Acne (from the Greek word acme, meaning “peak”) is an inflammatory disorder involving the pilosebaceous unit and results from the complex interplay of genetics, hormonal influences, innate and acquired immunity, and other environmental factors. Presentations range from comedones, papules and pustules, to cysts and scars. It is most prevalent in adolescents, affecting nearly 85% of young people between ages 12-24 years.

Acne has an equal sex incidence and tends to affect women earlier than men; although, the peak age for clinical acne is 18 years in both sexes. The incidence is higher in twins and those with a family history of acne.1 Globally, acne accounts for about 16% of the dermatologic disease burden.2 Treatments are designed to target as many pathogenic factors as possible to achieve disease control.

 

A variety of factors influence the pathogenesis of acne including:

    • Hormonal influences on sebum production and composition. Androgens produced locally in the sebaceous glands and androgen receptors found in the basal layer and sheath of the follicle are responsive to testosterone and DHT. Increased serum DHEAS levels in prepubescent children are associated with an increase in sebum production.3

 

    • Colonization with the bacterium Propionibacterium acnes. P. acnes is considered one of the normal colonizers of the skin, but can still illicit an innate inflammatory response dermatologically. It is a gram-positive, anaerobic rod found within the sebaceous follicle. Although it is found in increased numbers in acne patients, its density on the skin does not correlate with clinical severity.4

 

    • The effects of the local release of inflammatory mediators (e.g. cytokines, prostaglandins). Inflammation is seen early in acne lesion formation shown by an increased number of CD4+ T cells and IL-1.5 Included in an acne lesion are keratin, sebum, P. acnes, and cellular debris, which significantly intensify inflammation.

 

  • Resultant microanatomical changes in the pilosebaceous unit (e.g. ductal hyperkeratosis). A hyper-keratotic plug and bottleneck structure, often called a microcomedo and later comedo, are formed when corneocytes accumulate due to an increase in proliferation and cohesiveness of follicular cells. These skin changes result in the peaks seen with acne and further exacerbate the inflammatory and sebaceous accumulation process.

 

Pathogenesis of Acne

Picture adapted from Dermatology, Fourth Edition Copyright © 2018 Elsevier, Inc

 

Proper education of patients will ensure a successful therapy regimen.

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References:

  1. Ghodsi SZ, Orawa H, Zouboulis CC. Prevalence, severity, and severity risk factors of acne in high school pupils: a community-based study. J Invest Dermatol 2009; 129:2136–41.
  2. Karimkhani C, Dellavalle RP, Coffeng LE, et al. Global skin disease morbidity and mortality: an update from the global burden of disease study 2013. JAMA Dermatol 2017; 153:406–12.
  3. Lucky AW, Biro FM, Huster GA, et al. Acne vulgaris in premenarchal girls. An early sign of puberty associated with rising levels of dehydroepiandrosterone. Arch Dermatol 1994; 130:308–14.
  4. Leyden JJ, McGinley KJ, Mills OH, Kligman AM. Propionibacterium levels in patients with and without acne vulgaris. J Invest Dermatol 1975; 65:382–4.
  5. Jeremy AHT, Holland DB, Roberts SG, et al. Inflammatory events are involved in acne lesion initiation. J Invest Dermatol 2003; 121:20–7.

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