AIM: The proven ability of Mitomycin-C of inhibiting fibroblasts in vitro, has stimulated its use in research animals and in humans to control healing. The objective of this prospective experimental study was to follow the healing process of surgical wounds in the dorsum of rats treated topically with Mitomycin-C. It also evaluates the skin response to injections of different concentrations of this drug. STUDY DESIGN: Experimental. MATERIAL AND METHOD: Two distinct surgical wounds were made to the dorsum of ten adult rats, one of them received topical Mitomycin-C diluted at 0.5 mg/mL during 5 minutes and the other wound was used as a control. Three other rats were submitted to intradermal injections of Mitomycin C at different concentrations. The healing process of all three groups of rats was followed clinically and histologically after sacrificing the rats at different post-treatment periods. The degree of fibrosis was evaluated histologically by two distinct pathologists. RESULTS: Surgical wounds treated with Mitomycin-C presented delayed healing when compared to the untreated wounds, with remission of scabs 7 days after the control wounds. Histological analysis at one month post-treatment revealed a significant reduction in fibrosis of the wounds treated with Mitomycin-C when compared to the untreated wounds. After the third month the degree of fibrosis was comparable in both wounds. As for the injected dilutions, clinical and histological necrosis was proportional to the concentration (0.5; 0.1; and 0.05 mg/ml). The only concentration at which no necrosis was observed was 0.01 mg/ml. CONCLUSION: Topical Mitomycin-C delays the healing of surgical wounds in rats up to the forth week following treatment, but the degree of fibrosis is comparable in both wounds after 12 weeks. Its intradermal use cased necrosis only at high concentrations. In otolaryngology this characteristic of the drug may be useful in the treatment of external ear canal stenosis, coanal atresias, nasal cicatricial stenosis, laryngeal stenosis and keloids.
mitomycin-C; fibroblast inhibition
