Atrophic acne scar is a persistent sequela from acne and is undesirably troubling to many patients because of its cosmetic and psychosocial aspects. Although some reports have emphasized the role of early inflammatory responses in atrophic acne scarring, growing perspectives on the detailed pathogenic processes are promptly needed.

A study by Moon J. et al. examined the histological, immunological, and molecular changes in early acne lesions susceptible to atrophic scarring to provide new insights into understanding the pathophysiology of atrophic acne scar.

They experimentally validated several early fundamental hallmarks for the transition of early acne lesions to atrophic scars by contrasting molecular profiles of skin and acne lesions between patients prone to scar (APS) or those not (ANS).

They observed devastating degradation of elastic fibers and collagen fibers in the dermis, followed by their incomplete recovery APS, compared with ANS. They also noticed abnormally excessive inflammation mediated by innate immunity with T helper 17 and T helper 1 cells and significantly decreased epidermal proliferation. Transforming growth factor (TGF)-β1 was substantially more in APS, indicating aberrant TGF-β1 signaling to be an underlying modulator of all of these pathological processes.

This study′s results may provide a foundation for understanding the pathogenesis of atrophic acne scarring. Reduction of excessive inflammation and TGF-β1 signaling in early acne lesions may promote the protection of normal extracellular matrix metabolism and, eventually, prevent atrophic scar formation. 

Moon J, Yoon JY, Yang JH, Kwon HH, Min S, Suh DH. Atrophic acne scar: a process from altered metabolism of elastic fibers and collagen fibers based on transforming growth factor-β1 signaling. Br J Dermatol. 2019 Dec;181(6):1226-1237. Doi: 10.1111/bjd.17851. Epub 2019 Jul 9. PMID: 30822364.