Immunohistochemical Expression of TGF-β1 in Keloids and Hypertrophic Scars

Abstract

Aberrant wound healing of skin injury may lead to 2 pathologic entities, termed keloids and hypertrophic scars (HS). There has been growing evidence suggesting a role for transforming growth factor beta (TGF-β) family members in the pathogenesis of fibrosis. The aim of the present work was to investigate the role of TGF-β1 in the pathogenesis of keloids and HS. TGF-β1 was analyzed on skin biopsies of 30 patients presenting with keloids (16) or HS (14) and 10 normal surgical scar and 10 age- and sex-matched normal subjects (controls). TGF-β1 was expressed in dermal fibroblasts, inflammatory cells, and endothelial cells of normal surgical scar (60%) and aberrant scar (86.7%) with an absence of statistical difference. Although it is expressed in 90% of epidermis of aberrant scar (diffuse expression) compared with 60% of normal surgical scar (basal layer expression) and 20% of normal skin biopsies (basal layer expression) with highly significant differences. Dermal TGF-β1 expression in aberrant scar lesions was significantly associated with lesions of shorter duration (P = 0.01) and older age group (P = 0.02). The intense dermal expression was also associated with lesions of shorter duration (P = 0.0001) and immature scars (P = 0.002). TGF-β1 is involved in the pathogenesis of both keloids and HS with maximum effect at early stages. Keratinocytes are not passive partners but rather may have an active role in the induction of fibrosis. Targeting of TGF-β1 may be of benefit if applied early and if directed against keratinocytes as an unusual target of therapy.