Acne Vulgaris: Inflammation of Hair Follicles and Sebaceous Glands
Reviewed by Dr C. J. Odike, MRCGP
Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit, which contains a hair follicle and sebaceous gland. Androgen sensitive sebum production, follicular blockage, Cutibacterium acnes and immune inflammation interact to produce comedones and inflammatory lesions. Early effective treatment can reduce pain, pigmentary change, permanent scarring and psychological harm.
What acne vulgaris is Acne vulgaris is a chronic inflammatory disorder affecting hair follicles and their associated sebaceous glands. It commonly affects the face, upper chest, shoulders and back because these areas contain many large sebaceous glands. Visible lesions include comedones, papules, pustules, nodules and deeper cyst like swellings. Acne is not contagious and does not result from dirty skin, poor hygiene or inadequate washing. The pilosebaceous unit A pilosebaceous unit contains a hair follicle, a hair shaft and one or more sebaceous glands. The follicle is a narrow channel connecting structures within the skin to the surface. Sebaceous glands release sebum into the follicle, which then spreads across nearby skin and hair. Acne begins within this unit rather than from surface dirt becoming trapped after inadequate cleansing. What sebum normally does Sebum is a lipid rich substance containing triglycerides, wax esters, squalene and other components. It lubricates hair and supports the flexibility and water resistance of the skin surface. Sebum also interacts with the normal skin microbiome and local immune defences. Having oily skin is not itself a disease, although greater sebum output creates conditions favouring acne development. Androgens and sebaceous glands Androgens are hormones that stimulate sebaceous gland growth and sebum production. Their effects become particularly noticeable during puberty, when androgen activity increases in all sexes. Some people develop acne despite normal blood androgen concentrations because their sebaceous glands are particularly sensitive. An acne pattern alone does not prove that someone has excessive testosterone or another endocrine disorder. The four interacting processes Acne develops through four closely connected processes within the pilosebaceous unit. These are increased sebum production, abnormal follicular keratinisation, Cutibacterium acnes activity and inflammation. Genetic susceptibility, hormones, medicines, friction, cosmetics and environmental factors influence these mechanisms. Treatment works best when it targets several processes rather than repeatedly drying individual visible spots. Follicular hyperkeratinisation Keratinocytes normally mature and separate as they move through the follicular opening. In acne, these cells become excessively cohesive and accumulate with sebum inside the follicle. This process is called follicular hyperkeratinisation and creates a microscopic blockage called a microcomedone. The microcomedone is the precursor of visible comedones and many inflammatory acne lesions. Closed comedones A closed comedone develops when a blocked follicle remains covered by a thin epidermal layer. It appears as a small pale, white or skin coloured bump and is commonly called a whitehead. Closed comedones can remain non inflammatory or develop into papules, pustules and deeper lesions. They are not collections of dirt and should not be repeatedly squeezed or pierced. Open comedones An open comedone develops when the blocked follicular opening becomes widened and exposed to air. It is commonly called a blackhead. The dark colour results mainly from oxidation and light absorption within compacted keratin and sebum. It does not represent trapped dirt, and vigorous scrubbing can increase irritation and inflammation. Cutibacterium acnes Cutibacterium acnes is a bacterium normally living within sebaceous follicles on healthy skin. It was previously called Propionibacterium acnes and favours the low oxygen, lipid rich follicular environment. Within an obstructed follicle, bacterial density and activity can increase while bacterial products activate immune pathways. Ordinary acne is therefore not a simple contagious infection, although antimicrobial treatments can reduce part of its inflammatory mechanism. Inflammation begins early Inflammation can be present around a follicle before a visible inflamed lesion develops. Cutibacterium acnes, altered sebum, keratinocyte signals and immune cells activate one another. The follicular wall can weaken and release keratin, sebum and inflammatory material into the surrounding dermis. The depth and extent of this rupture influence whether a papule, pustule, nodule or scar develops. Papules A papule is a small raised inflammatory lesion without an obvious collection of pus. It may appear red or pink on lighter skin and brown, purple, grey or subtly darker on deeper skin tones. Papules can feel tender or itchy and may develop from previously unnoticed comedones. Picking them increases inflammation and the risks of persistent pigment change and scarring. Pustules A pustule is an inflamed lesion containing visible white or yellow inflammatory material. This material consists mainly of neutrophils, keratin and cellular debris. A pustule does not necessarily indicate an invasive bacterial infection requiring oral antibiotics. Pustules commonly occur alongside papules and comedones in inflammatory acne. Nodules A nodule is a deep, firm and often painful inflammatory lesion extending into the dermis or deeper tissue. Nodules persist longer than superficial papules and carry a greater