Dental Caries Seminar

DENTAL CARIES PRESENTED BY:-

MANVA MOHNISH ZULFIKAR PG STUDENT DEPARTMENT OF CONSERVATIVE DENTISTRY AND ENDODONTICS

DENTAL CARIES 1.

2. 3. 4. 5. 6. 7.

DEFINITION THEORIES OF DENTAL CARIES ETIOLOGY CLINICAL ASPECTS OF DENTAL CARIES HISTOPATHOLOGY OF DENTAL CARIES DIAGNOSIS OF DENTAL CARIES METHODS OF CARIES CONTROL

DEFINITION  Dental

caries is defined as a microbial disease of the calcified tissues of the teeth, characterized by demineralization of the inorganic portion and the destruction of the organic substances of the teeth.

 Affects

persons of both genders in all races, all socioeconomic strata and every age group.

THEORIES OF DENTAL CARIES

A. THE EARLY THEORIES: a] The legend of worms b] Endogenous theories c] Chemical theories d] Parasitic theories B.

a] Miller’s Chemo-parasitic / Acidogenic theory b] The proteolytic theory c] The sucrose-chelation theory

A. THE EARLY THEORIES: a) The legend of Worms: 

The earliest reference to tooth decays is probably from the ancient Sumerian text known as the ‘The legend of Worms'.



This dates from about 5000 B.C.Euphrates valley of the lower Mesopotamian area.



The idea that caries is caused by worms was universal as is evident from the writings of Homer who made a reference to worms as the cause of toothache.

b)Endogenous theories: 

It was advocated by Greek physicians, who proposed that dental caries is produced by internal action of acids and corroding humors. And an imbalance in these humors resulted in disease.

c) Chemical theory: 

In the 1820s observed that dental decay affected externally, not internally, as had been claimed.

 It

was proposed that an unidentified ‘chymal agent’ was responsible for caries.

 Support

for the chemical theory came after Robertson in 1835 proposed that dental decay was caused by acid formed by fermentation of food particles around the teeth.

 d)

Parasitic theory:



Apparently the first to relate microorganisms to caries on a causative basis as early as 1843 was Erdl who described filamentous organisms in the membrane removed from teeth.



Shortly thereafter, Ficnus in 1847, a German physician in Dresden, definitely attributed dental caries to ‘denticolae’ the generic term he proposed for decay related microorganisms.

B. 1) MILLER’S CHEMICO-PARASITIC THEORY (ACIDOGENIC THEORY): W

D Miller, an American, in beginning of 1890 gave the following hypothesis in which he stated: “Dental decay is a chemico-parasitic process consisting of two stages, the decalcification of enamel, which results in its total destruction and the decalcification of dentin as a preliminary stage, followed by dissolution of the softened residue.

 The

acid which affects this primary decalcification, is derived from the fermentation of starches and sugar lodged in the retaining centres of the teeth.

 Subsequently,

he isolated numerous microorganisms from the oral cavity, many of which were acidogenic and some were proteolytic.

 The

significance of W D Miller’s observation is that he assigned an essential role to three factors in the caries process : -the oral microorganisms in acid production and proteolysis; -the carbohydrate substrate; and -the acid which causes dissolution of tooth minerals.

×

Miller's chemico-parasitic theory is the backbone of current knowledge and understanding of the etiology of dental caries.

 Miller’s

theory was unable to explain the predilection of specific sites on a tooth to dental caries and the initiation of smooth surfaces was not accounted for by this theory.

 Also

miller’s theory doesn’t explain why some populations are caries-free and the phenomenon of arrested caries

2) THE PROTEOLYTIC THEORY 



Offered as an alternative explanation is the proteolytic theory where it has been proposed that the organic or protein elements are the initial pathway of invasion by microorganisms. It has been established that enamel contains approx. 0.56% organic matter, of which 0.18% is a type of keratin, 0.17% a soluble protein, possibly a glycoprotein, and the remainder citric acid and peptides.



Heider and Wedl, Bodecker, Abbot demonstrated that certain enamel structures are made up of organic material, such as enamel lamellae and rd sheaths.



Baumgartner and Fleischmann demonstrated that microorganisms could invade the enamel lamellae, and stated that acids produced by these bacteria were capable of destroying the inorganic portion of the enamel.



Gotlieb(1944) and Gottlieb, Diamond and Applebaum(1946) postulated that caries is essentially a proteolytic process: -the microorganisms invade the organic pathways and destroy them in their advance. -They did admit that acid formation acccompanied the proteolysis -Gotlieb held that yellow pigmentation was characteristic of caries and that this was due to pigment production by proteolytic organisms.

 Pincus

proposed that Nysmuth’s membrane and other enamel proteins are mucoproteins, yielding sulphuric acid upon hydrolysis. -Gram-ve bacilli capable of producing the enzyme sulphatase. -This enzyme releases the combined sulphuric acid from the mucoprotein, but only reluctantly unless the protein is first hydrolyzed to free the polysaccharide. -The liberated acid dissolves the enamel, combining with the calcium to form calcium sulphate

 Manley

and Hardwick attempted to reconcile the two chief theories concerning the etiology of dental caries. They pointed out that, while the acidogenic and the proteolytic mechanisms may be seperate and distinct , they need not be. Many bacteria produce acid from carbohydrate substrate, some bacteria capable of producing acid form carbohydrate may even degrade protein in the absence of carbohydrate.



