ABSTRACT
Pathology RA is characterized by both extravascular immune complex disease and disordered cell-mediated immunity producing chronic inflammation, granuloma formation and joint destruction. There is an initial synovitis, with infiltration by T-lymphocytes, plasma cells and macrophages followed by hypertrophy of the synovium and pannus formation. The pannus spreads across the joint surface, destroying the underlying cartilage and subchondral bone. Bone erosions occur earliest at the sites of synovial reflection. The joint capsule and its associated ligaments are progressively weakened by the inflammatory process. Muscles adjacent to affected joints atrophy. The result is progressive destruction of the joint with instability and subluxation. Subcutaneous ‘rheumatoid’ nodules, with characteristic central fibrinoid necrosis and granulomata, occur over bony prominences in 20% of cases.
