The Role of the Skin Microbiota in Acne Pathophysiology

S. Ramasamy; E. Barnard; T.L. Dawson Jr; H. Li

Disclosures

The British Journal of Dermatology. 2019;181(4):691-699. 

In This Article

Acne Vulgaris

Acne vulgaris (commonly called acne) is one of, if not the, most common chronic skin disorders. It is a disease of the pilosebaceous unit, most often starting in early adolescence, causing pain, disfiguring lesions and scarring, along with other negative physiological and psychological effects on patient well-being and self-esteem, particularly in youth.[1–3] Clinical features of acne include seborrhoea, noninflammatory lesions (microcomedones and comedones), inflammatory lesions (papules, pustules, nodules and cysts) and, in severe cases, scarring.[1] Primarily affecting sebaceous regions, acne can be distributed across the face, neck, upper chest, shoulders, and back, varying in degree with the number and size of pilosebaceous units.

Although acne is common, the aetiology of the disorder remains unclear, and has long been considered multifactorial. Changes in the hair follicle and the sebaceous gland, collectively referred to as the pilosebaceous unit, are implicated in acne onset.[4] Acne lesions are thought to arise as a result of excess sebum production, pore hyperkeratinization and abnormal growth of lipophilic anaerobic bacteria such as Cutibacterium acnes (formerly referred to as Propionibacterium acnes), resulting in overcolonization and follicle blockage, and subsequent inflammation.[5–7] There remains significant confusion and controversy regarding the name of this ubiquitous and historic organism, so throughout this review we will refer to it using the new name, C. acnes. Acne development stages are not known to be sequential and it is not clear which stage precedes which, or how these stages are interconnected. Equipped with advances in sequencing technologies, recent research efforts have focused on microbiome-level DNA-based involvement in acne pathogenesis.[8–13]

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