Acne — Causes, Types, Treatments & Skin Care Guide — Symptoms, Causes & Treatment | MyMedicPlus

Acne vulgaris is the most common chronic skin condition worldwide, affecting up to 85% of people between ages 12 and 24 at some point in their lives, and persisting into adulthood in approximately 12% of women and 3% of men over age 25 ('adult acne'). The pathological process begins in the pilosebaceous unit — the hair follicle and its associated sebaceous gland — where keratinocyte hyperproliferation (follicular hyperkeratinisation) causes plugging of the follicular canal, combined with excess sebum production from enlarged sebaceous glands and colonisation by Cutibacterium acnes (formerly Propionibacterium acnes), triggering an inflammatory immune cascade. The result is a spectrum of lesions ranging from non-inflammatory comedones to severely inflamed nodules and cysts. Acne is classified by lesion type and severity: Grade I (mild — predominantly open and closed comedones); Grade II (moderate — comedones, papules, and pustules); Grade III (moderately severe — papules, pustules, and early nodules); and Grade IV (severe nodulo-cystic acne — large, deep, painful nodules and cysts, high scarring risk). Affected areas mirror the distribution of sebaceous glands: face (forehead, cheeks, chin, perioral region — present in almost all acne patients), neck, upper chest (décolletage), upper back, and shoulders. Acne has a profound impact on psychosocial wellbeing — causing depression, anxiety, reduced self-esteem, and social withdrawal — particularly in adolescents and young adults; studies show health-related quality of life impairment comparable to chronic systemic conditions such as asthma, epilepsy, and diabetes mellitus. The condition is globally ubiquitous, with the highest prevalence in industrialised Western countries, and accounts for enormous dermatology consultation volumes.

Acne pathogenesis involves four interdependent mechanisms. (1) Excess sebum production: androgens (testosterone converted to the more potent DHT by 5-alpha-reductase in sebaceous glands) are the primary driver of sebaceous gland enlargement and sebum overproduction during puberty; elevated androgens from PCOS, adrenal hyperplasia, or exogenous androgen use also stimulate sebum production. Sebum provides the nutritional substrate for C. acnes proliferation. (2) Follicular hyperkeratinisation: abnormal keratinocyte shedding and adhesion within the follicular canal creates a plug (microcomedone — the earliest acne lesion), obstruct sebum drainage, creating an anaerobic environment. (3) Cutibacterium acnes proliferation: a Gram-positive commensal bacterium normally residing in sebaceous follicles — in acne-susceptible individuals, it proliferates in the plugged follicle, producing lipases (hydrolyse sebum triglycerides to proinflammatory free fatty acids), proteases, and biofilm; C. acnes activates toll-like receptors (TLR-2) on follicular keratinocytes and macrophages, driving IL-1β, IL-8, TNF-α, and LTB4 production. (4) Inflammation: the combined effect of C. acnes products and sebaceous lipid mediators (arachidonic acid metabolites) drives recruitment of neutrophils and macrophages to the follicle, causing rupture and the surrounding tissue destruction that determines acne scarring severity. Hormonal risk factors: puberty (rising androgens); premenstrual flares (progesterone-driven sebum increase in the luteal phase); PCOS (hyperandrogenism — causing adult female acne with irregular menses, hirsutism, acanthosis nigricans); pregnancy (first trimester acne flare); and exogenous androgens. Dietary factors: high-glycemic index foods (refined carbohydrates, white bread, sugary drinks — elevate IGF-1 and insulin, driving androgen production and mTORC1-mediated sebocyte lipogenesis); dairy products — particularly skimmed milk (whey protein and casein raise IGF-1 levels); these dietary effects appear most prominent in genetically susceptible individuals. Other risk factors: family history (genetics — monozygotic twin concordance approximately 80%); certain medications (anabolic steroids, corticosteroids, lithium, isoniazid, phenytoin, iodides — drug-induced acne); heavy oil-based cosmetics and hair products (acne cosmetica); tropical acne (heat and humidity); and mechanical friction on skin (acne mechanica — from helmets, straps, headbands).