risk of permanent scarring. Several connected nodules and abscess like spaces can form severe acne conglobata. Nodular disease warrants early effective treatment and often specialist referral. Cysts and cyst like lesions The word cyst is commonly used for deep fluctuant acne lesions containing inflammatory material. Many so called acne cysts are actually pseudocysts without the complete lining of a true cyst. Clinically, nodules and cyst like lesions are grouped because both are deep, painful and strongly associated with scarring. They should not be drained or injected outside an appropriately trained clinical setting. Acne severity exists on a continuum Severity assessment considers lesion type, number, distribution, scarring, pigment change, pain and psychological impact. Comedonal acne without inflammation is usually at the milder end of the spectrum. Numerous papules or pustules indicate greater inflammatory burden, while nodules and scarring indicate more severe disease. A small number of lesions can still be clinically severe when they scar or cause major psychological distress. Common body sites Facial acne often affects the forehead, cheeks, nose, chin and jawline. Truncal acne affects the upper chest, shoulders and back and can be missed when assessment focuses only on the face. Truncal lesions can be deep, painful and difficult to treat with small quantities of topical medicine. Clothing friction, sweating and inaccessible application sites can complicate management without causing the underlying disease. Acne through adolescence Acne commonly begins around puberty as androgen activity and sebaceous gland output increase. It can affect confidence, school attendance, sport, relationships and willingness to appear in photographs. Dismissing acne as a harmless teenage phase can delay treatment until permanent scars have formed. Adolescents should be included directly in treatment decisions while receiving appropriate family support where helpful. Adult acne Acne can persist from adolescence or begin for the first time during adulthood. Adult women commonly report lower face or jawline lesions and worsening before menstruation. This distribution can suggest androgen sensitivity but does not diagnose polycystic ovary syndrome. New abrupt or severe adult acne should prompt review of medicines, hormonal symptoms and alternative diagnoses. Hormonal acne patterns Hormonal influence is suggested by cyclical flares, persistent jawline lesions and changes associated with reproductive hormones. Pregnancy, stopping contraception, perimenopause and some fertility treatments can alter acne activity. The pattern reflects sebaceous sensitivity and changing androgen effects rather than one universal hormone abnormality. Topical therapy remains useful when hormonal treatment is added because follicular blockage and inflammation continue locally. Polycystic ovary syndrome Polycystic ovary syndrome, shortened to PCOS, is associated with ovulatory dysfunction, androgen excess and metabolic risk. Acne may occur with irregular or absent periods, hirsutism, scalp hair thinning or fertility difficulty. Acne alone is a relatively weak predictor of biochemical androgen excess, particularly during adolescence. Assessment becomes more important when several features coexist or symptoms become rapidly progressive. Signs suggesting another endocrine cause Rapid onset severe acne with new coarse facial hair, voice deepening, increased muscle mass or clitoral enlargement requires prompt assessment. These virilising features are not typical of ordinary acne or uncomplicated PCOS. Cushing syndrome, androgen producing tumours, congenital adrenal disorders and medicines are uncommon alternative causes. Testing should follow the complete clinical pattern rather than routine hormone panels for everyone with acne. Medicine related acne Anabolic androgenic steroids and testosterone treatment can increase sebum production and inflammatory acne. Systemic corticosteroids can produce a sudden eruption of similar papules and pustules with few comedones. Lithium, some anti seizure medicines and selected cancer treatments can cause acneiform eruptions. Do not stop an essential medicine independently because the indication and possible alternatives require clinical review. Acne mechanica Pressure, friction, heat and occlusion can provoke acneiform lesions in susceptible follicles. Examples include tight helmets, shoulder pads, straps, masks and repeatedly occlusive clothing. This local aggravation is sometimes called acne mechanica. Practical equipment adjustment can reduce worsening, but treatment of the underlying follicular process may still be required. Cosmetics and hair products Oil rich or comedogenic cosmetics and hair products can contribute to follicular blockage around the hairline and face. Non comedogenic products are designed to be less likely to block follicles, although no label guarantees perfect tolerance. Make up can be used when desired and should be removed gently ultimately. Repeatedly changing complex skin care routines can increase irritation and make treatment response difficult to interpret. Acne is not caused by poor hygiene Washing more frequently does not stop androgen activity, microcomedone formation or deep follicular inflammation. Harsh scrubs, abrasive brushes and alcohol based toners can damage the barrier and worsen soreness. NICE recommends a skin pH neutral or slightly acidic synthetic detergent cleanser twice daily on acne prone skin. Gentle cleansing supports treatment but should not be presented as a cure or measure of personal discipline. Picking