On this basis there may be two types of carious lesion

In one type, microorganisms invade enamel lamellae, attack the enamel and involve the dentin before there is clinical evidence In the other, no enamel lamellae are present and there is alteration of enamel prior to invasion produced through decalcification by acids formed by bacteria in a dental plaque overlying the enamel. The early lesion produced are those typically described as “chalky enamel”

3) SUCROSE-CHELATION THEORY 

Eagglers-Lura proposed that sucrose itself, and not the acid derived from it, can cause dissolution of enamel by forming an ionized calcium saccharate.



The theory is that calcium saccharates and calcium complexing intermediaries require inorganic phosphate which is subsequently removed from enamel by phosphorelating enzymes

ETIOLOGY OF DENTAL CARIES

I. PRIMARY FACTORS: 1.TOOTH a. Susceptible tooth surface b. biochemical characteristic of tooth 2.DENTAL PLAQUE 3.DIET 4.TIME

II.MODIFYING FACTORS: 1. SALIVA 2. SYSTEMIC HEALTH 3. SEX 4. HEREDITY 5. RACE 6. GEOGRAPHIC ENVIRONMENT 7. OCCUPATION

TOOTH a) Susceptible tooth surface:

• non-self cleansable areas are more prone ,as they provide stagnation areas for dental plaque • Pits & fissures have the highest prevalence , provide mechenical shelter for m.org • Proximal areas immediately gingival to contact area are the next common site, as they are protected from effects of mastication, tongue movement and salivary flow

• Enamel at the cervical aspects of the teeth near the gingiva and exposed root surface are other potential site for plaque retention • Plaque retention can also occur near the margins of existing restorations if they are rough, overhanging or exhibit wide marginal gaps

• Crowding

b) Biochemical characteristics of teeth: •The enamel surface of a newly erupted tooth is highly susceptible to caries because of highly carbonate content of enamel crystals. •Any deficiencies of vit-A and D, minerals like calcium phosphorus and flourides predisposes to caries occurrence. •Devlopmental disturbances of enamel hypoplasia or hypomineralization •With age, the surface enamel becomes more resistant to caries because of posteruptive maturation ,

•flouride, zinc and nitrogen level increases , provides resistance to caries

DENTAL PLAQUE •Soft, translucent, tenaciously adherent mass accumulating on tooth surface •Composed of an aggregate of bacteria, salivary glycoprotiens and inorganic salts •Also called “microbial biofilm” •Dental plaque associated with dental caries has high concentration of streptococcus mutans and lactobacillus acidophilus(acidogenic bacterias)

•Diet rich in sucrose favours the accumulation of strep.mutans in plaque •Sucrose rich environment allows the strep.mutans to produce large amount of extracellular polysacharide like glucan, which enables the bacteria to tenaciouly adhere to tooth surface and limits the salivary buffers. •With the local environment being highly acidic, dissolution of the tooth surface begins • once the tooth surface becomes cavitated, filamentous bacteria with poor adhesion abilities like lactobacilli becomes established in lesion

DIET •Less fibrous, more refined, soft and sticky diet favours the stagnation of food on tooth surface •Chemically diet is composed of carbohydrates which are cariogenic. •Modern diet contains more of refined carbohydrates (sucrose,fructose,glucose,etc) makes it more cariogenic

•Modern diet lacks of phytates, which is anticariogenic •Another factor promoting caries is the comsumption of snacks between meals, this lowers the plaque pH for prolonged time leads to dvelopment of caries. •Protective factors in diet against caries are: calcium lactate(cheese), milk, flourides, vit-D & B6

TIME •Significant factor

•During long intervals of undisturbed plaque stagnation, the plaque pH is lowered down , favours the production of organic acids that demineralize tooth structure

SALIVA •Has a protective role in preventing caries •Helps to flush away food debris and bacteria •Buffers the acids released , due to its bicarbonate concentration, phosphate content and presence of sialin

•Antimicrobial property due to the presence of lysosomes, immunoglobulinA, lectoperoxidase, lactoferrin, salivary protien and mucin •Helps in remineralization of early caries lesions due to presence of calcium, phosphate and flouride. •Salivary flow reduced-------> increased incidence of caries •Xerostomia – high risk of caries

SYSTEMIC HEALTH: •Any condition which predisposes to poor oral hygiene can increase the incidence of dental caries eg; neurological disorders, mental retardation

•Caries risk is highly associated with sjogren’s syndrome •Prolonged use of drugs like anti depressants, antihistamine, diuretics, etc, may cause xerostomia, which predisposes occurrence of caries

•Diabetes mellitus is associated with increased risk of caries •Pt under going radiotherapy or chemotherapy are prone to caries due to reduction in adult flow

SEX: •Females are more susceptible to caries than males due to early eruption of teeth