Acne lesions are classified into non-inflammatory (comedonal) and inflammatory types. Non-inflammatory comedones: open comedones ('blackheads') — dilated follicular ostia filled with oxidised sebum and keratin debris (the dark colour is from melanin oxidation, not dirt); closed comedones ('whiteheads') — follicular orifice tightly closed, appearing as small 2-3 mm flesh-coloured or white dome-shaped bumps beneath the skin surface — the precursor to inflammatory lesions. Inflammatory lesions: papules — small (below 5 mm), raised, firm, red/pink lesions without pus, caused by follicular wall disruption and perifollicular inflammation; pustules — similar to papules but with a central white or yellow pus-filled head (superficial rupture of follicular wall, abscess formation); nodules — large (above 5 mm), firm, deeply embedded in the dermis, painful, tender, and slow to resolve — the high-risk lesion for scarring due to depth of dermal involvement; cysts — fluctuant, deep, pus-filled, compressible lesions representing severe follicular disruption with liquefying necrosis — highest risk for permanent scarring and sinus tract formation. Distribution: facial acne predominantly involves the forehead ('T-zone' — forehead, nose, chin), cheeks, and jawline — adult female hormonal acne characteristically affects the lower face, jawline, and chin (influenced by premenstrual hormone fluctuations); truncal acne affects the upper chest and back (sebaceous-gland-rich areas). Acne severity scales: Global Acne Grading System (GAGS), Investigator's Global Assessment (IGA), and Leeds scale — used in clinical trials and specialist practice. Acne scars develop during active disease and worsen with squeezing or picking — identifying scar risk early (nodulo-cystic disease) justifies prompt aggressive treatment. Post-inflammatory hyperpigmentation (PIH) — brown or purple flat marks persisting for months after lesion resolution — is particularly problematic in patients with Fitzpatrick skin types IV-VI (Asian, Black, and Hispanic skin).

Acne diagnosis is clinical — a trained dermatologist or general practitioner identifies and classifies acne lesion types (comedones, papules, pustules, nodules, cysts), their distribution, density, and associated features (scarring, PIH, seborrhoea, rosacea, folliculitis) through visual examination of the skin in good lighting. Severity grading guides treatment selection: mild (predominantly comedonal with scattered inflammatory lesions — Grade I-II), moderate (mixed comedonal and inflammatory — Grade II-III), and severe (predominantly inflammatory nodules and cysts — Grade IV). Specific investigations: laboratory tests are not routinely required for typical adolescent acne, but are indicated in specific circumstances. Hormonal evaluation — in adult women with acne, especially with features suggestive of hyperandrogenism: serum total and free testosterone, DHEA-S (dehydroepiandrosterone sulphate), androstenedione, LH/FSH ratio (polycystic ovary syndrome — LH:FSH ratio above 2:1), fasting glucose and insulin (insulin resistance/metabolic syndrome); sex hormone binding globulin (SHBG — reduced in PCOS). Pelvic ultrasound for suspected PCOS (polycystic ovarian morphology). Total blood count and liver function tests (LFTs) before and during isotretinoin treatment — LFTs and fasting lipid profile monitored monthly during isotretinoin therapy (risk of transaminase elevation and hypertriglyceridaemia). Pregnancy test (urine hCG) mandatory before initiating isotretinoin and monthly throughout treatment — teratogenicity is the primary safety concern. DHEA-S and 17-hydroxyprogesterone for late-onset congenital adrenal hyperplasia if suspected (usually with deep facial and truncal acne in women, irregular periods).

Acne treatment follows a stepped approach based on severity, with combination therapy more effective than monotherapy. Topical treatments (first-line for mild-moderate acne): benzoyl peroxide (BPO) 2.5-10% — the cornerstone of acne treatment; bactericidal against C. acnes (including antibiotic-resistant strains); reduces comedones and inflammatory lesions; available as wash, gel, or cream; may cause dryness and bleaching of fabrics. Topical retinoids — adapalene 0.1-0.3% (most studied, mildest tolerability profile; most widely used), tretinoin 0.025-0.1% (stronger, more irritating), tazarotene 0.045% (potent, often reserved for refractory disease) — normalise follicular keratinisation, preventing microcomedone formation and promoting comedolysis; applied nightly; require 8-12 weeks for full efficacy; essential components of acne treatment as they address the primary pathological process. Topical antibiotics — clindamycin 1% gel/lotion (most used); erythromycin 2% — reduce C. acnes and inflammation; never used as monotherapy (accelerates antibiotic resistance) — always combine with BPO. Fixed-dose combination products (BPO + antibiotic; retinoid + BPO) improve efficacy and adherence. Azelaic acid 15-20% — alternative with antibacterial, anti-inflammatory, and anti-pigmentary properties — particularly useful for PIH. Niacinamide 4% — adjunct for anti-inflammatory and anti-seborrhoeic effects. Oral antibiotics (for moderate-severe inflammatory acne): doxycycline 50-100 mg once daily — first-choice oral antibiotic (tetracycline class; anti-inflammatory and antibacterial; take with food to avoid oesophageal irritation; photosensitivity); lymecycline 408 mg once daily (UK preference); minocycline (effective but autoimmune side effect risk with prolonged use — systemic lupus-like syndrome, pigmentation). Duration: 3-6 months maximum; always combine with topical BPO and retinoid; review at 6-8 weeks for response. Oral antibiotics for acne should not exceed 6 months of use due to resistance implications. Hormonal therapy (women): combined oral contraceptives (ethinylestradiol + anti-androgenic progestins — cyproterone acetate in Dianette, drospirenone in Yasmin/Yaz) — reduce androgen-driven sebum production; 4-6 months for full effect; use as contraception simultaneously; not suitable in smokers over 35 or with vascular risk factors. Spironolactone 25-100 mg/day — androgen receptor antagonist; effective in women with hormonal/adult acne; monitor potassium; avoid in pregnancy. Oral isotretinoin (0.5-1 mg/kg/day, cumulative dose target 120-150 mg/kg) — the most effective acne treatment: achieves long-term remission in approximately 85-90% of patients after a single course; acts on all four pathological mechanisms (reduces sebum 90%, C. acnes, follicular hyperkeratinisation, and inflammation); course duration typically 16-24 weeks; mandatory pregnancy prevention programme (females — two methods of contraception during and 1 month post-treatment; monthly pregnancy tests; MHRA Pregnancy Prevention Programme in the UK); monitoring: LFTs, fasting lipids monthly; common side effects: cheilitis (lip dryness — universal; managed with petroleum jelly), skin dryness, epistaxis; rare serious effects: pseudotumour cerebri (severe headache, visual disturbance — stop immediately), severe depression. Topical dapsone 5-7.5% (USA) — anti-inflammatory; preferred in women. Procedures: chemical peels (salicylic acid 20-30%, glycolic acid) for comedonal acne and PIH; intralesional triamcinolone injections (2.5 mg/mL) for individual large nodular lesions; photodynamic therapy (PDT with 5-ALA); laser treatments and microneedling for scar revision.

