Osteoarthritis (OA) is a disease of unknown etiology that involves degeneration of articular cartilage, limited intraarticular inflammation manifested by synovitis, and changes in the subchondral bone. Mechanical, biochemical, and genetic factors contribute to the loss of joint integrity and the initiation and progression of cartilage destruction. Chondro-cytes, which are the unique cellular component of adult articular cartilage, react to structural changes in the surrounding cartilage matrix by responding to and producing catabolic cytokines and anabolic factors, which act in an autocrine-paracrine manner. Since the initial stages of OA involve increased cell proliferation and synthesis of matrix proteins, proteinases, growth factors, cytokines and other inflammatory mediators by chondrocytes, research has focused on the chondrocyte as the cellular mediator of OA pathogenesis. The adult articular chondrocyte, which normally maintains the cartilage with a low turnover of matrix constituents, has limited capacity to regenerate the normal cartilage matrix architecture, however, and damage becomes irreversible unless the destructive processes are interrupted. Interactions between the cartilage and the other cells and tissues of cartilage damage with the joint, including the synovium and subchon-dral bone, also contribute to pathogenesis in ways that are largely undefined. Thus, further understanding of the roles of cytokines and growth factors in the initiating events in cartilage destruction and in mediating interactions between the different joint tissues that influence disease progression is needed to develop new approaches that help prevent initiation or progression of OA.

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