HEREDITY: •May be related to his genetic makeup. •Several studies have demonstrated that caries may be inherited from parents, especially mother to child •It has been shown that children are frequently colonized with strains of streptococcus mutans identical toi strains carried by their mothers

RACE: •Related to their culture and dietary influences

GEOGRAPHIC INVOLVEMENT: •Regions where there is high content of phosphate in food and water, caries prevalance is less

OCCUPATIONS: •Where frequent food sampling is required eg; bakery workers, confectionary industry workers, etc •Where regular meals scheduke is disturbed eg; night shift workers, truck drivers, etc

CLASSIFICATION OF DENTAL CARIES

Acc.to

Location 1. Pits & Fissures caries 2. Smooth surface caries 3. Root Surface caries

Acc.

to Rapidity of Dental caries 1. Acute Dental caries (Rampant caries 2. Chronic Dental Caries (Slow D.C) 3. Arrested Caries



Acc. to whether its new or recurrent lesion: 1. Primary caries(Initial)

2. Secondary caries(Recurrent)   Acc.

to extent of caries: 1. Incipient caries (Reversible) 2. Cavitated caries (non reversible)



Acc. to the pathway of caries: 1.Forward caries 2.Backward caries



Acc. to number of tooth surface involved 1.Simple caries 2.Compound caries 3.Complex caries



Acc. to treatment and restoration design 1. Class-I caries 2. Class-II caries 3. Class-III caries 4. Class-IV caries 5. Class-V caries 6. Class-VI caries

Acc. to the age of patient: 1. Nursing bottle caries 2. Adolescent caries 3. Senile caries Acc. to the tooth surface to be restored: 1.Occlusal 2.Mesial 3.Distal 4.Facial 5.Buccal 6.Lingual * combination of above are possible

WORLD HEALTH ORGANISATION(WHO) SYSTEM: - the shape and depth of the lesion can be scored on a four point scale D1- Clinically detectable enamel lesion with intact surface D2- clinically detectable cavities limited to enamel D3- clinically detectable cavities in dentine D4- lesions extending into pulp

A NEW CLASSIFICATION OF CARIES LESION BASE ON SEVERITY (DEPTH) 

Over time, to determine whether the caries risk is high, moderate

or low  E0

– No lesion

 E1

– Lesion on outer half of enamel

 E2

– Lesion extended into inner half of enamel

 D1

– Lesion in outer 1/3 of dentin

 D2

– Lesion in middle 1/3 of dentin

 D3

– Lesion in inner 1/3 of dentin

PITS & FISSURE CARIES  Occlusal

surface of molars & premolars – buccal & lingual surface of molars & lingual surface of maxillary incisors.  Early caries appears brown or black – slightly soft – provides catch  The enamel around caries may appear opaque bluish -> undermined  Lateral spread of caries at the D.E.J – May cause a large caries lesion with small point of opening

SMOOTH SURFACE CARIES  Proximal

surface to teeth or on gingival 1/3 of buccal & lingual surfaces (non-self cleansing areas)  Usually starts below the contact point of teeth  It appears as a yellow or brown area, initially,  As caries goes occurs on buccal or lingual surfaces  Extents from area opposite the gingival crest to the height of contour of the tooth.  It may extend laterally towards the proximal surface & also beneath free margin of the gingival  This typical cervical lesion is a crescent shape cavity and is always an open cavity

ACUTE DENTAL CARIES  Rapid  Early

clinical course

pulpal involvement

 Occurs

mostly in children & young adults

(dentinal tables are large and open and don’t show sclerosis)  Dentin  Pain

has a light yellow color

is present

CHRONIC DENTAL CARIES 

Progresses slowly

Late

pulpal involvement

More The

entrance of lesion is larger than acute

More Less

seen in adults

entry of saliva

food retention

Dentin

is dark – brown- cavity is shallow – minimum softening of dentin

Cavity

is not undermined, as pain is usually absent.

RECURRENT CARIES  Usually

occurs around the

restoration  May

be due to inadequate extension

of cavity or poor adaptation of restoration that produces leaky margin & has retention of food

ARRESTED CARIES 







 

This kind of caries become stationary and does not progress further if affects both deciduous & permanent dentition The superficial dentin is soft decalcified but gradually gets burnished (shinny) and has a brown polished appearance is hard This is called Eburnation, of dentin sclerosis of dentinal tubules & secondary dentin formation are seen. Another type of arrest carries seen on proximal surface of teeth when adjacent tooth is extracted It shows brown area at or below the contact point of tooth This type of caries is early caries which get arrested after extraction due to formation of self-cleaning area.

RAMPANT CARIES  This

is defined by massler as suddenly appearing wide spread rapidly burrowing type of caries resulting in early involvement of the pulp and affecting those teeth which are usually regarded as immune to dental decay  it is seen ion patients which suffer from xerostemia or drymouth  this caries is atypical and cervical area is attacked involving cementum and dentin  it progresses inwards until the crown is removed  there is a heavy brownish black discoloration of tooth  in children this is called as nursing bottle caries.

