Acne — Causes, Types, Grading & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit (the hair follicle and associated sebaceous gland), characterised by comedones (blocked follicles — blackheads and whiteheads), papules, pustules, nodules, and cysts. It is the most common skin disorder worldwide, affecting approximately 85% of adolescents aged 12-24 and persisting into adulthood in 15% of women and 8% of men. Adult acne (onset or persistence after 25 years) disproportionately affects women and is often hormonally driven. Acne predominantly affects the face (95%), back (60%), and chest (15%) — body regions with high sebaceous gland density. Beyond physical manifestations, acne causes significant psychological morbidity — depression, anxiety, reduced self-esteem, and social withdrawal — that is often disproportionate to physical disease severity. Early and effective treatment prevents scarring (which can be permanent) and preserves long-term psychological wellbeing.

Acne involves four key pathogenic processes occurring in the pilosebaceous unit: sebum overproduction (stimulated by androgens — DHEA-S and testosterone — acting on sebaceous glands; sebum provides substrate for Cutibacterium acnes growth and contributes to comedone formation); follicular hyperkeratosis (abnormal proliferation and reduced shedding of follicular epithelium — blocks the follicle ostium forming microcomedones — the precursor to all acne lesions); Cutibacterium acnes (C. acnes — formerly Propionibacterium acnes — colonises the anaerobic, lipid-rich follicular environment; activates toll-like receptors and triggers the innate immune inflammatory cascade); and inflammation (inflammatory cytokines — IL-1, IL-17, TNF-alpha — drive the progression from microcomedo to papule, pustule, and nodule). Hormonal factors: androgens stimulate sebum production — explains acne onset at puberty, premenstrual flares, adult female acne, and association with PCOS. Genetics: strong familial clustering. Aggravating factors: occlusive cosmetics and skincare products (comedogenic), high-glycaemic diet (dairy and refined carbohydrates — modest but real association), certain medications (systemic corticosteroids, lithium, androgens, certain anticonvulsants), and friction or pressure from sports equipment (acne mechanica).

Non-inflammatory (comedonal) acne: open comedones (blackheads — dilated follicle filled with oxidised sebum and keratin; the dark colour is from melanin oxidation, not dirt) and closed comedones (whiteheads — follicle blocked with trapped sebum; no surface opening). Inflammatory acne: papules (raised, solid, erythematous, up to 5 mm), pustules (elevated lesions with visible purulent centre), nodules (deep, large, painful, solid lesions — more than 5 mm; high scarring risk), and cysts (fluctuant, deep, pus-filled lesions; often coalesce — risk of significant scarring). Acne grading: mild (predominantly comedones with few papulopustules — affecting only the face); moderate (extensive papulopustules on the face, possibly some truncal involvement); severe (widespread papulopustules plus nodules/cysts, or acne involving the face, back, and chest; significant risk of scarring). Post-inflammatory hyperpigmentation (PIH): flat, dark marks that persist for months after lesions resolve — more prominent in darker skin tones. Acne scars: atrophic (ice pick, rolling, boxcar), hypertrophic, or keloidal — result from inadequate collagen remodelling after follicular rupture and inflammation.

Acne is diagnosed clinically based on the pattern of lesion types, distribution, and clinical history. No routine investigations are required for typical acne in adolescents. Investigations to consider in adult female acne with other signs of hyperandrogenism (irregular periods, hirsutism, weight gain): free and total testosterone, DHEAS, LH:FSH ratio, fasting glucose and insulin (polycystic ovary syndrome — PCOS); thyroid function. Microbiological swabs: if atypical presentation or concern about gram-negative folliculitis (which can complicate long-term antibiotic use — presents with sudden worsening with mainly pustular lesions around the nose). Acne conglobata: very severe, interconnected nodular cysts with sinus tracts — predominantly in males; may require systemic investigation. Acne fulminans: acute severe inflammatory acne with systemic features (fever, arthralgia, weight loss, elevated ESR/CRP) — rare; requires systemic corticosteroids before isotretinoin. Differential diagnoses: rosacea (adult, central face, erythema, telangiectasia — no comedones), folliculitis (uniform follicular pustules, often on trunk — usually from Staphylococcus or Malassezia), perioral dermatitis, sebaceous hyperplasia.

