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Adolescent acne: Etiological factors, clinical presentation, and pathophysiological pathways
*Acne vulgaris*, commonly referred to as "adolescent acne," represents one of the most prevalent dermatological conditions, affecting nearly the entire population at some point in life, with peak incidence during puberty. The disorder is clinically characterized by the presence of non-inflammatory comedones (both open and closed) alongside inflammatory lesions—such as papules, pustules, nodules, and cysts—predominantly localized to sebum-rich areas, including the face, back, and upper chest. The pathogenesis of acne is multifactorial, encompassing both endogenous and exogenous contributors. Key mechanisms include: **abnormal keratinization of the follicular infundibulum**, leading to pore obstruction and microcomedone formation; **excessive sebum secretion** driven by androgenic stimulation; **colonization and proliferation of *Cutibacterium acnes*** (formerly *Propionibacterium acnes*), which triggers an inflammatory cascade; and **the host immune response**, marked by the release of pro-inflammatory cytokines. Epidemiological data confirm that nearly 100% of individuals experience at least mild acne symptoms during adolescence, with disease severity modulated by genetic predispositions, hormonal fluctuations (e.g., elevated testosterone levels), and environmental influences (diet, stress, cosmetic products). Of particular note is **acne fulminans**, a rare but severe variant of adolescent acne, distinguished not only by cutaneous manifestations but also by systemic symptoms—including fever, myalgia, arthralgia, weight loss, and laboratory abnormalities (elevated erythrocyte sedimentation rate, leukocytosis).
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