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CONNECTIVE TISSUE DYSFUNCTION Victoria Merell, Donna K.Everix CHAPTER OUTLINE Objective Pathology Systemic Lupus Erythematosus Rheumatoid Arthritis Spondyloarthropathies Polymyalgia Rheumatica Polymyositis and Dermatomyositis Scleroderma Sjogren’s Syndrome Crystal-induced Arthropathies Juvenile Rheumatoid Arthritis Examination Patien History Systems Review Test and Measures Evaluation, Diagnosis, and Prognosis Intervention Rheumatoid Arthritis and other Inflammatory Conditions Spondyloarthropathies Polymyalgia Rheumatica Polymyositis and Dermatomyositis Scelroderma Case Study Chapter Summary Additional Resources Glossary References OBJECTIVE After reading this chapter, the reader will be able 1. Describe the pathologhy , clinical manifestations, and prognosis of nine different types of connective tissue dysfunvtions 2. Accuretly and efficiently take a history of patient with connective tissue dysfunction 3. Apply rheumatologhy specific outcome tools, tests, and measurement technique 4. Detremine a diagnosis and prognosis for a patient with connective tissue dysfunction. 5. Apply effective rehabilitation intervention for patients with connective tissue dysfunction, including patient education, exercise, modalities, and aquatic therapy.

Connective tissue dysfunctions result from a group of disease thar generally share clinical and pathological features of widespread inflammation. These disease are commonly known as rheumatoid disease. With the exception of osteoarthritis, the majority of rheumatic disease are chronic systemic inflammatory conditions with an autoimmune etiology. All of these disease can cause joint inflammation known as arthritis, as well as a range of other adverse effects. Rheumatic diseases encompass over 100 different conditions with different clinical manifestations. All are characterized by chronic pain an progressive damage to joints and soft tissue resulting in functional impairment. Arthritis, or joint inflammation, is the most prevalent chronic condition in the United States and is the leading cause of disability.1,2 Arthritis and the rheumatic disease significantly limit the ability of more than 7 million Americans to participate in activities of daily living (ADLs) and in vocational and leisure activities.3 The prevalence of rheumatic disease is expected to rise so that by the year 2020, these disease will limit an estimated 11.6 million individuals in their ability to perform daily activities. 3 This chapter focuses on a subset of rheumatic diseases that commonly cause connective tissue dysfunction, including rheumatoid arthritis and other inflammatory types of arthritis, disorders of soft tissue, and diffuse disease of the connective tissues. The care of individuals with rheumatic disease must be individualized and is founded on a early and accurate diagnosis. One of the challenges of working with patients with rheumatic disease is patients can have very different persentations, manifestating diverse signs and symptoms. Effective management requires an understanding of the disease process, a comprehensive examination and evaluation, and implementation of appropriate interventions to achiev realistic goals consistent with the patient’s preferences. Since the rheumatic disease involve multiple systems and have significant psychosocial ramifications, patients are the best treated with a multidisciplinary approach. 4,5 Rehabilitation plays critical role in the management of the patients with rheumatic disease and physical therapy has been identified as an integral component of care. 6,7 Rehabilitation clinicans may provide a wide range of interventions that may be benefical adjuncts to medication and surgery. These interventions may include patient education about the disease and components of management, instructions in joint protection and energy conservation, therapeutic exercise, physical agents, and aquatic therapy. This chapter include informations on pathology; examination; evaluation, including functional outcome assessment tools; and interventions for the rheumatic disease most commonly encountered by rehabilitation professionals. These include systemic lupus erythematosus, rheumatoid arthritis, spondyloarthophaties, polymyalgia rheumatica, polymyositis and dermatomyositis, scleroderma, sjogren’s syndrome, crystal-induced arthropathies, and juvenile rheumatoid arthritis. PATHOLOGY SYSTEMIC LUPUS ERYTHEMATOSUS Etiology. Systemic lupus erythematosus (SLE) is an autoimmune disease that results from the body producting antibodies directed against its own tissue (autoantibodies). In SLE, autoantibodies react with the antigents to produce circulating immune complexe that deposite in tissue producting a range of effect. The clinival spectrum of SLE is board, ranging from fatigue and mild arthralgias to severe and unremitting kidney inflammation (nephritis) that may ultimately cause renal failure (see box 6-1). SLE may impact any or all organ system, including the skins, oral mucosa, joints, lungs, heart, kidneys, blood, and brain, and is most damaging if there is kidney, heart, or neurological involvement. Although no single cause of SLE has been identified, numerous influential factors, including viral, genetic, environmental, and hormonal, are proposed.

