Joint erosion in rheumatoid arthritis

by Nathan Wei, MD, FACP, FACR

Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.

Click here: Second Opinion Arthritis Treatment Kit

Rheumatoid arthritis (RA) is a systemic inflammatory disease that leads to cartilage and bone destruction.

RA is a disease that affects the lining of the joint capsule which is called the synovium. Destruction of the joint as a result of inflammation in the synovium leads to deformities and loss of function.

RA is characterized by diffuse cartilage loss and erosion of bone and cartilage. Inflammation starts in the synovial membrane, with edema, neovascularization (formation of new blood vessels which invade tissue), and abnormal growth of the synovial lining. Proliferation of synoviocytes and macrophages causes thickening of the synovial lining and, together with lymphocytes, plasma cells, and mast cells, develops into pannus- an inflammatory mass of tissue that acts like a slow growing malignancy.

Pannus is a sheet of invasive cellular tissue that consists of synovium packed with both inflammatory cells as well as the products produced by the inflammatory cells. Pannus causes erosion of bone and cartilage at the margin of joints. Large fingers of inflamed synovium form as does inflammatory fluid (effusion). The effusion causes capsule distension and stretching of the ligamentous tissues, resulting in laxity of the capsule. With further progression of disease, the joint becomes unstable and begins to deform.

At the cellular level, cytokines, such as tumor necrosis factor alpha (TNF-alpha) and interleukin 1 (IL-1), stimulate synoviocytes to produce cartilage-degrading enzymes. Cytokines also regulate production and of adhesion molecules, which allow pannus to attach to cartilage and bone.

Hyperplastic synovium and pannus produce several enzymes that are capable of degrading components of bone and cartilage. One group of enzymes is the matrix metalloproteinases, which are secreted from synoviocytes and cartilage cells in response to cytokines. Other protein degrading enzymes also play a contributory role. Genetically, RA has been shown to be associated with positive human leukocyte antigen DR4.

The primary effect of RA is in joint deformity and fusion, which occurs in the advanced stages. Permanent disability occurs in approximately 10-20% of patients.

In the hands, the metacarpophalangeal (MCP), proximal interphalangeal (PIP), and thumb interphalangeal (IP) joints are involved most frequently. The distal IP (DIP) joints are involved only in the presence of coexisting MCP or PIP disease. Tenosynovitis (inflammation of tendon sheaths) causes a reduction in finger flexion and grip strength. Nodular thickening in the tendon sheath also may produce a trigger finger.

With progression of arthritis, deformities of RA become apparent. These include ulnar deviation of the fingers at the MCP joints, subluxation of the MCP joints, hyperextension of the PIP joint with flexion of the DIP joint (swan-neck deformity), flexion of the PIP joint with hyperextension of the DIP joint (boutonnière/button-hole deformity), Z-shaped deformity of the thumb from subluxation of the first MCP joint and compensatory hyperextension of the IP joint, and "finger drop" of the ring and little fingers resulting from rupture of the extensor tendons at the point of crossing the inflamed eroded ulnar styloid.

In the wrist, early stages of RA cause tenosynovitis of the extensor tendons, forming a swelling over the distal wrist. The ulnar styloid may become tender, which indicates inflammatory synovitis. The distal end of the ulna tends to sublux (dislocate) dorsally, and the carpal bones sublux anteriorly to the distal radius and ulna. The ulnar styloid erodes.

In addition, RA is a systemic disease and a number of important extraarticular manifestations have been identified. Fatigue, malaise, and weight loss are prominent features and may reflect disease activity.

MRI provides the most early and accurate assessment of erosion. Diagnostic ultrasound may have an important role as well.

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