[The pathogenesis of joint destruction in chronic polyarthritis]

Abstract

Joint destruction, a hallmark of rheumatoid arthritis, is described with respect to different mechanisms: destruction by inflammatory cells of the synovial fluid, pannus tissue and even ischemic bone necroses. Destruction via the synovial fluid is due to polymorphonuclear neutrophils (PMN) that can invade the pannus-free cartilage surface. In the absence of anti-proteases as a result of direct contact between the PMN and cartilage, enzymatic degradation can occur. Pannus tissue usually develops from the synovial insertion. Increased cellular proliferation in this area leads to a superficial pannus tissue that covers the cartilage (Fig. 4b); granulation tissue from the synovial insertion can destroy cortical bone and invade the subchondral tissue. The problem of isolated subchondral inflammatory foci is briefly discussed. The effector cells of cartilage destruction are identified as macrophages, PMN, and mast cells -cells that produce or activate destructive enzymes. Bone destruction is due to osteoclasts and even macrophages. Acute destruction via the granulation tissue may be followed by defect healing-scar tissue or chondroid metaplastic tissue can be present in the final stages of the disease. Ischemic bone necrosis leading to pseudocysts may also contribute to joint destruction.