Genetic.There is evidence that genetic factors predispose individuals to SLE. SLE occurs more often in relatives than in the general population. The prevalence of Lupus in first-degree relatives between 0.4% and 5%, which is a several hundred-fold increase over the prevalences in the general population. 8 The prevalence of SLE is also three times higher in African Americans than would be expected given their representation in the general population, and SLE is more common in certains native Americans tribes, particulary in females within that population.9 Environmental Factors. Environmental factors, including chemical exposure, ultraviolet radiation, diet, and viral infections, may trigger the expression of SLE in some individuals. 10 Drug-induced lupus comes on in response to a drug and resolves when the drug is no longer present and is almost always associated with exposure to one of three medications: hydralazine, procainamide, or methyldopa. 11 Aromatic amines (used in certain hair dyes) have also been associated with drug-induced lupus. The mechanism of thie effect remains unclear and only a small propotion of the people exposed to these drugs or chemical develop lupus.12,13Exposure to ultraviolet (UV) radiation, particulary UVA and UVB, may exacerbate lupus symptoms, possibly by promoting the formation of anti-DNA antibodies 12The effects of diet on SLE are poorly substantied and are based only on expert opinion or observational studies. Hormonal influences. Ninety percent of patients with lupus are women, and 90% of these patients develop lupus in their childbearing years. 14 It is thought that is because of the profound differences between the impact of female sex hormones (estrogens) and male sex hormone (androgens) on the immune system. Estrogens promote immune responses and increase the production of autoantibodies while androgens are more immunosuppressive. Thus female sex hormones appear to promote both disease activity and etiology.15 Diagnosis. The diagnosis of SLE is based on the criteria devised by the American College of Rheumatology. The presence of 4 of the 11 criteria listed in Box 6-1 confrim the diagnosis of SLE.

BOX 6-1 Diagnostic Criteria for Systemic Lupus Erythematosus 1. Malar rash: Fixed erythema, flat, or raised, over the malar eminences, tending to spare the nasolabial folds.

