A biomechanical analysis of passive-motion induced reparative monkey articular cartilage was undertaken to investigate the hypothesis that such a treating modality is effective for biological resurfacing of large full-thickness defects. An interspecies comparisons study was also performed to apply the results from this and other studies of animal models to the understanding of human cartilage.

In situ biphasic creep indentation experiments were performed in high and low-weight bearing knee femoral cartilage from five species to examine if anatomical and functional differences correspond to analogous variations of the intrinsic material properties. The results indicate that major differences exist in some of the material properties among species and sites within the same joint. In all species tested except rabbit, the patellar groove has the lowest aggregate modulus, smallest Poisson's ratio and iargest permeability. These material properties lead to the hypothesis that in an incongruent articulation (e.g., patello femoral joint), greater and faster compression occurs under load to satisfy lubrication requirements.

For the healing study, osteochondral defects were created in the high and low weight regions of the condyles and the patella of cynomolgus monkey knee joints. The animals were then treated for two weeks with either intermittent passive motion (IPM) or cast immobilization. Some defects exhibited remarkable repair based on gross examination, while others showed little or no repair at all. Joints subjected to passive motion did not heal any better than immobilized joints. To obtain the intrinsic material properties of the healed tissue in situ, optimization techniques were used coupled with finite element methods based on the linear KLM biphasic theory. It was found that normal monkey cartilage is four times stiffer than healed tissue. This study rejected the conjecture that large osteochondral defects in monkey knee joints can be managed more effectively with passive motion than with IPM.

Finally, a hypothesis was examined that a steep stiffness gradient in the underlying subchondral bone may be an initiating mechanism of osteoarthritis. Using a finite element analysis, it was shown that physiologic stiffness gradients in the subchondral bone do not affect the stress fields in cartilage.