Acne keloidalis nuchae (folliculitis keloidalis nuchae)

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Meet the patient

A 23-year-old man of West African descent is referred to dermatology for a "keloid" across the back of his neck that has been slowly growing for two years. He rides a motorcycle and keeps the nape shaved to the skin for his helmet. Along the occipital hairline, in a tidy horizontal band, sit firm dome-shaped papules coalescing into a keloidal plaque — with tufts of five or six hairs emerging from single widened ostia, and two discharging sinuses.[6]

The referral calls it a keloid. The biopsy will call it a foreign-body granuloma around a hair shaft. The barber calls it Tuesday. Three names for one process — and the one that decides treatment is the third.[1][3]

Two exam questions are now live, and the whole topic exists to answer them: is this really a keloid? (no) and what stops it coming back? (removing the trigger and the culpable follicles). Hold those two and every section below slots into place.[1]

"Acne" without a sebaceous gland, "keloid" without the collagen

The name is the trap, and the trap is the teaching point. Two words, both misleading, and each one sends a trainee down the wrong treatment path if taken literally.[1]

• It is NOT true acne. There is no sebaceous-gland dysfunction and no role for Cutibacterium acnes. The early papulopustular stage merely looks acneiform, which is how the word clung to the name a century ago and never let go.
• It is NOT a true keloid pathologically. The plaques feel keloidal — firm, bossellated, extending past the original follicle — but histology shows a foreign-body granulomatous fibrosing reaction around an ingrown hair shaft, not the disorganised type-III collagen dump of a spontaneous keloid.[1][5]

The modern name — folliculitis keloidalis nuchae — is the one to use in the viva: it frames a primary inflammatory folliculitis with secondary keloidal scarring, and it stops you reaching for the keloid-only playbook.[1][3]

AKN sits within the primary cicatricial alopecias as a fibrosing subtype, and it keeps predictable company — folliculitis decalvans and the follicular occlusion tetrad (hidradenitis suppurativa, dissecting cellulitis of the scalp, acne conglobata, pilonidal sinus). Look for the company it keeps.[3][10]

Etymology for viva gold: nuchae is Latin for "of the nape"; keloid comes from the Greek chele, a crab's claw — Alibert thought the lesions reached outward like claws. Both words outlived their metaphors; the pathology they mis-describe is exactly what you must unlearn.[1]

The classic trap: treating AKN as a keloid with intralesional steroid alone. You flatten a papule, ignore the follicular trigger, and the disease marches back the day he next visits the barber. The whole ladder below exists to break that cycle.[1]

The three stages — papule, plaque, tumour

Stage dictates therapy, so stage the patient first. AKN evolves through three clinical stages, and the stage sitting in front of you decides every rung that follows.[1][7]

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A second axis — by dominant lesion type (papular, plaque, nodular, tumoural, sinus-subtype) — matters only when you are choosing the surgical technique, not at the bedside.[7][8]

Who gets it — and why it lives on the nape

AKN is a disease of young Black men with tightly curled, closely-clipped hair. The male-to-female ratio is about 20:1, onset typically falls between 14 and 25 years, and it is uncommon in white, Hispanic and Asian populations — though it appears in anyone whose hair type and grooming line up the trigger.[1][6]

The strongest predisposing factor is tightly curled ("woolly") nuchal hair: the acute angle of emergence and the tight curl mean a closely-clipped tip re-enters or pierces the skin the moment it grows. Skin of colour independently primes keloidal-type scarring in response to any follicular inflammation.[1][11]

The mechanical triggers are the levers you can actually pull:[1]

• Close clipping of the nape with clippers or a razor — the dominant precipitant; the shorter the cut and the sharper the blade, the higher the risk.
• Friction and pressure — tight collars, helmet straps (motorcycle, construction, military), backpacks, headrests, traction braids.
• Traction and chemical relaxers, especially in the rare female patient who also trims the nape close.[12]

Athletes, military recruits, police officers and motorcyclists are over-represented for the same reason — helmets plus close crops.[6]

