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No evidence for follicular keratinocyte hyperproliferation in acne lesions as compared to autologous healthy hair follicles.

DOI: exd.13544  PMID: 29582469  

Abnormal hyperkeratinization in sebaceous hair follicles has long been believed to play an important role in acne pathogenesis. Several early reports purported to provide histological evidence for hyperproliferation of keratinocytes in acne lesions by showing a higher expression of the Ki67 as well as certain keratins. The evidence is, however, not robust and a number of methodological and technical pitfalls can be identified in these studies. In this study we looked at the expression of proliferation, mitosis and apoptosis markers directly at acne skin lesions in 66 patients with acne vulgaris. Ki67 was assessed using immunohistochemistry and ⍺-tubulin, phospho-histone H3 and cleaved-PARP with immunofluorescence microscopy. Allogenic unaffected hair follicles from the same acne patients were used as an internal control. In both acne and control hair follicles the α-tubulin staining was universal, approaching 100% cells and showed no signs of changed assembly. Expression of cleaved-PARP – the apoptosis marker was a rare event. Cell proliferation rate measured by the expression of Ki67 and phospho-histone H3 was virtually identical between acne and the two control groups. Our findings show the absence of increased keratinocyte proliferation in acne vulgaris. Alternative mechanisms are likely responsible for infundibular hyperkeratinization in acne pathogenesis. This article is protected by copyright. All rights reserved.

Persson G,  Johansson-Jänkänpää E,  Ganceviciene R,  Karadag AS,  Bilgili SG,  Omer H,  Alexeyev OA

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