ROOT CARIES  Called

as cementum caries  Defined as soft progressive lesion found anywhere on thereof surface that has lost gingival attachment and is exposed to the oral cavity  Enamel may also be involved if it is undermined during progress of the lesion  Dental plaque & micro-organisms are the main cause of lesion  Teeth most frequently affected are:- mandibular molar premolar – maxillary canine  Mandibular incisor are least affected

 In

the maxillary teeth the proximal surfaces are mostly affected – in mandibular arch buccal surface mostly affected  The lesion starts in cementum by sub surface deminirelization with an intact surface layer.  The cementum is easily attacked due to it’s greater porosity & high organic contain  The development of lesion is same as that of enamel caries.

INCIPIENT CARIES (REVERSIBLE) 

It is the first evidence of caries activity in the enamel which has not extended to the DEJ and enamel is hard & intact, it appears opaque white when air-dried and it can be demineralized if immediate corrective measures after the oral environment including plaque removal control

CAVITATED CARIES (NON-REVERSIBLE) Enamel lesion

surface is broken

is advanced into dentin

Remineralization Treatment

is not possible

by tooth preparation are

restoration indicated

BACKWARD CARIES



When the spread of caries along the DEJ exceeds the caries in the contiguous enamel, caries extends into this enamel from the junction

is called as backward caries

FORWARD CARIES



Whenever the caries come in enamel is larger or at least the same size as that is dentin

RESIDUAL CARIES 

caries that remains in completed tooth preparation whether by operator intention or by accident



It is not acceptable if at the DEJ or on the prepared enamel tooth wall



It may be acceptable when it is affected dentin, specially near the pulp

OCCULT OCCLUSAL CARIES  It

Represents dentinal caries – only on radiographs – unrecognized on visual examination

 Prevalence

– 2.2% to 50%

 This

caries may start as fissure caries, that after misdiagnosis progressed to early caries

 The

dentinal radiolucency may present in affected teeth even before the teeth erupted, as pre eruptive into a coronal resorptive defects

HISTOPATHOLOGY OF DENTAL CARIES a] CARIES OF ENAMEL

b] CARIES OF DENTIN

a] ENAMEL CARIES 

On smooth enamel surface , the earliest macroscopic evidence of incipient caries is the appearance of an area of decalcification beneath the dental plaque which resembles a smooth chalky white area.



Scott and his assocites, has revealed that the first change is usually a loss of the interprismatic or inter-rod substance of the enamel with increased prominence of the rods.

•In some instances, the initial change seems to consist of roughening of the ends of the enamel rods, suggesting that the prism may be more susceptible to early attack. •Another change in early enamel caries is the accentuation of the incremental striae of Retzius. •due to loss of minerals which causes the organic structure to appear more prominent.

Early smooth surface caries. Ground section shows body of lesion, enhanced striae of Retzius, between the dark zone and peripheral translucent zone.



There may also be accentuation of perikymata.



As this process advances and involves deeper layers of enamel



It forms a triangular or actually a cone-shaped lesion with the apex toward the DEJ and base toward the surface of the tooth.



There is eventual loss of continuity of the enamel surface, and the surface feels rough to the point of an explorer.



The roughness is caused by the disintegration of the enamel prisms after decalcification of the interprismatic substance and the accumulation of debris and microorganisms over the enamel rods.



The small lesion has been divided into different zones based upon its histological appearance when longitudinal ground sections are examined with the light microscope.



Four zones are clearly distinguishable, starting from the inner advancing front of the lesion.

* Zone 1: The transluscent zone. 

Lies at the advancing front of the enamel lesion



first recognizable zone of alteration from normal enamel.



About half of the lesions demonstrate a transluscent zone at their advancing front, which is seen only when a longitudinal ground section is examined in a clearing agent having a refractive index identical to that of enamel.



Quinoline is more suitable since its refractive index is identical to that of enamel(RI 1.62).



When ground section is examined under transmitted light, after imbibition with quinoline, the translucent zone appears structureless.



It is not always present.



By means of polarized light it has been shown that this zone is slightly more porous than sound enamel, having a pore volume of 1% compared with 0.1% in sound enamel.



Chemical studies carried out on various zones showed that the fluoride content of transluscent zone enamel was found to be increased relative to adjacent sound enamel.



The overall findings suggested that carious that attack had preferentially removed magnesium and carbonate rich mineral from translucent zone and not organic material.

* Zone 2: The dark zone. 

It has been referred to as the positive zone, because it is usually present.



This zone is formed as a result of demineralization and appears dark brown in ground sections examined by transmitted light after imbibition with quinoline.



Polarized light studies showed that the dark zone has a pore volume of 2-4%



These effects have been shown to be due to the presence of very small pores in the zone besides the relative large pores that are present in the first stage, the translucent zone.



If a ground section is examined in an aqueous medium having a small molecule which penetrates the micro pores, the dark zone is no longer seen.

* Zone 3: The body of the lesion. 

This zone lies between the relatively unaffected surface layer and the dark zone.



It is the area of greatest demineralizaiton.



