Pre and Post Mechanical Trauma Treatment Studies to ‘Save’ Chondrocytes

INTRODUCTION: Post -traumatic arthritis is one of the most common causes of secondary osteoarthritis (OA). While the mechanisms leading to a posttraumatic OA are currently not well understood, in acute experiments severe traumatic insults to chondral and osteochondral explants have documented both extensive cartilage matrix damage and chondrocyte death. These in vitro tissue damages closely resemble in vivo animal experimental data that exhibit chronic development of early stage joint disease. Intriguingly, chondrocyte death alone in an in vivo animal study results in early stage joint disease after 12 months. These studies suggest that preservation of chondrocyte viability and functionality in a joint may be a significant factor in the potential mitigation of a posttraumatic OA. Severe blunt trauma to chondral explants results in acute necrosis of chondrocytes. While the mechanisms of chondrocyte death are largely unknown, severe blunt mechanical loading of joint cartilage likely results in the development of large shear stresses and excessive deformation of chondrocytes. Post -trauma administration of a nonionic synthetic surfactant, poloxamer 188 (P188), has previously been shown to rescue chondrocytes from necrotic death in severe, mechanically traumatized chondral explants. 7 Interestingly, the biotechnology literature suggests that this amphiphilic tri-block polymer also exhibits the ability to mechanically strengthen animal cell plasma membranes and prevent damage caused by agitation and sparging in suspension cultures. 8 The hypothesis of the current study was that pre-treatment of chondral explants with P188 surfactant would strengthen the plasma membrane of chondrocytes and alter the degree of necrosis that develops in the initial 24 hours following a severe blunt impact trauma to joint cartilage.