Improvement of flexor tendon reconstruction with carbodiimide-derivatized hyaluronic acid and gelatin-modified intrasynovial allografts: study of a primary repair failure model.

摘要

BACKGROUND: Tendon grafts play an important role in flexor tendon reconstruction. This study was an investigation of the effects of surface modification of allograft intrasynovial tendons with carbodiimide-derivatized hyaluronic acid and gelatin in an in vivo canine model. To mimic the actual clinical situation, a novel and clinically relevant model of a failed primary flexor tendon repair was used to evaluate the flexor tendon grafts. METHODS: Twenty-eight flexor digitorum profundus tendons from the second and fifth digits of fourteen dogs were lacerated and repaired in zone II in a first-surgery phase. The dogs were allowed free active motion postoperatively. In a second phase, six weeks later, the tendons were reconstructed with use of a flexor digitorum profundus allograft. In each dog, one graft was treated with carbodiimide-derivatized hyaluronic acid and gelatin (the CHG group) and the other was treated with saline solution, as a control. The dogs were restricted from free active motion, but daily therapy was performed beginning on postoperative day 5 and continued until six weeks after the operation, when the animals were killed. The outcomes were evaluated on the basis of digit work of flexion, gliding resistance, healing at the distal attachment, graft cell viability, histological findings, and findings on scanning electron microscopy. RESULTS: In the first phase, all twenty-eight repaired tendons ruptured, with scar and adhesion formation in the repair site. Six weeks after allograft reconstruction, the mean work of flexion was 0.37 and 0.94 N-mm/degree in the CHG group and the saline-solution control group, respectively; these values were significantly different (p < 0.05). The gliding resistance in the CHG group was also significantly less than that in the saline-solution control group (0.18 versus 0.28 N) (p < 0.05), but no difference between groups was observed with regard to the distal tendon-bone pullout strength. Histological analysis showed that tenocytes in the host tendon proliferated and migrated toward the acellular allograft. CONCLUSIONS: This primary repair failure model was reproducible and reliable, with a uniform failure pattern, and provides an appropriate and clinically relevant animal model with which to study flexor tendon reconstruction. The surface modification of allografts with carbodiimide-derivatized hyaluronic acid and gelatin improved digital function and tendon gliding ability.