and squeezing Squeezing can rupture the follicular wall and push inflammatory material deeper into surrounding skin. This increases swelling, pain, pigment change and the likelihood of permanent scars. Picking can become compulsive and may reflect anxiety, body dysmorphic disorder or acne excoriée. Care should address both skin inflammation and the psychological drive to manipulate lesions without blame. Post inflammatory colour change Inflamed acne can leave darker or lighter areas after the active lesion settles. Post inflammatory hyperpigmentation is particularly frequent and persistent in darker skin tones. These flat colour changes are not the same as permanent textural scars, although both can coexist. Preventing new inflammation and using suitable sun protection are central to management. Acne in darker skin Inflammation may appear purple, grey, dark brown or only slightly different from surrounding skin. Severity can be underestimated when assessment relies on visible redness alone. Irritating treatment can produce disproportionate post inflammatory hyperpigmentation despite eventually controlling acne. Gradual introduction, moisturiser and early review can preserve effective treatment while reducing unnecessary irritation. Atrophic acne scars Atrophic scars sit below surrounding skin because inflammation has destroyed collagen and supporting dermal tissue. Icepick scars are narrow and deep, resembling small punctures. Boxcar scars have wider, sharply defined depressions, while rolling scars create broad undulating surface changes. One person can develop several scar patterns, and each responds differently to later procedures. Raised acne scars Hypertrophic scars and keloids contain excessive collagen and rise above the skin surface. They are more common on the chest, shoulders and jawline and occur more frequently in some darker skin types. Keloids extend beyond the boundaries of the original inflammatory lesion. Prompt acne control is particularly important when someone has previously formed keloids after injury or piercing. Why early treatment prevents scarring Scarring risk increases with deeper inflammation, longer disease duration, repeated manipulation and delayed effective treatment. Nodules can scar even when they are relatively few in number. Treating ongoing acne prevents new scars more reliably than attempting to remove established scars later. NICE recommends specialist referral when acne is causing scarring or persistent pigmentary change. Treating established scars Scar procedures are generally considered after active acne is controlled because continuing inflammation creates new damage. Options include subcision, microneedling, punch techniques, chemical reconstruction and laser treatment. The best procedure depends on scar type, skin tone, keloid tendency, cost and available expertise. NICE recommends specialist assessment when severe scarring persists one year after acne has cleared. Psychological impact Acne can cause embarrassment, shame, anxiety, depression, social withdrawal and avoidance of school or work. Impact can be severe even when a clinician sees relatively few lesions. Scarring and pigment change may continue affecting confidence after active acne improves. Assessment should ask directly about mood, daily functioning, bullying and thoughts of self harm. Body dysmorphic disorder Body dysmorphic disorder involves intense preoccupation with perceived appearance flaws and repetitive checking or concealment. The distress is real and can occur with mild, severe or successfully treated acne. Escalating cosmetic procedures alone may worsen the cycle without treating the underlying disorder. Suspected body dysmorphic disorder requires sensitive mental health assessment alongside appropriate acne care. Diet and acne Diet is not the sole cause of acne, and no specific diet reliably clears everyone. NICE concludes that evidence remains insufficient to prescribe a particular acne treatment diet. Systematic reviews suggest that high glycaemic load eating patterns may worsen acne in some people. Evidence concerning dairy is mixed and appears influenced by product type, population and study design. Glycaemic load High glycaemic foods produce rapid rises in blood glucose and insulin and may influence insulin like growth factor signalling. These pathways can promote androgen activity, sebum production and follicular keratinisation. Choosing whole grains, pulses, vegetables and less refined carbohydrates supports general health and may help some people. This complements proven treatment and should not become a rigid diet causing nutritional deficiency or guilt. Dairy evidence Observational studies have linked milk intake, particularly some skimmed or low fat milk patterns, with acne in certain populations. Results for total dairy, yoghurt and cheese are inconsistent, and association does not prove causation. Routine dairy exclusion is not recommended, particularly for children or anyone at nutritional risk. A time limited change can be discussed when someone notices a reproducible relationship and can maintain adequate nutrition. Chocolate and greasy foods Chocolate is not proven to cause acne simply because it contains fat. Products high in sugar or refined carbohydrate may contribute through glycaemic load rather than surface greasiness. Eating oily food does not transfer cooking oil directly into sebaceous glands. Dietary discussion should remain proportionate and should not distract from effective medical treatment. Diagnosing acne Acne is usually diagnosed clinically by finding comedones with or without inflammatory