2. Discoid rash: Erythemathosus rasied patches with adherent keratotic scaling and folicular plugging; atrophic scarring may occur in older lesions. 3. Photosensitivity: Skin rash as a result of unusual reaction to sunlight, by patient history or physician observation 4. Oral ulcer: Oral or nasopharyngeal ulceration, usually painless, observed by a physician. 5. Arthritis: Nonerosive arthritis involving two or more peripheral joints, characterized by tenderness, swelling, or effusion. 6. Serositis A. Pleuritis: Convincing history of pleuritic pain or rub heard by a physician or evidence of pleura effusion OR B. Pericarditis: Documented by electrocardiogram (ECG) or rub or evidence of pericardial effusion. 7. Renal Disorder A. Persistent proteinuria ?0,5 gm per day or >3+ if quantitation not perform OR B. Cellular casts may be in red cell, hemoglobin, granular, tubular, or mixed. 8. Neurologic disorder A. Seizure: in the absence of offending drugs or known metabolic derangements OR B. Psychosis: In the absence of offending drigs or known metabolic derangement 9. Hematologic disorder A. Hemolytic anemia B. Leukopenia C. Thrombocytopenia 10. Immunologic disorder A. Positive LE cell preparation OR B. Anti-DNA: Antibody to native DNA in abnormal titer OR C. Anti-Sm: Presence of antibody to Sm nuclear antigen OR D. False positive test for syphilis 11. ANA: An abnormal titer of ANA by immunofluorescence or equivalent assay at any point in time and in the absence of drugs known to be associated with drug-induced lupus syndrome. A person has SLE if any 4 or more of the 11 criteria are present, serially or simultaneously, during any interval of observation. From Tan EM, Cohen AS, Fries JF, et al; Arthritis Rheum 25:1271-1277,1982. LE, Lupus errythematosus; ANA, antibuclear antibody; SLE, Systemic lupus erythematosus. Clinical Features. Although SLE can involve all organ systems, its most common symptoms are fatigue and arthralgia (joint pain). Artharlgia occur in 80% to 90% of patients with SLE.; however, arthritis (joint inflammation) occurs in fewer than half of these cases. The joint pain and inflammation, when present, tends to be symmetrical with predilection for the knees, wirst, and interphalangeal joints. The shoulders, hips, ankles, and elbows are less commonly involved. 14 When arthritis is present in patients with SLE it is generally not deforming; however 10% of patients with SLE develop nonerosive deforming arthropathy of the hands, refferd to as Jaccoud’s arthritis (Fig 6-1). Which mostly effect the joint capsule and surrounding ligamnets, causing joint instability and subluxation rather than the joint contractures and bony ankylosis associated with erosive arthritides.

Avascular necrosis occurs in 3% to 52% of patients with SLE, and involvement is frequentlt bilateral and asymptomatic. Avascular necrosis is thought to be caused by the corticosteroid used to treat SLE rather than by the disease itself because patients who have been treated with higher doses of steroids for prolonged periods are at greatest risk for developing this problem. Prolonged corticosteroid use may also cause or accelerate osteoporosis in this population 14 Systemic manifestations of SLE include fever, malaise, weight loss, anorexia, and weakness. Fatigue occurs in 80% to 100% of patients and is often the most debilitating symptom, affecting quality of life and interfering with family and social relationship. 14 Myalgias, muscle tenderness, and muscle weakness may be present in up to 69% of patients with SLE.16 SLE commonly cause skin rashes, including, malar, discoid, or subacute lesions. The term lupuswas derived from the Latin word for “wolf” and is used to describe the butterfly-shaped rash (Fig.6-2) reported by 35% of patients with lupus. 17Acute inflammatory rashes may occur on the malar regions of the face, on the trunk, and upper extremities, or between the interphalangeal joints. Discoid lupus is manifested by a chronic, scaly, and scaring rash with a prediclection for the sun exposed areas of the body. Subacute nonscarring symmetrical rashes resembling psoriatic skin lesions are seen ini 9% of patients with lupus, and patients may also have mouth ore nose sores, alopecia, urticaria, purpura, Raynaud’s phenomenon, livedo reticularis, vasculitis, and panniculitis.12

