The limitation in the healing response of the anterior cruciate ligament (ACL) are well recognized. Several hypotheses have been proposed to explain why this tissue fails to heal, including mechanical retraction of the ends, and nutritional deprivation resulting from a limited blood supply. Others propose that synovial fluid may exert a deleterious effect on repair, because of proteolytic enzymes which may be harmful to immature proliferating cells and matrix at the repair site. It is presently believed that the failure of ACL repair is most likely the result of a multifactorial process. In contrast, we have demonstrated intrinisic repair of flexor tendon in the flexor tendon sheath when intermittent passive motion is utilized. The healing occurs more rapidly and with greater strength than with traditional techniques which permit tissue ingrowth from the tendon sheath of the immobilized digit. The tendon sheath environment is seemingly as """"""""hostile"""""""" as that of the ACL, with similar limitations of blood supply and nutrition in both cases. Why is intrinsic healing so effective in the case of tendon, but so limited in the case of the ACL? Our laboratory has recently developed a model of ACL injury which demonstrates healing in a reproducible manner. We have also developed a new methodology which standardizes biomechanical testing of the ACL. These will be valuable tools in understanding the biology of this ligament. These advances will be incorporated into a multidisciplinary investigation involving histological, biochemical, biomechanical and nutritional studies. ACL repair rate and repair quality will be compared to those of the medial collateral ligament, a ligament with a soft tissue environment. In light of the fact that passive motion was useful in flexor tendon healing, the influrence of past-injury activity on ACL healing will also be studied. We have also demonstrated successful ACL reconstruction in rabbits, and plan a multidisciplinary study of the natural history of ACL autografts of patellar tendon origin. We have shown that these autografts undergo a gradual metamorphosis, acquiring histological and biochemical properties very similar to normal ACL with time. These advances in model development will allow a detailed study of the healing and reconstructed ACL and should provide valuable insight as to the most appropriate treatment for injuries of this ligament.
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