Osteoarthritis is the leading cause of disability in the United States, associated with joint pain and loss of mobility of an increasing proportion of the population. The disease erodes and disrupts the articular surface, which when healthy provides a low-friction, load-bearing, wearresistant surface for articulation in joints. Osteoarthritis is most frequently idiopathic, but also results from traumatic joint injury. An understanding of the link between joint injury and the degeneration of articular cartilage and potential for protecting the articular surface depends on an understanding of both the biological and mechanical responsiveness of articular cartilage to injury. This thesis investigates this link, exploring the frictional behavior of articular cartilage and how it responds to mechanical and biochemical damage.