The Use of Corticosteroid for Scar Management
The International Advisory Panel on Scar Management recommended the use of intralesional steroid injections for the treatment of hypertrophic scars (1). Corticosteroids were proved to induce scar regression through many different mechanisms. Firstly, they suppress inflammation by inhibiting leukocyte and monocyte migration and phagocytosis (2). Second, they are powerful vasoconstrictors, thus reducing the delivery of oxygen and nutrients to the scar bed (2). Third, they have an antimitotic effect that inhibits keratinocytes and fibroblasts, slowing reepithelialization and new collagen formation. Furthermore, they may reduce plasma protease inhibitors, thus allowing collagenase to degrade collagen.
Corticosteriods also induces a significant plunge in alpha-1-antitrypsin and alpha-2-macroglobulin levels, which tend to be greater in scar tissue and are natural inhibitors of collagenase in human skin (3). Corticosteroids affect fibroblast proliferation and production capabilities and are responsible for their degeneration. Moreover, decreased levels of TGF-β, insulin-like growth factor-1 (IGF-1) and hydroxyproline were found in scar tissues treated with methylprednisolone (4).
(1) Mustoe TA, Cooter RD, Gold MH, et al; International Advisory Panel on Scar Management. International clinical recommendations on scar management. Plast Reconstr Surg. 2002;110(2):560–571.
(2) Roques C, Tèot L. The use of corticosteroids to treat keloids: a review. Int J Low Extrem Wounds. 2008;7(3):137–145.
(3) Leventhal D, Furr M, Reiter D. Treatment of keloids and hypertrophic scars: a meta-analysis and review of the literature. Arch Facial Plast Surg. 2006;8(6):362–368.
(4) Carroll LA, Hanasono MM, Mikulec AA, Kita M, Koch RJ. Triamcinolone stimulates bFGF production and inhibits TGF-beta1 production by human dermal fibroblasts. Dermatol Surg. 2002;28(8):704–709.
