jaw Odontogenic tumors Epithelial • Ameloblastoma • Adenoameloblastoma • Enameloma • Pindborg tumor (CEOT) Mesenchymal • Dentinoma • Cementoma • Cementoblastoma Mixed • Ameloblastic fibroma • Ameloblastic fibro-odontoma • Ameloblastic odontoma
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Appendix 1: Causes and Classifications 1067 • • • •
Odontogenic myxoma Compound composite odontoma Complex composite odontoma Odontogenic fibroma
• • • •
Developmental • Dense invaginatus or dilated odontome • Dense evaginatus
Oncocytoma Oxyphilic adenoma Warthin’s tumor Pleomorphic adenoma
Classification of Tumor Epithelial tumors
Non-odontogenic tumors Epithelial tissue • Papilloma • Keratoacanthoma • Adenoma Fibrous connective tissue • Fibroma • Myxoma • Fibrous hyperplasia • Fibrous epulis • Fibrous histiocytoma
Mesenchymal
Cartilage • Chondroma • Chondroblastoma • Chondromyxoid fibroma Adipose tissue • Lipoma Bone • Osteoma • Osteoid osteoma • Osteoblastoma • Exostosis and tori- torus palatinus, torus mandibularis • Enostosis Vascular tissue • Hemangioma • Lymphangioma • Glomus tumor • Hemangiopericytoma Neural tissue • Neurofibroma • Neurilemmoma • Schwannoma • Ganglioneuroma • Traumatic neuroma • Melanotic neuroectodermal tumor of infancy Muscle • Leiomyoma • Rhabdomyoma • Myoblastoma Giant cell tumors • Central and peripheral giant cell tumor • Giant cell granuloma • Giant cell reparative granuloma • Giant cell tumor of hyperthyroidism
Mixed tumors
Tissue of origin
Benign
Malignant
Squamous epithelium Transitional epithelial Glandular epithelium Basal cell layer Neuroectodermal Hepatocyte
Squamous cell papilloma Transitional cell papilloma Adenoma
Squamous cell carcinoma Transitional cell carcinoma Adenocarcinoma
Adipose tissue Adult fibrous tissue Embryonic fibrous tissue Cartilage Bone Synovium Skeletal muscle Smooth muscle Mesothelium Blood vessels Lymph vessels Glomus cell Meninges Hemopoietic cell Lymphoid tissue Nerve sheath Nerve cell Salivary gland
Tumor of more Totipotent cells than one germ in gonads or in cell layer embryonal rests
—— Basal cell carcinoma Nevus Melanoma Liver cell adenoma Hepatocellular carcinoma Lipoma Fibroma Myxoma
Liposarcoma Fibrosarcoma Myxosarcoma
Chondroma Osteoma Benign synovioma Rhabdomyoma Leiomyoma
Chondrosarcoma Osteosarcoma Synovial sarcoma Rhabdomyosarcoma Leiomyosarcoma Mesothelioma Angiosarcoma Lymphangiosarcoma
Hemangioma Lymphangioma Glomus tumor Meningioma Neurilemmoma Ganglioneuroma
Invasive meningioma Leukemia Malignant lymphoma Neurogenic sarcoma Neuroblastoma
Pleomorphic adenoma
Malignant salivary gland tumor
Mature teratoma
Immature teratoma
Malignant Tumor of the Jaw Odontogenic tumor • Ameloblastic sarcoma and Fibrosarcoma • Odontogenic sarcoma • Carcinoma in odontogenic cyst Non-odontogenic tumor Epithelial • Squamous cell carcinoma • Mucoepidermoid carcinoma • Adenocarcinoma • Basal cell carcinoma • Transitional cell carcinoma • Melanoma • Verrucous carcinoma • Intraepidermoid carcinoma Fibrous connective tissue • Fibrosarcoma
Teratoma
Adipose tissue • Liposarcoma
Salivary gland tumors • Adenoma
Cartilage • Chondrosarcoma
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1068 Textbook of Oral Medicine Bone • Osteosarcoma • Osteochondrosarcoma
Lipid • Gaucher’s disease • Niemann-Pick disease
Vascular • Hemangioendothelioma
Malignant • Wegener’s granulomatosis • Midline lethal granuloma • Hodgkin’s disease
Neural tissue • Neurosarcoma • Neurofibrosarcoma
Gingival Hyperplasia (Clinical Classification)
Muscle • Leiomyosarcoma • Rhabdomyosarcoma
Localized • Marginal • Papillary • Discrete
Lymphoid tissue • Hodgkin and non-Hodgkin lymphoma • Lymphosarcoma • Reticular cell sarcoma • Ewing sarcoma • Burkitt’s lymphoma • Multiple myeloma • Leukemia
Gingival Hyperplasia (Etiological Classification) Inflammatory Acute • Gingival or periodontal abscess • Acute exacerbation of chronic inflammatory enlargement
Tumor of salivary gland • Mucoepidermoid carcinoma • Adenocystic carcinoma • Adenocarcinoma • Acinic cell carcinoma • Malignant change in pleomorphic adenoma Granulomatous Diseases Specific or infective type • • • • • • • • • • • • • • • • •
Syphilis Yaws and Bejel Tuberculosis Leprosy Melkersson Rosenthal syndrome Heerfordt’s syndrome Blastomycosis Coccidioidomycosis Cryptococcosis Rhinosporidiosis Pyostomatitis vegetans Actinomycosis Candidiasis Aspergillosis Mucormycosis Lymphogranuloma venereum Granuloma inguinale
Non-lipid • Eosinophilic granuloma • Hand–Schüller–Christian disease • Letterer-Siwe disease
Chronic Local irritants • Calculus • Food lodgment area • Occlusal trauma • Mouth breathing • Overhanging restoration • Foreign bodies • Poor oral hygiene Infection • Bacterial • Viral • Fungal • Fusospirochetal • Parasitic • Saprophytic
Non-specific • Periapical granuloma • Pyogenic granuloma • Peripheral and central giant cell granuloma • Foreign body granuloma • Traumatic granuloma • Crohn’s disease • Pulsating granuloma Histiocytosis
Generalized • Diffuse • Marginal • Papillary
Allergy Non-inflammatory • Familial or hereditary • Developmental • Congenital • Idiopathic • Drug induced • Dilantin sodium • Phenobarbitone • Nifedipine • Cyclosporine Combined Conditional • Hormonal (puberty and thyroid dysfunction) • Leukemic enlargement—myelogenous or monocytic • Polycythemia vera • Vitamin C deficiency • Non-specific conditional enlargement • Epulis—fibrous • Epulis fissuratum • Eosinophilic granuloma • Plasma cell granuloma
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Appendix 1: Causes and Classifications 1069 • Black hairy tongue • Poor oral hygiene
• Crohn’s disease • Peripheral giant cell granuloma • Wegener’s granulomatosis
Hypopigmentation and de-pigmentation • Albinism • Vitiligo • Pernicious anemia • Hormonal disturbances • Parasitic infection • Chédiak-Higashi syndrome • Tuberous sclerosis • Cross syndrome • Severe burns • Extensive traumatic injury
Cyst • Eruption • Gingival Neoplastic Benign • Fibroma • Granular cell myoblastoma • Papilloma • Hemangioma • Peripheral ameloblastoma • Peripheral odontogenic fibroma
Endogenous
Malignant • Squamous cell carcinoma • Fibrosarcoma • Reticular cell sarcoma • Melanoma • Malignant lymphoma • Malignant hemangioendothelioma or hemangioendotheliosarcoma • Metastasis from lung, colon, testis, kidney and cervix Syndrome associated with gingival hyperplasia • Rutherford • Cannon’s disease • Cross • Zimmermann-Laband • Cowden’s • Papillon Lefevre • Tuberous sclerosis • Sturge-Weber • Melkersson-Rosenthal Oral Pigmentation 1st Classification Exogenous Occupational • Lead industry—lead • Match industry—phosphorus • Fluorescent lamp industry—mercury • Photography—silver
Physiologic • Ethnic, racial variation • Physiologic melanotic macule and papule • Fordyce’s granules • Postmenopausal changes in sex hormones • Pregnancy Pathological • Addison’s disease • Acromegaly • Peutz-Jeghers syndrome • Lentigo • Nevi (intradermal, compound, junctional, blue) • Neurofibromatosis • Metastatic carcinoma • Malnutrition • Acanthosis nigricans • Cyanosis • Hemolytic anemia • Jaundice • Hemochromatosis • Hemosiderosis • Porphyria • Carotenemia • Hematoma-ecchymoses-varicosities-purpura • Niemann-Pick disease • Diabetic melanosis • Simmond’s disease 2nd Classification
Habits • Tobacco—in the form of smoking, chewing and snuff dipping • Pan—catechu, pan and pan masala • Food—food stuff, black berries, blue grapes, coloring agent of sweets and chocolates Therapeutic • Drugs—anti-malarial drugs and contraceptives • Metallic salts—gold for tuberculosis, bismuth for diarrhea, silver for nasal drop, mercury for diuretic Others • Amalgam tattoos • Other self made tattoos—graphite, methylene blue
Benign melanocytic lesions • Racial pigmentation • Physiologic pigmentation • Smoking associated pigmentation • Ephelis • Lentigo • Oral melanotic macules • Nevi • Hematoma Neoplastic conditions • Melanoma • Multiple neurofibromatosis • Neuroectodermal tumor of infancy • Hemangioma • Kaposi’s sarcoma
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1070 Textbook of Oral Medicine Different type of pigmentation and their features Condition
Appearance
History
Age
Frequency
Melanoplakia
Macule of varying size, shape and location of oral mucosa
No symptoms
Birth to 1 year
Common in dark race
Amalgam tattoo
Macule on gingiva or edentulous ridge
Amalgam filled teeth
5 years and older
Common
Petechiae and ecchymosis Macule anywhere in oral cavity or skin
Recent trauma bleeding diathesis
Young children
Occasional
Melanotic macule
Small macule < 2 cm on lower lip gingiva or buccal mucosa
——
41-42 years
M/F 1:2.2
Superficial spreading melanoma
Enlarging macule on palate or maxillary sinus
Several years Slowly enlarging
Mean age 50.5
Rare M/F=2:1
Junctional nevus
Macule occurs anywhere in oral cavity
Mean age 38
Rare in oral cavity
Heavy metal poisoning
Macular lesion— free gingiva
Malaise anemia
Working age
Rare
Peutz-Jeghers syndrome
Macule around lip buccal mucosa, finger body orifice
Melanin intestinal polyposis
Distinct at puberty
Rare
Albright syndrome
Café au lait spot on skin and mucous membrane
Skeletal endocrine
—
——
Firm lesions Amalgam fragment
Macule on gingiva or edentulous ridge
Firm mass in tissue
5 years and older
Common
Late hematoma
Mass and swelling
Previous trauma
—
Occasional
Giant cell granuloma
Moderately firm macule and nodule on gingiva and alveolar
Slowly expanding
30 years and over
Occasional
Pigmented lesion
Papule nodule or polypoid Present for some mass usually on buccal mucosa time
—
Occasional
Intramucosal nevus
Papule nodule or polypoid mass Present from birth
—
Rare
Compound nevus
Same
Same
—
Same
Melanoma
Pigmented or amelanotic nodule polypoid mass on palate and maxillary gingiva
Rapidly enlarging
—
Rare M/F 2:1
Neuroectodermal tumor
Expansion of labial sulcus pigmented or pink
Slowly expanding mass in anterior maxilla
Birth to 1 year
Rare
Pigmentation due to exogenous deposits • Amalgam tattoo • V Graphite tattoo • Heavy metal pigmentation • Drug induce pigmentation Miscellaneous condition • Peutz-Jeghers syndrome • Addison disease • Pigmented lichen planus • Hairy tongue • Mucocele • HIV-associate oral pigmentation • Endocrinopathic pigmentation