lesions in a typical distribution. Comedones are particularly useful because many acne like eruptions do not produce them. The clinician assesses the face and trunk, lesion depth, scarring, pigment change and psychological impact. Laboratory tests are unnecessary for typical acne unless the history suggests endocrine disease or another diagnosis. Folliculitis Folliculitis produces inflamed papules or pustules centred on hairs. Bacterial folliculitis, Malassezia folliculitis and shaving related inflammation can resemble acne. Malassezia lesions are often itchy and appear very similar to one another, with few or no comedones. Microbiology or skin sampling can help when distribution and treatment response are atypical. Rosacea Rosacea can cause facial papules and pustules with flushing, central redness and visible vessels. Comedones are absent, which helps distinguish rosacea from acne vulgaris. Eye irritation and burning are more common in rosacea, while truncal disease is unusual. Topical corticosteroids can worsen or mask rosacea and should not be used as an acne substitute. Periorificial dermatitis Periorificial dermatitis causes small papules around the mouth, nose or eyes, often sparing the immediate lip border. It can be triggered or worsened by topical corticosteroids and some heavy facial products. Comedones and deep nodules are usually absent. Stopping corticosteroids can cause temporary rebound, so management benefits from a structured clinical plan. Hidradenitis suppurativa Hidradenitis suppurativa causes recurrent painful nodules, abscesses and tunnels within armpits, groins and buttocks. It is a separate follicular inflammatory disease rather than ordinary acne in a hidden area. Scarring, double ended comedones and recurrent drainage support the diagnosis. Early recognition matters because repeated incision or short antibiotic courses do not control tunnel forming disease. The stepped treatment approach Treatment is selected according to lesion type, severity, distribution, scarring risk, pregnancy potential and preference. Most first line regimens are used for twelve weeks before effectiveness is judged. Improvement often begins after six to eight weeks because existing microcomedones require time to resolve. The treatment plan should cover the whole acne prone area rather than visible spots alone. Skin care foundation Cleanse acne prone skin gently twice daily with a pH neutral or slightly acidic non soap cleanser. Use non comedogenic moisturiser and sunscreen when needed, particularly during irritating or photosensitising treatment. Avoid repeated scrubbing, abrasive exfoliation and frequent product changes. Skin care reduces irritation and supports adherence but does not replace active treatment. Topical retinoids Topical retinoids include adapalene and tretinoin. They normalise follicular keratinisation, reduce microcomedone formation and provide anti inflammatory effects. Because microcomedones generate future lesions, retinoids treat current acne and help prevent new comedones. They are foundation medicines for comedonal and mixed acne and are commonly combined with benzoyl peroxide. Applying a topical retinoid Apply a thin layer across the whole acne prone area rather than large amounts on visible lesions. A pea sized amount is usually sufficient for the entire face, although individual product instructions should be followed. Start on alternate evenings or use short contact application when irritation risk is high. Moisturiser before or after treatment can improve tolerability without removing the clinical benefit. Retinoid irritation and pregnancy Dryness, stinging, peeling and temporary inflammation are common during the first treatment weeks. Severe irritation does not mean that applying more treatment will clear acne faster. Reducing frequency temporarily and avoiding other irritants can allow treatment to continue. Topical retinoids should not be used during pregnancy, and conception plans should be discussed with the prescriber. Benzoyl peroxide Benzoyl peroxide reduces Cutibacterium acnes through oxidative activity and has anti inflammatory effects. Bacterial resistance does not develop to benzoyl peroxide as it does to antibiotic treatment. It can be used alone when other treatments are unsuitable and is commonly combined with adapalene or antibiotics. It can irritate skin and permanently bleach hair, towels, bedding and clothing. Introducing benzoyl peroxide Lower strengths and less frequent application can be as effective as stronger preparations with fewer adverse effects. NICE suggests alternate day or short contact use when starting an irritating topical treatment. Apply it to the full affected area and wash hands afterwards. Moisturiser and non comedogenic sunscreen improve comfort when dryness or sensitivity develops. Azelaic acid Azelaic acid reduces follicular keratinisation, Cutibacterium acnes activity and inflammation. It can be useful for inflammatory acne and post inflammatory hyperpigmentation. Stinging and irritation can still occur during early treatment. It is an important alternative when retinoids are not tolerated or are contraindicated, including during pregnancy after review. Topical antibiotics Topical clindamycin can reduce inflammatory lesions but promotes antimicrobial resistance when used alone. NICE advises against topical antibiotic monotherapy. When used, it is combined with benzoyl peroxide or included within another approved combination regimen. Benzoyl peroxide reduces selection of antibiotic resistant Cutibacterium acnes. Oral antibiotics Oral lymecycline or doxycycline can be