Traumatic injury has been shown to cause osteoarthritis. A mature bovine articular cartilage explant system was developed to evaluate the effects oftraumatic (30 or 40 MPa) and physiological (15 MPa) loads compared to cytokine treatment. Proteoglycan (PG) and nitric oxide (NO) release, as well as cell death, were evaluated. In all ofthe experiments, impacted explants were found to have minimal NO release compared to controls, while in cytokine treatments, interleukin-1B (IL-1) and lippopolysaccharide (LPS), were significantly elevated. Proteoglycan release was minimal in cytokine treatments but varied with load and rate for impacted treatments. Proteoglycan release in the 30 MPa slow (1 sec) load was found to be the greatest, while the lower and faster rate of 15 MPa and 50 msec did not produce the same significant response. Glucosamine-sulfate was used to pre-treat the impacted samples, and found to have no significant effect on cell death, NO or PG release, which is contrary to its ability to inhibit cytokine-induced cartilage degradation. Cell death was increased for all impacted treatments with significant cell death at 30 MPa slow and a trend for greater cell death with higher loads and longer rates of loading. Cytokine treatments gave minimal cell death. Analysis for apoptosis following acute traumatic impact, revealed no significant increase in apoptosis compared to controls. Acute 30 MPa load at slow rate of impact caused necrosis ofthe chondrocytes and degradation ofthe matrix, while cytokine treatment caused increased NO production.