In polarized light, the zone shows a pore volume of 5% in spaces near the periphery, to 25% in the center of the intact lesion.



When a longitudinal ground section is examined in quinoline with transmitted light, the body of the lesion appears relatively translucent compared with sound enamel.

* Zone 4: Surface zone. 

When examining a small initial carious lesion with the polarizing microscope, the surface zone is an important feature.



Quantative studies of the surface layer indicate the partial demineralization equivalent to about 1-10% loss of mineral salts has taken place and the pore volume of the surface zone is less than 5% of spaces.



The greater resistance of the surface layer may be due to a greater degree of mineralization and/or a greater concentration of fluoride in the surface enamel and perhaps a greater amount of insoluble protein in the surface enamel.



The surface zone remains intact and also well mineralized because it is a site where calcium and phosphate ions, released by subsurface dissolution, become reprecipitated. This process is referred to as remineralization.

CARIES OF THE DENTIN 

Caries of the dentin begins with the natural spread of the process along the DEJ and the rapid involvement of great numbers of dentinal tubules, each of which acts as a tract leading to the dental pulp along which the microorganisms may travel at a variable rate of speed.

* Early dentinal changes 

The initial penetration of the dentin by caries may result in alterations in the dentin previously described as dentinal sclerosis or ‘transparent dentin’.



This dentinal sclerosis is a reaction of vital dentinal tubules and a vital pulp in which there is calcification of the dentinal tubules that tends to seal them off against further penetration by microorganisms.



The formation of sclerotic dentin is minimal in rapidly advancing caries and is most prominent in slow chronic caries.



The term ‘transparent dentin’ has been applied because of the peculiar transparent appearance of the tooth structure when a ground section is viewed by transmitted light.



By reflected light the sclerotic dentin appears dark.



The appearance of fatty degeneration of Tomes’ dentinal fibers, with the deposition of fat globules in these processes, precedes even the early sclerotic dentinal changes.



Two types of lipid staining have been seen,



one of which is more superficial and probably of bacterial origin.



The other type may be due to unmasking of lipids present in the intratubular dentin, by demineralization.

 The

rate at which the carious destruction progresses tends to be slower in older adults than in young persons because of the generalized dentinal sclerosis that occurs as a part of the aging process.

 In

the earliest stages of caries, when only a few tubules are involved, microorganisms may be found penetrating these tubules before there is any clinical evidence of the carious process.

 These

have termed ‘pioneer bacteria’.



The initial decalcification involves the walls of the tubules, allowing them to distend slightly as they become packed with masses of microorganisms.



It is evident that these microorganisms as they penetrate farther and farther into the dentin, become more and more separated from the carbohydrate substrate upon which the bacteria responsible for the initiation of the disease depend.



The high protein content of the dentin would favor the growth of those microorganisms which have the ability to utilize this protein in their metabolism.



Thus proteolytic organisms would appear to predominate in deeper caries of the dentin, while acidogenic forms are more prominent in early caries.

* Advanced dentinal changes A thickening and swelling of the sheath of Neumann may sometimes be noted at irregular intervals along the course of involved dentinal tubules. Tiny ‘liquefaction foci’ described by Miller, are formed by foccal coalescence and breakdown of a few dentinal tubules. This focus is an ovoid area of destruction parallel to the course of the tubules and filled with necrotic debris which tends to increase in size by expansion. This produces compression and distortion of adjacent dentinal tubules so that their course is bent around the ‘liquefaction focus’.



In areas of globular dentin, decalcification and confluence of dentinal tubules occur rapidly.



The destruction of dentin through a process of decalcification followed by proteolysis occurs at numerous focal areas which eventually coalesce to form a necrotic mass of dentin of a leathery consistency.



Clefts are rather common in this softened dentin, although they are rare in chronic caries, since the formation of a great deal of softened necrotic dentin is unusual.



These clefts extend at right angles to the dentinal tubules and appear to be due to extension of the carious process along the lateral branches of the tubules or along the matrix fibres which run in this direction.



The cleft account for the manner in which carious dentin often can be excavated by peeling away thin layers with hand instruments.



As the carious lesion progresses, various zones of carious dentin may be distinguished which grossly tend to assume the shape of a triangle with the apex toward the pulp and the base toward the enamel. Beginning pulpally at the advancing edge of the lesion adjacent to the normal dentin, these zones are as follows:



Zone 1: zone of fatty degeneration of Tomes’ fibres Zone 2: Zone of dentinal sclerosis characterized by deposition of calcium salts in dentinal tubules.



  

Zone 3: Zone of decalcification of dentin, a narrow zone, preceding bacterial invasion. Zone 4: Zone of bacterial invasion of decalcified intact dentin. Zone 5: Zone of decomposed dentin.

* Secondary dentin involvement 

The carious involvement of secondary dentin does not differ remarkably from the involvement of the primary dentin, except that it is usually somwhat slower because the dentinal tubules are fewre in number and more irregular in their course, thus delaying penetration of the invading microorganisms.



Sooner or later, however, the involvement of the pulp results with ensuing inflammation and necrosis. Occasionally, caries will spread laterally at the junction of the primary and secondary dentin and produce a seperation of the two layers.

