Posttraumatic arthrosis after joint injury occurs as a result of the disruption of the matrix components and chondrocyte death. Matrix components can be disrupted by mechanical and enzymatic means, and proteoglycan loss also has been shown to occur after cartilage injury. Until recently, chondrocyte death has been thought to occur primarily as a result of necrosis. However, new evidence shows that chondrocyte apoptosis can be stimulated to occur as a result of mechanical injury. The role chondrocyte death plays in the development of posttraumatic arthrosis currently is unknown. The development of in vitro cartilage injury models has made it possible to investigate some of the effects of impact load (acute injury) on cartilage. In vivo models of cartilage injury have made it possible to investigate changes in the integrity of the matrix components and of the chondrocytes in response to injury with time. However, considerably more information regarding this process is necessary before improvements in the prevention and treatment of posttraumatic arthrosis can be developed.
