ARTICULAR CARTILAGE HEALING AND PASSIVE MOTION

关节软骨紊乱致残的人比其他任何群体都多

Disorders of articular cartilage disable more people than any other group of musculoskeletal problems. Any treatment that improves repair of articular cartilage would be invaluable. Reports that continuous passive motion (CPM) promotes healing of 1 mm diameter full thickness defects in rabbit articular cartilage have stimulated use of CPM to promote chondrogenesis in humans. However, the value of CPM in treatment of defects that closely resemble clinical problems in humans has not been demonstrated and our preliminary studies did not show a positive effect of PM in healing three types of 4 mm diameter defects in primate articular cartilage. The aims of this investigation are to: 1) verify previous reports that CPM facilitates cartilage healing; and to determine: 2) if defect size affects the healing of articular cartilage treated with CPM; 3) if the healing induced by CPM (24 hours of PM per day) differs from the healing induced intermittent passive motion, IPM, (16 hours of PM per day); and 4) if healing of articular defects treated with PM or casting is the same in rabbits and cynomolgus monkeys whose knees more closely resemble human knees. To confirm previous reports, assess the importance of defect size, and compare CPM and IPM, 1 mm and 3.2 mm diameter full thickness defects will be made in rabbit weight bearing femoral articular surfaces and treated with CPM, IPM or casting. To evaluate the effects of PM in joints that more closely resemble human knees, 1 mm diameter and 3.2 mm diameter drill hole defects will be made in the articular surfaces of primates and treated with cast immobilization or IPM and compared with the results of the rabbit experiments. Cartilage repair will be evaluated by a new morphologic-histochemical index of cartilage repair tested for reliability and based on the sequence of events in cartilage injury and repair. The validity of the index will be assessed by comparing the index values with the biochemical composition of the repair cartilage. Information gained from this study will enhance our understanding of the role of PM in the healing of articular defects that more closely resemble clinically significant defects in humans. If this study shows that PM facilitates articular cartilage healing, proposals will be developed to study the effect of PM in other types of articular cartilage defects and in animal models of osteoarthritis and to explore the basic mechanism of the PM effect on chondrogenesis.