Transforming Growth Factor-? Effect on Soft Tissue Repair

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Abstract
Previous studies have demonstrated that TGF-beta possesses many of the biologic properties necessary for acceleration of the normal wound healing process. We report that recombinant human TGF-beta 2 (rhuTGF-beta 1) increases wound strength and accelerates wound closure when applied topically to experimental wounds. Doses of 5 to 1,000 ng/wound increased wound strength in a dose-response manner and wound strength increase as high as 161% above control in the rat incisional wound model. Increased wound strength was observed as early as 3 days following rhuTGF-beta 1 application and continued to Day 28. In the rabbit ear ulcer model, acceleration of wound closure was observed following doses of 5 to 100 ng/wound applied a single topical application. No adverse effects of rhuTGF-beta 1 were observed. The amount of fibrous tissue, scar formation, and mitotic figures were not significantly greater than control. Epithelialization of rhuTGF-beta 1-treated wounds was not impeded. rhuTGF-beta 1 induced bone formation in the rabbit ear ulcer model but not in the rat incisional model, suggesting that precursor cells, such as perichondrial cells, are required for the bone forming activities of TGF-beta 1.