Fractional Ablative Laser Therapy for The Treatment Of Severe Burn Scars: A Pilot Study Of The Underlying Mechanisms

Mr Stewart Ross1,3, Ms Josephine Malcolm2,3, Dr Joanneke Maitz2,3, Dr Yiwei Wang2,3, Prof Peter Maitz2,3,4, Dr Zhe Li2,3,4, Dr Andrea Issler-Fisher2,3,4

1Faculty of Engineering, University of Sydney, Camperdown, Australia, 2Burns Unit, Concord Repatriation General Hospital, Concord, Australia, 3Burn Injury and Reconstructive Surgery Research Group, ANZAC Research Institute, Concord, Australia, 4Concord Clinical School, University of Sydney, Concord, Australia

Abstract:

Ablative fractional resurfacing is clinically a very efficient treatment modality for burn scar management. The aim of this pilot study was to investigate the currently poorly understood mechanisms underlying ablative fractional CO2 laser (AFL- CO2) therapy in relation to two particular biomarkers, S100 and 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). S100 stains for Langerhans cells (LCs) in the epidermis and neuronal cells in the dermis, potentially representing the pruritus experienced by patients. 11β-HSD1 catalyses the interconversion of active cortisol and inactive cortisone in cells, potentially modulating the proliferation of keratinocytes and fibroblasts, promoting tissue remodelling.

In this study, immunohistochemical analysis of S100 and 11β-HSD1 protein expression in the dermis and the epidermis of the skin from human skin biopsies was performed on normal skin, before and after AFL-CO2 therapy.

We recruited 8 patients who were treated with AFL-CO2 therapy. LC population decreased by 39% after 2nd treatment compared to after 1st treatment. Dermal neuronal cells were overexpressed before treatment in the scar tissue by 91% but levels returned to that resembling normal skin after successive AFL-CO2 therapy. 11β-HSD1 expression in keratinocytes was significantly higher after laser treatment compared to before in scar tissue (p<0.01), an area increase from 16% of the epidermis to 59%. 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 further research to investigate this complex relationship


Biography:

Stewart is currently studying at the University of Sydney completing a combined degree of Biomedical Engineering (Hons.) and Medical Science majoring in physiology. Stewart worked as a Summer Intern at the Burns Injury and Reconstructive Surgery Research Group in 2020/2021, the results of the project he will be presenting. Stewart is currently in the final year of his studies working on an honours project investigating the thrombogenicity of ePTFE using a microfluidic design.

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