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      Tools & Reference>Dermatology

      Acne Vulgaris

      Updated: Aug 26, 2025
      • Author: John Samuel Barbieri, MD, MBA; Chief Editor: William D James, MD  more...
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      Overview

      Background

      Acne vulgaris is a common chronic inflammatory skin disease of the pilosebaceous unit (hair follicles and their accompanying sebaceous gland). It is characterized by comedones (see the image below), inflammatory papules and pustules, and deeper nodules and cysts. Acne vulgaris typically affects the areas of skin with the densest population of sebaceous follicles (eg, the face, the upper part of the chest, and the back). Facial involvement is most common, but approximately half of those with acne will have involvement of the chest or back as well. [1]  

      Acne, grade I; multiple open comedones. Acne, grade I; multiple open comedones.
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      In addition to the aforementioned lesions, local symptoms of acne vulgaris may include pain, tenderness, or erythema. Systemic symptoms are most often absent in acne vulgaris. In rare but severe cases, acne vulgaris could lead to acne conglobata, with highly inflammatory nodulocystic acne and interconnected abscesses. Acne fulminans can present with systemic symptoms, such as fever, joint pain, and general malaise. Additionally, acne vulgaris may have substantial psychosocial effects. [2, 3, 4]

      Acne vulgaris is a clinical diagnosis, based on the history and physical findings (see Presentation). However, laboratory testing (see Workup) may be indicated in the following situations:

      • Polycystic ovarian syndrome (PCOS) [5]  
      • Cases where long-term antibiotic treatment is ineffective or where improvement gained with antibiotics is not maintained

      Treatment of acne vulgaris should be directed toward the known pathogenic factors, including follicular hyperproliferation, excess sebum, Cutibacterium acnes (formerly Propionibacterium acnes), and inflammation. The most appropriate treatment is based on the grade and severity of the acne, as well as patient preferences. Available therapies include topical and systemic pharmacotherapy, various procedures, and dietary and nutritional strategies. (See Treatment.)

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      Pathophysiology

      Acne develops from the following four factors [6] :

      • Follicular epidermal hyperkeratinization with subsequent plugging of the follicle
      • Excess sebum production
      • Presence and activity of the commensal bacterium C acnes
      • Inflammation  

      Follicular hyperkeratinization involves increased keratinocyte proliferation and decreased desquamation, leading to sebum- and keratin-filled microcomedones. [7]  Androgens can also contribute to follicular hyperkeratinization. [8]

      Sebum production and excretion are regulated by a number of different hormones and mediators. In particular, androgen hormones (eg, testosterone and dehydroepiandrosterone sulfate [DHEAS]) promote sebum production and release. [9] The degree of acne in prepubertal girls correlates with circulating levels of DHEAS. [10, 11]  Insulin growth factor (IGF)-1 can also stimulate sebaceous gland activity and may explain the relationship between a high-glycemic-index diet and acne. 

      C acnes is an anaerobic organism present in acne lesions. It contributes to inflammation by producing proinflammatory mediators and activating Toll-like receptor 2 (TLR2) on monocytes and neutrophils. [12] Activation of TLR2 then leads to the production of multiple proinflammatory cytokines, including interleukin (IL)-8, IL-12, and tumor necrosis factor (TNF). [13]  Certain strains of C acnes (eg, phylotype IA) are associated with the development of acne, whereas others (eg, II and III) are more often found in healthy skin. [14, 15]

      Both innate and adaptive immune responses have an important role in acne pathogenesis. C acnes stimulates proinflammatory cyotokines (eg, TLR2 and IL-1β). T helper 17 (Th17) cells also play a central role in acne pathogenesis. IL-17 is increased in acne lesions, which results in recruitment of neutrophils and monocytes that contribute to inflammation. However, Th17 cells can also produce IL-10, which can decrease inflammation, as well as antimicrobial molecules (eg, T-cell extracellular traps), which can be protective against acne. [16]  

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      Etiology

      The main underlying cause of acne is a genetic predisposition. Acne is highly heritable in a polygenic manner, with some studies estimating that approximately 80% of the variability in acne risk is explained by genetics. [17, 18]  In addition, other aggravating factors are recognized, including the following:

      • Occlusive cosmetic agents and hair pomades [19]
      • Medications, including steroids, testosterone, epidermal growth factor receptor (EGFR) inhibitors, Janus kinase (JAK) inhibitors, lithium, phenytoin, and halogens (iodides and bromides) [20]
      • Congenital adrenal hyperplasia (CAH), PCOS, and other endocrine disorders associated with excess androgens may trigger the development of acne vulgaris; in addition, acne often worsens during pregnancy [21]
      • Mechanical occlusion with headbands, headphones, back packs, helmets, shoulder pads, or other clothing [22]
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      Epidemiology

      Acne is the most common skin condition in the United States, affecting as many as 50 million Americans annually and affecting an estimated 80-90% of the US population at some point during their lives. [23, 24] Acne affects approximately 85% of adolescents.

      Acne is more common among males in adolescence and among females in adulthood. Approximately 50% of women will experience acne in their 20s and 30-40% in their 30s; approximately 25% of adult women with acne will not have had acne during adolescence (adult-onset acne). [25] Approximately 40% of men will experience acne in their 20s and 20% in their 30s. [23]

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      Prognosis

      Although acne can often be managed with available treatments, it may cause long-lasting and detrimental psychosocial and physical effects. It is associated with depression and anxiety, particularly among those with more severe disease. In addition, acne may cause permanent scarring and long-lasting dyspigmentation. [26]

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      Patient Education

      Because many acne treatments can be complicated by side effects such as dryness and irritation, it is important to educate patients regarding appropriate use of these treatments, as well as strategies for mitigating their side effects. In addition, it is crucial to inform patients that most treatments take at least 8-12 weeks to yield results. Patience and consistency are essential for successful treatment.

      For patient education resources, see the Skin Conditions and Beauty Center, as well as Acne.

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