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Sports-Medicine Kalyan-Dombivali
Rheumatoid Arthritis
Evidence of immune activity in RA
Postulated role of humoral and cellular immunity in pathogenesis of RA
Histology of rheumatoid nodules
Clinical features
Joints affected in RA
Stages of Rheumatoid Arthritis
Deformities in Rheumatoid Arthritis
Extra articular manifestations
Laboratory findings
Special investigations
Sinovial fluid examination
Radiographic evaluation
Revised criteria for the classification of Rheumatoid Arthritis
Laboratory differentiation in RA
Management of Rheumatoid Arthritis
Treatment methods
Staged therapy in Rheumatoid Arthritis
Disease modifying antirheumatic drugs
  Parenteral gold and D- pencillamine
  Cytotoxic and Immunosupressive agents
  Cyclosporin A
Newer therapeutic approaches
Role of leflunomide in RA
Toxic effects of immunosuppresive drugs
Orthopaedic treatment
Clinical manifestation - urgent clinical problems
Rheumatoid arthritis (RA) is an immuno – inflammatory disease that affects joints and extra articular tissues.  


·        The reported prevalence of RA in adults varies from 0.5% to 3.8% but is slightly less in the tropics. varying from 0.2% to 1.2%.

·        The sex ratio is 4: 1 in favour of females.

·        The prevelence increases with age and sex differences diminish in the older age group.

·        The onset is most frequent during the fourth and fifth decades of life, with 80% of all patients developing the disease between the age of 35 -50.


The theoretical causes proposed are following.

A.     Infectitious: Hemolytic and nonhemolytic types of streptococci has been isolated from joints and regional lymph nodes.

B.     Endocrine: This is suggested by clinical response to therapeutic steroids.

C.     Allergic: The patients frequently exhibit various allergic menifestations. Eosinophilia is frequent.

D.    Metabolic


Rheumatoid arthritis is an immunologically mediated event, although the original initiating stimulus has not been characterized. It is believed that the inflammatory process in the tissue is driven by the CD 4 + T cells infiltrating the synovium.

The tissue inflammation is reminiscent of delayed type hypersensitivity reaction occurring in response to soluble antigens or microorganisms. It remains unclear whether the persistent T-cell activity represent a response to a persistent exogenous antigen or to altered auto antigens such as collagen immunglobulin or one of the heat shock proteins or perhaps both. Alternatively it could represent persistent responsiveness to activated autologous cells such as might occur as a result of Epstein Barr virus infection or persistent response to a foreign antigen or superantigen in the synovial tissue. Finally rheumatoid inflammation could reflect persistent stimulation of T-cells by synovial derived antigens. Overriding the chronic inflammation in the synovial tissue is an acute inflammatory process in the synovial fluid. The exudative synovial fluid contains more polymorphonuclear cells than mononuclear cells. The precise mechanism by which bone and cartilage destruction occurs has not been completely resolved, the majority of destruction is in juxtaposition to the inflamed synovium or pannus, that spreads to cover the articular cartilage. This vascular granulation tissue is composed of proliferating fibroblasts, small blood vessels and a variable number of mononuclear cells. It produces a large amount of degradation enzymes including collagenase and stromelyin, that may facilitate tissue damage. The cytokines IL-I and TNF- µ play an important role by stimulating the cells of the pannus to produce collagenase and other neutral proteases.

Evidence of immune overactivity in RA:

1.      The presence in the serum of an abnomal immunoglobin –rheumatoid factor

2.      The infilteration of the synovial tissue by immunological competent cells, lymphocytes, and plasma cells, which are reponsible for the local production of immunoglobins including rheumatoid factor.

3.      The presence of immune antigen-antibody complexes within leucocytes in synovial fluid and peripheral blood

4.      The finding of lowered complement levels in the synovial fluid

Postulated role of humoral and cellular immunity in pathogenesis of rheumatoid arthritis:
Chart showing details. Click here

Histology of rheumatoid nodules:

It reveals distinct zones:

·        A central area of necrosis

·        A palisade of elongated, connective tissue cells arranged radially in a corona about the necrotic zone.