Mild acne (comedonal or mild inflammatory): topical retinoid (adapalene 0.1-0.3% or tretinoin 0.025-0.05% — normalises follicular keratinisation, prevents microcomedo formation; apply at night; start every other day and build up to avoid irritation) combined with topical benzoyl peroxide (2.5-5% — antibacterial, reduces C. acnes resistance, comedolytic; use in the morning). NICE recommends combining a topical retinoid with topical benzoyl peroxide as first-line for all types of acne. Moderate acne: add a combined hormonal OCP (for women — combined OCP with a low-androgenic progestogen: Dianette/co-cyprindiol, Yasmin; reduces sebum production and androgen effect; typically effective within 3-6 months); or short-course topical antibiotic (clindamycin or erythromycin — only for 12 weeks maximum due to antibiotic resistance; never as monotherapy — always with benzoyl peroxide). Oral antibiotics (doxycycline 100 mg daily or lymecycline 408 mg daily): for moderate acne with significant inflammation — 12-week maximum; always co-prescribe with topical benzoyl peroxide to prevent resistance development. Severe and nodulo-cystic acne: oral isotretinoin (Roaccutane, 0.5-1 mg/kg/day for 16-24 weeks cumulative dose 120-150 mg/kg) — the only treatment targeting all four pathogenic factors; highly effective with long-term remission in 80-90% of patients; teratogenic (mandatory pregnancy prevention programme in women of childbearing potential — iPLEDGE in USA, Pregnancy Prevention Programme in UK); side effects include dryness, elevated triglycerides, and rare psychiatric effects. Post-inflammatory hyperpigmentation: topical azelaic acid 15-20%, niacinamide, glycolic acid, and SPF daily — prevent further hyperpigmentation from UV exposure.

Acne vulgaris carries significant physical and psychological complications that can persist long after the active inflammatory lesions resolve. Scarring: permanent scarring is the most serious physical complication, affecting 30-40% of patients with moderate-to-severe acne. Subtypes include: ice-pick scars (deep, narrow, pitted depressions — most common in comedonal-dominant acne), rolling scars (broad, shallow, wave-like depressions from subcutaneous fibrotic bands), boxcar scars (broad, defined edges), and hypertrophic or keloid scars (raised, overgrown scars — more common in darker skin tones and the trunk). Post-inflammatory hyperpigmentation (PIH): flat, darkened macules persist for months to years after inflammatory lesions, particularly in patients with Fitzpatrick skin types IV-VI; distinct from post-inflammatory erythema (redness) in lighter skin. Psychological complications: acne has a disproportionate psychological impact relative to its physical extent — depression affects 30-40% of acne patients, anxiety and reduced self-esteem are very common; suicide risk is elevated in severe acne — particularly with isotretinoin use (requires monitoring). Social and occupational impairment: facial acne causes social withdrawal, school avoidance, and reduced career confidence. Acne fulminans: rare, severe systemic complication with ulcerating acne lesions, fever, arthralgia, and elevated inflammatory markers — requires urgent systemic treatment.

Establish a consistent gentle skin care routine: cleanse twice daily with a mild, non-comedogenic, sulphate-free cleanser; avoid over-washing (strip barrier and increase sebum production as compensation). Use non-comedogenic, oil-free moisturisers and sunscreens — particularly important during retinoid or isotretinoin treatment when the skin barrier is compromised. Sun protection: broad-spectrum SPF 30-50 daily reduces PIH and inflammation. Avoid picking or squeezing lesions — dramatically increases the risk of scarring, secondary infection, and PIH. Dietary considerations: high-glycaemic foods (white bread, sugar, dairy — particularly skimmed milk) may worsen acne in susceptible individuals — replacing with low-GI foods, reducing dairy, and increasing vegetables may modestly benefit acne. However, dietary changes alone are rarely sufficient for moderate-severe acne and should not replace medical treatment. Review potentially aggravating medications with your GP. Women with suspected PCOS or hormonal acne should seek endocrine evaluation.

See a GP for: acne not controlled with 2-3 months of over-the-counter treatments (benzoyl peroxide, salicylic acid cleansers), any nodular or cystic acne (high scarring risk — requires prescription-only treatment), acne causing significant psychological distress, or adult female acne associated with irregular periods, excessive hair growth, or weight changes (possible PCOS). Seek urgent or same-day GP review for acne fulminans (sudden severe acne with fever, joint pain, and systemic upset — rare but requires systemic corticosteroids). Referral to a dermatologist is appropriate for: severe nodulo-cystic acne, acne unresponsive to two adequate courses of oral antibiotics, acne requiring isotretinoin, or acne with significant scarring requiring procedural treatment (fractional laser, subcision, dermal fillers for atrophic scars). Never delay treatment of severe acne — every week of active nodulo-cystic acne is a week of preventable scarring.