Definition and epidemiology
Alopecia refers to hair loss, which can be localized or diffuse, scarring or non-scarring, and congenital or acquired. The term encompasses many distinct diseases rather than a single diagnosis, so classification is essential before counseling patients.
Major categories
- Androgenetic alopecia (AGA): most common cause of hair loss overall; affects up to 50% of men by age 50 and a significant proportion of women, usually postmenopausal
- Alopecia areata (AA): autoimmune, affects roughly 2% of people at some point in their lifetime, often starts in childhood or young adulthood
- Telogen effluvium: diffuse shedding, very common, often triggered by a physiologic stressor 2-3 months prior
- Scarring (cicatricial) alopecias: uncommon but important because hair follicles are permanently destroyed
- Tinea capitis, trichotillomania, traction alopecia: additional causes seen more often in children or specific populations
Androgenetic alopecia and telogen effluvium together account for the large majority of patients presenting with hair thinning in primary care and dermatology clinics.
- Scarring vs non-scarring is the single most important clinical branch point in alopecia.
- Exclamation point hairs at the margin are classic for alopecia areata.
- Telogen effluvium shedding appears about 2-3 months after the triggering event.
- Finasteride works by inhibiting 5-alpha-reductase, blocking testosterone to DHT conversion.
- Alopecia areata is T-cell mediated and associated with other autoimmune diseases, especially thyroid disease.
- Scalp biopsy with horizontal sectioning is the test of choice when scarring alopecia is suspected.
- Minoxidil is first-line and available over the counter for androgenetic alopecia in both sexes.
- JAK inhibitors carry a boxed warning for serious infections, MACE, malignancy, and thrombosis.
Etiology and risk factors
- Androgenetic alopecia: genetically determined sensitivity of hair follicles to dihydrotestosterone (DHT); family history is the strongest risk factor
- Alopecia areata: autoimmune, T-cell mediated attack on hair follicles; associated with other autoimmune disease (thyroid disease, vitiligo, atopic dermatitis) and family history
- Telogen effluvium: triggered by childbirth, severe illness, major surgery, high fever, crash dieting, iron deficiency, thyroid dysfunction, or new medications (e.g., retinoids, anticoagulants, beta-blockers)
- Scarring alopecia: lichen planopilaris, discoid lupus erythematosus, folliculitis decalvans, and central centrifugal cicatricial alopecia (more common in women of African descent)
- Traction alopecia: tight hairstyles (braids, weaves, ponytails) causing mechanical follicle damage
- Trichotillomania: psychiatric compulsive hair-pulling disorder
- Tinea capitis: dermatophyte infection, mainly in children
- Nutritional: iron deficiency, zinc deficiency, severe protein-calorie malnutrition, biotin deficiency (rare)
Pathophysiology
Normal hair cycling moves follicles through anagen (growth, years), catagen (brief transition), and telogen (rest, ~3 months) before shedding and restarting. Disease processes disrupt this cycle in characteristic ways.
- Androgenetic alopecia: DHT binds androgen receptors in genetically susceptible follicles, progressively shortening anagen and miniaturizing terminal hairs into vellus-like hairs, producing a receding/thinning pattern rather than complete baldness in most cases
- Alopecia areata: loss of immune privilege at the hair follicle allows CD8+ T cells to attack anagen follicles, causing abrupt, non-scarring, often well-circumscribed round patches of hair loss
- Telogen effluvium: a stressor prematurely pushes a large proportion of anagen follicles into telogen simultaneously; shedding becomes clinically apparent about 2-3 months after the trigger because of the lag between telogen entry and shedding
- Scarring alopecia: inflammation destroys the follicular stem cell niche in the bulge region, replacing it with fibrosis, so regrowth is not possible once scarring is established
Clinical features
- Androgenetic alopecia: gradual, patterned thinning; bitemporal recession and vertex balding in men (Hamilton-Norwood scale); diffuse crown thinning with preserved frontal hairline in women (Ludwig scale)
- Alopecia areata: sudden, well-demarcated round or oval patches of complete hair loss, smooth scalp without scarring; exclamation point hairs at the margin; nail pitting in some patients; can progress to alopecia totalis (scalp) or universalis (entire body)
- Telogen effluvium: diffuse increased shedding (positive hair pull test), no scarring, scalp otherwise normal, history of a trigger 2-3 months earlier
- Scarring alopecia: patches with loss of visible follicular openings, erythema, scaling, or scarring plaques; often symptomatic (itching, burning, pain)
- Tinea capitis: scaling patches, broken hairs, possible kerion (boggy inflamed mass) in children
- Traction alopecia: thinning along the frontal/temporal hairline in patients with tight hairstyling habits
- Trichotillomania: irregular patches with hairs of varying length, often in reachable areas, no inflammation
Diagnosis
Diagnosis is largely clinical, supported by targeted tests when the picture is unclear.
