Topical tamoxifen to prevent excessive scar tissue
I forget who posed the question recently about the possibility of using transdermal tamoxifen to prevent gyno, but after finding some time to read up on it, it turns out it has been used in a completely different application to prevent the development of disfiguring scar tissue. Evidently tamoxifen suppresses the secretion of TGF from fibroblasts, limiting their proliferation.

Br J Plast Surg 1998 Sep;51(6):462-9

Topical tamoxifen--a potential therapeutic regime in treating excessive dermal scarring?

Hu D, Hughes MA, Cherry GW.

Department of Dermatology, Churchill Hospital, Headington, Oxford, UK.

Abnormal dermal scarring which affects a large number of people is aesthetically disfiguring and can be functionally disabling. Existing medical and surgical strategies to prevent or to treat scars are frequently disappointing and more effective therapies are needed. Tamoxifen, which has been used extensively in the treatment of breast cancer over the last 20 years has recently been shown to inhibit the proliferation of fibroblasts cultured from keloid biopsies. Successful treatment of retroperitoneal fibrosis and desmoid tumours with tamoxifen has also been reported. We have investigated the potential of tamoxifen as an inhibitor of wound contraction, using fibroblast-populated collagen lattices as an in vitro model. From these studies we postulate that tamoxifen may have potential clinical significance in the treatment of abnormal scarring. Normal adult human skin fibroblasts were embedded within type I collagen, then medium either with or without addition of tamoxifen was added to the collagen lattices. Lattice diameters were measured at intervals to assess the influence of tamoxifen on the lattice contraction. The reversibility of the inhibitory effect of tamoxifen on lattice contraction was investigated by 'washing out the tamoxifen' at different time-points. To visualise changes in the morphology of fibroblasts MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] was added to the lattices. Tamoxifen at 1 and 5 microM had no significant influence on lattice contraction but higher concentrations of 50 and 100 microM completely inhibited contraction. At intermediate concentrations from 10 to 20 microM the degree of lattice contraction was dose-dependent. The reversibility of the inhibition was both dose- and time-dependent. Both the inhibition of contraction and the reversibility of inhibition appeared to correlate with changes in fibroblast morphology. The dose- and time-dependent inhibition of contraction by fibroblasts suggests that tamoxifen could be investigated as a novel potential therapeutic agent in treating abnormal dermal scarring.

Arch Facial Plast Surg 2001 Apr-Jun;3(2):111-4

Effect of tamoxifen on transforming growth factor beta1 production by keloid and fetal fibroblasts.

Mikulec AA, Hanasono MM, Lum J, Kadleck JM, Kita M, Koch RJ.

Division of Otolaryngology/Head and Neck Surgery, Stanford University Medical Center, 300 Pasteur Dr, Stanford, CA 94305-5328, USA.

BACKGROUND: Evidence suggests that keloid scar formation may be mediated, in part, by deranged growth factor activity, including that of transforming growth factor (TGF) beta1. 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 micromol/L). Cell counts were performed and supernatants collected at 24, 48, and 96 hours. Cell-free supernatants were quantitatively assayed for TGF-beta1 expression. RESULTS: Keloid fibroblasts show increased per-cell TGF-beta1 production compared with fetal fibroblasts. Tamoxifen appeared to decrease per-cell TGF-beta1 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-beta1 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-beta1.