Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Detect follicular destruction before it becomes irreversible, distinguish inflammatory, infective and traction patterns, and obtain correctly sited photographs, samples and biopsy without delaying specialist care.
Scarring alopecia is a clinicopathological outcome in which inflammation destroys the follicular unit and permanent fibrous tissue replaces it. Primary forms target follicles; secondary scarring follows burns, radiotherapy, tumour, severe infection or trauma. The practical recognition rule is disappearance of follicular openings in an area of hair loss, supported by shiny surface change, perifollicular inflammation or tufting. Early active disease may have subtle density loss but prominent itch, tenderness or burning.
Patterns guide but do not prove cause. Lichen planopilaris produces irregular patches with scale cuffing individual hairs; frontal fibrosing alopecia creates a band of recession and eyebrow loss; central centrifugal cicatricial alopecia expands from the crown; discoid lupus may leave dyspigmented atrophic plaques; folliculitis decalvans adds pustules and polytrichia. These appearances must be assessed in every skin tone. Erythema may appear red, violaceous, grey or dark brown, while scale and loss of ostia remain visible with magnification.
Lichen planopilaris, frontal fibrosing alopecia, CCCA and discoid lupus direct immune injury toward follicular structures that sustain regrowth.
Folliculitis decalvans and dissecting disease combine pustulation, microbial interactions and destructive inflammation, often producing tufted hairs and crust.
Longstanding traction, burns, radiation, severe infection, tumour and trauma can destroy follicles even when they were not the original immune target.
Genetic background, mechanical stress and product exposure may modify selected conditions, but no single practice or ancestry explains every case.
Inflammation attacks the bulge region that contains epithelial stem cells, removing the follicle's capacity to regenerate a cycling hair shaft.
Destroyed units collapse and are replaced by fibrous tissue, causing smooth skin and permanent disappearance of follicular openings.
Inflammatory disease often spreads around remaining peripheral hairs, leaving a quieter scarred centre and a diagnostically valuable active edge.
Fungal invasion or pustular bacterial-neutrophilic inflammation can rapidly damage follicles, making organism-directed treatment and inflammatory control time sensitive.
Smooth shiny skin without regular ostia in an alopecic area is the central sign that follicles have been replaced by scar.
Scale collars, erythema, hyperkeratosis, itch, pain or burning around remaining edge hairs identify a useful active zone for urgent assessment.
A pale scarred band behind the former hairline with isolated lonely hairs and eyebrow reduction supports frontal fibrosing alopecia.
Reduced density and loss of ostia beginning at the vertex and spreading outward, sometimes with tenderness or breakage, suggests CCCA.
Crust, pustules and several shafts emerging from one enlarged opening suggest folliculitis decalvans or another neutrophilic destructive process.
Broken hairs and marginal loss at sites of sustained pull may retain a fringe early; shiny skin later indicates irreversible traction scar.
Smooth patches retain follicular openings and may show exclamation-mark hairs or nail pitting without the perifollicular scale of active scar.
Patterned density loss shows miniaturised variable-calibre hairs but preserves ostia and lacks pain, pustules and shiny replacement fibrosis.
Scale, broken hairs, nodes and boggy inflammation require mycology; severe kerion can become a secondary scarring cause rather than a benign mimic.
Irregular patches with shafts broken at multiple lengths and no primary loss of openings suggest repeated manipulation, though chronic trauma can complicate appearance.
A firm, ulcerated, bleeding or rapidly enlarging scalp lesion with alopecia needs urgent biopsy to exclude infiltrative primary or metastatic disease.
Fibrosis prevents regrowth from destroyed follicles, so delayed inflammatory control leaves an expanding and irreversible visible hair deficit.
Pustules, erosions and treatment immunosuppression create bacterial or fungal complications that can accelerate pain and tissue damage.
Long courses of potent topical, injected or systemic immune treatment can cause skin, infection, metabolic, organ and reproductive adverse effects.
Visible permanent loss, insensitive advice and loss of valued styling options can affect identity, confidence, relationships and engagement with care.
Burning, tenderness or itch may precede obvious density loss, offering a window to diagnose and suppress inflammation before widespread destruction.
A smooth bald centre proves previous destruction but contains little active inflammation; its margin is usually more useful for diagnostic biopsy.
Active inflammation can appear violaceous, grey or dark brown in richly pigmented skin, so perifollicular scale and symptoms prevent under-recognition.
Tension and chemicals may modify risk, but ancestry or a culturally important style is not itself a diagnosis or sufficient explanation.
Because scarred follicles cannot regrow, preserved remaining density and resolution of symptoms are meaningful outcomes even without filling bald areas.
Waiting for a large shiny bald area before referring painful perifollicular inflammation.
Taking a biopsy from the featureless scarred centre rather than an active hair-bearing margin.
Calling every central loss in a Black woman traction and overlooking CCCA.
Giving repeated topical antifungals for pustular destructive disease without adequate hair or pus sampling.
Assuming normal red colour excludes inflammation in deeply pigmented skin.
Promising regrowth from an area in which follicular openings have already disappeared.
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A patient has a smooth scarred central scalp patch surrounded by painful perifollicular scale and erythema with remaining hairs. Where should a diagnostic biopsy be planned?
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
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