Approximately 50% of patients with lupus develop kidney disease (lupus nephritis), and 78% of patients develop proteinuria (protein in the urine), the most common real abnormality caused by lupus, at some period during the disease.14Lupus also has hematological manifestations, including anemia, leukopenia or lymphopenia, thrombocytopenia, and a false positive syphilis test. In addition, lupus may affect the cardiopulmonary system by causing pleurisy or pericarditis, or more rarely, endocarditis, pneumonitis, thrombophlebitis, and coronary artery disease. Neuropsychiatric symptoms occur in 25% to 80% of patients with SLE at some time during the course of the illness. SLE can also cause seizure, stroke, headaches, psychosis, and organic brain syndroms, nut depression is the most common psychiatric disorder in patients lupus and may be caused by the disease itself or be a reaction to the stresses associated with chronic illness. RHEUMATOID ARTHRITIS Rheumatoid arthritis (RA ) is chronic, systemic inflammatory disease of unknown etiology. It is characterized by symmetrical polyarthritis of the peripheral joints, morning stiffness, malaise, and fatigue. The disease course is variable, although there are often excerbations and remissions, and the disease may completely remit or progress aggressively to result in profound disability. The cause of RA has not been identified; however research suggest that there are genetic influences. 18 The concordance rate for RA in monozygotic twins is 15% which is four times higher than in dizygotic twins.19 Disease transmission in RA is complicated and may involve numerous genetic loci. The inflammation and tissue destruction in RA are caused by complex interactions between antigenpresenting cells and T cells. Clonal expansion of T cells stimulates synovial secretion of proinflammatory sytokines, including interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α). 20 RA also cause synovial proliferation, with the synovium changing from single cell layer to a multicellular composition containing growth factors, lymphocytes, and inflammatory cytokines. The over grown synovium, reffered to as pannus, invades an destroy articular cartilage and bone. Diagnosis. There is no diagnostic test for RA that is 100% sensitive or specific. The diagnosis criteria for RA drafted by the American College of Rheumtology (ACR) are listed in Box 6-2. Disease may vary among individualsan over time, delaying, the initial diagnosis. Although rheumatoid factor is detectable in the serum of most patients with rheumatoid arthritis, it can also be found in patients with other disease

including SLE, Sjogren’s syndrome, and liver or chroninc lung disease. Furthermore, 20% to 30% of patients with RA do not have a positive rheumatoid factor test. BOX 6-2 Diagnostic Criteria for Rheumatoid Arthritis 1. Morning stiffness: Morning stiffness in and around the joints lasting at least 1 hour before maximal improvment. 2. Arthritis of 3 more joint areas: At least 3 joint areas simultaneuosly have had soft tissue swelling or fluid observed physician. The 14 possible areas are right or left PIP, MCP, wirst, elbow, knee, ankle, and MTP joints. 3. Arthritis of hand joints: At least one area swollen in a wirst, MCP, or PIP joint. 4. Symmetrical arthritis: Simultaneous involvement of the same joint areas on both sides of the body. 5. Rheumatoid nodules: Subcutaneus nodules, over bony prominences, or extensor surface, or in juxtaarticular regions, observed by physician. 6. Serum rheumatoid factor: Demonstration of abnormal amounts or serum rheumatoid factor by any method for which the result has been positive in 0,5 gram per hari atau> 3+ jika hasil kuantitatif tidak melakukan OR B. Cellular casts mungkin berasal dalam sel darah merah, hemoglobin, granular, tubular, atau campuran. 8. gangguan neurologis A. kejang: Dengan tidak adanya penggunaan obat-obatan atau dikerahui gangguan metabolik OR B. Psikosis: Dengan tidak adanya dpenggunaan obat menyinggung atau dikenal gangguan metabolik 9. gangguan hematologi A. Anemia hemolitik B. Leukopenia C. Trombositopenia 10.Gangguan imunologi A.Persiapan sel Positif LE OR B. Anti-DNA: antibodi untuk DNA asli di titer normal OR C. Anti-Sm: Kehadiran antibodi terhadap antigen nuklir Sm OR D. Tes positif palsu untuk sifilis 11. ANA: Sebuah titer abnormal ANA oleh imunofluoresensi atau uji setara di setiap titik waktu dan tidak adanya obat yang diketahui terkait dengan sindrom drugs-induced lupus. Seseorang memiliki SLE jika ada 4 atau lebih dari 11 kriteria yang hadir, seendiria atau bersamaan, selama setiap interval pengamatan. Dari Tan EM, Cohen AS, Fries JF, dkk; Arthritis Rheum 25:1271-1277,1982. LE, Lupus errythematosus; ANA, antibuclear antibody; SLE, Systemic lupus erythematosus.