Diseases of the Maxillary Sinus Traumatic • • • •
Fracture of maxilla, nasal bone, zygoma and orbital floor Hematoma Foreign bodies—root piece, bullet injury, antroliths Oroantral fistula
Inflammatory • • • •
Acute and chronic sinusitis Local hyperplasia from odontogenic infection Antral polyp Osteomyelitis
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Appendix 1: Causes and Classifications 1071 Cysts
Sexually Transmitted and Blood Born Disease
Intrinsic • Mucus retention cyst (mucocele) • Serous cyst • Pseudo cyst
Bacterial and chlamydial STD (potentially curable and rarely blood borne) • Gonorrhea and related clinical syndrome (urethritis, cervicitis, salpingitis, pelvic inflammatory disease, disseminated systemic infection, arthritis, proctitis, pharyngitis) • Non- and post-gonococcal urethritis and related clinical syndrome (cystitis, epididymitis, Reiter’s disease, pelvic inflammatory disease) • Syphilis and other treponemal infection (yaws pinta bejel) • Chancroid • Granuloma inguinale • Lymphogranuloma venereum • Gay bowel syndrome associated pathogen
Extrinsic • Odontogenic • Radicular • Dentigerous • Primordial • Keratocyst • Non-odontogenic • Globulomaxillary • Traumatic • Aneurysmal bone cyst (ABC)
Viral STD (currently incurable some frequently blood born) Neoplasm Odontogenic • Ameloblastoma • Adenoameloblastoma • Calcifying Epithelial Odontogenic Tumor (CEOT) Nonodontogenic • Exostosis • Enostosis Malignant • Squamous cell carcinoma • Midline lethal granuloma* Metabolic
* It is controversial issue to consider midline lethal granuloma as a malignancy as many investigators in spite of taking repeated biopsies have not found neoplastic tissue in these lesions.
• • • • • • • • • • • • • • • • •
Syphilis Yaws and Pinta Gonorrhea Genital herpes Genital warts Nonspecific genital infection Trichomoniasis Pediculosis pubis Scabies Molluscum contagiosum Chancroid Lymphogranuloma venereum Lymphogranuloma inguinale Hepatitis B Cytomegalovirus inclusion body Infectious mononucleosis AIDS
Herpes simplex virus infection by HSV I and II Infectious mononucleosis Cytomegalovirus infection Viral hepatitis • Hepatitis A • Hepatitis B • Hepatitis D • Hepatitis C • Hepatitis E • Hepatitis F • AIDS • T cell lymphoma and leukemia • Molluscum contagiosum Miscellaneous bacterial fungal and parasitic infection which sometime manifested as STD (usually curable and rarely blood born except candida)
• Fibrous dysplasia • Leontiasis ossea
Sexually Transmitted Diseases
• • • •
• • • • • •
Vulvovaginal candidiasis Trichomoniasis Vaginitis, cervicitis and cystitis Bacterial vaginosis Intestinal protozoa infection Ectoparasitic skin infection
Other blood born infection with no evidence of sexual transmission • • • •
Toxoplasmosis Malaria Babesiosis Trypanosomiasis
Autoimmune Disorder Associated with Mucocutaneous Lesion • • • • • •
Recurrent aphthous ulcer Behcet’s disease Pemphigus Bullous pemphigoid Cicatrical pemphigoid Dermatitis herpetiformis
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1072 Textbook of Oral Medicine • Myeloblastic leukemia • Decrease of eosinophils
Salivary gland • Mikulicz’s disease • Sjögren’s syndrome
Disorders of platelet Purpura • Idiopathic thrombocytopenic purpura • Secondary thrombocytopenic purpura • Thrombotic thrombocytopenia • Drug-associated thrombocytopenia • Thrombocytopathia • Glanzmann’s thrombasthenia • von Willebrand’s disease • Bernard-Soulier syndrome • Aldrich syndrome
Blood disorder • Pernicious anemia • Purpura Collagen disorder • Systemic lupus erythematous • Scleroderma • Rheumatic arthritis Miscellaneous
Thrombocytosis
• Myasthenia gravis • Dermatomyositis • Oral submucus fibrosis
Disorders of coagulation • • • • •
Blood Disorders Disorders of RBC Deficiency • Iron deficiency anemia • Pernicious anemia • Normocytic anemia • Aplastic anemia • Hemolytic anemia
Fibro-osseous Lesions Lesions arising from periodontal ligament
Extra-corpuscular causes • Infection and toxin • Hypersplenism • Rh factor incompatibility (hemolytic disease of newborn, erythroblastosis fetalis) • Chronic liver disease • Autoimmune diseases • Transfusion reaction Intra-corpuscular causes • Hereditary spherocytosis • Sickle cell anemia • Thalassemia • Cooley’s anemia • Glucose-6 phosphate dehydrogenase deficiency • Pyruvate kinase deficiency • Folic acid and B12 deficiency Polycythemia • Relative • Secondary • Vera (malignant) Disorders of WBC Qualitative • Lazy leukocyte syndrome • Chédiak-Higashi syndrome Quantitative • Agranulocytosis • Cyclic neutropenia
Hemophilia A Hemophilia B Factor XI deficiency Factor X deficiency von Willebrand’s disease
• • • • •
Periapical cemental dysplasia Localized fibro-osseous cemental lesion Florid osseous dysplasia Ossifying fibroma Cementifying fibroma
Fibrous dysplasia • Monostotic • Polyostotic • Familial Fibro-osseous neoplasm of uncertain origin or debatable origin • • • • • • • •
Cementoblastoma Osteoblastoma Osteoid osteoma Juvenile ossifying fibroma Fibro-osteoma or osteofibroma Cementifying fibroma Paget’s disease Ossifying fibrous epulis
Giant cell lesion • Central giant cell tumor or central giant cell reparative granuloma • Brown tumor of hyperthyroidism • Aneurysmal bone cyst • Cherubism Mucocutaneous Disorder Genodermatoses • White sponge nevus
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Appendix 1: Causes and Classifications 1073 • • • • • • •
Darrier’s disease Peutz-Jeghers syndrome Dyskeratosis congenita Hereditary benign intraepithelial dyskeratosis Pachyonychia congenita Hyalinosis cutis et mucosa oris Pseudoxanthoma elasticum
Non-infective disease Vesicular • Erythema multiforme • Pemphigus • Benign mucous membrane pemphigoid • Bullous pemphigoid • Epidermolysis bullosa • Bullous Lichen planus Non-vesicular disease • Lichen planus • Benign migratory glossitis Collagen disorder • Lupus erythematous • Scleroderma • Polyarteritis nodosa • Vasculitis • Ischemic lingual necrosis • Wegner granulomatosis • Midline lethal granuloma Degenerative and relative disorder • Amyloidosis • Oral submucous fibrosis • Senile solar elastosis Pigmentation • Racial pigmentation • Endocrinopathy • Addison disease • Albert syndrome • Bronze diabetes • Anemia Oral Hamartomas Odontogenic Those involving teeth • Dens invaginatus • Dens evaginatus • Talon’s cusp Those not involving teeth • Enameloma • Odontoma • Gigantiform cementoma • Dental lamina cyst of newborn Non-odontogenic Epithelial origin • Epstein pearls and Bohn’s nodule
• Oral and labial melanotic macule • Pigmented cellular nevus Vascular origin • Hemangioma • Lymphangioma • Glomus tumor Osseous origin • Torus palatinus • Torus mandibularis Adipose tissue • Lipoblastomatosis Neural tissue • Neurofibromatosis Unknown or doubtful origin • • • •
Granular cell myoblastoma Congenital epulis of newborn Melanotic neuroectodermal tumor of infancy Fibromatosis gingivae
Disorders of the Salivary Glands Developmental • • • • • • •
Congenital aplasia or agenesis Congenital hypoplasia Atresia Aberrance or ectopic gland Diverticuli Accessory duct Congenital fistula
Inflammatory • Acute and chronic • Staphylococcus • Streptococcus • Actinomycosis • Tuberculosis • Viral infection • Mumps • Cytomegalovirus inclusion disease • Para-influenza • Sarcoidosis • Melkersson-Rosenthal syndrome • Heerfordt’s syndrome • Allergy • Secondary to sialolithiasis • Post-irradiation to oral tumor • Salivary fistula Sialolithiasis • • • •
Due to stricture of the duct Due to trauma or infection Due to salivary stone calculi Mucus plug
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1074 Textbook of Oral Medicine Cysts
Syndrome
• • • •
• Mikulicz’s disease of syndrome • Sjögren’s syndrome
Mucocele Ranula Lymphoepithelial cyst Branchial cyst
Disorders of the Temporomandibular Joint
Frey’s syndrome
Developmental
Sialadenosis • Non-inflammatory swelling of salivary gland Sjögren’s syndrome
• • • •
Agenesis of the condyle Hypoplasia of the condyle Hyperplasia of the condyle Exostosis of the joint
Necrotizing sialometaplasia Traumatic
Neoplasms
• • • • • • •
Benign epithelial • Adenoma • Oncocytoma • Warthin’s tumor • Pleomorphic adenoma Malignant epithelial • Adenocarcinoma • Mucoepidermoid carcinoma • Adenocystic carcinoma • Acinic cell carcinoma • Malignant pleomorphic adenoma
Trauma to disc Trauma to developing condyle or growth center Trauma to ligament Subluxation or dislocation or dislocation within displacement Ankylosis Foreign body in the joint space Trauma to muscle
Inflammatory Infective • Pyogenic infection from staphylococci • Syphilis • Tuberculosis • Actinomycosis • Rheumatic arthritis • Osteomyelitis • Psoriasis • Secondary to hepatitis B infection
Mesenchymal benign • Hemangioma • Lymphangioma • Neurofibroma • Schwannoma • Xanthoma • Lipoma
Non-infective • Still’s disease • Systemic lupus erythematosus • Ankylosis spondylitis • Synovitis
Malignant mesenchymal • Rhabdomyosarcoma • Hemangioendothelioma Others • Lymphoma—Hodgkin and non-Hodgkin • Metastatic
Non-articular arthritis • Myositis • Myositis ossificans • MPDS
Oral Lymphoid Tissue Lesion Metabolic Disorders Developmental lesions • Reactive lymphoid aggregates • Lymphoid hamartomas • Angio-lymphoid hyperplasia with eosinophilia Cystic • Lymphoepithelial cyst
• • • • • •
Gout Chondrocalcinosis Oxalosis Amyloidosis Wilson’s disease Gaucher’s disease
Neoplasms
Neoplastic • Benign—Warthin’s tumor • Malignant—lymphoepithelioma (epithelial) and malignant lymphoma, Burkitt’s lymphoma, non-Hodgkin lymphoma and leukemia (connective tissue)
Benign • Osteoma • Chondroma • Osteochondroma • Fibromyxoma • Synovioma
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Appendix 1: Causes and Classifications 1075 Malignant • Osteosarcoma • Chondrosarcoma • Synovial sarcoma • Malignant lymphoma
• • • •
Midline lethal granuloma* Burkitt’s lymphoma Reticular cell sarcoma Pseudosarcomatous fascitis
* It is controversial issue to consider midline lethal granuloma as a malignancy as many investigators in spite of taking repeated biopsies have not found neoplastic tissue in these lesions.
