Residency · Residency · Dermatology
Approach to Alopecia: Scarring vs. Non-Scarring
Introduction
Hair loss is one of the most common reasons for dermatology consultation and carries significant psychological impact. The fundamental diagnostic question is whether the alopecia is scarring (cicatricial) or non-scarring (non-cicatricial), as this distinction determines the urgency of intervention, prognosis, and therapeutic approach. Scarring alopecia involves permanent destruction of the hair follicle, making early diagnosis and treatment essential to prevent irreversible hair loss.
Initial Evaluation
History
A thorough history should address onset and duration (acute versus gradual, with attention to recent triggers such as stress, illness, medication changes, or pregnancy), pattern (focal, multifocal, diffuse, or patterned), and associated symptoms. Pruritus, pain, and burning are common in scarring alopecia, while non-scarring forms are typically asymptomatic. Hair care practices should be reviewed, including chemical treatments, tight hairstyles, and heat styling. Medication history is important, particularly anticoagulants, retinoids, chemotherapy, antithyroid drugs, lithium, and valproic acid. Relevant medical history includes thyroid disease, iron deficiency, autoimmune conditions, recent surgery, and hormonal changes. Family history of androgenetic alopecia, alopecia areata, and autoimmune diseases should be assessed.
Physical Examination
The examination should assess distribution and pattern across the vertex, frontal hairline, temporal areas, and occipital scalp. The scalp surface is evaluated for erythema, scaling, pustules, atrophy, and loss of follicular ostia. Hair shafts are examined for broken hairs, exclamation point hairs, vellus hairs, and hair caliber variation. The pull test is performed by grasping 40 to 60 hairs near the base and applying gentle traction; more than 6 hairs extracted indicates active shedding. Trichoscopy (dermoscopy of the scalp) is invaluable for distinguishing scarring from non-scarring alopecia and narrowing the differential diagnosis.
Key Distinguishing Features
| Feature | Non-Scarring | Scarring |
|---|---|---|
| Follicular ostia | Preserved | Absent (replaced by fibrosis) |
| Scalp surface | Normal or mildly inflamed | Atrophic, shiny, or fibrotic |
| Reversibility | Potentially reversible | Permanent once destroyed |
| Symptoms | Usually asymptomatic | Often symptomatic (pain, itch, burn) |
Non-Scarring Alopecias
Diffuse Non-Scarring Alopecia
Telogen Effluvium
Telogen effluvium is the most common cause of diffuse hair loss, resulting from a premature shift of anagen hairs into the telogen phase. Triggers include physiologic stress (surgery, high fever, crash dieting), postpartum changes (2 to 4 months after delivery), medication changes, and emotional stress. The presentation is diffuse thinning with a positive pull test but no scalp abnormalities. Trichoscopy shows an increased proportion of short regrowing hairs without miniaturization. The condition is self-limited in most cases, with hair regrowth occurring over 3 to 6 months after removing the trigger. Chronic telogen effluvium (persisting beyond 6 months) is a diagnosis of exclusion, often idiopathic, and predominantly affects middle-aged women.
Anagen Effluvium
Anagen effluvium results from abrupt interruption of actively growing (anagen) hair by cytotoxic agents (chemotherapy), radiation, or toxin exposure. Hair loss occurs within days to weeks of exposure, much faster than the 2 to 3 months seen in telogen effluvium. Trichoscopy reveals tapered or pencil-point fractures of the hair shaft. The condition is reversible upon discontinuation of the offending agent.
Focal Non-Scarring Alopecia
Alopecia Areata
Alopecia areata is an autoimmune-mediated non-scarring alopecia targeting the hair follicle bulb. It presents as well-circumscribed, smooth, round patches of hair loss with characteristic exclamation point hairs (3 to 4 mm dystrophic hairs that taper proximally) at the margins. It is covered in detail in Lecture 47.
Tinea Capitis
Tinea capitis is a dermatophyte infection of the scalp and the most common cause of alopecia in prepubertal children. The black dot pattern results from broken hairs at the scalp surface in endothrix infection (Trichophyton tonsurans), while the gray patch pattern shows scaly patches with broken hairs in ectothrix infection. A kerion is a boggy, inflammatory, pustular mass representing a vigorous immune response. Diagnosis is established through KOH preparation, fungal culture, and trichoscopy (which may reveal comma hairs, corkscrew hairs, and broken hairs). Treatment requires oral antifungals (griseofulvin or terbinafine for 6 to 8 weeks), as topical therapy alone is insufficient.
Trichotillomania
Trichotillomania is a hair-pulling disorder producing irregularly shaped patches with hairs broken at varying lengths. Trichoscopy shows black dots, V-sign, flame hairs, tulip hairs, and coiled hairs. There is no scalp inflammation, and the distribution often favors the frontal or temporal area on the dominant-hand side. The Friar Tuck sign describes short hairs remaining in the patch that are too short to grasp. Management involves behavioral therapy (habit reversal training) with or without psychiatric referral.
Traction Alopecia
Traction alopecia is covered in detail in Lecture 48.