6. DIAGNOSIS OF DENTAL CARIES METICULOUS CLINICAL EXAMINATION  TACTILE EXAMINATION  RADIOGRAPHIC EXAMINATION  TOOTH SEPARATION  FIBEROPTIC TRANSILLUMINATION  XERORADIOGRAPHY  DIGITAL RADIOGRAPHIC METHODS  COMPUTER AIDED RADIOGRAPHIC METHODS  DIGITAL FIBEROPTIC TRANSILLUMINATION 

METICULOUS CLINICAL EXAMINATION: Careful examination under clean and dry condition with good illumination can reveal varios signs of caries like:- brown discoloration of pits and fissures - opacity beneath pits and fissures or marginal ridges - frank cavitation of the tooth surface

TACTILE EXAMINATION: • Use

of dental explorer may help in detection of dental caries. •Tactile findings suggestive of caries are: - softness at the base of a pit and fissures and discontinuity of enamel surface - catch at the explorer tip - cavitation at base of pit and fissure •Cautions:excassive pressure with explorer can cause cavitation where was not present earlier  infective m.org may be transferred to uninfected area

RADIOGRAPHIC EXAMINATION: -Conventional , intraoral periapical and bitewing radiograph are employed to daignose dental caries - bitewing is of more duagnostic value Uses of bitewing: • detecting proximal caries •Examinig many teeth in one radiograph •Checking cervical margin of restoration •Monitering the progress of arrest caries

Scoring the progress of caries on bitewing: 0= sound enamel 1= radiolucency only in enamel 2= radiolucency in enamel extending upto DEJ 3= radiolucency in enamel and outer half of dentine 4= radiolucency in enamel reaching inner half of dentine

Cervical burnout: “a radiolucent appearance mimicing proximal caries seen at cervical aspect of teeth. This is perfectly a normal appearance at the gap between the dense enamel over the crown of the tooth and the crest of the alveolar ridge where xray pass tangentially through the root dentine.

TOOTH SEPARATION: •To detect initial proximal caries, separation of the contacting teeth can be achieved using wedges or mechanical separator •Once the proximal surface is accessible, visual examination and gentle probing may help in diagnosis of the carious lesion

FIBEROPTIC TRANSILLUMINATION: •Carious lesion have lowered index of light transmission, when teeth are examined with the fiberoptic light source, caries appears as a dark shadow •After drying the tooth, a fiberoptic probe can be placed in the buccal or lingual embrassures directly beneath the contact area between two adjacent teeth. •If caries is present , dark shadow is seen beneath the marginal ridge •Non invasive •No radiation hazard •No permanent record •Difficulty in placing probe

XERORADIOGRAPHY: •Image is recorded on an aluminium plate coated with a layer of selenium particles •These selenium particles are charged uniformly and stored in a unit called condition •When x-ray is passed onto the film , it causes selective discharge of the particles which forms a latent image. •This is converted into positive image by a process known as development in the processper unit •Less radiation exposure •No wet processing •Electric charge over the film may cause discomfort

DIGITAL RADIOGRAPHIC METHODS: • offers more superior means of detecting caries •Can be obtained by 2 methods i)video recording and digitization of a conventional radiograph ii)direct digital radiography •The direct digital radiography system was RVG •It uses a charged couple device which works like a miniature video camera •This records images produced by conventional x-ray and stores it in the computer memory for image processing and viewing •Reduced radiation dose ,no need of dark room,no processing error, instant image visualization and can be magnified

COMPUTER AIDED RADIOGRAPHIC METHOD: •This method uses the measurement potential of computers in assessing and recording the size of carious lesions. •Provides graphic visualization of the size and progression of the carious lesion especially approximal caries. •Computer software have been developed for automated interpretation of digital radiographs in order to standardize image assessment •Helps in monitering the carious process •Time consuming and expensive

DIGITAL FIBEROPTIC TRANSILLUMINATION: •New technique which combines fiberoptic transillumination and digital ccd camera. •Images captured by the camera are sent to a computer for analysis, which produces digital images that can be viewed •This method overcomes the shortcomings of FOTI •Non invasive •Can detect incepient and recurrent caries very early •Does not measure the depth of the lesion

METHODS OF CARIES CONTROL 

The control of dental caries presents one of the greatest objectives that must be met today by the dental profession.

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The suggested methods of control may be classified into three general types: 1. Chemical measures 2. Nutritional measures, and 3. Mechanical measures

CHEMICAL MEASURES •

Chemicals used for caries control include: •

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Substances which alter the tooth surface or tooth structure Substances which interfere with carbohydrate degradation through enzymatic alteration Substances which interfere with bacterial growth and metabolism

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* Substances which alter the tooth surface or tooth structure •

The exposure of the teeth to fluoride through profesional application of fluoride solutions, gels, foams and varnishes plus exposure from dentrifices and other fluoride preparations used at home is beneficial in preventing dental caries.