·        Enveloping granulation tissue with chronic inflammation cells

Diagram : Click here

Clinical features:

Rheumatoid arthritis is characterized by joint pain, stiffness and symmetrical swelling of a number of peripheral joints. Initially, pain may be experienced only on movement of joints but rest pain and prolonged early morning stiffness develop gradually. Characteristically, RA is a chronic polyarthritis. In approximately two – thirds of patients it begins with fatigue, anorexia. Generalized  weakness and vague musculoskeletal symptoms.

In the typical case the small joints of the fingers and toes are the first to be affected. As the disease progresses, it tends to spread to involve the wrists, elbows, shoulders, knees, ankles, subtalar and midtarsal joints. The hips becomes involved only in the more severly affected, but neck pain and stiffness from cervical spine disease is common.

Clinically. synovial inflammation cause swelling. tenderness and limitation of motion. Warmth is usually evident on examination. especially of large joints such as the knee joints. Swelling results from accumulation of synovial fluid. hypertrophy of the synovium and thickening of the joint capsule. Motion is limited by pain.

Joints affected in rheumatoid arthritis:




Less common              


- Wrist knee, ankles and elbows

- MP joints of hand

- PI P joints of fingers

- Hip joint

- Atlanto-axial joint

- Cervical spine facet joints


As the disease advances, muscle atrophy and tendon sheath and joint destruction result in limitation of joint motion, joint instability and deformities. At first, deformities are correctable, but later permanent contractures develop resulting in characteristic deformities in feet, the knees, hips and elbow. Anterior subluxatin of the metacarpophalangeal joints is common with ulnar deviation of the fingers. Other finger

deformities lead to greater loss of hand function. These include the "swan neck" deformity, the boutonniere or button -hole deformity (fixed flexion of the proximal interphalangeal joint and extension of the terminal interphalangeal joint) and deformity of the thumb. Dorsal subluxation of the ulnar styloid of the wrist is common and may contribute to rupture of the 4th and 5th extensor tendons when these are already the site of tenosynovitis.

In the forefoot, subluxation of the metatarsophalangeal joints is followed by clawing of the toes and callosities over the exposed metatarsal heads, tenosynovitis and bursitis are integral of RA, as tendon sheaths and bursae are also lined with synovium.

Stages of rheumatoid arthritis:

1.      Potentially reversible soft tissue proliferations: In this Stage the disease is limited to the synovium with associated hypertrophy and effusion.

2.      Controllable but irreversible soft tissue destruction and early cartilage erosions: X-rays shows a reduction in the joint space but the articular congruency is well maintained.

3.      Irreversible soft tissue and bony changes: There is erosion of subchondral bone, subluxation or dislocation of joint or fibrous ankylosis.

Deformities in rheumatoid arthritis:













- Drop fingers from rupture of extensor tendon

- Fingers: Swan neck deformity

               Boutonniere deformity

- Ulnar drift of the hand

- Z- deformity of the thumbs

- Flexion deformity

- Early: Flexion deformity

- Late: Triple deformities: flexion, posterior

           Subluxation and lateral rotation

- Hallux valgus, hammer toe, etc

- Equinus deformity

Diagrams :  Diagram 1       Diagram 2

Figure 1.2

A.     Minimum damage occurs at the site of maximum compression.

B.     Fold of synovium over the cartilage is the site of maximum damage.

Diagram : Click here

Extra articular manifesations:

Rheumatoid arthritis is a systemic disease, Anorexia, weight loss, lethargy, myalgia and raynaud's phenomenon occur commonly throughout its course, Rheumatic nodules develop in 20% to 30% of persons with RA. They are usually found on periarticular structures, extensor surfaces or other areas subjected to mechanical pressure, but they can develop else where including the pleura and meninges. Nodules vary in size and consistency and are rarely symptomatic, but on occasion they break down as a result of trauma or become infected. They are found almost invariably in individuals with circulating rheumatoid factor.

