The severity of the acne is directly related to the secretion of sebum - a higher rate causes more irritation of the duct and subsequently, increased keratin production. Release of pilosebaceous contents into the surrounding dermis triggers the inflammatory response. This may be further aggravated by the release of exo-enzymes from the anaerobic bacterium, Propionobacterium acnes, commonly found in large quantities in the sebaceous glands of susceptible patients.
Lesions result from obstruction of the pilosebaceous follicle due to increased production of the keratinised epithelium lining the duct. The cells become more cohesive and form an organised keratotic plug which seals off the duct. The plug may dilate the pilosebaceos orifice and be extruded onto the skin - the open comedo or blackhead; or the wall of the duct may rupture with release of the contents into the dermis - the closed comedo or whitehead (1).
Four pathophysiological processes occur to produce acne:
- androgen driven increase in sebum production
- blockage of the sebaceous follicle by keratin and sebum
- colonisation of the follicle with Propionibacterium acnes
Increased androgen production causes abnormal epithelial desquamation and follicular obstruction leading to formation of the microcomedone, the precursor lesion in acne, invisible to the naked eye.
- androgens also promote sebum production, causing the obstructed follicles
to fill with lipid rich material forming visible open and closed comedones
- the increased incidence at puberty may be associated with elevated levels of androgenic hormones which control the activity of the sebaceous glands
- hormonal levels are often normal in acne patients so that the condition may represent an over-responsiveness of the gland to normal hormone levels (1)
- in older patients, there may be an elevated testosterone level (1)
- sebum promotes bacterial growth, leading to proliferation of P acnes
- Propionobacterium acnes, commonly found in large quantities in the sebaceous glands of susceptible patients (1)
- releases chemicals that promote inflammation, propagated by traumatic rupture of comedones into the surrounding dermis (2)
- inflammation presents in the form of papules, pustules, nodules and cysts
- other local commensals - Staphylococcus epidermis and Pityrosporum ovale
- may have a pathogenic role (1)
- severity of the acne is directly related to the secretion of sebum - a higher rate causes more irritation of the duct and subsequently, increased keratin production (1)
Immune-mediated inflammatory process might involve CD4+ lymphocytes and macrophages that stimulate the pilosebaceous vasculature precede follicular hyperkeratinisation (3). Defective keratinocyte differentiation leads to comedo formation under the influence of androgens and changes in sebum lipids that induce interleukin-1 secretion. Sebaceous glands are also influenced by corticotrophin releasing hormone, which might mediate the link between stress and acne (2). Vitamin D also regulates sebum production, and insulin like growth factor might increase sebum through sterol-response element binding proteins. Oxidised lipids can increase keratinocyte proliferation and other inflammatory responses mediated by leukotriene B4. Matrix proteases in sebum also influence inflammation, cell proliferation, degradation of the dermal matrix, and treatment responsiveness (2)
Risk factors and genes associated with acne prognosis and treatment are unclear. Twin studies have pointed to the importance of genetic factors for more severe scarring acne (4,5)
Diet, sunlight and skin hygiene have been linked to acne, but there is little evidence relating to these (6)
The black colour of open comedones is oxidised melanin not dirt.
There is a significant dose dependent association between smoking and acne severity (7)
High serum dehidroepiandrosterone and increased insulin resistance might explain acne in polycystic ovary syndrome. Occlusion of the skin with greasy products can result in pomade acne; clothing and sweat can worsen acne. Anti-epileptics and some anticancer drugs (e.g. genfitinib) can produce acne, as can anabolic steroids. Dioxin exposure can cause severe comedonal acne (3).
Contributor: Dr Maryanne Hammon (GP; 24/3/2014)
- Clinical Knowledge Summaries 2006.Acne Vulgaris
- Williams HC, Dellavalle RP, Garner S. Acne Vulgaris. Lancet 2012;379:361-72
- Jeremy AH, Holland DB, Roberts SG, Thompson KF, Cunliffe WJ. Inflammatory events are involved in acne lesion initiation, J Invest Dermatol 2003;121:20-27.
- Ballanger F, BAudry P, Gyen JM, Khammari A, Dreno B. Heredity: a prognostic factor for acne.
- Dermatology 2006;212:145-149.
- Magin P, Pond D, Smith W, Watson A. A systematic review of the evidence for 'myths and misconceptions' in acne management: diet, face-washing and sunlight. Fam Pract 2005;22:62-70.
- Dawson A, Dellavalle RP. Acne Vulgaris. Clinical Review. BMJ 2013; 346:2634
Last reviewed 10/2021