The sequence of inflammation, relevant biomarkers, and the pathogenesis of acne vulgaris: what does recent research show and what does it mean to the clinician?

Abstract

Acne vulgaris (AV) remains one of the most common skin disorders seen in dermatology practices worldwide. Despite an abundance of publications, AV continues to be a formidable therapeutic challenge due to its complex pathogenesis and chronicity. Regarding the sequence of AV lesion formation, the traditional model teaches that the primary lesion is the microcomedone, a subclinical lesion caused by follicular hyperkeratinization. From the microcomedone, visible AV emerges with development of comedonal ("noninflammatory") and inflammatory lesions. Research published over the past decade has provided information about inflammatory mechanisms that warrant us reconsidering the traditional model of AV pathogenesis. More specifically, there is evidence that specific cascades of inflammation occur early during the initial subclinical formation and visible emergence of AV lesions, later during progression, and finally during resolution including scarring. It has also been shown that subclinical inflammation occurs before or concurrently with microcomedone formation. This article reviews an updated model of acne lesion development and its progression based on a literature review that highlights the role of inflammatory mediators, cellular infiltration patterns, and expression of receptors that signal specific immunologic and inflammatory responses. Clinical relevance related to this updated model is also addressed.