The other extra articular features of the disease, are listed below:

Click here for table showing features of Rheumatoid Arthritis


Rheumatic fever: As a rule large joints are involved with associated fever, leukocytosis, tonsillitis and cardiac. pulmonory and kidney inflammatorv lesions. Relatively younger people are involved

Radiological features are absent and also titre is raised. It responds very well to salicylates.

Osteoarthritis: The older age group is affected, mainly involving DIP and large weight bearing joints with osteophyte formation. Systemic symptoms are absent, subchondral scierosis is seen on x-rays and ESR is not elevated.

Laboratory findings:

Rheumatoid factor: No tests are specific for diagnosing RA. However rheumatoid factors are found in more than two thirds of adults with the disease. The presence of rheumatoid factors is not specific for RA as it is found in 5% of healthy persons.


The presence of rheumatoid factor can be of prognostic significance because patients with high titres tends to have more severe and progressive disease with extraarticular manifestations.

Index 1.1

Occurance of rheumatoid factor in selected conditions

Rheumatic Disease

·        Adult rheumatoid arthritis

·        Sjogrens syndrome

·        Systemic lupus erythmatosus

·        Scleroderma

·        Mixed connective tissue disease

·        Polymyositis

Actual viral infections

Chronic Inflammatory disease

·        Tuberculosis

·        Syphilis

·        Infective endocarditis



·        Elderly but otherwise healthy individuals

·        Sarcoidosis

·        Chronic hepatitis

·        After transfusions

·        After renal transplantations

Methods of testing RA factor:

              I.      Latex screening

           II.      Latex test (Normal < 20)

         III.      Sheep cell agglutination test (Rose waaler) (SCAT) (normal < 32)

        IV.      Differential agglutination test (normal < 16)

Other laboratory findings:

Normochromic normocytic, anaemia is frequently present in active RA Eosinophilia  when present usually reflects severe systemic disease. The erythrocyte sedimentation rate (ESR) is useful for assessment of disease activity. It is increased in nearly all patients with active RA. C-reactive protein (CRP) is a useful marker or acute phase reactant and valuable in the management. High levels of CRP at the onset of disease correlates with poor prognosis.

Special Investigation:

a.       Synovial biopsy: Rheumatoid pattern (villus formation with thickening nf synovial layer and infiltration with abnormal cells in rheumatoid arthritis (also in SLE, stills disease).

b.      Synovial fluid: May show positive Rose- Waaler test in joint fluid before it can be detected in blood. Fluid may show polymorphonuclear or mononuclear leucocytes containing cytoplasmic inclusion bodies.

c.       Arthoscopy: In accute RA synovium is diffusely erythematous and friable. In chronic presentation. It is usually polypoid and thickened.

Synovial fluid examination:
Click here for the table

Radiographic evaluation:

The primary value of radiography is to determine the destruction and bone erosion produced by the disease is monitoring the impact of theraphy with disease -modifying drugs or surgical intervention.

The sequence of early radiological sign in RA are.

1.      Soft tissue swelling due lo joint effusion

2.      Perarticular symmetrical osteoporosis with reduction in the width of shaft cortices and loss of normal trabecular pattern.

