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Corinna Wicke, MD; Betty Halliday; Daniel Allen, MD; Nanette S. Roche, MS; Heinz Scheuenstuhl; Martin M. Spencer, MD, PhD; Anita B. Roberts, PhD; Thomas K. Hunt, MD

Arch Surg. 2000;135:1265-1270.

Hypothesis  Anti-inflammatory corticosteroids significantly impair wound healing. Retinoids partially, but significantly, reverse this effect. Little is known about the mechanism of steroid retardation or retinoid reversal. We hypothesized that corticosteroids lower transforming growth factor- (TGF-) and insulin-like growth factor-I (IGF-I) levels and tissue deposition in wounds and that retinoids stimulate corticosteroid-impaired TGF- and IGF-I release and collagen production.

Design  Randomized controlled trial.

Setting  Wound healing research laboratory.

Participants  Animal study.

Interventions  Four wire mesh wound cylinders were implanted subcutaneously into the backs of 72 male Sprague-Dawley rats. Wound healing was impaired by a single subcutaneous injection of 6 mg of methylprednisolone acetate (Depo-Medrol). Two preparations of retinoids were used in separate experiments: all-trans-retinoic acid and 9-cis-retinoic acid that were fed orally.

Main Outcome Measures  Hydroxyproline content was measured in the healing tissue and TGF- and IGF-I levels were analyzed in the wound fluid.

Results  Methylprednisolone treatment significantly decreased TGF- and IGF-I levels in the wound fluid and hydroxyproline content in the tissue (P<.05). Oral all-trans- and 9-cis-retinoic acid partially reversed the TGF- and IGF-I decrease and significantly increased hydroxyproline content toward normal levels (P<.05). Oral all-trans-retinoic acid enhanced collagen deposition, TGF- and IGF-I levels over normal chow fed control animals (P<.05).

Conclusions  Steroids and retinoids have antagonistic effects on growth factors and collagen deposition in wound healing. These effects can be relevant for treatment options in a clinical setting.

From the Departments of Surgery, University of Tübingen, Tübingen, Germany (Dr Wicke), University of California, San Francisco (Ms Halliday, Mr Scheuenstuhl, and Dr Hunt); Division of Plastic Surgery, University of California, Davis (Dr Allen); Laboratory of Cell Regulation and Carcinogenesis National Cancer Institute, Bethesda, Md (Drs Roche and Roberts); and the Laboratory of Growth and Development, Davies Medical Center, San Francisco (Dr Spencer). The authors have no commerical, proprietary, or financial interest in the products and companies described in this article.

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