Approach
- History: onset (sudden vs gradual), pattern, associated symptoms, medication changes, recent illness/surgery/delivery, family history, hairstyling practices, psychiatric history
- Hair pull test: gentle traction removes more than a few hairs in active shedding (telogen effluvium, active AA)
- Trichoscopy (dermoscopy of scalp): yellow dots and exclamation point hairs in AA; miniaturized hairs with hair diameter variability in AGA; peripilar casts/perifollicular erythema in scarring alopecia
- Scalp biopsy: reserved for diagnostic uncertainty or suspected scarring alopecia; horizontal sectioning assesses follicle density and ratio; essential to confirm scarring process and guide urgency of treatment
- Laboratory tests: TSH, ferritin, CBC when telogen effluvium or diffuse thinning is suspected; consider ANA if lupus-related scarring alopecia suspected
- Fungal culture or KOH prep for suspected tinea capitis
| Type | Pattern | Scarring | Key test finding |
|---|---|---|---|
| Androgenetic | Patterned thinning | No | Miniaturized hairs on trichoscopy |
| Alopecia areata | Round patches | No | Exclamation point hairs |
| Telogen effluvium | Diffuse shedding | No | Positive hair pull test |
| Scarring alopecia | Patches, variable shape | Yes | Loss of follicular openings on biopsy |
Differential diagnosis
- Androgenetic alopecia vs telogen effluvium: AGA is gradual and patterned; telogen effluvium is diffuse and often has an identifiable trigger
- Alopecia areata vs tinea capitis: tinea capitis usually shows scale and broken hair stubs, more common in children, confirmed by fungal culture
- Alopecia areata vs trichotillomania: trichotillomania shows hairs of irregular length and an irregular, non-round patch, usually without exclamation point hairs
- Scarring alopecia vs severe alopecia areata: biopsy distinguishes follicular destruction (scarring) from preserved but miniaturized/absent follicles (areata)
- Secondary syphilis: can cause a moth-eaten alopecia pattern, consider in sexually active patients with other systemic signs
- Nutritional/endocrine causes: iron deficiency and hypothyroidism can mimic or worsen diffuse thinning and should be screened for
Management
Treatment depends entirely on the underlying type; there is no universal therapy for "alopecia."
