Fractional ablative laser therapy for the treatment of severe burn scars: A pilot study of the underlying mechanisms

Abstract

Ablative fractional resurfacing is clinically an efficient treatment for burn scar management. The aim of this pilot study was to investigate the poorly understood mechanisms underlying ablative fractional CO2 laser (AFL-CO2) therapy in relation to biomarkers S100 and 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). S100 stains for Langerhans cells and neuronal cells, potentially representing the pruritus experienced. 11β-HSD1 catalyses the interconversion of cortisol and cortisone in cells, promoting tissue remodelling. Immunohistochemical analysis of S100 and 11β-HSD1 protein expression in the dermis and epidermis of the skin was performed on normal skin, before and after AFL-CO2 therapy. Data assessing outcome parameters was collected concurrently with the skin biopsies. 13 patients were treated with AFL-CO2 therapy. Langerhans cells decreased by 39% after 2nd treatment. Neuronal cells were overexpressed before treatment in the scar tissue by 91% but levels returned to that resembling normal skin. 11β-HSD1 expression in keratinocytes was significantly higher after laser treatment compared to before in scar tissue (p <0.01). No clear correlation was found in dermal fibroblast numbers throughout the treatment course. Whilst the role of the explored mechanisms and their association with clinical outcomes cannot conclusively be stated, this pilot study demonstrates promising trends that encourages investigation into this relationship.

Keywords: 11β-HSD1; Ablative fractional CO(2) laser; Hypertrophic burn scars; Immunohistochemistry; S100; Scar resurfacing.