Because AKN belongs to the follicular occlusion spectrum, screen for hidradenitis suppurativa, dissecting cellulitis, acne conglobata and pilonidal sinus. Severe disease has also been linked to ciclosporin and other post-transplant immunosuppression, and to anabolic steroid use.[1]

Four steps from a sharp tip to a keloidal plaque

The mechanism is pseudofolliculitis barbae transposed to the nape — the same hair-shaft foreign body on a different anatomical stage. Four steps, in order:[1][11]

Step 1 — Close clipping of tightly curled nuchal hair. Clippers cut the shaft obliquely, leaving a sharp tip; because the follicle is curved, the cut hair retracts below the surface.[1]

Step 2 — Extrafollicular or transfollicular penetration. As the hair grows, the sharp tip either curves back out and pierces the skin next to the follicle (extrafollicular) or breaches the follicular wall into the dermis (transfollicular). Either way, keratin and hair-shaft protein land inside the dermis — foreign material.[1][5]

Step 3 — Foreign-body granulomatous reaction. The immune system walls off the hair fragment with multinucleated giant cells, histiocytes, lymphocytes and plasma cells; Staphylococcus aureus may superinfect and add an acute neutrophilic folliculitis.[1]

Step 4 — Fibrosis and follicular destruction. Chronic inflammation drives dense keloidal-type fibrosis that destroys the follicle, its sebaceous gland and the arrector pili — leaving the firm keloidal plaque and the permanent cicatricial alopecia of late disease.[1]

Why the nape and not elsewhere? A uniquely dense population of curved follicles, constant friction and occlusion from collars and helmets, and the site the barber shaves shortest — three forces converging on one strip of skin.[1]

Why "keloid-like" yet not a keloid? A true keloid is a benign fibroproliferative tumour of disorganised type-III collagen that extends beyond the wound, recurs after excision, and has no follicular trigger. AKN fibrosis is centred on a ruptured follicle and is trigger-dependent — stop the clipping and progression halts. That single difference is why trigger avoidance and laser sit at the centre of treatment, not excision-and-hope.[1][9]

At the bedside — site is the diagnosis

Site, morphology, demographic — in that order — make AKN a bedside diagnosis. The lesion is confined to the nape and lower occipital scalp, almost always as a horizontal band along and just below the occipital hairline, bilateral and symmetric. It does not touch face, chest, back or beard — which separates it from acne vulgaris and pseudofolliculitis barbae on the spot.[1][6]

By stage, expect:[1]

• Stage I — 2–5 mm firm follicular papules and tiny pustules in the hairline, often itchy; easily mistaken for ordinary folliculitis.
• Stage II — firm, dome-shaped, skin-coloured to hyperpigmented keloidal papules coalescing into a plaque, with tufted hairs (polytrichia) — multiple shafts from one dilated ostium — the single most characteristic sign.
• Stage III — a large lobulated, bossellated keloidal mass with discharging sinus tracts, abscesses and scarring alopecia; hard, fixed, tender.[1][7]

Symptoms are often quieter than the appearance suggests. Many patients are asymptomatic apart from the cosmetic concern; when present, expect pruritus, pain (with abscess or sinus), discharge of pus or keratin, foul odour from chronically infected sinuses, and bleeding. The cosmetic and psychological burden is usually the chief complaint — measure it with the DLQI.[6]

The course is chronic, indolent, progressive and relapsing over years to decades; spontaneous resolution is rare, and without intervention most patients progress to permanent scarring alopecia, punctuated by acute infective flares.[1]

The mimics — site is the discriminator

A face-off table forces the discriminator to the surface. The single highest-yield exam skill on AKN is naming what it is not, using site as the blade.[1][3]

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One-line discriminators: AKN owns the nape; pseudofolliculitis barbae owns the beard; folliculitis decalvans owns the vertex; dissecting cellulitis owns the whole boggy scalp. If the lesion is not on the nape, it is not AKN.[11]

Other considerations:[1]