Neuropathic • Charcoat joint • Ritter’s sympathetic dystrophy
Enamel Pathology
Internal derangement
Developmental
• Disc displacement • Disc fracture
• Amelogenesis imperfecta • Dens invaginatus • Enameloma
Giant Cell Disorders
Environmental pathology
Traumatic
• Attrition • Abrasion • Erosion
• • • • • • •
Peripheral giant cell granuloma Central giant cell granuloma Traumatic granuloma Epulis fissuratum Pyogenic granuloma Internal resorption Periapical granuloma
Enamel caries • Pit and fissure • Smooth surface • Caries at cementoenamel junction
Infection • • • • • • • • • • • • •
Pigmentation
Tuberculosis Syphilis Leprosy Blastomycosis Sarcoidosis Histoplasmosis Candidiasis Aspergillosis Actinomycosis Cryptococcosis Mucormycosis Rhinosporidiosis Lymphogranuloma
• Endogenous • Exogenous Enameloma Dentin Pathology Developmental • • • •
Cystic
Dentinogenesis imperfecta Dentinal dysplasia Regional odontodysplasia Dentin hypocalcification
Dentinal caries
• ABC • Traumatic bone cyst • Calcifying epithelial odontogenic cyst (CEOC)
Neoplastic • Dentinoma • Odontoma
Metabolic • • • • •
Hyperparathyroidism Paget’s disease Fibrous dysplasia Cherubism Histiocytosis
Regressive changes • Secondary dentin • Dentinal sclerosis Verrucous-papillary Lesion
Neoplasms
Reactive lesion
• • • • •
• • • • •
Giant cell tumor Osteoblastoma Osteosarcoma Malignant lymphomas Wegener’s granulomatosis
Papillary hyperplasia of palate Condyloma latum Squamous papilloma Oral warts Oral papillomatosis
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1076 Textbook of Oral Medicine • Condyloma acuminatum • Heck’s disease Neoplasm • Keratoacanthoma • Verrucous carcinoma Unknown Etiology • Pyostomatitis vegetans • Verruciform xanthoma Disorders of Tongue Developmental • • • • • • • •
Aglossia or hypoglossia Ankyloglossia Bifid tongue Lingual polyp Macroglossia Midline fistula Teratoma Median rhomboid glossitis
Infectious • • • •
Bacterial Fungal and saprophytic Parasitic Viral
Cystic • • • • • • • •
Epidermoid Dermoid Lymphoepithelial Mucus Anterior median lingual cyst Gastric mucosal cyst Parasitic cyst Bronchogenic cyst
Neoplastic Benign • Fibroma • Granular cell myoblastoma • Glomus tumor • Leiomyoma • Rhabdomyoma • Neurofibroma • Keratoacanthoma • Traumatic neuroma • Papilloma • Pyogenic granuloma • Adenoma • Hemangioma • Lymphangioma Malignant • Squamous cell carcinoma
• • • • • • • • • •
Adenocarcinoma Transitional cell carcinoma Verrucous carcinoma Mucoepidermoid carcinoma Reticular cell carcinoma Lymphosarcoma Angiosarcoma Kaposi’s sarcoma Melanoma Rhabdomyosarcoma
Metastatic lesions from • Kidney • Liver • Stomach • Lung Red and white lesions • • • • • • • • • • •
Leukoplakia Erythroplakia Lichen planus Oral submucus fibrosis Candidiasis Psoriasis Focal epithelial hyperplasia White sponge nevus Pemphigus Syphilitic mucus patches Verruca vulgaris
Neurological • • • • • • • •
Dyskinesia—involuntary movements Glossodynia Trigeminal neuralgia Glossopharyngeal neuralgia Polyneuritis Neurofibromatosis Tongue thrusting Dysgeusia
Papillary changes in tongue Atrophic • Median rhomboid glossitis • Geographic tongue • Pernicious anemia • Protein deficiency • Lichen planus • Oral submucous fibrosis • Scleroderma Hypertrophic • White and black hairy tongue • After antibiotic therapy • After steroid therapy • Hydrogen peroxide mouthwash • Immunosuppressive drugs • Smoking • High fever • Constipation • Hyperacidity
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Appendix 1: Causes and Classifications 1077 Fissured tongue
Miscellaneous
• • • • • •
• • • • •
Congenital Syphilis Amyloidosis Melkersson Rosenthal syndrome Papillon Lefevre syndrome Traumatic bite
Pulp calcification Hypervitaminosis Chronic osteomyelitis Systemic sclerosis Dystrophic calcification in areas of tissue necrosis
Vascular Tissue Disorders Systemic diseases manifested in tongue • • • • •
Infection—bacterial, viral and fungal Blood disorders Metabolic disorders Dermatological disorders Collagen and autoimmune disorders
Calcification of Oral Soft Tissue
Arteritis • Polyarteritis nodosa Midfacial granuloma syndrome • • • •
Wegner’s granulomatosis Stewart type of midfacial granuloma Giant cell arteritis Radiation arteritis
Lymph nodes • Chronic infection (tuberculosis) • Calcification following necrosis • Calcification in metastatic tumor
Vascular hamartomas
Sialoliths
Telangiectasia
• In submandibular gland • In minor salivary gland Antroliths
• Hemangioma • Lymphangioma
• Hereditary hemorrhagic telangiectasia • Radiation telangiectasia Vascular tumor
• Eagle’s syndrome
• • • • •
Osteomas
Oral Ulcerative Lesions
• Osteoma cutis • Osteoma of the tongue
According to duration
• In maxillary antrum Calcified ligament
Calcified blood vessels • Arteriosclerosis of facial artery • Sturge-Weber syndrome • Phleboliths Myositis ossificans • Localized • Progressive myositis ossificans Cysticercosis • Calcification of worm larvae Neoplasms • • • • •
Ossifying fibroma Calcifying epithelial odontogenic cyst Calcifying epithelial odontogenic tumor Cementifying fibroma Calcifying fibroma
Hemangioendothelioma Hemangiopericytoma Kaposi sarcoma Angiolymphoid hyperplasia with eosinophils Kimura’s disease
Acute • Acute herpetic stomatitis • Acute aphthous stomatitis • Erythema multiforme • Allergy • ANUG • Herpes zoster • Herpangina Chronic • Traumatic ulcer • Tuberculosis ulcer • Syphilitic ulcer • Actinomycosis ulcer • Erosive lichen planus • Malignant ulcer Recurrent • Recurrent aphthous ulcer • Recurrent herpetic stomatitis • Cyclic neutropenia • Allergic reaction • Erosive lichen planus
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1078 Textbook of Oral Medicine Systemic
• Ulcer due to nutritional deficiency • Erythema multiforme
Blood disorders • Agranulocytosis • Cyclic neutropenia • Polycythemia • Leukemia • Aplastic anemia
According to Etiology Local trauma • Trauma due to sharp and malposed teeth • Trauma due to appliance or restoration • Trauma due to epileptic seizure • Trauma during whooping cough • Trauma from injecting needle Chemical irritant • Local use of chemical agents like phenol, TCA, formocresol, eugenol, phosphorus • Local use of caustic drugs Thermal • Hot foods (pizza burn) • Hot instrument • Reverse smoking • Cold ice, CO2 snow or local anesthetic or ether spray • Actinic radiation Infection Viral • Herpes simplex • Herpes zoster • Chickenpox • Smallpox • Measles • Rubella • Hand foot and mouth disease • Herpangina • Acute lymphonodular pharyngitis • Infectious mononucleosis • AIDS Bacterial • Tuberculosis • Syphilis • ANUG • Scarlet fever • Diphtheria Fungal infection • Candidiasis • Histoplasmosis • Blastomycosis • Mucormycosis • Cryptococcosis Allergy • Local (stomatitis venenata) • Systemic (stomatitis medicamentosa) Neoplastic • Squamous cell carcinoma • Mucoepidermoid carcinoma • Basal cell carcinoma • Melanoma • Malignant lymphoma
Nutritional deficiency • Vitamin B complex • Protein deficiency • Diabetes mellitus • Uremia • Metal poisoning • Xerostomia • Gastric hyperacidity or peptic ulcer • Constipation or malabsorption syndrome • Histiocytosis-X Disease of unknown origin • • • • • • • •
Aphthous ulcer Erythema multiforme Epidermolysis bullosa Systemic lupus erythematosus Lichen planus Pemphigus BMMP Acrodermatitis enteropathica
Syndrome • Stevens-Johnson • Behcet’s • Reiter’s Disorders of Teeth (WHO) Abnormalities of size and form • • • • • • • • • • • •
Concrescence Fusion Gemination Dens evaginatus Dens in dente Dens invaginatus Enamel pearls Peg shaped Taurodontism Tuberculum paramolar Macrodontia Microdontia
Mottled teeth • Dental fluorosis • Mottling of enamel • Non-fluoride enamel opacity Disturbances in tooth formation • Aplasia and hypoplasia of cementum
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Appendix 1: Causes and Classifications 1079 • Dilaceration of toot • Enamel hypoplasia (neonatal, postnatal, prenatal) • Regional odontodysplasia (Turner tooth) Hereditary disturbance in tooth structure • • • •
Amelogenesis imperfecta Dentinogenesis imperfecta Odontogenesis imperfecta Dentinal dysplasia shell teeth
Microdontia • • • • • • •
Supernumerary teeth Idiopathic Peg shaped lateral Cleft lip and palate Hereditary hypohidrotic ectodermal dysplasia Radiotherapy during childhood Hypopituitarism
Malformed crown Disturbances in tooth eruption • • • • • •
• • • • • • • • • • • • • • •
Dentia praecox Natal teeth Neonatal teeth Premature eruption of tooth Premature shedding of primary tooth Retained primary teeth
Supernumerary teeth • • • • •
Distomolar Fourth molar Mesiodens Paramolar Supplementary teeth
Mesiodens Enamel hypoplasia Peg shaped lateral incisor Turner tooth Talon cusp Amelogenesis imperfecta Dens evaginatus Dentinogenesis imperfecta Regional odontodysplasia Congenital syphilis Vitamin D resistant rickets Renal osteodystrophy Hypoparathyroidism Epidermolysis bullosa Radiotherapy during childhood
