Abstract

Objectives: TGF-beta is a growth factor that stimulates the production of extracellular matrix molecules and reduces inflammation. Diabetes is characterized by a delay in periodontal tissue healing. Therefore, it is tempting to speculate whether TGF-beta activity is altered during diabetic wound healing. In the present study we have analyzed the regulation of TGF-beta activity, the development of inflammation and the amount of wound closure and connective tissue regeneration in gingivectomies performed in type I diabetic and non-diabetic rats. Methods: Type I diabetes was induced in Sprague Dawley rats by injecting streptozotocin and periodontal wounds were created in the upper gingiva. Wound healing was evaluated histologically at 2, 5, 7 and 14 days through H/E staining and immunohistochemistry for pSmad2 and cell nuclei (DAPI). Collagen was evaluated through Red Sirius staining. The amount of inflammatory infiltrate was quantified at each time point. Epithelial migration was evaluated by morphometric assessment using image J. Statistical analysis was performed using the student’s t test. Results: Epithelial cell migration was delayed and a reduction in connective tissue healing was observed in diabetic rats when compared to non-diabetic animals. At two days post wounding inflammatory infiltrate was increased in nondiabetic rats. However, the amount of inflammatory infiltrate was increased at 5, 7 and 15 days in the diabetes group when compared to the non-diabetic rats. Smad2 phosphorylation was decreased in the diabetic group at 5 and 7 days when compared to its control. Conclusions: Delayed wound healing in diabetes is associated an increase in the inflammatory infiltrate. The delayed regeneration in connective tissue can be explained by a decrease in pSmad2 activation. Further studies are needed to identify critical pathways in the regulation of pSmad in diabetic wound healing.