Osteoarthritis is defined largely as a disease of cartilage, since the chondrocytes, which constitute the unique cellular component of adult articular cartilage, are able to respond to mechanical injury, joint instability due to genetic factors, and biologic stimuli such as cytokines and growth and differentiation factors (Fig. 3.1). In young individuals without genetic abnormalities, biomechanical factors due to trauma are strongly implicated in initiating the OA lesion [95,114], and mechanical disruption of the association between chon-drocytes and matrix may lead to changed metabolic responses in the chondrocyte [6,82]. The aberrant behavior of OA chondrocytes is reflected in the appearance of fibrillations, matrix depletion, cell clusters, and changes in quantity, distribution, or composition of matrix proteins . In the early stages of OA, a transient increase in chondrocyte proliferation is associated with increased synthesis of cartilage matrix proteins. This is often interpreted as a repair response. At the same time, there is increased synthesis of the catabolic cytokines and matrix-degrading enzymes. Local loss of proteoglycans and cleavage of type II collagen occur initially at the cartilage surface. This results in an increase in water content
Mechanical injury Hereditary factors Aging_
Repetitive injury Subchondral bone changes
Imbalance in cytokine/growth factor expression, activity and signaling
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