Objectives: Scar formation is the one of critical issues for patients who undergo surgical procedures. Repair of cleft lip in infants and youths often results in severe scar formation. It is well known that TGF-beta signaling is involved in wound healing. Specifically, TGF-beta signaling mediator Smad3 affects the quality of scar formation. The effect of Smad2, however, is unknown in the process of wound healing. In this study, we hypothesized that Smad2 has specific affect for the process of wound healing. Methods: K14-Smad2 transgenic mice which overexpress Smad2 under the control of K14 promoters, were used in this study. We made 1 cm full-thickness incisional wound on the dorsal skin of 4 week-old mice. Samples were collected at 3, 5, and 7 days following surgery. Histological and immunohistochemical analyses were done to compare the wound healing process between the wild type and K14-Smad2 transgenic mice. Results: The quality of wound healing in K14-Smad2 mice was poor at 7 days post surgery. The basal cell layer along with the basement membrane was not visible in the K14-Smad2 mice. The failure of basal cells to cover the wound region was likely due to their migration defect. Instead, the suprabasal layer of epithelial cells migrated into the wound region in the K14-Samd2 mice. Statistical analysis revealed that the re-epithelization was delay in K14-Smad2 mice when compared to the one of the wild type littermate (P<0.05). Conclusion: These results suggest that Smad2 affects the ability of keratinocytes migration in the early stage of wound healing and influences the quality of wound healing. Supported by R01 NIDCR, NIH.

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