Anodontia
Enamel loss
• Hypodontia • Oligodontia
• • • • • •
Other developmental disorders • • • •
Embedded teeth Impacted teeth Teething syndrome Color change during tooth formation
Caries Attrition Abrasion Erosion Amelogenesis imperfecta Dentinogenesis imperfecta
Extrinsic stain • • • •
Causes Teeth Pathology
Tobacco Coffee, tea Cold drink Chromogenic bacteria
Hyperdontia • • • •
Idiopathic Cleft lip and cleft palate Gardner’s syndrome Cleidocranial dysplasia
Intrinsic discoloration
Hypodontia • • • • •
Idiopathic Cleft lip and palate Hereditary hypohidrotic ectodermal dysplasia Incontinentia pigmenti Radiotherapy during childhood
• • • • • • • • • •
Aging Death of pulp Fluorosis Tetracycline Internal resorption Calcific metamorphoses Dentinogenesis imperfecta Amelogenesis imperfecta Congenital erythropoietic porphyria Erythroblastosis fetalis
Macrodontia
Abnormal shaped root
• • • • •
• • • • •
Idiopathic Fusion Gemination Facial hemihyperplasia Gigantism
External root resorption Dilaceration Hypercementosis Supernumerary roots Concrescence
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1080 Textbook of Oral Medicine • • • • • •
• Cryptococcosis • Toxoplasmosis
Taurodontism Enamel pearl Benign cementoblastoma Radiotherapy during childhood Dentinogenesis imperfecta Dentin dysplasia type I
Necrosis • Chemicals like phosphorus, arsenic • Osteoradionecrosis • Noma
Enlarged pulp chamber • • • • • • •
Internal resorption Taurodontism Dentinogenesis imperfecta Regional odontodysplasia Vitamin D resistant rickets Hypophosphatasia Dentin dysplasia type II
Odontogenic cysts • • • • • •
Radicular Residual Dentigerous Primordial Lateral periodontal cyst Gingival
Pulpal calcification
Non-odontogenic cysts
• • • • • •
• • • • • • •
Idiopathic pulp stone Secondary dentin Calcific metamorphosis Dentinogenesis imperfecta Dentin dysplasia type I Dentin dysplasia type II
Early exfoliation • • • • • • • • • • • • •
Trauma Aggressive periodontitis Immunocompromised stages Diabetes mellitus Osteomyelitis Cyclic or chronic neutropenia Langerhan’s cell disease Dentin dysplasia type I Regional odontodysplasia Papillion-Lefevre syndrome Down syndrome Hypophosphatasia Scurvy
Neoplasm • Benign • Malignant Endocrine and metabolic disorders • • • • • • •
Fibrous dysplasia Paget’s disease Hyperthyroidism Histiocytosis Caffey’s disease Pregnancy tumor Leontiasis ossea
Salivary gland disorders
Swellings of the Palate
• Mucocele • Tumor • Necrotizing sialometaplasia
Traumatic • • • •
Nasopalatine or incisive canal cyst Globulomaxillary Traumatic Median alveolar and median palatine cyst Aneurysmal bone cyst Mucocele Botryoid cyst
Fracture of maxilla, alveolar process Hematoma Epulis Denture hyperplasia
Developmental • Torus palatinus • Hyperplasia of palatal gland
Inflammatory • Periapical, periodontal, gingival abscess of anterior maxillary teeth • Osteomyelitis—acute and chronic • Syphilis • Tuberculosis • Actinomycosis • Quinsy (peritonsillar abscess) • Infected cyst • Mucormycosis • Aspergillosis
Miscellaneous • • • • • • • •
Impacted and supernumerary teeth Angioneurotic edema Teratoma Wegener’s granulomatosis Gingival hyperplasia Midline lethal granuloma Tuberous sclerosis Papillomatosis in acanthosis nigricans
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Appendix 1: Causes and Classifications 1081 Swellings in the Submandibular (angle of mandible) Region
Neoplasm
Traumatic
Allergy
• Hematoma—post-traumatic, postoperative and postextraction • Fracture of mandible in symphysis area and body of mandible • Denture hyperplasia • Epulis fissuratum • Pyogenic granuloma • Traumatic granuloma • Myositis ossificans Cysts
• Urticaria • Angioneurotic edema • Allergic macrocheilia
Tumors
• • • • • • •
Metastasis Inflammatory • • • • • • •
Periapical, pericoronal Osteomyelitis Periostitis Cellulitis Ludwig’s angina Tuberculosis Actinomycosis
• Congenital—double lip Miscellaneous Amyloidosis Keratoacanthoma Papillomatosis Tuberous sclerosis Melkersson-Rosenthal syndrome Papillon Lefevre syndrome Cheilitis glandularis
Swellings in the Floor of the Mouth Traumatic • • • • • •
Salivary Gland Dysfunction Endocrine • Fibrous dysplasia • Cherubism • Caffey’s disease
Hematoma Fracture of alveolar process in symphysis region Denture granuloma Foreign body granuloma Epulis on lingual aspect of mandibular anterior teeth Epulis fissuratum, denture irritation hyperplasia
Inflammatory
Lymphadenitis Swelling of the Lip Traumatic • • • •
Developmental
From fall, assault, accidental, injury Lip sucking or lip biting or pipe smoking Trauma during epileptic and hysteric seizures Actinic cheilosis
• Abscess—periapical, gingival, periodontal, in anterior mandibular teeth • Cellulitis—Ludwig’s angina • Infection following trauma • Infection of Wharton’s duct Necrosis • Chemical • Post-irradiation
Inflammatory • Secondary to dental infection • Carbuncle or abscess from mucus glands or hair follicle or acne • Infected traumatic lesion • Tuberculosis • Leprosy • Syphilis—chancre-gumma • Actinomycosis • Molluscum contagiosum • Secondary to irradiation • Condyloma acuminatum Cyst • Mucus extravasation or mucocele • Lympho-epithelial cyst • Epidermoid cyst • Nasolabial cyst
Cysts Odontogenic • Radicular • Dentigerous • Gingival • Residual • Keratocyst • Primordial Non-odontogenic • Traumatic • Ranula • Mucocele • Sublingual dermoid cyst • Lympho-epithelial cyst • Cystic hygroma
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1082 Textbook of Oral Medicine Syndrome • Sturge-Weber syndrome
Extraoral Discharging Sinus
Neoplasms
• Salivary fistula • First or second branchial arch sinus or fistula • Congenital lip pit
Benign epithelial tumors • Papilloma • Adenoma • Oncocytoma • Oxyphilic adenoma Malignant epithelial tumors • Squamous cell carcinoma • Malignant melanoma • Mucoepidermoid carcinoma • Adenocarcinoma • Transitional cell carcinoma Benign connective tissue tumors • Hemangioma • Lymphangioma • Neurofibroma • Leiomyoma • Rhabdomyoma • Fibroma • Lipoma • Granular cell myoblastoma Malignant mesenchymal and other tumors • Fibrosarcoma • Hemangioendothelioma • Reticular cell sarcoma • Rhabdomyosarcoma • Malignant lymphoma
Developmental
Inflammatory • Periapical, periodontal and dentoalveolar abscess pointing extraorally • Chronic osteomyelitis • Syphilis • Tuberculosis of jaw bone • Actinomycosis • Osteoradionecrosis • Salivary fistula from suppurative sialadenitis • Infected lymph node • Infected cyst • Infection secondary to trauma, injury • Infection of various facial space • Oronasal fistula Neoplastic • Intraoral malignancy with secondary growth • Salivary gland malignancy Perforations of the Palate Congenital • Cleft palate Inflammatory
Salivary gland swelling • • • • • •
Sialadenitis Sialolithiasis Sjögren’s syndrome Mikulicz’s disease Salivary gland tumors Cysts of salivary gland
Allergy • Angioneurotic edema Swelling of Neck Lateral neck swelling • • • • • • • •
Lymphadenitis Metastatic carcinoma to lymph nodes Lymphoma Parotid lesion Metabolic diseases Carotid body tumor Epidermoid cyst Cystic hygroma
Midline neck swelling • Thyroglossal duct cyst • Thyroid tumor • Dermoid cyst
• • • • • • • • •
Osteomyelitis Syphilitic gumma Tuberculosis Infection of traumatic and chronic wound Mucormycosis Toxoplasmosis Blastomycosis Leprosy Wegener’s granulomatosis
Traumatic • Fracture of maxilla • Use of suction disc for dentures • Pizza burn, thermal burn Neoplasm • • • • • •
Squamous cell carcinoma Mucoepidermoid carcinoma Adenocystic carcinoma Osteosarcoma Lymphoma Midline lethal granuloma
Glossodynia Local causes • Traumatic injury
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Appendix 1: Causes and Classifications 1083 • • • • • • • • • • • • • •
Median rhomboid glossitis Geographic tongue Lichen planus Oral submucus fibrosis Candidiasis Denture irritation Allergic reaction to denture material Malignant lesions Ulcerative and erosive lesions on tongue due to infection, trauma, allergy and systemic disease Xerostomia Trauma to lingual nerve Fusospirochetal infection TMJ dysfunction Chronic mouth breathing
Systemic diseases • • • • • • • • • • •
Diabetes Neuralgia—lingual, glossopharyngeal and facial Neuritis Nutritional deficiency Allergy Anemia Sjögren’s syndrome Chronic gastritis Hypothyroidism Mercurialism AIDS
• Pharyngitis • Habits—smoking, tobacco and catechu Systemic conditions • Odor from nasopharynx—due to adenoma, rhinitis, sinusitis, postnasal drip, tonsillitis, tonsillar abscess, pharyngitis • From lung and bronchi—bronchitis, lung abscess, pulmonary tuberculosis, lung malignancy • Diseases of gastrointestinal tract—hyperacidity, gastritis, peptic ulcer, malignancy • Metabolic disorders—diabetes, uremia and liver disease • Blood disorders—anemia, agranulocytosis, leukemia, thrombocytopenia • Salivary gland dysfunctions causing xerostomia • Dehydration states—diarrhea, vomiting, diabetes insipidus, • Drug—isosorbide dinitrate, iodine derivatives, diuretics phenothiazines, immunosuppressive drugs and dimethyl sulfoxide Enlargement of Cervical Lymph Nodes Inflammation and Infection