• Acne vulgaris — face, chest, back; comedones; never the nape alone.
• Tinea capitis or tinea barbae — scaly annular patch with hair loss; KOH positive.
• Discoid lupus — well-demarcated erythematous plaques with follicular plugging, carpet-tack scale and scarring; biopsy shows interface dermatitis; immunofluorescence a lupus band.
• Basal cell carcinoma — pearly papule with rolled border and telangiectasia; solitary; biopsy.
• Squamous cell carcinoma (Marjolin's ulcer) — a non-healing ulcer within a long-standing AKN plaque; biopsy, always.[1]

Confirm it clinically — and biopsy the ulcer

AKN is a clinical diagnosis; reach for the blade only when the picture is atypical or the ulcer will not heal. History and examination do the work in the overwhelming majority.[1][4]

Take a focused history: how short the nape is clipped and how often (clippers vs razor, "fade to skin"), mechanical exposure (helmets, collars, backpacks, traction braids), itch, pain, discharge, odour, bleeding, cosmetic and psychological impact (DLQI), family history of keloids, and the follicular occlusion tetrad (axillary or inguinal boils, boggy scalp nodules, conglobate acne, pilonidal sinus). Consider HIV or immunosuppression if the disease is severe or atypical.[1]

Examine the whole scalp, beard, axillae, groins and gluteal cleft — not just the nape. Palpate the plaque for firmness, fixity, fluctuation (abscess) and sinus tracts; use dermoscopy to show tufted hairs, perifollicular scale, dilated ostia, broken shafts and white structureless areas of fibrosis.[1]

Reserve a 4 mm punch biopsy for three situations: atypical morphology or site where a mimicker (discoid lupus, BCC, sarcoidosis) is plausible; a non-healing ulcer within a long-standing plaque to exclude Marjolin's ulcer; and refractory disease. Histology shows a ruptured follicle, a naked hair shaft in the dermis ringed by a foreign-body granuloma with giant cells, and dense keloidal-type fibrosis — not always separable from folliculitis decalvans, hence the overlap debate.[3]

A bacterial swab from any pus or sinus typically grows Staphylococcus aureus (including MRSA in endemic areas); fungal studies are negative and only worth doing if tinea is genuinely in play. Before systemic therapy or surgery send FBC, U&E, LFTs, and HIV and hepatitis serology if surgery is planned; add baseline FBC, U&E and LFTs for the rifampicin-plus-clindamycin combination.[1][10]

The management ladder — five rungs, one direction

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The ladder is stage-based, and every rung has the same goal: remove the trigger and destroy the culpable follicles. Skip a rung and the disease comes back; the order matters.[1][7][8]

Rung 1 — Trigger avoidance and topical therapy (all stages; first-line for stage I)

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Rung 2 — Intralesional corticosteroid (stage II plaque; adjunct at all stages)

• Agent: triamcinolone acetonide, intralesional.
• Concentration: 10 mg/mL for softer papules, 40 mg/mL for firm keloidal plaques.
• Volume: 0.05–0.1 mL per papule through a 30-gauge needle; total 20–30 mg per session, never over 40 mg.
• Frequency: every 4–6 weeks until flattening, typically 3–6 sessions.
• Effect: flattens papules, settles pruritus and pain.
• Warn first: atrophy, telangiectasia and hypopigmentation — the last especially visible in skin of colour, so counsel before you inject.[1][2]

Adjuvant or alternative intralesional agents for refractory plaques include 5-fluorouracil (50 mg/mL, alone or mixed with triamcinolone) and verapamil (2.5 mg/mL).[2]

Rung 3 — Systemic therapy (moderate to severe; sinus or abscess; refractory)

Anti-inflammatory tetracycline: doxycycline 100 mg BD orally for 8–12 weeks (or minocycline 100 mg OD), continued long-term at the lowest effective dose if it helps. Warn about photosensitivity, gastrointestinal upset and oesophagitis (take upright with water); avoid in pregnancy and in children.[1]

The follicular-occlusion combination for refractory or sinus-stage disease borrows the regimen proven in folliculitis decalvans:[10]

