Clinical studies of traumatic joint injury often document early pain and development of chronic diseases, such as osteoarthritis (OA). Various studies from the literature suggest that OA can be initiated by cell death that occurs in articular cartilage during mechanical trauma to the joint. The current study investigates chondrocyte cell death following blunt trauma and the roles of apoptosis and necrosis. TUNEL analysis was used to determine that a small degree of apoptotic cell death was observed in bovine chondral explants 48 hours following blunt impact. In previous studies on chondral explants from our laboratory it was observed that 30 — 4O % of the cells die in the first 24 hours following this same mechanical insult, therefore it was concluded that necrosis, rather than apoptosis, must be the primary mechanism of cell death. A nonionic surfactant, Poloxamer 188 (P188), was explored as a potential tool for early intervention into the disease process, as this surfactant has been shown to repair damaged cell membranes in other cell types. Bovine cartilage explants were treated with P188 following trauma and showed a significant decrease in the amount of cell death versus explants not treated with P188. When explants pre-treated with P188 were compared with those pre-treated and post—treated following trauma, it was determined that the posttreatment of cartilage with P188 had a greater effect than pre-treatment. In these studies, P188 was found to have a greater effect at lower levels of impact stress than at higher levels of trauma. Finally, the effectiveness of P188 was investigated in the in vivo