Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit and remains one of the most prevalent dermatologic conditions worldwide. Although commonly associated with adolescence, acne can persist into adulthood or present for the first time later in life. The image presented illustrates severe inflammatory acne, characterized by numerous erythematous papules, pustules, and deeper nodular lesions involving the cheek and jawline. Such presentations are clinically significant due to their association with scarring, post-inflammatory hyperpigmentation, and substantial psychosocial impact.
Clinical Presentation
Severe inflammatory acne typically manifests as a combination of:
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Inflammatory papules: Firm, erythematous, tender lesions resulting from follicular inflammation
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Pustules: Papules containing visible purulent material
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Nodules: Large, deep, painful lesions extending into the dermis
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Diffuse erythema: Reflecting active inflammation of surrounding skin
In the image, the cheek shows dense clustering of pustules and papules, with background erythema and uneven skin texture, suggesting ongoing inflammation and a high risk of permanent scarring. The distribution over the cheek and jawline is typical of hormonally influenced acne, especially in adults.
Pathophysiology
The development of inflammatory acne is multifactorial and involves four primary pathogenic mechanisms:
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Follicular hyperkeratinization
Abnormal desquamation of keratinocytes leads to obstruction of the pilosebaceous unit and formation of microcomedones. -
Increased sebum production
Androgen-mediated sebaceous gland activity results in excess sebum, providing an ideal environment for bacterial proliferation. -
Cutibacterium acnes colonization
Formerly known as Propionibacterium acnes, this anaerobic bacterium contributes to inflammation by activating innate immune responses. -
Inflammatory cascade activation
Release of pro-inflammatory cytokines, including interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-α), and matrix metalloproteinases, leads to follicular wall rupture and dermal inflammation.
In severe cases, inflammation extends into deeper skin layers, resulting in nodules and cyst-like lesions, as seen in this presentation.
Differential Diagnosis
Conditions that may resemble severe inflammatory acne include:
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Acne conglobata – severe nodulocystic acne with interconnected abscesses
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Rosacea (papulopustular type) – lacks comedones and often involves flushing
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Folliculitis – usually uniform lesions centered on hair follicles
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Perioral dermatitis – typically spares the vermilion border
The presence of comedonal and nodular inflammatory lesions supports a diagnosis of severe acne vulgaris.
Complications
Untreated or poorly controlled severe acne may lead to:
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Atrophic scars (ice-pick, boxcar, rolling scars)
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Hypertrophic or keloid scars
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Post-inflammatory hyperpigmentation or erythema
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Psychological distress, including anxiety, depression, and reduced quality of life
Early recognition and aggressive management are essential to prevent irreversible sequelae.
Management Strategies
Treatment of severe inflammatory acne requires a multimodal and often systemic approach.
Topical Therapy
Adjunctive topical agents include:
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Topical retinoids (adapalene, tretinoin, tazarotene)
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Benzoyl peroxide to reduce bacterial resistance
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Topical antibiotics (used short-term and always combined with benzoyl peroxide)
Systemic Therapy
For severe disease, systemic treatment is usually indicated:
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Oral antibiotics (e.g., doxycycline, minocycline) for anti-inflammatory effects
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Oral isotretinoin, considered the treatment of choice for severe nodulocystic acne
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Hormonal therapy in appropriate patients, including combined oral contraceptives or anti-androgens
Supportive Care
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Gentle cleansers and non-comedogenic moisturizers
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Strict photoprotection to reduce post-inflammatory changes
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Avoidance of lesion manipulation to prevent scarring
Prognosis
With timely and appropriate treatment, severe inflammatory acne can be effectively controlled. However, delayed intervention increases the likelihood of permanent scarring. Long-term follow-up is often required, particularly in patients receiving systemic therapies such as isotretinoin.
Conclusion
Severe inflammatory acne vulgaris is a complex dermatologic condition with significant clinical and psychosocial implications. The image presented demonstrates active inflammatory disease with pustular and nodular lesions, underscoring the need for early, aggressive, and individualized treatment. A comprehensive understanding of acne pathogenesis and evidence-based management strategies is essential for optimizing outcomes and minimizing long-term complications.