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Other systemic agents in resistant disease: isotretinoin (off-label; 0.5 mg/kg/day for 16–24 weeks; only in patients past childbearing potential, with strict contraceptive cover) for the follicular occlusion overlap, and a short tapering course of prednisolone (0.5 mg/kg/day over 2–3 weeks) only for an acute severe inflammatory flare — not as routine.[2]

Rung 4 — Laser and physical modalities (adjuvant; the recurrence key)

Laser hair removal is the single most important adjuvant, because it destroys the culpable nuchal follicles and removes the trigger.[9]

• Laser of choice in skin of colour: long-pulsed Nd:YAG 1064 nm — deepest penetration, lowest melanin absorption, safest in Fitzpatrick IV–VI.
• Alternatives: diode 810 nm and long-pulsed alexandrite 755 nm (the latter for lighter skin types only).
• Protocol: 4–8 sessions at 4–8 week intervals after a test patch, with topical anaesthetic; counsel about transient erythema or oedema and a small risk of pigmentary change.
• Indication: any active disease (to cut the follicular load) and, crucially, after any surgical excision to prevent new lesions at the periphery.[9]

Cryotherapy, electrodessication and radiofrequency ablation of individual papules are options for small-volume disease; cryotherapy is unpredictable in skin of colour (hypopigmentation) and has largely yielded to laser. Intralesional 5-FU and verapamil sit here too. Superficial radiotherapy is rarely used as a post-excision adjuvant for severe keloidal diathesis — the risk-benefit balance is poor in young patients.[1]

Rung 5 — Surgical excision (stage III tumoural; refractory plaque or sinus disease)

Surgery is definitive for extensive, tumoural or sinus/abscess disease that has failed medical therapy.[7][8]

• Principle: complete excision of all involved skin and subcutaneous tissue down to the deep cervical fascia or occipital periosteum, to remove every culpable follicle.
• Closure by defect size: primary closure for small defects; second-intention healing (excise and leave open — surprisingly well tolerated on the nape, slow over 8–12 weeks, low recurrence); split-thickness skin grafting; or local rotation or advancement flaps for large defects.
• Outcome: wide excision has the lowest recurrence of any single modality — under 10–15 percent in most series; recurrence is highest with incomplete excision or when close clipping resumes.
• Post-op adjuvants: intralesional triamcinolone to the healing scar at 4–6 weeks, laser hair removal to the surrounding nuchal skin, and a custom nuchal pressure garment for 12–18 hours a day over 4–6 months in keloidal-prone patients.[7][8]

Escalation triggers:[1]

• No response to rung 1 after 8–12 weeks → add rung 2 (intralesional triamcinolone).
• Active papular or plaque disease despite rungs 1–2, or sinus or abscess → add rung 3 (doxycycline, or rifampicin 300 mg BD + clindamycin 300 mg BD) and arrange laser.
• Tumoural plaque, persistent sinuses, or failure of medical therapy → rung 5 (surgical excision).
• Any non-healing ulcer in a chronic plaque → biopsy for Marjolin's ulcer before proceeding.[1]

Marjolin's ulcer — the one thing you must not watch

A non-healing ulcer inside a long-standing AKN plaque is squamous cell carcinoma until the biopsy says otherwise. Chronic scarring alopecia is a recognised soil for scar-associated SCC, and the threshold to biopsy is, deliberately, very low.[1]

This is the single preventable-harm line on the page: any ulcer in a plaque that has been there for years and will not heal gets a 4 mm punch — not a trial of antibiotic, not a wait-and-see, not another course of intralesional steroid. Biopsy first, treat after.[1]

The same-day decisions — abscess, sepsis, distress

AKN is rarely an emergency, but three scenarios move today. Recognise them at the door.[1]

Acute abscess in a plaque — fluctuant, painful — gets incision and drainage (or punch drainage for a recurrent sinus), a swab, and a 7–10 day anti-staphylococcal course guided by local sensitivities (flucloxacillin 500 mg QDS oral, or clindamycin 300 mg QDS if MRSA is suspected or confirmed), with paracetamol and a short NSAID course.[1]