Psychological
Bacterial infections • Specific bacterial infection • Syphilis • Tuberculosis • Non-specific • Periodontal disease • Pericoronitis • Periapical infections
• • • • •
Viral infections • Infection caused by herpes simplex • Human immunodeficiency virus • Cat scratch disease • Infectious mononucleosis
Emotional stress and strain Depression Neurosis Schizophrenia Mood disorders
Fungal infection • Histoplasmosis • Oral candidiasis
Halitosis Physiological During infancy—sweet odor During development of dentition—pungent odor Menstruation Food habits—alcohol, garlic, lemon, other aromatic beverages or food substances • Old age—due to metabolic changes in periodontal tissue • Hunger breath
Parasitic infection • Rickettsial infections
Pathological
• Lymphoma
• • • •
Local oral conditions • Retention of food around the teeth (interdental area, flaps) • Gingival and periodontal disease • Deep carious lesion and necrotic pulp • Coating of tongue • Mouth breathing • Denture and orthodontic appliance • Oral soft tissue lesion • Stomatitis • Glossitis
Allergic conditions • Serum sickness Primary neoplasm
Metastasis tumors • Oral squamous cell carcinoma • Metastasis carcinoma from the breast Miscellaneous conditions • • • •
Non-tender lymphoid hyperplasia Collagen disease Sarcoidosis Leukemia
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1084 Textbook of Oral Medicine Trismus Traumatic Intra-articular • Trauma to growth center or developing condyle • Monoarticular arthritis like spasm or subluxation (due to chronic malocclusion) • Trauma to articular disc • Trauma to capsular or temporomandibular ligament • Fracture with or without dislocation and displacement of condylar head • Ankylosis • Foreign body in the joint area Extra-articular • Trauma to muscle • Trauma during extraction • Faulty mandibular block • Fracture of coronoid process • Fracture of zygomatic arch • Fracture of styloid process • Misplaced fixative or augmentative device
• Cancrum oris or noma • Abscess in various fascial spaces like infratemporal, lateral pharyngeal, submasseteric, and pterygomandibular spaces • Phosphorus necrosis • Quinsy (peritonsillar abscess) • Infection of ear or otitis media • Mumps • Acute generalized stomatitis • Angular cheilitis • Pharyngitis Congenital and developmental disorders • • • • •
Unilateral or bilateral condylar hyperplasia Unilateral or bilateral exostosis of coronoid Hyperplasia of coronoid process and zygomatic arch Fusion of coronoid process with zygomatic arch Absence of coronoid process
Neoplastic Intra-articular Benign • Osteoma • Chondroma • Osteochondroma • Myxoma • Benign giant cell tumor • Trotter’s syndrome
Inflammatory Intra-articular • Pyogenic infection • Rheumatic fever • Rheumatoid arthritis • Gout • Tuberculosis • Syphilis • Actinomycosis • Osteomyelitis • Synovitis
Malignant • Osteosarcoma • Chondrosarcoma • Fibrosarcoma • Metastatic carcinoma
Extra-articular • Pericoronitis • Acute and chronic osteomyelitis • Acute and chronic dentoalveolar abscess
Extra-articular • Benign and malignant tumors of mandible and maxilla mainly in premolar and molar area
Summary table of the effects of different inflammatory processes on the periapical tissues and the resultant radiographic appearances Stage of inflammation
Underlying inflammatory changes
Radiographic appearance
Initial acute inflammation
Inflammatory exudate accumulates in the apical periodontal ligament space— acute apical periodontitis
Widening of the radiolucent line of periodontal ligament space or no apparent changes evident
Initial spread of inflammation
Resorption and destruction of the apical bony socket—periapical abscess
Loss of radiopaque line of lamina dura at the apex
Further spread of inflammation
Further resorption and destruction of the apical alveolar bone
Area of bone loss at the tooth apex
Initial low-grade chronic inflammation
Minimal destruction of the apical bone. The body’s defense systems lay down dense bone in the apical region
No apparent bone destruction but dense sclerotic bone evident around the tooth apex (sclerosing osteitis)
Latter stages of chronic inflammation Apical bone is resorbed and destroyed and dense bone is laid down around the area of resorption—periapical granuloma or radicular cyst
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Circumscribed well defined radiolucent area of bone loss at the apex, surrounded by dense sclerotic bone
Appendix 1: Causes and Classifications 1085 • Malignant tumors of nasopharynx • Malignant tumors of maxillary sinus • Parotid tumors Cystic Extra-articular • All large cystic lesion affecting mandible, ramus and posterior part of maxilla
Tetanus Tetany Fibrous dysplasia Paget’s disease Acromegaly
Miscellaneous • • • • • • • • • • • • • • • •
Epilepsy and hysteria Hydrophobia Sudden physical, chemical and electrical shock Hemorrhage in medulla oblongata Brain tumor Scleroderma Strychnine poisoning Myelofibrosis Amylotrophic lateral sclerosis Oral submucus fibrosis Osteoradionecrosis Myositis ossificans Disuse atrophy Myofascial pain dysfunction syndrome (MPDS) Extensive burns of face with keloid and scar formation Dystrophic epidermolysis bullosa
Hemorrhage
von Willebrand’s disease Deficiency of Stuart factor Multiple myeloma Systemic lupus erythematosus Diffuse intravascular coagulation Macroglobulinemia
Hemorrhage due to systemic diseases • • • • • • • • •
Systemic • • • • •
• • • • • •
Scurvy Diabetes mellitus Septic embolism in bacterial endocarditis Meningococcemia Systemic viral infection Allergy Anti-coagulant therapy Graft versus host reaction Sturge-Weber syndrome
Angular cheilitis • Infections • Candidiasis • Herpes labialis • Unhygienic appliances • Malabsorption syndrome • Diabetes • Change in vertical dimension • Xerostomia • Nutritional deficiency • Anemia • Vitamin deficiency • Protein deficiency • Plummer-Vinson syndrome • Split papule of syphilis • Allergic reaction to lipstick • Cold sore
Local causes • • • •
Post-extraction, post-surgical and post-traumatic Infections—viral, bacterial, fungal, parasitic and spirochete Oral ulcerative lesions—stomatitis, glossitis Oral exophytic soft tissue lesions—pyogenic granuloma, pregnancy tumor • Local irritants leading to gingivitis and periodontitis • Rupture of blood containing bulla • Congenital hamartomas—hemangioma, hereditary hemorrhagic telangiectasia, arteriovenous malformation Hemorrhage due to platelet disorders • • • • •
Thrombocytopenia Thrombocytosis Thrombasthenia Glanzmann’s disease Aldrich syndrome
Sialorrhea • • • • • • • • • • • • •
Acute inflammation of oral mucosa Fracture of jaw bone During eruption of teeth in infants Mental retardation Neurosis Psychosis Parkinsonism Schizophrenia Epilepsy Acrodynia (mercury poisoning) Rabies Familial dystonia Drugs like sialogogue
Xerostomia
Hemorrhage due to coagulation diseases
Factor affecting salivary center
• Hemophilia • Christmas disease
• Emotional disturbance like stress, strain • Depression
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1086 Textbook of Oral Medicine • Hysteria • Neurosis Factor affecting autonomous nervous system • Encephalitis • Brain tumor • Neurological operation Factor affecting salivary gland • • • • • • •
Developmental Inflammatory Tumor of salivary gland Sialolithiasis Sjögren’s syndrome Mikulicz’s disease Atrophy of gland
Alteration in fluid and electrolyte balance • • • • • • • •
Dehydration Diarrhea Vomiting Diuresis Diabetes insipidus Congestive cardiac failure Ascites Liver cirrhosis
Drugs • • • • • • • • • • •
Anticholinergic Antidepressants Sympathomimetics Opium derivatives Antipsychotic Antihistamine Diuretics Sedatives Digitalis Steroids Chemotherapeutic agents
Miscellaneous • • • • • •
Malnutrition Nutritional and vitamin deficiency Radiation Toxemia Habits (smoking, betel nut chewing) Chronic alcoholism
Saliva Drooling at Corner of Mouth • • • • • • •
Oral infection, throat infection Jaw fracture Psychosis Schizophrenia Rabies Acrodynia During eruption of teeth in infant
Discoloration of the Teeth Extrinsic • • • • • • • •
Habits—tobacco, catechu Chromogenic bacteria Poor oral hygiene Oral drugs Iatrogenic Tattoo made by patient Chlorhexidine mouthwash Medicaments like AgNO3, iodine, iron
Intrinsic • • • • • • • • • • • • • •
Erythroblastosis fetalis due to Rh incompatibility Neonatal jaundice Congenital porphyria Tetracycline therapy during formation of teeth Cystic fibrosis Osteogenesis imperfecta Dentinogenesis imperfecta Amelogenesis imperfecta Fluorosis Enamel opacities Non-vital teeth or internal resorption Congenital heart disease Acute exanthematous disease Turner’s teeth
