What Causes Pimples: Sebum, Bacteria, and Inflammation

Acne vulgaris develops from four interacting factors:

1. Excess sebum production: Androgen-stimulated sebaceous glands secrete more oil, especially at puberty.
2. Follicular hyperkeratinization: Abnormal shedding of keratinocytes blocks the pilosebaceous unit → microcomedone.
3. Cutibacterium acnes proliferation: Anaerobic bacterium thrives in lipid-rich, occluded follicle; produces lipases, proteases, and biofilms.
4. Inflammation: C. acnes activates innate immunity (TLR2, NLRP3 inflammasome) → neutrophils, cytokines (IL-1, IL-17, TNF-α) → papules, pustules, nodules. Rupture spreads inflammation.

White blood cells (neutrophils) accumulate in the follicle, forming pus (pustules). Their enzymatic digestion of follicular wall leads to scarring.

Treatment Targets

• Retinoids (normalize keratinization).
• Benzoyl peroxide/antibiotics (reduce C. acnes).
• Anti-inflammatories (niacinamide, dapsone).
• Hormonal therapy (anti-androgens for females).