Severe pain or systemic symptoms — fever, cellulitis beyond the nape — need same-day assessment, intravenous antibiotics and consideration of drainage. Psychological distress is real; offer reassurance, an explicit plan, and counselling or psychology referral, and screen for depression and anxiety.[1][6]

Refer urgently for a non-healing ulcer, extensive tumoural disease amenable to excision, refractory disease after first- and second-line therapy, or diagnostic uncertainty.[1]

Special situations

Pregnancy. Avoid tetracyclines (doxycycline, minocycline) and systemic retinoids (isotretinoin) — both teratogenic. Favour physical measures (trigger avoidance, laser — safe in pregnancy), topical clindamycin or erythromycin, and intralesional triamcinolone in single small doses (avoid high cumulative doses). Defer elective surgery until after delivery.[1]

Women (rare). Usually milder and often mislabelled as acne vulgaris or folliculitis decalvans; address chemical relaxers, traction braids and overzealous nape trimming, prefer laser over shaving, and withhold systemic retinoids unless contraception is reliable.[12]

Adolescents. Increasingly recognised, driven by barbershop clipping and sports helmets; manage as in adults with extra attention to cosmetic and psychological impact, and avoid systemic retinoids in adolescent girls of childbearing potential without contraception.[6]

Immunosuppressed (renal transplant on ciclosporin, HIV, chemotherapy). AKN may be more severe, atypical and refractory; reduce ciclosporin where possible (it has been implicated as a trigger), treat staphylococcal superinfection aggressively, and optimise the patient before any surgery.[1]

Evidence and the names that score marks

AKN has no single global guideline; recommendations converge from the AAD and StatPearls or UpToDate (US), the BAD and NICE CKS (UK), EADV consensus (Europe) and IADVL (India) — all on the same stage-based ladder.[1][4]

The rifampicin 300 mg BD + clindamycin 300 mg BD combination is best evidenced for folliculitis decalvans (Miguel-Gómez et al, JAAD 2018, multicentre series, response over 70 percent) and is extrapolated to AKN as part of the same spectrum.[10]

Long-pulsed Nd:YAG 1064 nm is the laser of choice in skin of colour (Roberts, J Drugs Dermatol 2019), with the lowest pigmentary risk in Fitzpatrick IV–VI; surgical series (Madura 2021; Umar 2019) show excision to the fascia with second-intention healing or primary closure gives the lowest recurrence, and lesion-tailored selection improves cosmesis. Doche et al (Int J Dermatol 2019) argue AKN and folliculitis decalvans share a final common pathway of follicular rupture and granulomatous scarring, supporting overlapping therapy.[3][7][8][9]

Khumalo et al (Br J Dermatol 2007) documented the high prevalence of traction and traumatic scalp disorders in African adults tied to tight hairdressing — the evidence base for the mechanical triggers you counsel every patient about.[12]

The mantra, and the mnemonic

[1] [1]

The mantra: stop the clipping, lose the follicles, or it comes back. Every rung of the ladder — topicals, steroid, antibiotic, laser, surgery — is a different way of doing those two things; miss either and relapse is near-certain.[1][9]

The consultant confession: I tell every patient, on the day we operate, that the surgery is the easy part — the lifelong ban on close clipping is the hard part, and it is non-negotiable. Recurrence after excision is almost always resumed clipping, not failed surgery.[8]

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Ward-round test — three stems, thirty seconds each

Stem 1 — the man from the top of the topic (answer)

The 23-year-old motorcyclist with a two-year "keloid" across the nape, tufted hairs and two discharging sinuses. The GP called it a keloid and gave a topical steroid. What is wrong with that plan? Model: Two errors. First, this is AKN, not a true keloid — tufted hairs and sinus tracts on the nape in a young Black man who shaves to the skin are pathognomonic; a keloid would have no follicular tufting and no sinus. Second, topical steroid alone ignores the follicular trigger: the disease marches back the day he next visits the barber. Stage him (this is stage II–III), add intralesional triamcinolone 10–40 mg/mL every 4–6 weeks, start doxycycline 100 mg BD or the rifampicin-plus-clindamycin combination, arrange long-pulsed Nd:YAG 1064 nm laser, and counsel a lifelong ban on close clipping. Biopsy any ulcer.[1][6]