Macroglossia Congenital or developmental • Mongolism • Lingual thyroid or polyp Inflammatory • • • • • • • • •
Syphilis Amoebic dysentery Ludwig’s angina Pneumonia Typhoid Tuberculosis Blastomycosis Infected wound Actinomycosis
Neoplasms • Hemangioma (diffuse type) • Neurofibromatosis • Lymphangioma (diffuse type) Systemic • • • • • • • •
Pellagra Down’s syndrome Myxedema Acromegaly Amyloidosis Uremia Gardner’s syndrome Diabetes
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Appendix 1: Causes and Classifications 1087 • • • • • • •
Differentiation pain syndrome • Atypical odontolgia • Traumatic neuroma • Neuritis • Reiter’s sympathetic dystrophy
Scurvy Dyskinesia chorea Melkersson-Rosenthal syndrome Sturge-Weber syndrome Hurler’s syndrome Beckwith’s hypoglycemia syndrome Tuberous sclerosis
Psychogenic pain • Anxiety and depression • Delusional or hallucination pain • Hysterical or hypochondriac pain
Orofacial pain Extra-cranial causes Dental and oral • Dentinal hypersensitivity • Pain from disorders of pulp • Hyperemia • Acute pulpits • Chronic pulpits • Pain from disorders of periodontium • Mucogingival pain • Stomatitis • Gingivitis • Glossitis • Glossodynia • Osseous and periosteal pain • Dry socket • Periostitis • Osteomyelitis • From disorders of ear and eye • Enlargement of salivary glands
Classification by Bells Somatic • Superficial—mucogingival • Deep visceral—musculoskeletal Neurogenic • Neuropathy—neuralgia and neuritis • Deafferentation syndrome Psychogenic • Conversion hysteria • Delusional pain Sloughing Pseudomembranous Necrotic White Lesion • • • • • • • • • • • •
Pain from paranasal sinuses • Sinusitis • Tumors of the sinus Musculoskeletal • • • • •
Myofacial pain Temporomandibular joint arthropathy Cervical spine disorders Trotter’s syndrome Eagle’s syndrome
Osteoporosis
Intra-cranial causes • • • •
Traction disorders of pain sensory structure of the brain Neoplasms, aneurysms, hematoma, hemorrhage or edema Displacement of great venous sinus Distortion and dilation of intracranial vessels
Vascular pain • • • • • •
Migraine headache Cluster headache Tension headache Temporal headache Carotodynia Angina pectoris or myocardial infarction
Plaque Traumatic ulcer Diffuse gangrenous stomatitis Diphtheria Noma Candida endocrinopathy syndrome Chemical burns ANUG Candidiasis Eosinophilic granuloma Superficial abscess Syphilitic chancre and mucous patches
• • • • • • • • • • • • •
Osteogenesis imperfecta Post-menopausal osteoporosis Hyperthyroidism Diabetes Old age Gonadal osteoporosis Idiopathic osteoporosis Renal acidosis Oxalosis Acromegaly Adaptation syndrome Hypervitaminosis D Hypovitaminosis C
Depapillation of Tongue
Neurogenic pain
Congenital cause
Paroxysmal • Trigeminal neuralgia • Glossopharyngeal neuralgia • Geniculate neuralgia
• • • •
Familial dystonia Epidermolysis bullosa Dyskeratosis congenita Endocrine candidiasis
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1088 Textbook of Oral Medicine • • • • • •
Developmental • Geographic tongue • Median rhomboidal glossitis • Central papillary atrophy Chronic trauma Nutritional and hematological abnormalities • Pellagra • Riboflavin • Conditional deficiency • Plummer-Vinson syndrome Medication • Antibiotic • Anticholinergic agent • Cancer chemotherapeutic agent
Abnormal crypt position Overcrowding Additional teeth Retention of deciduous predecessor Dentigerous and eruption cyst Hereditary gingival fibromatosis
Systemic causes • • • • • •
Congenital hypopituitarism Congenital hypothyroidism Down syndrome Cleidocranial dysplasia After radiation Rickets
Loosening or Early Loss of Teeth Local causes
Peripheral vascular disease
• Inflammatory periodontal disease • Trauma • Juvenile periodontitis
Chronic candidiasis Tumor • Squamous cell carcinoma • Epidermoid carcinoma
Systemic causes • • • • • • •
Miscellaneous • Diabetes mellitus • Oral submucous fibrosis Atrophic Lesion of Oral Mucosa of Tongue
Down syndrome Diabetes mellitus Neutropenia Hypophosphatasia Papillon lefevre syndrome Ehlers-Danlos syndrome AIDS related disorders
Developmental
Others
• Benign migratory glossitis • Median rhomboidal glossitis
• Acrodynia • Neoplasm • Eosinophilic granuloma
Systemic condition • Endocrine—diabetes mellitus • Vitamins like B2, B5, B6, B9 and B12 deficiency • Blood disorders—pernicious anemia and iron deficiency anemia Infection • Syphilis • Chronic candidiasis
Malformed Teeth • • • • • •
Local infection or trauma Radiotherapy Congenital syphilis Down syndrome Ectodermal dysplasia Rickets
Hairy Tongue Oral submucus fibrosis Mucocutaneous • • • • •
Atrophic lichen planus Discoid lupus erythematosus Dyskeratosis congenita Scleroderma Xerostomia
• • • • •
Dehydration Debilitated patient Long illness Painful oral condition restricted tongue movement Use of local and systemic medication like systemic antibiotic, topical H2O2 and perborate
Causes that Cause Red Lesions Retarded Eruption of Teeth Local causes
Marked increased in hemoglobin concentration of articulating blood
• Loss of space
• Polycythemia
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Appendix 1: Causes and Classifications 1089 Vascular dilation from Inflammation (erythema) • Mechanical trauma (cheek biting, ill fitting denture) • Thermal trauma (hot food) • Chemical trauma • Infection (cellulitis and Ludwig angina) • Allergy or autoimmune disease • Ulcer with inflamed rim (recurrent herpetic ulcer) Congenital defect • Hemangioma
Agents occasionally associated with leukopenia apparently as a result of individual sensitivity • Analgesics, sedative and anti-inflammatory • Antithyroid drug • Anticonvulsant • Sulfonamides • Antihistamine • Antimicrobial agents • Tranquilizers Physical agents
Extravasation of blood (trauma or homeostatic disease) Atrophy or thinning of mucosa
• X-ray radiation and radioactive substance Anaphylactic shock and early stages reaction of foreign protein Disease of unknown etiology • Liver cirrhosis • Disseminated erythematosus • Cyclic neutropenia
Leukopenia Infections Bacterial • Typhoid • Paratyphoid fever • Brucellosis • Tularemia (early)
Basophilia Blood disorders • Chronic myelocytic leukemia • Chronic anemia • Hodgkin’s disease
Viral and rickettsial • Influenza • Measles • Rubella • Chickenpox • Infectious hepatitis • Colorado tick fever • Dengue • Yellow fever
Splenectomy Infection • Chronic inflammation of accessory tissue • Smallpox • Chickenpox
Protozoal • Malaria • Relapsing fever • Kala azar
Myxedema
Any overwhelming infection • Miliary tuberculosis • Septicemia
Neutrophilia
After injection of foreign proteins Some cases of nephrosis
Acute infection • • • • • • • •
Hemopoietic disorders • • • • • •
Gaucher’s disease Pernicious anemia Aplastic anemia Chronic hypochromic anemia Aleukemic leukemia Agranulocytosis
Coccal Bacilli Fungi Spirochetes Virus Rheumatic fever Diphtheria Smallpox
Inflammatory Chemical agents Agents commonly producing leukopenia in all patient if given in sufficient dose • Mustards (sulfur and nitrogen mustards) • Urethane • Busulfan • Benzene • Antimetabolites
• • • • •
Coronary thrombosis Gout Collagen vascular disease Burns Hypersensitivity reaction
Intoxication • Uremia
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1090 Textbook of Oral Medicine • Diabetes acidosis • Poisoning by chemical and drugs like lead, mercury, digitalis, insect venoms, black widow spider Acute hemorrhage Acute hemolysis
Miscellaneous • Pulmonary infiltration with eosinophilia • Tropical eosinophilia • Polyarteritis nodosa • Rheumatoid arthritis • Sarcoidosis • Certain poison
Malignant tumor of
Inherited
• Gastrointestinal tract • Liver • Bone marrow
Idiopathic
Blood disorders
Acute infection
• • • • • •
• Infectious mononucleosis • Acute infectious lymphocytosis • Infectious hepatitis
Myelocytic leukemia Polycythemia Myelofibrosis Myeloid metaplasia Chronic idiopathic neutropenia Hereditary neutrophilia
Miscellaneous • • • • • •
Physiologic in the newborn During labor After repeated vomiting Convulsion Paroxysmal tachycardia After epinephrine injection
Lymphocytosis
Chronic infection • Tuberculosis • Secondary and congenital syphilis • Undulant fever Lymphocytic leukemia Lymphosarcoma Heavy chain disease Hemopoietic disorders • Neutropenia • Exanthema
Eosinophilia Allergic • Bronchial asthma • Urticaria • Angioneurotic edema • Hay fever • Allergic rhinitis • Drug sensitivity Skin disease • Pemphigus • Dermatitis herpetiformis • Bullous pemphigoid Parasitic infection • Trichinosis • Echinococcosis disease Blood disorders • Chronic myelocytic leukemia • Polycythemia vera • Hodgkin’s disease • Pernicious anemia Infection • Scarlet fever • Chorea • Erythema multiforme Malignant disease of any type Following irradiation
