ABSTRACT
Etiopathologic evaluations of arthritis have implicated multiple processes regulating cartilage degradation, including genetic predisposition, aging, and immunologic, endocrine, biochemical, and biomechanical mechanisms. The cartilage degradation in rheumatoid arthritis appears to take place both at the synoviocar-tilage junction and on the free surface of cartilage. Neutral metalloproteinases and other degradative proteinases appear to play a central role in the cartilage destruction and inflammation associated with arthritis. Recently, several potent synthetic inhibitors were described for the aminophenylmercuric acetate-activated form of proteoglycan- and collagen-degrading metalloproteinases obtained from Interleukins-1 stimulated chondrocytes. Tissue inhibitor of metalloproteinase may be useful in the control of arthritis and other diseases in which metalloproteinases are increased. A network of interactions between cells, cellular factors, and matrix components appear to be involved in the destructive process that occurs in arthritis. In the early stages of osteoarthritis, cartilage is usually hypermetabolic and further stimulation may not be required.