Stem 2 — the ulcer in the plaque (answer)

A 45-year-old has had a keloidal AKN plaque on the nape for twelve years. Three months ago a painful ulcer appeared in the middle of it and will not heal, with a foul discharge. Next step? Model: Biopsy — now. A non-healing ulcer within a long-standing scarring alopecia is squamous cell carcinoma (Marjolin's ulcer) until proven otherwise, and chronic AKN is a recognised soil for scar-associated SCC. Do not trial another antibiotic or more intralesional steroid; a 4 mm punch of the ulcer edge is the single decisive step. If SCC is confirmed, treat as a cutaneous malignancy (wide local excision, staging) — not as a flare of AKN.[1]

Stem 3 — the pregnant woman with papules on the nape (answer)

A 28-year-old, 16 weeks pregnant, develops itchy follicular papules on the nape; she uses chemical relaxers and trims the nape close. How does pregnancy change the ladder? Model: The diagnosis is still AKN (rare in women, but relaxers, traction and close nape trimming are the triggers). Tetracyclines (doxycycline, minocycline) and systemic retinoids are teratogenic — stop them. Build the plan around what is safe in pregnancy: trigger avoidance (stop close trimming, switch the relaxer), topical clindamycin or erythromycin, a retinoid-free anti-inflammatory, intralesional triamcinolone in small single doses, and long-pulsed Nd:YAG 1064 nm laser, which is safe in pregnancy. Defer any elective excision until after delivery.[1][12]

References

1. [1]Olagun-Samuel C, Manduca S, Adotama P Acne Keloidalis Nuchae JAMA Dermatol, 2025.PMID 40601307
2. [2]Alves JP, Heck R Acne Keloidalis Nuchae J Cutan Med Surg, 2022.PMID 36124546
3. [3]Doche I, Coelho EQ, Quaresma MV, et al. Acne keloidalis nuchae and folliculitis decalvans: same process affecting the follicle or coexisting diseases? A retrospective study Int J Dermatol, 2019.PMID 31241169
4. [4]Al Aboud DM, Badri T Acne Keloidalis Nuchae 2026.PMID 29083612
5. [5]Kolve J, Crutchfield C Acne keloidalis nuchae Dermatol Nurs, 2003.PMID 14735606
6. [6]Patel A, Pippin M, Marshall D A Classic Presentation of Acne Keloidalis Nuchae in a Black Male Cureus, 2025.PMID 40656282
7. [7]Madura C, Kareddy S, Kusuma MR, et al. Multimodality Surgical Treatment Approach to Acne Keloidalis Nuchae Based on Lesion Morphology J Cutan Aesthet Surg, 2021.PMID 34566374
8. [8]Umar S Selection criteria and techniques for improved cosmesis and predictable outcomes in laser hair removal treatment of acne keloidalis nuchae JAAD Case Rep, 2019.PMID 31205997
9. [9]Roberts WE, et al. Laser Treatment of Skin of Color for Medical and Aesthetic Uses With a New 650-Microsecond Nd:YAG 1064nm Laser J Drugs Dermatol, 2019.PMID 31017752
10. [10]Miguel-Gómez L, Rodrigues-Barata AR, Molina-Ruiz A, et al. Folliculitis decalvans: Effectiveness of therapies and prognostic factors in a multicenter series of 60 patients with long-term follow-up J Am Acad Dermatol, 2018.PMID 29864465
11. [11]Ogunbiyi A Pseudofolliculitis barbae; current treatment options Clin Cosmet Investig Dermatol, 2019.PMID 31354326
12. [12]Khumalo NP, Jessop S, Gumedze F, et al. Hairdressing and the prevalence of scalp disease in African adults Br J Dermatol, 2007.PMID 17725667