History ofjoint injury due to participation in SRE, particularly to the knee or hip, increases the risk of developing a chronic joint disease, osteoarthritis. 0A is one of the most common and widespread rheumatic diseases responsible for deterioration of articular cartilage, subchondral bone and synovium, ultimately leading to the failure of synovial joints. Experimental studies with animal models have sought to understand the association between acute joint trauma and the development of 0A. The research presented in the current thesis makes use of an in viva rabbit model to examine the acute and chronic responses of articular cartilage and subchondral bone to blunt force trauma. Chapter 2 addressed the issues of acute damage to chondrocytes following a single, severe insult to the flexed TF joint. Chapter 3 describes chronic studies where a single impact was again delivered to the TF joint of anesthetized rabbits and the changes in the mechanical and histological properties of the articular cartilage were evaluated six months and one year following trauma. Chapter 4 documented the development of an in vivo model of traumatic ACL rupture. Chapter 5 evaluated the efficacy of a mild nonionic surfactant, poloxarner 188 (P188), in ‘repairing’ damaged cells after an in vivo impact to the rabbit TF joint. Future studies can utilize the data presented to investigate the progression of chronic joint disease and the efficacy of various intervention methods.