Traumatic injury to a joint is known to increase the risk for the development of secondary osteoarthritis, but it is unclear how this process occurs. The existence of such a discrete event that can lead to an increased risk of osteoarthritis has spurred interest in developing in vitro models of traumatic joint injury. The current authors review some of the recent insights gained from these model systems into the pathogenesis of osteoarthritis, including the evidence for an initial, irreversible insult to chondrocytes during mechanical injury, the occurrence of apoptotic chondrocyte death, and attempts to identify the effects of trauma on chondrocyte metabolic response. Results also are presented from the authors' ongoing studies of the degradative pathways initiated by traumatic mechanical loads, the mechanism by which chondrocytes are affected during compression, and possible contributions of the joint capsule to posttraumatic cartilage degradation.