Metabolic studies in early experimental osteoarthritis (OA) have shown that the rate of proteoglycan synthesis in the diseased articular cartilage may be markedly enhanced relative to normal; elevated rates of synthesis were however accompanied by increased release of new molecules from the tissue so that the response was apparently non-reparative. Described here are experiments with immature and mature chondrocytes in culture which show that aging of chondrocytes in vivo is accompanied by a marked fall in the capacity of these cells to synthesize link protein and to assemble a proteoglycan-rich matrix. It is suggested that poor deposition of proteoglycan by mature chondrocytes in OA may result from insufficient synthesis of link protein for stabilization of aggregates.