Fitur klinis. Meskipun SLE dapat melibatkan semua sistem organ, gejala yang paling umum adalah kelelahan dan arthralgia (nyeri sendi). Artharlgia terjadi pada 80% sampai 90% dari pasien yang menderita SLE. Namun, arthritis (radang sendi) terjadi dalam waktu kurang dari setengah dari kasus-kasus ini. Nyeri sendi dan peradangan, saat ini, cenderung simetris dengan kecenderungan nyeri biasanya pada lutut, sendi pergelangan tangan , dan interphalangeal . Bahu,

pinggul, pergelangan kaki, dan siku kurang terlibat dan jarang menimbulkan nyeri. 14 Ketika arthritis hadir pada pasien dengan SLE umumnya tidak deformasi; Namun 10 % dari pasienpasien dengan SLE mengembangkan nonerosive deformasi arthropathy tangan, yang akan berlanjut menjadi arthritis Jaccoud (Gambar 6-1),yang sebagian besar mempengaruhi kapsul sendi dan ligamen sekitarnya, menyebabkan ketidakstabilan sendi dan subluksasi daripada kontraktur sendi dan ankilosis tulang terkait dengan artritis erosif.

Gambar 6-1 Jaccoud’s arthritis. Deformasi arthropati nonerosif pada tangan Timbul pada pasien dengan sistemik lupus eritematosus. Reprinted from the clinical Slide collection on the rheumatic Disease, copyright 1997. Used by permission of the American Collage of Rheumatology Nekrosis avaskular terjadi pada 3% sampai 52% dari pasien dengan SLE , dan keterlibatan yang frekuensi bilateral dan asimtomatik. Neksrosis avascular diduga disebabkan oleh kortikosteroid yang digunakan untuk mengobati SLE bukan oleh penyakit itu sendiri, karena pasien yang telah diobati dengan dosis tinggi steroid untuk waktu yang lama berada pada risiko terbesar untuk mengembangkan permasalahan ini. Penggunaan kortikosteroid berkepanjangan juga dapat menyebabkan atau mempercepat osteoporosis di populasi.14 Manifestasi sistemik dari SLE termasuk demam, malaise, penurunan berat badan, anoreksia, dan kelemahan. Kelelahan terjadi pada 80% sampai 100% dari pasien, dan sering gejala yang paling melemahkan, yang mempengaruhi kualitas hidup dan mengganggu keluarga dan hubungan interaksi sosial.14 Mialgia, nyeri otot, dan kelemahan otot dapat hadir pada sampai dengan 69 % dari pasien dengan SLE.16 SLE sering menyebabkan ruam kulit, termasuk malar, diskoid, atau lesi subakut.Lupus merupakan istilah yang berasal dari kata Latin untuk "serigala" dan digunakan untuk menggambarkan bentuk ruam seperti kupu-kupu (Fig.6-2) dilaporkan oleh 35% pasien yang menderita lupus.17Ruam inflamasi akut dapat terjadi pada daerah malar wajah, pada trunkus, dan ekstremitas atas, atau antara sendi interphalangea. Lupus diskoid dimanifestasikan oleh gejala kronis, bersisik, dan ruam akan sangat sensitif terhadap sinar matahari jika terkena tempat yang menjadi predileksi. Ruam nonscarring subakut berbentuk simetris menyerupai lesi kulit psoriasis terlihat 9% dari pasien dengan lupus, dan pasien juga mungkin memiliki mulut luka, luka pada hidung, alopecia, urtikaria, purpura, fenomena Raynaud, livedo reticularis, vaskulitis, dan panniculitis.12

