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THE aetiology of rheumatoid arthritis remains unknown, though much is known about the immunopathogenic mechanisms involved in joint destruction [1]. Although a systemic disease, it primarily attacks synovial joints. The synovial membrane becomes an organized lymphoid tissue suggesting a chronic hypersensitivity reaction to an exogenous or self antigen [2]. The primary site of joint destruction is the articular cartilage, and yet it may also be the tissue responsible for driving the immune response as, once it is destroyed, the synovitis usually subsides within that joint. This suggests that inciting exogenous antigens or autoantigens may be sequestered within the cartilage framework.

AUTOANTIBODIES TO CARTILAGE COLLAGENS IN RHEUMATOID ARTHRITIS. DO THEY PERPETUATE THE DISEASE OR ARE THEY IRRELEVANT?