3.      Periosteal reaction with new osteogenesis along the shaft near the capsular attachment.

4.      Subchondral cyst formation.

5.      Subchondral erosions due to actual loss of bone substance by erosion along the marginal areas of the joint.

Click here for the table

Revised criteria for the classification of Rheumatoid Arthritis

1.      Guidelines for classification:

a.      Four of seven criteria are required to classify a patient as having rheumatoid arthritis (RA).

b.      Patients with two or more clinical diagnosis are not excluded

      2.   Criteria:

a.       Morning stiffness: Stiffness in and around the joints lasting 1 hr. before maximal improvement.

b.      Arthritis of three or more joint areas: At least three joint areas, observed by a physician simultaneously, have soft tissue swelling or joint effusions, not just bony over growth. The 14 possible joint areas involved are right or left proximal interphalangeal metacarpophalangeal, wrist. Elbow, knee, ankle and metatarsophalangeal joints.

c.       Arthritis of hand joint. Arthritis of wrist, metacarpophalongeal joint or proximal interphalangeal joint.

d.      Symmetric arthritis: simultaneously involvement of the same joint areas on both sides of the body.

e.       Rheumatoid nodules. Subcutaneous nodules over bony prominences, extensor surface or juxtarticular regions observed by a physician.

f.        Serum rheumatoid factor: Demonstration of abnormal amounts of serum rheumatoid factor by any method for which the result has been positive in less than 5% of normal control subjects.

g.       Radiographic changes: Typical changes of RA on posterroanterior hand wrist radiographs which must include erosions or unequivocal bony decalcification localized in or most marked adjacent to the involved joints.

Major differences between rheumatoid arthritis and spondyoarthropathies:

Refer to table : Click here

Clinical differentiation between RA and OA:
Refer to table : Click here

Laboratory Differentiation in rheumatoid arthritis:

Click here for the table

Management of rheumatoid arthritis:


  • Control of joint inflammation

  • Arrest and / or retard the disease process

  • Maintain joint function and prevent deformities

Goal: The goal of treatment is to control inflammation sufficiently to prevent or retard joint damage with ultimate goal being to induce complete remission.

Treatment Methods:


  • By NSAIDS (Non - Steroidulantiin flammamatory agents)

  • By corticosteroids and

  • By disease modifying antirheumatic drugs (DMARDs)

Simple analgesics: Paracetamol 500mg with or without dextropro poxyphene hydrochloride 65mg three times a day is useful in pain management.


NSAIDS: NSAIDS reduce joint and swelling and may improve, they do not alter disease progression. Nevertheless predictable course of rheumatoid arthritis at presentation they are used as initial treatment. If patients continue to experience persistent symptoms, morning stiffness and fatigue for 2 -3 months, treatment with DMARDs is indicated.


Corticosteroids: Although corticosteroid usually produce immediate and dramatic antinflammatory effects in RA, they do not alter progression of the disease. Further more, clinical manifestations of the active disease reappear when the drug is discontinued.


DMARD: DMARDs are drugs, which modify the course of the disease. The aim of resorting to DMARD in rheumatoid arthritis is to postpone or preclude the use of corticosteroids, which have their well known side effects. These drug can reduce the activity of rheumatoid arthritis including pain, stiffness and swelling. Most disease modifying drugs take six to twelve weeks before a beneficial effects is noted.


Drugs of this type do not possess immediate anti -inflammatory effect but will improve joint pain, stiffness, swelling and reduce systemic symptoms. Their main benefit is in inducing, a symptomatic remmissin for 1 -2 years in 40 -60% of patients. They are usually introduced in a pyramidal fashion. Starting with the safest determined by the severity of the disease.

The current treatment startegy invloves the early use of DMARD to limit joint damage and preserve function.

Indications for disease-modifying drugs:

  • Persistent symptoms and signs of inflammatory arthritis

  • Evidence of progressive radiological damage

  • Troublesome extra -.articular manifestations

  • Palindromic (returning / recurrent) rheumatoid arthritis.

Examples: Methodtrexate gold compounds, D -penicillamine, the antimalarials and sulfasalazine.


Advantages of DMARDs:

  • Reduce disease progression

  • Improve functional disability

  • Decrease pain.

  • Interfere with inflammatory processes.

  • Retard development of joint erosion.

