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Background Female patients undergoing arthroscopic anterior cruciate ligament reconstruction with hamstring tendon graft developed increased post-operative laxity compared to male and female patients who had been reconstructed using patellar tendon graft.
Hypothesis Supplementary tibial fixation in female patients will reduce laxity.
Study Design Prospective, randomized, double-blinded clinical trial.
Methods Fifty-six female patients divided into two groups (standard tibial fixation versus supplementary staple fixation) were followed for 2 years.
Results After 2 years the mean side-to-side difference utilizing KT-1000 arthrometer manual maximum measurements was 1.8 mm (standard group) and 1.1 mm (staple group) (p=0.05). A Grade 0 Lachman test was present in 63% of the standard group and 86% of the staple group (p=0.04). Kneeling pain was experienced by 7% of the standard group and 29% of the staple group (p=0.05).
Conclusions Supplementary tibial fixation in female patients undergoing ACL reconstruction with hamstring tendon graft and interference screw fixation with a single screw size significantly improves laxity measurements and clinical stability assessment 2 years postoperatively. However, this is at the cost of increased kneeling pain.
Statement of purpose: To study the biology of tendon – bone integration in human hamstring tendon autograft at the femoral tunnel interface
Methods: A total of 70 patients undergoing revision anterior cruciate surgery for both traumatic and atraumatic injury were studied. All surgery was performed under the supervision of the senior author. At time of surgery tissue was taken from the residual graft and femoral tunnel. The demographics of the original surgery, mechanism of failure, patient characteristics were recorded. We have also recorded variables such as tunnel positioning, early rehabilitation, associated ligamentous laxity. Local ethical committee approval has been granted. The specimens were analysed for gross evidence of cell necrosis, macrophage and fibroblast ingrowth (H&
E). Vascularity was quantified by multiple high powered field counting. The influence of makers of cell turnover and matrix degradation have been determined by cell staining for TIMP-1, -2 and –3 (Immunohistochemistry) and early correlations drawn between the histological findings and patient factors such as mechanism of reinjury. We have also examined the graft expression of receptors of IGF1, FGF, MMP-1, 7, 8, 11, and 13 as key markers of collagen remodelling.
Results: We have found novel expression of MMP-13 in collagen graft tissue. There is clear evidence in a subgroup of certain patients exhibiting aggressive vascular ingrowth in association with IGF and MMP-11 and −13 expression suggesting a possible regulatory process. Areas of poor cellularity appear to exhibit low levels of MMP-13 but moderate levels IGF-II suggesting an alternative cellular response to graft fixation at the femoral tunnel. There appear to be distinct subgroups of cellular response in patients with atraumatic failure.
Conclusion: This is the first study to the biology of ACL graft failure at the bone tendon interface in a human model. Previous work has been case reports or using a canine model. These have limited application to the clinical work. We have found clear evidence of a processs of graft – host bone integration through neovascularisation. There is evidence of the graft remodelling through local expression of collagen resorptive agents. This work is being extended to look at the role of exogenous factors in augmenting graft integration at the host site.
