Osteoarthritis is a painful and debilitating disease characterized by progressive degenerative changes in the articular cartilage and other joint tissues. Biomechanical factors play a critical role in the initiation and progression of this disease, as evidenced by clinical and animal studies of alterations in the mechanical environment of the joint caused by trauma, joint instability, disuse, or obesity. The onset of these changes after joint injury generally has been termed posttraumatic arthritis and can be accelerated by factors such as a displaced articular fracture. Within this context, there is considerable evidence that interactions between biomechanical factors and proinflammatory mediators are involved in the progression of cartilage degeneration in posttraumatic arthritis. In vivo studies have shown increased concentrations of inflammatory cytokines and mediators in the joint in mechanically induced models of osteoarthritis. In vitro explant studies confirm that mechanical load is a potent regulator of matrix metabolism, cell viability, and the production of proinflammatory mediators such as nitric oxide and prostaglandin E2. Knowledge of the interaction of inflammatory and biomechanical factors in regulating cartilage metabolism would be beneficial to an understanding of the etiopathogenesis of posttraumatic osteoarthritis and in the improvement of therapies for joint injury.