THE feasibility of whole-joint transplantation as a means of replacement of destroyed joints has long intrigued surgeons interested in reconstruction. Although it has been shown that articular cartilage of autogenous whole joints appears to survive transplantation, it ultimately undergoes progressive destruction.1,2 While the sequence of changes has been studied extensively, the mechanism is not yet understood. It would be considerably more practical, if it were possible, to replace the destroyed joints with homografts, but even without the genetic factors of rejection, the autografts are not able to withstand the long-term effects of transplantation.
In previous experiments from this Department attempts have been made to analyze the factors contributing to the ultimate destruction of articular cartilage.1,3 The following have been considered as possible contributing factors: mechanical stress, disturbance of vascular and nerve supply, and alteration of synovial fluid. However, with whole-joint transplants it was not possible to differentiate the