<image>Trichoscopy comparison images showing: exclamation point hairs and yellow dots in alopecia areata, comma hairs and black dots in tinea capitis, and flame hairs with V-sign in trichotillomania</image>
Scarring (Cicatricial) Alopecias
Classification
Scarring alopecias are classified by the predominant inflammatory infiltrate on histopathology. Lymphocytic forms include lichen planopilaris (LPP), frontal fibrosing alopecia (FFA), central centrifugal cicatricial alopecia (CCCA), discoid lupus erythematosus (DLE), and pseudopelade of Brocq. Neutrophilic forms include dissecting cellulitis and folliculitis decalvans. Mixed forms include acne keloidalis nuchae and erosive pustular dermatosis.
Lymphocytic Scarring Alopecias
Lichen Planopilaris (LPP)
Lichen planopilaris is the most common primary scarring alopecia, involving lymphocytic interface attack on the follicular bulge stem cells. It presents as multifocal patches of scarring alopecia with perifollicular erythema and perifollicular scale (follicular keratosis) at the active margin. Trichoscopy shows perifollicular scaling, perifollicular erythema, loss of follicular openings, and tubular perifollicular casts. LPP may coexist with lichen planus of the skin, nails, or mucous membranes. Treatment includes potent topical or intralesional corticosteroids, hydroxychloroquine, doxycycline, and mycophenolate mofetil.
Frontal Fibrosing Alopecia (FFA)
Frontal fibrosing alopecia is a variant of LPP characterized by progressive band-like recession of the frontal and temporal hairline. It predominantly affects postmenopausal women, and its incidence is increasing dramatically. It is often accompanied by eyebrow loss (50 to 80%) and loss of body hair. The lonely hair sign describes isolated retained hairs within the alopecic band. Perifollicular erythema and scaling are present at the recession margin. Treatment is similar to LPP, and finasteride or dutasteride may slow progression.
Discoid Lupus Erythematosus (DLE)
DLE presents as well-demarcated, erythematous, scaly plaques with follicular plugging, dyspigmentation (central hypopigmentation with peripheral hyperpigmentation), and atrophic scarring. The carpet tack sign describes keratotic spicules on the undersurface of removed scale. The scalp is the most common site of isolated DLE. Five to 10% of DLE patients progress to SLE, warranting ANA, CBC, and urinalysis testing. Treatment involves potent TCS, intralesional triamcinolone, and hydroxychloroquine as first-line systemic therapy.
Neutrophilic Scarring Alopecias
Dissecting Cellulitis (Perifolliculitis Capitis Abscedens et Suffodiens)
Dissecting cellulitis is part of the follicular occlusion triad (along with hidradenitis suppurativa and acne conglobata). It presents with boggy, fluctuant nodules and sinus tracts on the vertex and occiput with purulent drainage. Treatment options include isotretinoin, intralesional corticosteroids, oral antibiotics (rifampin plus clindamycin), and adalimumab for refractory cases.
Folliculitis Decalvans
Folliculitis decalvans is a chronic, relapsing condition characterized by follicular pustules and crusts with tufted folliculitis, in which multiple hairs emerge from a single dilated follicular opening. Staphylococcus aureus may play a pathogenic role. Treatment requires prolonged courses of rifampin plus clindamycin, with dapsone as maintenance therapy.
<image>Clinical photograph comparison of scarring alopecias showing lichen planopilaris with perifollicular erythema and scale at the active margin, discoid lupus with central scarring and peripheral hyperpigmentation, and folliculitis decalvans with tufted folliculitis and pustules</image>
Diagnostic Workup
Trichoscopy is the first-line, non-invasive tool to guide the differential diagnosis. Scalp biopsy should include two 4 mm punch biopsies: one processed for horizontal sectioning (which evaluates follicular density and inflammation pattern) and one for vertical sectioning (which evaluates depth of inflammation and scarring). Laboratory studies are obtained as indicated and may include CBC, ferritin, TSH, ANA, RPR, DHEA-S, free and total testosterone, and prolactin. Fungal culture is mandatory in children with focal alopecia. A pull test and hair mount evaluate for hair shaft abnormalities.
Key Clinical Pearls
Loss of follicular ostia on clinical exam or trichoscopy is the cardinal sign of scarring alopecia, and once follicles are destroyed, hair loss is permanent. Scalp biopsy with horizontal sections is the gold standard for classification, and this should be specified to the pathologist. Tinea capitis must always be excluded in children with focal alopecia before initiating corticosteroid therapy. Active scarring alopecia is a dermatologic urgency, as delayed treatment means irreversible follicular destruction. Trichoscopy has transformed alopecia diagnosis and should be performed at every hair loss evaluation.
<image>Flowchart algorithm for the systematic approach to alopecia: initial assessment dividing into scarring vs non-scarring, then focal vs diffuse, with key diagnostic features and conditions at each branch point</image>
References
- Olsen EA, Bergfeld WF, Cotsarelis G, et al. Summary of North American Hair Research Society (NAHRS): guidelines for the classification of cicatricial alopecias. J Am Acad Dermatol. 2003;48(1):103-110.
- Mubki T, Rudnicka L, Olszewska M, Shapiro J. Evaluation and diagnosis of the hair loss patient: Part I — History and clinical examination. J Am Acad Dermatol. 2014;71(3):415.e1-415.e15.
- Rudnicka L, Olszewska M, Rakowska A. Atlas of Trichoscopy: Dermoscopy in Hair and Scalp Disease. Springer; 2012.
- Harries MJ, Sinclair RD, Macdonald-Hull S, et al. Management of primary cicatricial alopecias: options for treatment. Br J Dermatol. 2008;159(1):1-22.
