Articular Cartilage and Osteoarthritis Research

Journal/Book: Z Rheumatol 1998; 57: 176. 1998;

Abstract: Klaus E. Kuettner Ph.D.; Department of Biochemistry Rush Medical College Chicago A consensus report of the 1996 NIH sponsored workshop "New Horizons in Osteoarthritis" defined the disease processes as "... a result of both mechanical and biologic effects that destabilize the normal coupling of degradation and synthesis of articular cartilage chondrocytes and extracellular matrix (ECM) and subchondral bone. Although they may be initiated by multiple factors including genetic developmental metabolic and traumatic osteoarthritic (OA) diseases involve all of the tissue of the diarthrodial joint. Ultimately OA diseases are manifested by morphologic biochemical molecular and biomechanical changes of both cells and matrix which lead to a softening fibrillation ulceration loss of articular cartilage sclerosis and eburnation of subchondral bone osteophytes and subchondral cysts ..." In early OA the cartilage seems to respond with imbalance between synthesis and degradation of macromolecules produced by the chondrocytes. Attempts by the chondrocytes to repair the damaged cartilage matrix and to replenish lost ECM components occur reflecting an attempted but gradually failing repair. A severe loss of ECM ensues based on a process called chondrocytic chondrolysis (chondrocyte mediated ECM breakdown) whereby select matrix metalloproteases degrade the ECM. Since OA is a non-inflammatory disease with rare inflammatory episodes fragments of components of the ECM may well be the driving force inducing catabolic events. The prevalence of symptomatic OA is higher in some joints e. g. the knee. It very rarely occurs in the ankle. Our investigations focus on a comparison of chondrocytes in normal articular cartilage from the knee and ankle joints of the same human donor obtained through the Regional Organ Bank of Illinois. ... le

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