The new treatment paradigm with respect to DMARDs: Earlier concept was to use DMARD for advanced cases and relatively later in rheumatoid arthritis. Recent data shows that damage to the bones and synovial tissue begin during the first couple of years of disease onset and aggressive use  of DMARDs during this phase helps in reduction of joint damage and subsequent deformity and disabiltity.


Many experts are now recommending that patients with moderate or severe, RA should start therapy with DMARDs as well as NSAID.

Refer to diagram : Click here

Staged therapy in rheumatoid arthritis:
Refer to table : Click here 

Disease modifying antirheumatic drugs:

Antimalarials: The successful use of antimalarials dates back several decades. Antimalarials used are chloroquine and its analogue hydroxychloroquine.

Meta -analysis of second line - therapy suggests that antimalarial drugs have a very favourable risk: benefit ratio. Response generally occurs in 40 to 50% of patients. After several decades of use, there is an impression that patients with milder disease have the greatest potential for a positive response of therapy.

The usual dose of hydroxychloroquine is 200 - 400mg/day. Clinical benefit with hydroxychloroquine is noted in about half the patients in 4 –12 weeks and the drug should be discontinued if there is no effect within 6 months.


Sulfasalazine: Sulafasalazine is the only drug currently used that was specially developed for the therapy of rheumatoid arthritis. The drug is useful as therapy of mild to moderate rheumatoid arthritis. It generally takes 12 -20 weeks for response to occur. The usual starting dose is 500mg/day for 1 week with dose escalations weekly until dose of 2 to 3g/day is achieved. Dose of 3g/day may be associated with greater toxicity. Side effects of sulfasalazine include gastrointestinal toxicity, rash, headaches, dizziness, haematologic toxicity (hemolytic anaemia, leukopenia) and fever. Routine monitoring of the blood count is required. The drug is most commonly used inpatients with mild to moderate disease and in combination with many other second line therapies including methotrexate.


Methotraxate: Methotraxate works more quickly than other DMARDs with significant improvement in symtoms in 4-6 weeks. It is currently a frequently used DMARD. Most rheumatologists recommend use of methotrexate as the initial DMARD, especially in individuals with aggressive RA. Maximal improvement is observed after 6 months of therapy. Major toxicity includes gastrointestinal upset, oral ulceration and liver function abnormalities that appears to be doses related and reversible. Full blood count and liver function tests must be monitored regularly and care must be taken to avoid drug interaction with sulphonamides. Liver biopsy is recommended for individuals with persistent liver function abnormalities. Acute pulmonary toxicity is an unpredictable problem in 5 -10% of patients. The salient development of progressive hepatic fibrosis has been recorded and the drug should not be given to chronic alcoholic patients.


Parenteral gold and D - pencillamine:

These are slow -acting suppressive antirheumatic drugs which have been shown to decrease the progression of erosive changes as well as reduce the activity of the disease in 50 -60% of patients. Due to a high incidence of toxic effects, treatment with these agents should only be considered as an addition to basic therapy when there are clear indications for the use of a disease modifying drug and the patients has failed to respond to antimalarials or sulfasalazine.

Two parenteral gold preparations are available aurothioglucose and sodium thiomolaste. The major difficulties with parenteral gold are its delayed action and side effect profile. Adverse events occur in approximately 40% of patients and include skin reactions, stomatitis,  proteinuria and nephrotic syndrome, thrombocytopenia, eosinophilia, agranulocytosis, aplastic anaemia, pneumonitis, colitis, hepatitis and neurotoxcity, hypotension, dizziness, weakness, nausea and vomiting. Auranofin is an orally absorbed gold preparation. Despite initial enthusiasm for auranofin there has been a reduction in interest in this drug. This is most likely due to the delayed onset of action and limited  efficacy. The most common side effects with auranofin are loose stools and diarrhea. Routine monitoring of the blood count and urinalysis is required.