added for moderate to severe inflammatory acne affecting the face or trunk. They reduce Cutibacterium acnes activity and inflammation but do not correct follicular blockage by themselves. They should be combined with non antibiotic topical treatment such as adapalene with benzoyl peroxide or azelaic acid. Oral antibiotic monotherapy is not recommended. Antibiotic stewardship Topical and oral antibiotics should not be used together because this increases unnecessary antibiotic exposure. NICE recommends reviewing first line treatment at twelve weeks. If acne has cleared, stop the oral antibiotic while continuing suitable topical treatment. Antibiotic containing treatment should continue beyond six months only in exceptional circumstances with regular review. Tetracycline safety Doxycycline and lymecycline can cause nausea, oesophageal irritation and photosensitivity. Take them exactly as directed with sufficient water and avoid lying down immediately afterwards when advised. Tetracyclines are not used during pregnancy and are generally avoided in children younger than twelve years. They should not be combined with oral isotretinoin because both can increase intracranial hypertension risk. Combined oral contraceptives A combined oral contraceptive can improve acne by reducing ovarian androgen production and increasing androgen binding proteins. It can be useful when effective contraception is also wanted and no important contraindication exists. Benefits take several months, and clotting, migraine, smoking and blood pressure risks require assessment. NICE generally prefers a combined pill over a progestogen only pill when hormonal contraception is requested for acne. Co cyprindiol Co cyprindiol combines ethinylestradiol with the anti androgen cyproterone acetate. It can be considered for selected moderate or severe androgen sensitive acne after first line treatment. It increases venous thromboembolism risk and is not chosen simply as routine contraception. NICE advises review at six months to discuss continuation or alternative treatment. Spironolactone Spironolactone blocks androgen receptors and reduces androgen driven sebaceous activity. Evidence supports it as an alternative to repeated oral antibiotics for persistent acne in adult women. It is used off label for acne in the UK and commonly works gradually over three to six months. It can be particularly useful for cyclical lower face acne or other androgen sensitive patterns. Spironolactone safety Spironolactone can cause increased urination, dizziness, breast tenderness, menstrual irregularity and headache. Kidney disease, adrenal disease, high potassium and interacting medicines can make treatment unsafe. Baseline kidney function and potassium are commonly checked, with further monitoring determined by age and risk. Pregnancy must be avoided because anti androgen effects could harm fetal sexual development. Treating PCOS associated acne NICE recommends beginning with standard evidence based acne treatment rather than assuming hormones are the only mechanism. A combined oral contraceptive or co cyprindiol can be added when first line treatment is ineffective and clinically suitable. Spironolactone is another option for appropriate adult women under an experienced prescriber. Additional hyperandrogenic features or diagnostic uncertainty can justify endocrinology or gynaecology referral. Maintenance treatment Maintenance treatment is not required after every successful acne course. It can help people who relapse frequently, particularly after antibiotics are stopped. Adapalene with benzoyl peroxide is a preferred option, with adapalene, azelaic acid or benzoyl peroxide alternatives. Maintenance should be reviewed after twelve weeks and continued only when its benefits justify treatment burden. When specialist referral is appropriate Urgent same day referral is required for acne fulminans. Dermatology referral is appropriate for acne conglobata, nodulocystic disease, diagnostic uncertainty or substantial scarring risk. Referral should also be considered after adequate first line treatments fail or psychological distress is persistent. Active treatment should continue while referral is pending rather than allowing preventable scarring to progress. Isotretinoin Isotretinoin is an oral retinoid and the most effective medicine for severe acne. It markedly reduces sebaceous gland activity, sebum production, follicular blockage and inflammation. NICE recommends it for people older than twelve with severe acne resistant to adequate systemic antibiotic and topical therapy. Examples include nodulocystic acne, acne conglobata, acne fulminans and acne at risk of permanent scarring. Isotretinoin is specialist treatment Treatment is initiated by a prescriber with expertise in systemic retinoids within an appropriate dermatology pathway. Expected benefit is weighed against teratogenicity, mental health concerns, sexual function concerns and other adverse effects. All patients complete current risk minimisation documentation and receive continuing monitoring. People younger than eighteen no longer require a second independent prescriber's approval under the updated 2026 requirements. Pregnancy prevention Isotretinoin can cause severe congenital abnormalities and miscarriage and must never be taken during pregnancy. Anyone with childbearing potential enters the MHRA Pregnancy Prevention Programme unless formal criteria show no pregnancy risk. The programme uses pregnancy testing and effective contraception or documented absence of pregnancy risk under current requirements. Pregnancy must be avoided during