Acne Vulgaris

Acne is an inflammatory disorder of the pilosebaceous unit, driven by four primary pathophysiological factors.

The Four Pillars of Pathogenesis

Understanding acne requires examining the chronological cascade of events within the follicle.

1. Follicular Hyperkeratinization

The normal desquamation (shedding) of keratinocytes within the follicle is disrupted. Cells cohere, forming a microcomedo—the invisible precursor to all acne lesions.

2. Increased Sebum Production

Driven primarily by androgens (specifically dihydrotestosterone or DHT) binding to receptors on sebocytes, the sebaceous glands enlarge and increase lipid output. The altered composition of this sebum (lower in linoleic acid) further promotes comedogenesis.

3. Proliferation of Cutibacterium acnes

C. acnes (formerly P. acnes) is a normal commensal bacterium that thrives in the anaerobic, lipid-rich environment of a blocked follicle. Its overgrowth triggers an immune response.

4. Inflammation

C. acnes metabolizes sebum triglycerides into pro-inflammatory free fatty acids and releases chemotactic factors, drawing neutrophils to the site and resulting in the inflammatory papules and pustules characteristic of clinical acne.

Treatment Modalities