Ligament injuries commonly lead to persistent disability and may result in degenerative joint arthritis. Surgical reconstruction of damaged ligaments have relied on the use of expendible host dense connective tissues from another site. These " autograft" reconstructions have been complicated by reduced post-operative strength and excessive laxity,, occasionally leading to recurrent symptomatic instability of the involved joint.
Abnormal graft loading at the time of ligament reconstruction has been suggested as a potential cause for post-operative graft weakening and abnormal graft laxity. After developing an animal model and appropriate methods to investigate the importance of graft loading, I studied the effects of this variable on subsequent graft healing over time. Adequate external control groups were developed for comparative purposes. My results showed that ligament autografts placed at abnormally reduced loads were mechanically inferior to normal or excessively loaded grafts at twelve weeks. This tensioning effect, however, was no longer present by 48 weeks post- operatively. These results suggest that normal or excessive graft tensioning at the time of surgery should result in improved early post-operative graft performance.
The second potentially important variable, which I chose to study, was graft cell viability. This has special relevance to allograft ligament reconstructions (tissue donated by another individual) where immune rejection has been a problem. Since the graft cells are thought to be the primary focus of rejection, it was postulated that acellular or " dead" grafts would be less immunogenic, and possibly could improve the results of ligament allografts. It was unknown, however, whether killing these intrinsic graft cells would impair graft healing. I therefore investigated the extremes of graft cell viability - "viable" or " dead" in a non- immunologic autograft model of ligament transplantation. I used a freezing protocol which had previously been shown to make ligament cells largely metabolically inactive. After investigating possible mechanical effects of the provocative freezing protocol immediately after treatment, we studied the effect of this freezing technique over time.
Although only subtle differences in the mechanical behaviour of the fresh and frozen- thawed ligaments were present initially, my results showed that marked differences were present after twelve weeks of graft healing and persisted over time. The "dead", frozen- thawed grafts, were mechanically inferior to the " alive", fresh grafts, at all healing intervals. This suggests that preserved graft cell viability at the time of autograft ligament transplantation yields improved results.