See a GP or dermatologist for: acne that does not improve after 2-3 months of over-the-counter treatments, any nodular or cystic acne (deep painful lumps — high scarring risk), acne causing significant psychological distress or affecting daily life, or adult female acne associated with irregular periods, unwanted hair growth, or weight gain (possible PCOS requiring hormonal evaluation). Seek urgent review for acne fulminans — a rare, sudden onset of severe ulcerating acne with systemic features including fever, joint pain, weight loss, and markedly elevated inflammatory markers — which requires immediate systemic corticosteroids. Do not delay: active nodulo-cystic acne causes permanent scarring with every week of inadequate treatment, and early specialist intervention prevents irreversible skin damage.

The most significant consequence of untreated or inadequately treated acne is permanent scarring — affecting an estimated 20% of acne sufferers. Severe inflammatory nodulo-cystic acne causes the most destructive scarring: ice-pick scars (deep, narrow pits from follicular damage), rolling scars (broad depressions from dermal tethering), and boxcar scars (well-defined depressions with vertical edges). Hypertrophic and keloid scars are more common in individuals with darker skin phototypes. Scarring is permanent without dermatological intervention — prevention through early effective treatment is far superior to scar revision. Post-inflammatory hyperpigmentation (PIH) — persistent flat dark marks after acne lesions — is particularly pronounced and prolonged in skin phototypes IV-VI, lasting months to years without treatment. The psychological impact of acne is substantial and frequently underestimated: acne is strongly associated with depression, anxiety, social withdrawal, reduced self-esteem, and impaired quality of life — comparable in some studies to the psychosocial burden of epilepsy and diabetes. Acne fulminans — a rare complication of severe acne, more common in young men — is a medical emergency presenting with sudden explosive, ulcerating, highly inflammatory acne with systemic features including fever, arthralgia, weight loss, and markedly elevated ESR and CRP, requiring immediate systemic corticosteroids. Delay in starting isotretinoin for fear of side effects frequently causes more permanent scarring than the medication itself causes in adverse effects.

Wash affected areas twice daily with a gentle, non-comedogenic cleanser — over-washing strips the skin and triggers compensatory sebum overproduction. Avoid touching, squeezing, or picking at lesions, which spreads bacteria and dramatically increases scarring risk. Use only oil-free, non-comedogenic skincare and makeup products — check labels for 'non-comedogenic' or 'oil-free.' A low-glycemic diet (reducing refined carbohydrates, sugary drinks, and high-glycemic foods) may help reduce breakouts in susceptible individuals. Limit dairy consumption if acne worsens around milk intake. Manage stress through regular physical exercise, adequate sleep (7-9 hours nightly — cortisol spikes worsen acne), and mindfulness techniques. Apply SPF 30+ non-comedogenic sunscreen daily to prevent post-inflammatory hyperpigmentation from UV exposure. Begin prescription treatment early in moderate acne — consistent adherence to retinoids, antibiotics, and prescribed regimens over 8-12 weeks is essential for sustained improvement.