Fluorine •

The history of fluorine and dental caries dates from the recognition by GV Black and Frederick S Mckay that teeth with even a severe degree of mottled enamel have a greater immunity to dental caries than normal teeth.In biological mineralized tissues such as bone and teeth, it occurs as the apatite salt of fluoridated hydroxy-apatite.

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Fluorine has been administered principally in two ways: through the communal water supply and by topical application.

Mechanism of action of ingested fluoride 

The mechanism of action of fluoride in the drinking water has been discussed by many workers, and several theories have been proposed. Since fluoride inhibits enzymes by inactivating the coenzyme portion of the enolase system, and specifically by inhibing the conversin of 2-phosphoglyceric acid to (enol) phosphopyruvic acid, it has been thought to protect against caries by preventing carbohydrate degradation.

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The most widely accepted theory on the mechamism of action of ingested fluoride is that of alteraiton of the structure of the developing tooth through systemic absorption of the element.

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The exact means whereby fluoride would alter the tooth structure to resist caries has not been completely established, but it is probably through the incorporation of fluorine in the crystal lattice structure of enamel, with the formation of a fluorapatite producing less acid soluble enamel.

Fluoride supplements 

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Where communal water fluoridation is not feasible, fluoride tablets, drops, or lozenges have been proven definitely to be effective cariostatic agents, provided such supplements are taken on a daily basis from birth to about 14 years. The correct dosage in prescribing fluoride supplements depends on two factors: the age of the child and the existing fluoride concentration in the water supply.

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For young infants, drops are more convenient and can be added to foods such as cereals or beverages such as milk formula, or juices.

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For older children, whose primary teeth have erupted, fluoride tablets or lozenges are indicated as these provide both systemic benefits when swallowed an topical benefits as they are swished around the mouth.

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The concentration of total fluoride in human milk is about 0.05 ppm and cow’s milk about 0.1 ppm. Nevertheless, in most cases there is no need to supplement breastfed children who reside in optimally fluoridated areas.

Topical application of fluoride  The second manner in which fluoride is used for the prevention of dental caries is by topical or local application to the teeth. 

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Although the exact mechanism is not known, it appears that there is formation of either a calcium fluoride or a calcium fluorapatite. Professionally applied topical fluoride preparations usually contain 2% sodium fluoride, 8% stannous fluoride, or 1.23% acidulated phosphate fluoride. Sodium Fluoride

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It was first proposed by Knutson et.al. which involved first the cleaning of the teeth with pumice paste followed by a four minute topical application of 2% sodium fluoride solution at pH 7.

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The initial topical application was then followed by three similar applications at weekly intervals, except that no prophylazis was carried out at these subsequent visits. The treatment series was recommended at ages 3,7,10, and 13 years.

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The disadvantage of this technique was that the patient had to make four visits to the dentist within a relatively short time. However, sodium fluoride as a topical agent had many advantages in that it is chemically stable, has an acceptable taste, non irritating to gingiva and does not discolor the teeth.

Stannous fluoride  The advantages of using SnF2 were rapid penetration of tin fluoride and formation of a highly insoluble tin fluorophosphate complex on enamel surfaces.  The disadvantages of aqueous SnF2 far outweighed advantages in that it is unstable and should be prepared fresh for every treatment, its naturally low pH make it astringent, it produces discoloration of the teeth particularly in hypocalcified areas and the solution has a metallic taste. 

In order to overcome some of the disadvantages of a freshly prepared 85-10% solution of SnF2, stannous fluoride gel containing 0.4 % SnF2 in methyl cellulose and glycerin base was developed. However, for fluoride ion to be released, the gel should be diluted with water following its application to the teeth.

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By far the most useful fluoride therapy is the application of acidulated phosphate fluoride (APF) in the form of a solution or gel. The use of these agents provides a 25-40% reduction in caries.

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APF agent has to be applied for four minutes usually in a disposable tray applicator. APF agents have a pH of approximately 3 and contain 1.23 % fluoride and 0.1M orthophosphoric acid.

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The low pH favors more rpid fluoride uptake by enamel and the presence of the orthophosphate prevents enamel dissolution by the common ion effect.

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The application of these solutions or gels is often preceded by a coronal polishing. This removes exogenous stains and plaque but doesn’t affect the cariostatic potential of topical fluoride gel.

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To allow topical fluoride to react with the enamel for more time and thereby increase its uptake, fluoride varnishes have been developed.

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One of the most effective means of caries reduction involves the daily self application of 0.5 % fluoride gel (5000ppm F) about 40% of the concentration used for professional office applications in custom fitted trays for five minutes.

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This form of self therapy is best suited for high caries risk patients who are sufficiently motivated to confirm to the daily regimen.

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It is appropriate for those school going children and for patients who have received therapeutic radiation in the headand neck region.

Fluoride dentifrices This is another method of applying fluoride. Although fluoride containing mouthwashes, lozenges and chewing gums have all been suggested, and in some cases tested, there is no evidence to indicate that their use produces any benificial effect. Sodium Monoflurophosphate (MFP) has been used as a therapeutic agent in dentrifices and in the USA, MFP at 0.76% or 1000 ppm is the most commonly used therapeutic ingredient in commercial toothpastes.