Gambar 6-2 Lupus rash. Rash eritem (rash kupu-kupu) meluas sampai menyebrang regio malar pada daerah wajah dan menyeberang kehidung seperti jembatan. Dari Hochberg MC, Silman Al, Simolen Sl, et al, Editors: Rheumatoid arthritis, Philadelphia, 2008. Mosby Sekitar 50 % pasien dengan lupus juka akan mengalami penyakit ginjal (nefritis lupus), dan 78 % dari pasie akan menunjukkan proteinuria (protein dalam urin), kelainan nyata yang paling umum disebabkan oleh lupus, di beberapa periode selama menderita penyakit. 14Lupus juga memiliki manifestasi hematologi, termasuk anemia, leukopenia atau limfopenia, trombositopenia, dan tes sifilis positif palsu. Selain itu, lupus dapat mempengaruhi sistem cardiopulmonary dengan menyebabkan radang selaput pembungkus jantung atau perikarditis, atau lebih jarang, endokarditis, pneumonitis, tromboflebitis, dan penyakit arteri koroner . Gejala neuropsikiatri terjadi pada 25% sampai 80% dari pasien dengan SLE pada beberapa waktu selama perjalanan penyakit . SLE juga dapat menyebabkan kejang, stroke, sakit kepala, psikosis, dan sindroma otak organik, depresi adalah gangguan kejiwaan yang paling umum pada pasien lupus dan dapat disebabkan oleh penyakit itu sendiri atau menjadi akibat yang timbul terhadap stres yang terkait dengan penyakit kronis. RHEUMATOID ARTHRITIS Rheumatoid arthritis (RA) adalah penyakit inflamasi sistemik kronis yang tidak diketahui penyebabnya. Hal ini ditandai dengan poliartritis simetris pada sendi perifer, kekakuan pada pagi hari, malaise, dan kelelahan. Penyakit ini banyak melibatkan variabel, meskipun sering ada eksaserbasi dan remisi, dan penyakit yang dapat benar-benar mengakibatkan atau kemajuan yang agresif untuk menjadikan cacat yang mendalam . Penyebab RA belum teridentifikasi; namun penelitian menunjukkan bahwa ada keterlibatan faktor genetik.18Tingkat konkordansi untuk RA pada kembar monozigot adalah sebesar 15 % yang empat kali lebih tinggi daripada di transmisi penyakit pada kembat dizigot. 19Penyakit Rheumatoid Artritis adalah penyakit yang rumit dan mungkin akan banyak melibatkan lokus genetik. Peradangan dan kerusakan jaringan pada RA disebabkan oleh adanya kompleks interaksi antara sel antigen dan sel T. Ekspansi klonal sel T akan merangsang sekresi sinovial dari

sytokines proinflamasi, termasuk interleukin-1 (IL-1) dan tumor necrosis factor alpha (TNF -α ).20 RA juga menyebabkan proliferasi sinovial, dengan sinovium yang berubah dari lapisan sel tunggal menjadi komposisi multiseluler yang mengandung faktor pertumbuhan, limfosit, dan sitokin inflamasi. Sinovium lebih berkembang, dirujuk sebagai pannus, menyerang dan menghancurkan sebuah artikular tulang rawan dan tulang . Diagnosis. Tidak ada tes diagnostik untuk RA yang 100% sensitif atau spesifik. Kriteria diagnosis untuk RA disusun oleh American College of Rheumtology ( ACR ) yang tercantum dalam Kotak 6-2 . Penyakit dapat bervariasi antara individual dari waktu ke waktu, dan dapat menunda, diagnosis awal. Meskipun faktor rheumatoid dapat dideteksi dalam serum, kebanyakan pasien dengan rheumatoid arthritis, juga dapat ditemukan pada pasien dengan penyakit lainnya termasuk SLE , sindrom Sjogren , dan penyakit yang menyerang hati atau penyakit paru-paru kronik. Selanjutnya, 20 % sampai 30 % dari pasien dengan RA tidak memiliki tes faktor rheumatoid positif. BOX 6-2 Kriteria Diagnosis pada rheumatoid arthritis 1. Kekakuan pada pagi hari: Kekakuan pada pagi hari didalam dan sekita sendi yang berlangsung selama satu jam sebelum mengalami perbaikan. 2. Arthritiss pada 3area sendi atau lebih: Setidaknya tiga daerah sendi hampir bersamaan telah mengalami pembengkakan jaringan lunak atau dari pengamatan cairan yang diamati dokter. Ada 14 daerah yang mungkin juga terkena antara lain PIP kanan atau kiri, MCP, sendi pergelangan tangan, sendi siku, dan sendi MTP 3. Arthritis pada sendi tangan: Setidaknya hanya satu daerang yang mengalami pembengkakan yaitu pada pergelangan tangan, MCP, atau sendi PIP. Arthritis of hand joints: At least one area swollen in a wirst, MCP, or PIP joint. 4. Arthritis simetris: Adanya keterlibatan pada area sendi atau pada kedua sisi tubuh. 5. Nodul rheumatoid: Nodul subkutan Lebih sering terlihat pada permukaan extensor, atau didaerah juxtaarticular berdasarkan pemeriksaan dokter. 6. Perubahan pada radiography yang sangat khas reumathoid artritis pada daerah tangan posteroanterior dan radiografi sendi pergelangan tangan yang harus mencakup erosi dari deklasifikasi tulang lokal di atau paling ditandai berdekatan dengan melibatkan sendi From Arnett FC, Edworthy SM,Bloch DA, et al: Arthritis Rheum 31: 315-324,1988. PIP, Proximal interphalangeal; MCP, metacarpophalangeal; MTP, Metatarsophalangeal; RA, rheumatoid arthritis.