treatment and for one month after the final dose. Mental health and isotretinoin Severe acne itself is associated with depression, anxiety, self harm and suicidal thoughts. Psychiatric symptoms have also been reported during and after isotretinoin treatment, although causation is complex. MHRA guidance requires mental health assessment before treatment and objective monitoring at every follow up appointment. New or worsening mood, anxiety, self harm thoughts or behavioural change requires prompt clinical advice. Sexual function monitoring Possible sexual function adverse effects have been reported with isotretinoin, sometimes continuing after treatment in individual reports. Current MHRA measures require discussion before treatment and monitoring during follow up. People should be able to raise concerns without embarrassment or fear that treatment will automatically be withdrawn. Severe or rapidly worsening symptoms require prompt advice and an individual treatment decision. Common isotretinoin effects Dry lips are extremely common and usually require frequent bland lip balm. Dry skin, dry eyes, nosebleeds and increased sun sensitivity are also common. Contact lenses may become uncomfortable, and eczema like irritation can develop. Moisturiser, sunscreen, gentle cleansing and early adverse effect management improve tolerability. Other isotretinoin safety issues Muscle aches, joint pain and back discomfort can occur, particularly during vigorous exercise. Headache with visual disturbance, nausea or vomiting requires urgent assessment for possible intracranial hypertension. People should avoid vitamin A supplements and must not share isotretinoin capsules. Blood donation is avoided during treatment and for one month afterwards. Liver and lipid monitoring Isotretinoin can raise triglycerides and liver enzymes. Baseline liver function and lipid tests are usually obtained, with repeat testing guided by the treatment pathway and individual risk. Marked abnormalities can require dose adjustment, interruption or investigation for another cause. Monitoring should not be presented as proof that serious toxicity is expected in everyone. Starting and finishing isotretinoin The dose is individualised according to body weight, response and adverse effects. Some people experience an initial flare before improvement begins. Treatment commonly lasts around six months but can be shorter or longer according to response and dose. Relapse can occur, and later management depends on its severity rather than automatically repeating isotretinoin. Acne fulminans Acne fulminans is a rare severe systemic variant with abrupt painful nodules, erosions and ulceration. Fever, malaise, joint pain, muscle pain and inflammatory blood test abnormalities can occur. It most often affects adolescent males but can occur in other groups. NICE requires same day referral to the on call dermatology team for assessment within twenty four hours. Treating acne fulminans Acne fulminans usually requires systemic corticosteroid treatment under specialist supervision before cautious low dose isotretinoin. Starting or rapidly increasing isotretinoin without controlling severe inflammation can worsen the eruption. Wounds, pain and systemic complications may require hospital level treatment. This condition is different from an ordinary temporary acne flare after beginning treatment. Managing individual severe nodules A trained specialist can inject a selected severe inflammatory cyst or nodule with dilute corticosteroid. This may reduce pain and inflammation quickly and lower local scarring risk. Incorrect depth or dose can cause skin thinning, visible vessels or pigment change. Injection does not replace broader acne treatment when new nodules continue forming. Physical treatments Light devices, chemical peels and other procedures are sometimes promoted for active acne. Evidence and availability vary, and procedures do not replace medical treatment for severe inflammatory disease. NICE allows consideration of photodynamic therapy for selected adults when other treatments are ineffective or unsuitable. Procedures can worsen pigment change or scarring when delivered without appropriate expertise. Treatment adherence Acne medicines commonly fail because irritation develops, instructions are unclear or improvement is expected within days. A written routine should specify the amount, body area, frequency and order of products. Reducing initial frequency often improves long term adherence more than abandoning an effective treatment. Review should distinguish true treatment resistance from insufficient duration, quantity or tolerability problems. General safety netting Seek review if acne becomes painful, nodular, rapidly progressive or begins leaving scars despite treatment. Report persistent pigment change, major irritation or failure after a completed twelve week treatment course. New menstrual disturbance, hirsutism or virilising symptoms require hormonal assessment rather than repeated skin treatment alone. Psychological distress, self harm thoughts or social withdrawal requires direct support regardless of the visible acne grade. The central safety message Acne develops through androgen sensitive sebum, follicular blockage, Cutibacterium acnes activity and inflammation, not poor hygiene. Topical retinoids and benzoyl peroxide target central mechanisms, while antibiotics must be combined and time limited. Early control of nodules and persistent inflammation reduces permanent scars and pigment change. Acne fulminans, suicidal thoughts and rapidly progressive endocrine symptoms require urgent escalation.