D-penicillamine has been demonstrated to be effective in randomized controlled trials. However, it has a delayed onset of action and side effects occur frequently. It has a similar toxicity profile to parenteral gold and additionally can cause rare autoimmune reactions including myasthenia gravis and lupus. D -penicillamine is believe to be more toxic than parenteral gold.


Cytotoxic and Immunosupressive agents:

A number of cytotoxic and immunosupressive agents have been found to have both symptomic and slow acting disease modifying activity in rheumatoid arthritis. The effect as mediated by their usefulness is limited by immediate and potential long term toxicity.


They include azathioprine, cyclophosphamide and cyclosprin A.

The indication for use of these agents at present are limited to:

  • Life -threatening extra -articular manifestations which have failed to corticosteroids or second line agents.

  • Severe active symptomatic and progressive joint disease that has failed to respond to all other forms of therapy.

  • Patients receiving unacceptably high doses of corticosteroids in whom dose reduction has not been possible.


An antimetabolite, is generally reserved for patients who have failed conventional therapy including methotrexate. The onset of action is generally after 12 to 24 weeks. A return in disease activity occurs with drug discontinuation. Side effects include gastrointestinal intolerance, nausea~norexia, vomiting, pancreatitis, hepatotoxicity, leukopenia macrocytic anaemia and rarely infection. Concern has been expressed regarding the potential for cancer with long term therapy routine and regular monitoring of the complete blood count and periodic monitoring of liver function tests are required.



Cyclophoshamide is a potent immunosuppressive drug that has been shown to be efficacious in rheumatoid arthritis. Despite its efficacy profile there is limited use of this drug due to long term toxicity concerns. With chronic administration. Carcinogenesis is a major concern and generally precludes its use in this chronic disease.


Cyclosporin A:

Cyclosporin A is generally reserved for patients with refractory rheumatoid arthritis who have failed a trial with azathioprinc or methotrexate. Discontinuation of cyclosprin A is associated with a flare of disease activity. Side effects include gastrointestinal intolerance, headaches, paraesthesias, flushing. gingival hypertrophy. tremors, hypertrichosis hypertension and renal toxicity. Its use in many patients is limited due to cost.

Monitoring parameters on long term use:
Click here to refer to table

Newer therapeutic approaches:

lnfliximab and etanercept have recently been approved for use in the treatment of rheumatoid anthritis. Both drugs have shown to reduce disease activity they directly target TNF -2. a proinflammatory cytokine, which  plays a key role in the pathological inflammatory process in rheumatoid arthritis. They have been associated with an increased risk of upper respiratory tract infection and more rarely with cases of serious infection. Their exact place in therapy of RA is not yet established and at present they are very expensive.

American College of rheumatology (ACR) criteria for measuring improvement in disease activity in patients with rheumatoid arthritis:
Refer to table : Click here

Role of leflunomide in RA:

Leflunomide has a unique mechanism of action. It acts by inhibiting denovo pyrimidine synthesis thus preventing proliferation of activated T lymphocytes.

It is known to improve functional scores of patient and retard radiological evidence of structural damage.

Dose schedule:

It is usually started for first 3 days as 100 mg/day (5 tables of 20 mg)

subsequently maintenance dose of 20 mg/daily can be given up to 2 years.

Adverse reactions:

These include diarrhoea, elevated liver enzymes (ACT and AST), alopecia, rash, sometimes acute skin reactions like toxic epidermal necrolysis and Stevens-Johnson syndrome.

Toxic effects of immunosuppressive drugs:

Click here to refer to the table

Orthopaedic treatment:

1)      Rest

2)      Splintage

a.       For relief of pain and inflammation

b.      Prevention of deformity

c.       Correction of deformity

d.      Postoperative.

3)  Hydrocortisone injection: When one or two large joints are involved not responding to systemic medication, intraarticular steroid injection can give dramatic relief.


