Articular cartilage, which makes possible the painless, low-friction movement of synovial joints, consists of a sparsely distributed population of highly specialized cells called chondrocytes that are embedded within a matrix and provide articular cartilage with remarkable mechanical properties. Chondrocytes form the tissue matrix macromolecular framework from three classes of molecules: collagens, proteoglycans, and noncollagenous proteins. The matrix protects the cells from injury resulting from normal joint use, determines the types and concentrations of molecules that reach the cells, acts as a mechanical signal transducer for the cells, and helps maintain the chondrocyte phenotype. Throughout life, articular cartilage undergoes internal remodeling as the cells replace matrix macromolecules lost through degradation. Aging decreases the ability of chondrocytes to maintain and restore articular cartilage and thereby increases the risk of degeneration of the articular cartilage surface. Progressive degeneration of articular cartilage leads to joint pain and dysfunction that is clinically identified as osteoarthritis. Investigation regarding the pathogenesis of posttraumatic osteoarthritis, the form of osteoarthritis that develops following joint injury, is helping to explain the development and progression of joint degeneration.