Acne is an inflammatory disease of the pilosebaceous unit rather than a cleanliness problem. Effective treatment targets follicular blockage, sebum, Cutibacterium acnes and inflammation early enough to prevent permanent scarring, pigment change and psychological harm.
Medical words made simple
- Acne vulgaris
- A chronic inflammatory disorder of hair follicles and their associated sebaceous glands.
- Pilosebaceous unit
- A hair follicle together with its hair shaft and connected sebaceous gland.
- Sebaceous gland
- A gland opening into a hair follicle and producing the oily substance called sebum.
- Sebum
- A lipid-rich substance that lubricates hair and skin and interacts with the skin microbiome.
- Androgen
- A hormone that can stimulate sebaceous gland growth and sebum production.
- Follicular hyperkeratinisation
- Abnormal accumulation of cohesive keratin-producing cells inside a hair follicle, creating blockage.
- Microcomedone
- A microscopic follicular blockage that develops before a visible acne lesion.
- Comedone
- A follicle blocked by keratin and sebum, appearing as a blackhead or whitehead.
- Closed comedone
- A blocked follicle covered by skin and appearing as a pale or skin-coloured bump.
- Open comedone
- A widened blocked follicle whose contents appear dark through oxidation and light absorption.
- Cutibacterium acnes
- A normal follicular bacterium that can contribute to inflammation within an obstructed pilosebaceous unit.
- Papule
- A small raised inflammatory acne lesion without an obvious collection of pus.
- Pustule
- An inflamed lesion containing visible white or yellow inflammatory material.
- Nodule
- A deep, firm and painful inflammatory acne lesion with a high scarring risk.
- Acne cyst
- A common clinical term for a deep fluctuant acne lesion, often representing a pseudocyst.
- Acne conglobata
- Severe nodulocystic acne with connected nodules, abscess-like spaces and sinus tracts.
- Acne fulminans
- A rare rapidly worsening ulcerative acne variant with fever, pain or other systemic symptoms.
- Acne mechanica
- Acneiform lesions worsened by repeated pressure, friction, heat and occlusion.
- Post-inflammatory hyperpigmentation
- Flat darkening remaining after inflammation, particularly common and persistent in darker skin.
- Atrophic scar
- A depressed scar caused by loss of collagen and supporting dermal tissue.
- Icepick scar
- A narrow deep atrophic acne scar resembling a small puncture.
- Boxcar scar
- A wider depressed acne scar with relatively sharp edges.
- Rolling scar
- A broad undulating depression caused partly by fibrous tethering beneath the skin.
- Hypertrophic scar
- A raised collagen-rich scar remaining within the original area of injury.
- Keloid
- A raised scar extending beyond the original inflammatory or injury boundary.
- Hormonal acne
- Acne influenced by androgen sensitivity or reproductive hormone changes, often showing cyclical or lower-face flares.
- Polycystic ovary syndrome
- An endocrine condition associated with ovulatory disturbance, androgen excess and metabolic risks.
- Hyperandrogenism
- Clinical effects of excessive androgen activity, including hirsutism, severe acne or androgen-pattern hair loss.
- Virilisation
- Rapid development of marked androgen effects such as voice deepening or clitoral enlargement.
- Comedogenic
- Likely to block follicles and contribute to comedone formation in susceptible skin.
- Topical retinoid
- A vitamin-A-related skin medicine that normalises follicular keratinisation and prevents microcomedones.
- Adapalene
- A topical retinoid used to treat and prevent comedonal and inflammatory acne.