Indication for use of local corticosteroid injection in rheumatoid arthritis

  1. Intra-articular injection for the patients with one or two active joints.

  2. For temperary relief in tendinitis and tendon nodules e.g. trigger finger.

  3. Capsular or ligamentous involvement e.g. shoulder

  4. As a palliative method in the treatment of carpal tunnel and other compression syndomes.


  1. Uncertain diagnosis

  2. Proven or possible infection

  3. Severe joint damage

  4. Severe local osteoperosis

  5. A neurological deficit: as it may produce charcot type arthropathy.

4)  Surgery: Surgical options are

  1. Synoviectomy

  2. Corrective surgeries including capsulotomies, tenotomy tendon transfer, bony osteotomies & arthrodesis.

  3. Joint replacement.


  1. When not responding to medication.

  2. Involving one or two joints.

  3. Threatening impending rupture of tendon.


  1. Open synoviectomy

  2. Laser synoviectomy

  3. Arthroscopic synoviectomy

  4. Radioisotope synoviectomy

Selection of patients for knee synovectomy.

1.      Those with persistent, painful synovitis with proliferative synovium not responding to medical therapy over a period of 3 months.

2.      There should be a useful range of movement (i.e. atleast 45° of flexion) without any persistent flexion contracture.

3.      The joint should be stable.

4.      There should not be severe destruction of joint space or subchondral bone loss.


·        When patient is relative younger > 55 years of age

·        Only partial involvement of joint.

·        Most commonly done at hip (intertrochanteric osteotomy and abduction osteotomy)


  • Provides long term relief

  • Usually reserved in peripheral joints where arthroplasty may not succeed or is not feasible

  • Puts extra stress on large joints which may lead to secondary OA

Treatment algorithm : Refer to chart - Click here


Various factors affecting the outcome in a rheumatoid case are as follows:

  1. Natural history of the disease: Which may be fulminant in some or punctuated with episodes of remissions and exacerbations.
  2. Sex & age at onset: Women of child bearing age with mainly upper extremity involvement has a progressively severe disease. Male with history of onset before 30 yrs. have a better prognosis.
  3. Type of onset: Insidous - onset disease has been found to have a more protracted course.
  4. E.S.R & creative protein: High levels of ESR is associated with more erosive arthritis.
  5. Rheumatoid factor : Higher titre are associated with poor prognosis.
  6. Anaemia: Anaemia is associated with progressive rheumatoid arthritis.
  7. Radiological erosions: Occurance before 2 years of onset is a bad prognosis sign.
  8. Histopathological changes: Excessive synovial proliferation with increased number of synovial cells with DR antigen, carry bad prognosis.

Clinical manifestation -urgent clinical problems

Acute cricoarytenoid arthritis:

This is a life threatening disorder that produces sudden hoarsness, dyspnea, stridor and tightness of the throat. On palpation, the cricoarytenoid joints are tender and examination of indirect laryngoscopy reveals marked erythema and swelling of the arytenoids and vocal cards. It usually responds well to corticosteroid (including local injection and inhalation).


Synovial cyst: Fluid filled synovial cysts may enlarge and rupture into the surrounding soft tissues. Sudden bending of the knee may precipitate rupture of a synovial cyst in the popliteal fossa behind the knee (Baker's cyst). Ruptured cyst usually respond quickly to aspiration and corticosteroid injection. Surgery is rarely indicated.


Tendon Rupture: Rupture occur most often in the extensor tendon over the dorsum of the hand leading to altered finger extension. It requires surgical intervention.


Septic Arthritis: It may occur in those patients treated with intraarticular steroids or immunosupressive agents. Unexplained persistent or progressive inflammation in a single joint may be an indication of joint aspiration. Arthrocentesis confirms the diagnosis.


Uncommon Complication: Amyloidosis: It is found at post-mortem in about 20% of cases. However few patients show signs of amyloidosis. Proteinuria leading to nephrosis is the usual presentation.