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Anthony A. Mikulec, MD; Matthew M. Hanasono, MD; Joanne Lum, BS; James M. Kadleck; Magdalena Kita; R. James Koch, MD, MS

Arch Facial Plast Surg. 2001;3:111-114.

Background  Evidence suggests that keloid scar formation may be mediated, in part, by deranged growth factor activity, including that of transforming growth factor (TGF) ß₁. Tamoxifen citrate has shown promise in the treatment of keloids.

Objective  To evaluate the effect of tamoxifen on autocrine growth factor expression in keloid and fetal dermal fibroblasts, which exhibit scar-free healing.

Design  Serum-free cell lines of keloid and fetal dermal fibroblasts were established. Cell cultures were exposed to different concentrations of tamoxifen solution (8 and 12 or 16 µmol/L). Cell counts were performed and supernatants collected at 24, 48, and 96 hours. Cell-free supernatants were quantitatively assayed for TGF-ß₁ expression.

Results  Keloid fibroblasts show increased per-cell TGF-ß₁ production compared with fetal fibroblasts. Tamoxifen appeared to decrease per-cell TGF-ß₁ production at each of the time points evaluated.

Conclusions  Keloids likely arise due to locally insufficient or excessive concentrations of specific growth factors. The higher level of TGF-ß₁ produced by keloid cells compared with fetal fibroblasts could be related to the aberrant wound healing seen with keloids. The addition of tamoxifen may lead to improved wound healing in keloids by decreasing the expression of TGF-ß₁.

From the Wound Healing and Tissue Engineering Laboratory, Division of Otolaryngology/Head and Neck Surgery, Stanford University Medical Center, Stanford, Calif.

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