Monocytosis Bacterial infection • • • • •
Tuberculosis Subacute bacterial endocarditis Syphilis Brucellosis Typhoid
Protozoan and rickettsial infection • • • • • •
Malaria Rocky Mountain spotted fever Typhus Kala azar Trypanosomiasis Oriental sore
Blood disorders • • • •
Lymphoma Leukemia Hodgkin’s disease Multiple myeloma
Lipid storage disease • Gaucher disease Malignant neoplasm • Carcinoma of ovary, breast and stomach
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Appendix 1: Causes and Classifications 1091
• Sarcoidosis • Ulcerative colitis • Regional arteritis
• Periapical scar • Giant cell granuloma • Benign and malignant tumor including secondary metastatic deposits • Lymphoreticular tumors of bone • Langerhan’s cell disease • Periapical cemental dysplasia • Surgical defect • Osteomyelitis
Chronic high dose steroid therapy
Monolocular and Multilocular Radiolucency
Collagen vascular disease • Lupus erythematosus • Rheumatoid arthritis Granulomatous disease
Monolocular lesion Peripheral Plasmocytosis Infection Viral • Rubella • Rubeola • Varicella • Infectious mononucleosis Bacterial • Streptococcal • Diplococcal • Syphilis • Tuberculosis Protozoal • Malaria • Trichinosis Serum Sickness Drugs • Penicillin • Sulfisoxazole Antitoxins • Equine tetanus • Equine diphtheria Neoplasm Hematological • Plasma cell leukemia • Chronic lymphocytic leukemia Nonhematological • Breast • Prostate Miscellaneous • Transfusion • Hyperimmunization • Trauma
• • • • • • • • • • • • • •
Radicular cyst Residual cyst Dentigerous cyst Lateral periodontal cyst Nasopalatine duct cyst Simple bone cyst Calcifying epithelial odontogenic tumor Adenomatoid odontogenic tumor Primary bone tumors Secondary metastasis tumor Multiple myeloma Eosinophilic granuloma Fibro-cemento-osseous lesion Stafne’s bone cavity
Multilocular lesion • • • • • • • • • • • • • •
Odontogenic keratocyst Ameloblastoma Ameloblastic fibroma Ameloblastic fibro-odontoma Odontogenic myxoma Central giant cell granuloma Brown tumor Cherubism Aneurysmal bone cyst Metastatic tumor of the jaw CEOT Fibrous dysplasia Burkitt’s lymphoma Squamous odontogenic tumor
Pericoronal Radiolucency • • • • • • • •
Dentigerous cyst Ameloblastoma Calcifying odontogenic cyst Adenomatoid odontogenic tumor Pericoronal space Unicystic ameloblastoma Ameloblastic fibroma Envelopmental primordial cyst
Periapical Radiolucency • • • • •
Acute apical periodontitis Periapical abscess Periapical granuloma Periapical cyst Dentigerous cyst
Inter-radicular Radiolucency • • • •
Primary tooth crypt Mental foramina Nutrient canal Bony periodontal pocket
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1092 Textbook of Oral Medicine • • • • • • • • • • • •
Malignancy Lateral periodontal cyst Median mandibular cyst Paradental cyst Furcation involvement Lateral radicular cyst Traumatic bone cyst Odontogenic tumor Globulomaxillary tumor Incisive canal cyst Histiocytosis-X Osteoradionecrosis
• Odontoma • Osteomyelitis chronic Pericoronal Mixed Lesion • • • • • • • •
Solitary Cyst-like Radiolucency not Necessary Contacting Teeth • • • • • • • • • • • • • •
Primordial cyst Traumatic cyst Residual cyst Odontogenic keratocyst Aneurysmal bone cyst Cementoma Central fibroma Ameloblastoma Giant cell granuloma Midpalatal cyst Cementifying ossifying fibroma Benign non-odontogenic tumor Central squamous cell carcinoma Myxoma
Odontoma—intermediate stage AOT Keratinizing and calcifying odontogenic cyst CEOT Odontogenic fibroma Eruption sequestrum Cystic odontoma Ameloblastic fibroma
Mixed Radiolucent-radiopaque Lesion not Necessary Contacting Teeth • • • • • • • • • • •
Chronic osteomyelitis Osteoradionecrosis Fibrous dysplasia Paget’s disease—intermediate stage Central hemangioma Osteoid osteoma Cementifying and ossifying fibroma Osteogenic sarcoma Chondroma and chondrosarcoma Ossifying subperiosteal hematoma Calcifying epithelial odontogenic tumor
Variable Radiopacities
Multiple Separate Well-defined Radiolucency
Abnormalities of the teeth
• • • • • • • •
• • • •
Multiple myeloma Basal cell nevus syndrome Multiple cyst or granuloma Histiocytosis-X Cherubism Nodular central masses Neurofibromatosis Hurler’s and Hunter’s syndrome
Condition affecting the bone Developmental • Exostosis including tori—mandibular or palatal Inflammatory • Low grade chronic infection—sclerosing osteitis • Osteomyelitis—sequestra involucrum formation
Generalized Rarefaction of Jaw Bones • • • • • • • • • •
Hyperparathyroidism Osteoporosis Osteogenic imperfecta Hypervitaminosis D Diabetes Osteomalacia Leukemia Paget’s disease Multiple myeloma Lymphosarcoma
Tumors odontogenic (late stages) • Calcifying epithelial odontogenic tumor • Adenomatoid odontogenic tumor • Calcifying odontogenic cyst Non-odontogenic tumor • Benign—osteoma, chondroma • Malignant—osteosarcoma, osteogenic secondary metastases
Mixed Radiolucent—Radiopaque Lesion Associated with Teeth • • • • • •
Unerupted and misplaced teeth including supernumeraries Odontoma—compound and complex Root remnants Hypercementosis
Calcifying crown of developing teeth Tooth root with rarefying osteitis Rarefying and condensing osteitis Cementifying and ossifying fibroma Periapical cementoma—intermediated stage Foreign bodies
Fibro-cemento-osseous • Fibrous dysplasia • Periapical cemental dysplasia • Gigantiform cementoma • Benign cementoblastoma • Cemeto-ossifying fibroma Other • Paget’s disease • Osteopetrosis
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Appendix 1: Causes and Classifications 1093 Superimposed soft tissue calcifications
Generalized Radiopacities
• • • • •
• • • • • • •
Salivary calculi Calcified lymph node Calcified vessels Phleboliths Calcified ACE scars
Foreign bodies • Intrabony • Within the soft tissue • On or overlying the skin
Thickened Periodontal Ligament Space • • • • • •
Periapical radiopacities True • • • • •
Condensing osteitis Periapical idiopathic osteosclerosis Mature periapical cementoma Foreign bodies Hypercementosis
Periapical abscess Current orthodontic therapy Increase occlusal friction Systemic sclerosis Sarcoma infiltration Carcinoma infiltration
Loss of Lamina Dura
Projected • • • • • •
Gardener’s syndrome Fluorosis Caffey’s disease Adenomatoid odontogenic tumor Metastatic carcinoma of prostate von Buchan disease Osteopetrosis
Sialoliths Phleboliths Arterial calcification Retained root tips Exostosis tori and periapical osteoma Calcified lymph nodes
Multiple Separate Radiopacities • Multiple chondroma • Sickle cell sclerosis • All solitary radiopacities not necessary contacting teeth
• • • • • • • • • • •
Periapical infections Fibrous dysplasia Paget’s disease Osteoporosis Normal anatomical variation Hyperparathyroidism Leukemia Cushing syndrome Hypophosphatasia Osteomalacia Multiple myeloma
Different Type of Periosteal Reaction and their Cause Regular type
Solitary Radiopacities not Necessary Containing Teeth True • • • • • • • • • • • • •
Tori, exostosis and periapical osteoma Unerupted, impacted and supernumerary teeth Retained root Idiopathic osteosclerosis Cementifying and ossifying fibroma Chondroma Chondrosarcoma Mature osteoblastoma Osteogenic sarcoma Fibrous dysplasia Mature cementoma Sclerosing osteomyelitis and diffuse sclerosing osteomyelitis Proliferative periostitis
Projected • • • • •
Anatomic radiopacities Foreign bodies Pathologic soft tissue Arterial calcification Rhinoliths and antroliths
Parallel type • Onion peel appearance • Eosinophilic granuloma • Chronic osteomyelitis • Codman’s triangle • Osteosarcoma Radiating type • Sunray appearance • Osteosarcoma • Hair on end appearance • Paget’s disease • Central hemangioma Irregular type • Osteomyelitis • Fracture • Osteogenic malignancy • Subperiosteal bleeding • Leukemia • Histiocytosis • Arthritis • Rheumatism
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1094 Textbook of Oral Medicine Typical Features of the Lesion Typical clinical feature Name of disease
Typical feature
Ameloblastoma
Egg shell cracking
Pyogenic granuloma
Hour-glass appearance
Hodgkin’s disease
Bimodal age incidence peak
Psoriasis
Auspitz’s sign
Lichen planus
Wickham’s striae
Pemphigus
Nikolsky’s sign
Scarlet fever
Strawberry and Raspberry tongue
Diphtheria
Diphtheritic membrane
Wegener’s granulomatous
Strawberry gingivitis
Tetany
Risus sardonicus
Behcet’s syndrome
Pathergy test positive
Measles
Koplik’s spot
Mild restricted muscular dystrophy
Tapir-lips
Leukokeratosis nicotina glossi
Golf ball appearance
Bell’s palsy
Masklike or expressionless appearance
Rickets
Rachitic rosary, pigeon breast
Pseudoxanthoma elasticum
Hound dog
Typical radiological feature Typical radiological feature
Name of disease
Soap bubble appearance
Ameloblastoma, aneurysmal bone cyst, central hemangioma
Honeycomb pattern
