Osteoarthritis is a joint disease characterized by cartilage degeneration and progressive disability. Excessive loading may lead to osteoarthritis via chondrocyte death. Much of the research on chondrocyte death has either been on tissue explants or impact loading in vivo. Little attention has been paid to the effects of in vivo muscle contractions on cartilage, even though chondrocyte death has been seen in tissue explants loaded to physiologically relevant stresses.

To explore the relationship between muscle loading and chondrocyte death, we developed an in vivo model system for applying impact and muscular loading (single maximal and repetitive submaximal) to the patellofemoral joint of the ACL-intact and ACL-deficient rabbits and we assessed cell death across the joint surfaces via confocal microscopy.

Maximal muscle contraction lead to greater chondrocyte death in the femoral groove cartilage (7.7±2.6% versus 1.2±0.4% in controls). Maximal muscle contraction plus impact did not lead to more chondrocyte death than an impact load alone (17.2±4.7% versus 22.5±4.5% for the femoral groove and 9.4±4.1% versus 14.4±4.3% for the patella). Repetitive submaximal muscle loading killed chondrocytes in both the retropatellar(10.7±3.5%) and femoral groove cartilage(6.7±2.5%) and made both surfaces more susceptible to cell death from subsequent impact loading(41.4±6.4% versus 14.4±4.3% in the patella and 44.6±13.9% versus 22.5±4.5% in the femoral groove). With interesting implications to cartilage damage after joint injuries, there was a shift in the cartilage cell death response (from femur to patella) in ACL-deficient joints subjected to impact loading (21.3±6.4% patella, 8.3±2.9% femoral groove) as compared to cartilage in normal impact loaded joints (12.6±2.7% patella, 17.5±3.3% femoral groove). A similar shift from femur to patella was seen in joints in which pressure-sensitive film was placed between the joint surfaces before impact. These results are consistent with the hypothesis that tensile overloading of the collagen network contributes to chondrocyte death. The differences in cell death between the femoral groove and the retropatellar cartilage may be do to their differing material properties and differences between ACLx and non-ACLx joints may be do to preferential weakening of the collagen in the patella. Further work will be required to define these mechanisms.