It has been suggested that altered joint loading may be a cause of the cartilage degeneration commonly observed following joint destabilizing events such as anterior cruciate ligament (ACL) injury [1]. Changes in the biochemical environment of the joint accompany these changes in joint loading, though, with acute and chronic increases in synovial concentrations of proinflammatory cytokines such as tumor necrosis factor-alpha (TNFα) [2, 3]. TNFα is a potent catabolic factor associated with increased expression [4] and synthesis [5] of matrix proteases in articular cartilage, and therefore may play in important role in the degenerative events following joint injury.

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