Calcifying epithelial odontogenic cyst, odontogenic myxoma, hemangioma, central giant cell granuloma
Driven snow appearance
Calcifying epithelial odontogenic cyst
Sun burst appearance
Hemangioma, osteosarcoma
Sunray appearance
Osteosarcoma, hemangioma, osteoblastoma
Hair on end appearance
Sickle cell anemia, thalassemia
Tennis racket
Odontogenic myxoma
Moth eaten
Early stage of osteosarcoma, squamous cell carcinoma, osteomyelitis, osteoradionecrosis, leukemia, malignant lymphoma
Teeth standing in space or floating teeth
Histiocytosis-X, severe periodontitis, malignant lymphoma
Ground glass
Fibrous dysplasia, Paget’s disease, hyperparathyroidism, ossifying fibroma
Orange peel
Fibrous dysplasia
Cotton wool
Paget’s disease
Downward bowing
Cemento-ossifying fibroma
Mass of coral
Calcified lymph node
Antral halo
Acute sinusitis
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Appendix 1: Causes and Classifications 1095 Typical radiological feature
Name of disease
Hanging drop appearance in maxillary sinus
Blow out orbital fracture
Ely’s cyst
Osteoarthritis
Pepper pot skull
Hyperparathyroidism
Step ladder pattern
Sickle cell anemia
Tree in winter appearance
Normal sialographic appearance of parotid gland
Bush in winter appearance
Normal sialographic appearance of submandibular gland
Sausage link appearance
Sialographic appearance of sialodochitis (ductal inflammation/infection)
Snowstorm appearance
Sialographic appearance of Sjögren’s syndrome
Sialectasis
Sialographic appearance of sialadenitis
Ball in hand appearance
Sialographic appearance of intrinsic benign tumor
Codman’s triangle
Osteogenic sarcoma
Balloon like appearance
Follicular cyst
Candlestick appearance
Pyknodysostosis and progressive systemic sclerosis
Chalk like appearance
Osteopetrosis, pyknodysostosis, hyperparathyroidism
Cherry blossom pattern
Sialographic appearance of Sjögren’s syndrome
Eggshell appearance
Ameloblastoma, multilocular cyst
Filling defect
Salivary gland tumor
Mottled appearance
Fibrous dysplasia, ossifying fibroma
Onion peel (skin) appearance
Chronic osteomyelitis, eosinophilic granuloma, Ewing’s sarcoma
Permeated type
Carcinoma of gingiva, squamous cell carcinoma of maxilla
Pear shaped appearance
Globulomaxillary cyst
Pencil line appearance
Ameloblastoma, traumatic bone cyst and CEOC
Pressure type appearance
Squamous cell carcinoma of the gingiva
Punched out appearance
Multiple myeloma
Sand like appearance
Adenoameloblastoma, CEOC and CEOT
Salt and paper appearance
Hyperparathyroidism, ABC and giant cell granuloma
Scalloping pattern (margins)
Dentigerous cyst, traumatic bone cyst, ABC and giant cell tumor
Spiked root
Malignant histiocytoma, Burkitt’s lymphoma
Beaten silver
Craniofacial dysostosis (Crouzon’ disease)
Sharpened pencil or mouth piece of flute
Rheumatoid arthritis of TMJ
Thumb print
Fibrous dysplasia
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1096 Textbook of Oral Medicine Typical histological features Typical histological features
Name of disease
Starry sky
Burkitt’s lymphoma, infective mononucleosis, polycythemia
Rushton bodies
Dentigerous cyst
Reed-Sternberg cell
Hodgkin’s disease
Dropping off effect
Junctional nevus
Saw tooth appearance
Lichen planus
Antoni type A and type B tissue
Neurilemmoma
Honeycomb or Swiss cheese pattern
Adenoid cystic carcinoma of salivary gland
Picket fence or tombstone
Primordial cyst
Liesegang ring
Calcifying epithelial odontogenic tumor
Safetypin appearance
Granuloma inguinale
Lipschutz bodies
Herpes simplex infection
Anitschkow cell
Aphthous ulcer, sickle cell anemia, megaloblastic anemia and iron deficiency anemia
Henderson-Paterson inclusion
Molluscum contagiosum
Dilapidated brick wall effect
Familial benign chronic pemphigus
Cartwheel or checkerboard appearance
Multiple myeloma
Tobacco cells or cell in cells
Hereditary benign intra-epithelial dyskeratosis
Lava flowing around boulder’
Dentin dysplasia (shield type I)
Various drug effect on oral cavity Tissue
Drug effect
Drugs used
Teeth
Discoloration
Tetracycline Chlorhexidine Phenytoin Cytotoxic
Root anomalies Gingiva
Swelling
Phenytoin Cyclosporine Nifedipine
Salivary gland
Dry mouth
Tricyclic antidepressant Phenothiazine Antihypertensive Lithium
Taste
Disturbed
Metronidazole Penicillamine
Facial movements
Dyskinesia
Phenothiazines Metoclopramide
Mucosa
Thrush Ulcers Lichenoid lesions Erythema multiforme
Broad spectrum antimicrobial Corticosteroids Cytotoxic drugs NSAID Barbiturates Sulphonamides
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Appendix 1: Causes and Classifications 1097 Summary of the main mandibular and maxillary fracture site and the common projection used for each side Mandibular Fracture site
Commonly used projection
Angle
Dental panoramic tomography or oblique lateral Postero-anterior of jaws
Condylar neck
Dental panoramic tomography or oblique lateral Postero-anterior of jaws (for low neck fracture) Reverse Towne’s (for high condylar neck)
Body
Dental panoramic tomography or oblique lateral Postero-anterior of jaws periapical of involved teeth, Lower 90o occlusal
Canine region
Dental panoramic tomography or oblique lateral Periapical of involved teeth, True lateral skull
Symphysis
Lower 45° occlusal, Lower 90° occlusal
Ramus
Dental panoramic tomography or oblique lateral Postero-anterior of jaws
Coronoid process
Dental panoramic tomography or oblique lateral 0o occipitomental
Maxillary Fracture type/site
Commonly used radiograph
Dento-alveolar
Periapical, Upper standard occlusal, Upper occlusal
Le Fort I
0° occipitomental, 30° occipitomental, True lateral skull (brow-up)
Le Fort II
0° occipitomental, 30° occipitomental, True lateral skull (brow-up)
Le Fort III
0° occipitomental, 30° occipitomental, True lateral skull (brow-up), Coronal section tomography, CT scan/3D reconstruction
Zygomatic complex
0° occipitomental, 30° occipitomental, Submentovertex
Nasoethmoidal
0° occipitomental, 30° occipitomental, True lateral skull (brow-up) Soft tissue lateral view of the nose, CT /3D reconstruction
Orbit
0° occipitomental, True lateral skull (brow-up), Postero-anterior 25° CT/3-D reconstruction
Various lymph nodes in the head and neck region and their area of drainage Lymph nodes
Area of drainage
Discharge
Occipital
Posterior scalp
Spinal accessory nodes
Retromandibular
Scalp, posterior ear, back of external auditory meatus
Internal jugular nodes
Superficial parotid
Lateral and frontal scalp, lateral ear, external auditory canal, eyelids
Superficial cervical nodes Internal jugular nodes
Deep parotid
Parotid gland, orbit, lateral eyelid, conjunctiva, superficial thyroid nodes
Internal jugular nodes
Buccal
Medial eyelids, skin and mucous membrane of the nose and cheeks
Mandibular nodes
Mandibular
Similar to buccal lymph nodes
Submandibular nodes
Submental
Tip of the tongue, anterior floor of mouth, anterior lower gingiva, middle lower lip, chin
Submandibular nodes
Submandibular
Salivary gland, upper and lower lips, cheeks, gingiva teeth, anterior palatine pillar, soft palate, anterior two-third of the tongue
Internal jugular nodes
Superficial cervical
Parotid nodes
Internal jugular nodes
Internal jugular
All the nodes mentioned above and pharynx, tonsil, tongue, palate, larynx
Subclavian vein, right side thoracic duct
Spinal accessory
Occipital nodes, retroauricular nodes, back of heads, nape and lateral aspect of the neck
Supraclavicular nodes
Supraclavicular
Spinal accessory nodes, posterior triangle submandibular nodes
Joins inferior internal jugular
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1098 Textbook of Oral Medicine Firm non-hemorrhagic soft tissue growth of oral cavity
Compressible soft tissue growth of oral cavity
• • • • • • • • • •
• • • • • • • • • • •
Fibromatosis Torus Irritation fibroma Peripheral fibroma Myxoma Neurofibroma Lipoma Granular cell myoblastoma Sialadenitis Tumor of salivary gland
Eruption cyst Mucocele Mucous cyst Ranula Gingival cyst Nasoalveolar cyst Epidermoid cyst Cavernous Capillary hemangioma Lymphangioma Cystic hygroma
Hemorrhagic or easily bleeding soft tissue growth of oral cavity • • • • • • • • • •
Various odors related to systemic disease
Parulis Eosinohilic granuloma Epulis fissuratum Peripheral giant cell granuloma Pyogenic granuloma Pregnancy tumor Squamous cell carcinoma Lymphomas Leukemia AIDS
• • • • • • • •
Sour—digestive dysfunction Fetid—ANUG Urinous—uremia, kidney dysfunction Acetone—diabetes mellitus Strench—gangrene, necrotic lesion Fruity—after use of ether for GA Mousy—chronic liver dysfunction Bloody—internal hemorrhage
Exophytic lesion Condition
Appearance
Fluctuance
Emtibility
Usual history
Age
Frequency
Black hairy tongue
Patch of hairy growth on dorsal surface of tongue
No
No
Feels like hair on tongue gagging sensation
Older than 40
Occasionally
Mucocele
Nodular swelling
Yes
No
Variation in size rupture and draining
