Acne Vulgaris

 Acne vulgaris is a chronic inflammatory disease of the pilosebaceous unit and remains one of the most common dermatologic conditions in adolescence, affecting over 80% of teenagers. The pathogenesis is multifactorial. During puberty, sebaceous glands become increasingly sensitive to rising androgen levels, which stimulate excess sebum production and promote follicular obstructions. Additional contributing factors include the use of steroids, ultraviolet exposure, mechanical occlusion from items such as sports gear or backpack straps, and the application of oil-based skin products. Dietary influences, such as high milk intake, as well as endocrine disorders, such as polycystic ovary syndrome, have also been associated with acne development. The relationship between body mass index and acne remains inconclusive, with conflicting findings across studies and the ongoing need for investigation.

A key microbiologic component of acne vulgaris is Cutibacterium acnes. C. acnes colonizes the pilosebaceous unit and contributes to inflammation via activation of innate immune pathways, stimulation of pro-inflammatory cytokines, and disruption of the follicular microenvironment.

Clinically, acne vulgaris presents with comedones, papules, pustules, and nodules involving the face, chest, back, and upper extremities. In Fitzpatrick I–II, inflammatory lesions appear bright red or pink, while open comedones containing dark keratinaceous material contrast sharply against the lighter surrounding skin, making erythema and inflammation readily appreciated. In Fitzpatrick III–VI, erythematous changes may be subtle or difficult to visualize, and inflammatory papules may blend into background pigmentation. In Fitzpatrick V–VI, the erythema presents more subtly and with less violaceous undertones. Because erythema is less visible in darker skin tones, the clinical severity of acne may be underestimated. In darker Fitzpatrick skin types, a primary visible concern is post-inflammatory hyperpigmentation (PIH), which results from increased melanin production following inflammation. PIH may appear more prominent than the inflammatory lesions themselves. The degree of hyperpigmentation varies by the depth of melanin deposition and individual skin type, and pigmentary alteration may persist even after active lesions resolve. Patients should be educated on this possibility.

Treatment for acne vulgaris is guided by disease severity, risk of scarring, and patient preference. First-line therapies include topical retinoids, which normalize follicular keratinization, and benzoyl peroxide, which reduces C. acnes proliferation. Topical or oral antibiotics may be employed for inflammatory acne. Combination formulations, such as retinoid and benzoyl peroxide or retinoid and antibiotic therapies, have demonstrated improved treatment efficacy in acne, and may be useful in minimizing inflammation that contributes to PIH in darker skin types. In our opinion, treatments to minimize pigmentary alterations as well as more aggressive early treatment is important to prevent, minimize and treat post inflammatory pigmentary disturbances. In darker Fitzpatrick skin types, agents such as azelaic acid are particularly beneficial, as they target both acne lesions and PIH. Additionally, irritant regimens should be introduced cautiously in Fitzpatrick IV–VI, as excessive irritation may worsen PIH. Counseling regarding rigorous photoprotection is essential, as ultraviolet exposure can also prolong or darken hyperpigmentation.

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