Fitur klinis Manifestasi artikular. Manifestasi artikular dari RA meliputi kekakuan pada pagi hari, peradangan pada sinovial, dan kerusakan struktural. Kekakuan pada pagi hari berkorelasi dengan tingkat peradangan dan biasanya berlangsung lebih dari dua jam, yang bertentangan dengan kekauan pada pagi hari yang singkat, yang terjadi pada osteoarthritis. Nyeri dan pembengkakan adalah fitur kunci dari sendi yang terkena RA. Sinovitis akut dapat menyebabkan kemerahan, hangat, dan bengkak pada sendi dangkal; Namun, sinovitis yang mempengaruhi sendi akan masuk lebih dalam, seperti pinggul dan bahu, mungkin sulit untuk menilai pada pemeriksaan fisik. Sinovitis Persisten dapat menyebabkan hilangnya tulang rawan, erosi tulang, dan akhirnya mengalami kerusakan struktur yang reversibel.22 Tangan. Pergelangan tangan dan metacarpophalangeal (MC) dan interphalangeal proksimal (IP) sendi tangan biasanya terlibat dalam RA.22 Penyimpangan radial di pergelangan tangan yang sering dikaitkan dengan deviasi ulnaris di jari (deformitas zig -zag )(Gambar 6- 3) 23. Deformitas

ini disebabkan oleh sinovitis kronis pada wirst dan sendi MC, melemahnya otot ekstensor karpi ulnaris, bias ulnar dari kekuatan genggam.24 dan tindakan yang tidak tepat dari otot intrinsik.25 Deformitas leher angsa, yang melibatkan fleksi dari MCP dan distal IP ( DIP ) bersama dan hiperekstensi dari sendi PIP, mungkin berkembang karena persistents MCP sinovitis dengan bersamaan kekakuan otot intrinsik (Gambar 6-4). Peradangan kronis pada sendi PIP dengan avulsi dari kap ekstensor dapat menyebabkan deformitas boutonniere (fleksi pada sendi PIP dan hyphersxtension pada sendi DIP)(Gambar.6-5) Pembengakakan dorsal dalam selubung sinovial tendon ekstensor di pergelangan tanga juga umumnya merupakan manifestasi awal

Fig.6-3 Deviasi pada pergelangan tangan radial dan deviasi jari ulnar (Deformitas zig-zag) pada pasien dengan RA. Dari Hochberg MC, Silman Al, Smolen Sl, et al, Editors: Rheumatoid arthritis, Philadelphia, 2008. Mosby