BACKGROUND:In terms of the histocompatibility, immune rejection and scar formation after repair, acel ular nerve al ograft is closer to autologous nerve cel s. At present, hyaluronic acid has been applied for autologous peripheral nerve repair;however, research on the nerve al ograft is rarely reported.
OBJECTIVE:To explore the effect of hyaluronic acid on the anastomotic scar in acel ular nerve al ograft repair of rat sciatic nerve defect.
METHODS:Thirty-six Sprague-Dawley rats were randomly divided into three groups (n=12 per group). The rat model of nerve defect of 10 mm was established by cutting the sciatic nerve of the left hind leg and then given nerve al ograft combined with the injection of hyaluronic acid at anastomosis (experimental group), only nerve al ograft (control group) and autologous nerve graft (nerve autograft group), respectively. Afterwards, the healing of the proximal anastomosis was observed and scar components were assessed.
RESULTS AND CONCLUSION:Gross observations showed that the rat skin and muscle fascia had no significant differences in healing among groups, while the surrounding tissue adhesion in the experimental group was milder than that in the control group (P<0.05). Masson staining found that col agen deposition in the epinerium could be observed in each group. In the experimental group, a smal amount of col agen fibers arranged orderly in the epineurium;in the control group numerous col agen fibers accumulated and arranged irregularly;in the nerve autograft group, sparse epineurial col agen fibers appeared in an order arrangement. The gray value of col agen type I in the experimental group was higher than that in the control group (P<0.05), while the gray value of col agen type III was lower than that in the control group (P<0.05). No significant differences were found in the sum gray values of col agen type I and III among groups (P>0.05). These findings indicate that in the peripheral nerve repair, hyaluronic acid abrogates the scar formation by increasing the deposition of col agen type III and reducing the deposition of col agen type I.