- Tretinoin
- A topical retinoid that reduces follicular blockage and inflammation.
- Benzoyl peroxide
- A topical antimicrobial and anti-inflammatory treatment that does not drive bacterial resistance like antibiotics.
- Azelaic acid
- A topical medicine reducing follicular blockage, bacterial activity, inflammation and sometimes pigment change.
- Antibiotic stewardship
- Using antibiotics only when necessary, in appropriate combinations and for the shortest effective duration.
- Lymecycline
- An oral tetracycline antibiotic used with non-antibiotic topical treatment for inflammatory acne.
- Doxycycline
- An oral tetracycline antibiotic with anti-inflammatory effects used for selected acne.
- Combined oral contraceptive
- A contraceptive containing oestrogen and progestogen that can reduce androgen-driven acne in suitable people.
- Co-cyprindiol
- A combined hormonal treatment containing cyproterone acetate and ethinylestradiol for selected androgen-sensitive acne.
- Spironolactone
- An oral anti-androgen medicine used off-label for persistent acne in appropriate adult women.
- Isotretinoin
- A highly effective oral retinoid used under specialist supervision for severe, scarring or treatment-resistant acne.
- Teratogenic
- Capable of causing severe harm or abnormalities in a developing fetus.
- Pregnancy Prevention Programme
- The MHRA safety system preventing pregnancy exposure during treatment with highly teratogenic oral retinoids.
- Triglyceride
- A circulating blood fat that can rise during isotretinoin treatment.
- Intracranial hypertension
- Raised pressure around the brain causing headache, visual symptoms, nausea or vomiting.
- Body dysmorphic disorder
- A mental health condition involving severe preoccupation with perceived appearance flaws.
- Glycaemic load
- A measure combining how quickly carbohydrate raises blood glucose with the amount eaten.
Quick recap
- Acne is a chronic inflammatory disorder of hair follicles and sebaceous glands.
- The pilosebaceous unit contains a follicle, hair shaft and connected sebaceous gland.
- Sebum normally lubricates skin and hair and interacts with the skin microbiome.
- Androgens increase sebaceous activity, but acne does not always mean excessive hormone levels.
- The central mechanisms are increased sebum, follicular hyperkeratinisation, Cutibacterium acnes activity and inflammation.
- A microcomedone is the microscopic blockage from which many visible lesions develop.
- Closed comedones are whiteheads, while open comedones are blackheads whose colour is not dirt.
- Papules and pustules are superficial inflammatory lesions.
- Nodules and cyst like lesions are deeper and more likely to cause permanent scars.
- Severity includes lesion depth, distribution, scarring, pigment change, pain and psychological impact.
- Jawline and perimenstrual flares suggest hormonal influence but do not diagnose PCOS.
- Irregular periods, hirsutism and scalp hair thinning make endocrine assessment more relevant.
- Rapid virilisation requires prompt investigation for significant androgen excess.
- Acne is not caused by poor hygiene, and abrasive over washing can worsen irritation.
- Picking and squeezing can deepen inflammation and increase pigment change and scarring.
- Post inflammatory hyperpigmentation is common in darker skin and is not identical to a textural scar.
- Icepick, boxcar and rolling scars are different forms of atrophic acne scarring.
- Early control of nodules and persistent inflammation prevents new scars more effectively than later procedures.
- Acne can cause depression, anxiety, body dysmorphic symptoms and social withdrawal at any visible severity.
- High glycaemic load diets may worsen acne in some people, while dairy evidence remains mixed.
- NICE does not recommend one specific acne treatment diet.
- Topical retinoids treat microcomedones and help prevent future lesions.
- Benzoyl peroxide reduces Cutibacterium acnes without driving antibiotic resistance.
- Azelaic acid can help inflammatory acne and post inflammatory pigment change.
- Topical antibiotic monotherapy and oral antibiotic monotherapy should not be used.
- Oral antibiotics are combined with non antibiotic topical treatment and reviewed at twelve weeks.
- Antibiotic treatment beyond six months is reserved for exceptional circumstances.
- Combined oral contraception and spironolactone can help appropriate androgen sensitive acne.
- Spironolactone is off label for acne in the UK and must not be used during pregnancy.
- Isotretinoin is reserved for severe, scarring or treatment resistant acne under specialist supervision.
- Isotretinoin is highly teratogenic and requires current pregnancy prevention measures when pregnancy is possible.
- Acne fulminans is a systemic dermatological emergency requiring same day referral.