Fluoride mouthwashes or rinses 

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There has been extensive clinical trial of mouthwashes or rinses containing fluoride used either as a mouthwash to flush the oral cavity, or in a few instances by application with a toothbrush in effort to prevent dental caries. For geographic areas where t is impossible to fluoridate the water supplies because of the lack of a central water system, alternative measures should be considered in the form of school based fluoride mouth rinse program. American Dental Association has recognized neutral sodium fluoride and acidulated phosphate fluoride rinses as effective caries preventive agents (1975) as well as stannous fluoride rinse(1980). Since the rinsing can be performed as an individual caries preventive measure at home or as a school based group preventive program, the dentist must be familiar with the different techniques involved, because they vary considerably with the different circumstances and objectives.

BIS-BIGUANIDES 

Chlorhexidine have received the most attention as potential anticaries agents, since they have been shown to be effective antiplaque agents. It has been shown by in vitro studies that chlorhexidine is adsorbed onto the tooth surfaces and salivary mucins, and then released very slowly in an active form.

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Unfortunately , it has a bitter taste, produces a brownish discoloration of hard and soft tissues and may produce a painful desquamation of mucosa.

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Due to stringent food and drug regulation, it is still not available for patient use.

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SILVER NITRATE 

The earlier workers believed that the silver plugged the enamel, either the organic invasion pathways such as the enamel lamellae or the inorganic pathways, combining with the soluble inorganic portion of enamel to form a less soluble combination

ZINC CHLORIDE AND POTASSIUM FERROCYANIDE 

Gottlieb in accordance with his theories of the importance of the protein matrix of the enamel in the dental caries process, proposed that the use of a solution of zince chloride and potassium-ferrocyanide-would effectively impregnate the enamel and seal off caries invasion pathway.

B. NUTRITIONAL MEASURES 

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On an individual basis, the dentist, dental hygienist and/or dietician consultant can provide information on safe foods and drinks. But the ultimate responsibility for diet modification lies in the individual. Voluntary dietary restriction may suit some patients and certainly reduce caries as evidenced by persons who have hereditory fructose intolerance.

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The function of the dental office personnel in diet modification is one of counselling, providing information, motivation and encouragment.

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The diet used in caries prevention is essentially a healthy, adequate, balanced diet and resembles a normal diet except for the exclusion of a few food components and eating practices.

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Changes in dietary habits are reflected within a couple of weeks in corresponding reductions in the numbers of oral lactobacilli and streptococcus mutans. Follow up visits are adivsed so that the patients diet can be rechecked and further modifications adopted if necessary. The control of dental caries through nutritional or dietary means is impossible to achieve on the basis of a mass prevention program and, for this reason, is relatively unimportant in public health preventive dentistry is contrast to fluoridation of water supplies.

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The chief nutritional measure advocated for the control of dental caries is restriction of refined carbohydrate intake. Only the most cooperative patient will adhere rigidly to the type of diet designed to reduce sugar consumption drastically.

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For this reason, clinical studies on large groups of patients for the purpose of ascertaining the extent of caries reduction that would occur with restriction of sugar consumption are difficult to carry out.

PHOSPHATE DIETS Stralfors mixed 2% dibasic calcium phosphate into the bread , flour, and sugar used in a school lunch program in Sweden and obtained a significant reduction in caries incidence in the maxillary incisors over a two year period. Ship and Mickelsen found no meaningful reduction in the caries attack rate of children consuming a diet in which flour used in the preparation of bakery products was supplemented with 2% calcium acid phosphate for three years. The cariostatic superiority of sodium dihydrogen phospate over calcium acid phosphate was attributd to the greater systemic action of the sodium salt as demonstrated by radiophosphorus uptake studies on sound and carious enamel.

PIT AND FISSURE SEALANTS 

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Pits and fissures of occlusal surfaces are among the most difficult areas on teeth to keep clean and from which to remove plaque. Because of this, it was suggested many years ago that prophylactic odontomy, the preparation of cavities in these areas and their restoration by some material such as amalgam before extensive decay had developed, be carried out. In this way, these caries susceptible pit and fissure areas would be made less susceptible to subsequent caries.

The sealant is not necessarily required to fill the entire depth of the fissure, but it must extend along its entire length, bonding firmly at the fissure entry.

 A major breakthrough in the efforts to produce an effective sealant occurred when Buonocore reported greatly improved retention of an acrylic filling material to an enamel surface that had been etched with a 50% phosphoric acid solution. The etchant, referred to as a conditioning agent, removes surface layers and a part of the enamel surface to about 5-10um and thereby produce surface irregularity into which the resin material penetrate and polymerize.

CONCLUSION Diagnosis prevention and treatment of dental caries must be the foremost objectives of operative dentistry. -Research efforts in understanding the caries process, maximizing the benefits of fluoride and chlorohexidine use, and perhaps, developing anti caries vaccines must be continued -patient education and motivation in the prevention and treatment of dental caries must be stressed. Finally the clinical treatment of cavitated carious teeth must be accomplished judiciously and appropriately.

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