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Rapid degeneration of the anterior cruciate ligament (ACL) has been observed following acute ACL rupture. An understanding of this process might explain some of the poor clinical results of primary ACL repair. We created a surgical rabbit model of acute ACL injury and developed an in vitro assay for collagenase activity in the ACL and menisci. Microscopic evaluation revealed a rapidly degenerative process in injured ACLs, with loss of cellularity and matrix organization. This was associated with a significant increase in collagenase activity and a decrease in total collagen of the injured ACLs as compared with sham-operated controls. These findings confirm the observation that cut ACL ligament ends rapidly degenerate. This degenerative process might be partly due to a response of cells intrinsic to the ACL to injury. Left unchecked, this process may be detrimental to surgical attempts for primary ACL repair.

The purpose of this study was to investigate the results or rib perichondrial grafting after the creation of a full thickness articular cartilage defect. In a rabbit model, rib perichondrium was used to repair defects created in the femoral condyle. The formation of repair tissue (neocartilage) and its chondrogenesis into a tissue resembling articular cartilage was found over time. The gross, histological and biochemical characteristics of the neocartilage were evaluated at intervals of 6, 12, 18, 26 and 52 weeks post transplant, and compared to normal articular cartilage. The neocartilage was characterized by the early formation of relatively large amounts of glycosaminoglycans. A steady increase in the proportion of type II collagen over the time periods was also observed. Improved attachment of the neocartilage to host tissues was seen over the period of 6 to 52 weeks. Successful grafts were seen to proliferate to fill the articular defect and to undergo a chondrogenesis over a post transplant time period of one year.

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