Androgenetic alopecia
- Topical minoxidil (over-the-counter in many countries) is first-line for both sexes
- Oral finasteride (or dutasteride in some regions) for men, blocking conversion of testosterone to DHT; not used in women who are or may become pregnant
- Spironolactone or other anti-androgens sometimes used off-label in women
- Hair transplantation for stable, advanced cases
Alopecia areata
- Intralesional corticosteroid injections for limited patchy disease; first-line in most guidelines
- Topical high-potency corticosteroids, especially in children
- Topical immunotherapy (e.g., diphencyprone) or systemic agents for extensive disease
- JAK inhibitors (e.g., baricitinib, ritlecitinib) are approved in several countries for severe alopecia areata and represent a major recent advance. These agents carry a boxed warning (shared across the JAK inhibitor class) for increased risk of serious infections, major adverse cardiovascular events (MACE), malignancy, and thrombosis, and require baseline and ongoing risk assessment before and during use
- Spontaneous remission occurs in many patients with limited patchy disease, so observation is reasonable in mild cases
Telogen effluvium
- Identify and correct the underlying trigger (iron repletion, thyroid treatment, stopping an offending drug)
- Reassurance that regrowth typically occurs within 6-12 months once the trigger resolves
Scarring alopecia
- Treated as a dermatologic emergency relative to other alopecias because damage is irreversible
- Anti-inflammatory therapy (topical/intralesional/systemic corticosteroids, hydroxychloroquine, doxycycline or other agents) to halt progression; choice depends on the specific subtype (lichen planopilaris, discoid lupus, folliculitis decalvans)
- Early dermatology referral is critical
General
- Psychological support and counseling are important across all types given the significant impact on quality of life and body image
- Wigs, scalp micropigmentation, and camouflage products are reasonable adjuncts
Complications and prognosis
- Androgenetic alopecia: slowly progressive, not reversible without treatment, but non-scarring so follicles remain potentially responsive to therapy
- Alopecia areata: unpredictable course; limited patchy disease often remits spontaneously, but relapse is common; progression to alopecia totalis/universalis carries a worse prognosis for regrowth
- Telogen effluvium: generally self-limited and fully reversible once the trigger is removed
- Scarring alopecia: hair loss is permanent in affected areas once fibrosis occurs; the main goal of treatment is halting further progression rather than regrowth
- Psychosocial impact: anxiety, depression, and reduced quality of life are common across all alopecia types and should be actively addressed
- Associated disease: alopecia areata patients should be screened for other autoimmune conditions, particularly thyroid disease
TELOGEN for telogen effluvium triggers: Thyroid disease, Emotional/physical stress, Low iron, Oral contraceptive changes, Giving birth (postpartum), Extreme diets, New drugs.
Practice questions
1. A 34-year-old man notices a single well-circumscribed, smooth, round bald patch on his scalp that developed over about one week. There is no scaling, erythema, or scarring. Examination of hairs at the margin shows hairs that are narrower proximally than distally. Which of the following is the most likely diagnosis?
2. A 28-year-old woman reports diffuse hair shedding for the past month. Three months ago she delivered a healthy baby after an uncomplicated pregnancy. Scalp examination shows no patches, no scarring, and a positive hair pull test. Which of the following is the most appropriate next step?
3. A 45-year-old woman of African descent presents with a slowly expanding area of hair loss at the vertex of the scalp. She reports itching and burning. Examination shows loss of visible follicular openings and perifollicular erythema. Which of the following is the most appropriate next step in management?
Frequently asked questions
What causes alopecia?
Alopecia has many distinct causes rather than one single cause: genetic androgen sensitivity in androgenetic alopecia, autoimmune follicle attack in alopecia areata, physiologic stress triggers in telogen effluvium, and inflammatory destruction of follicles in scarring alopecia. Infections like tinea capitis and mechanical damage from tight hairstyles or hair-pulling can also cause localized hair loss. Identifying which category applies determines both prognosis and treatment.
What are the first symptoms of alopecia?
The first sign is usually noticeable hair thinning or shedding, but the pattern varies by type. Androgenetic alopecia starts with gradual recession or crown thinning, alopecia areata presents as a sudden smooth round bald patch, and telogen effluvium causes diffuse increased shedding noticed on a pillow, in the shower drain, or on a hairbrush. Scarring alopecia often adds itching, burning, or visible scalp inflammation.
How is alopecia diagnosed?
Diagnosis starts with a focused history and scalp examination, often supported by trichoscopy to look for patterns like exclamation point hairs or miniaturized hairs. A hair pull test helps confirm active shedding, and blood tests (ferritin, thyroid function) are checked when telogen effluvium is suspected. A scalp biopsy is reserved for uncertain cases or when scarring alopecia is suspected, since this changes management urgency.
Is alopecia curable?
It depends on the type: telogen effluvium is usually fully reversible once the trigger resolves, androgenetic alopecia can be slowed or partially reversed with ongoing treatment but is not cured, and alopecia areata is unpredictable with possible spontaneous remission or relapse. Scarring alopecia causes permanent hair loss in affected areas because the follicles themselves are destroyed, so treatment focuses on stopping further progression rather than regrowth.
Alopecia areata vs androgenetic alopecia — what is the difference?
Alopecia areata is an autoimmune disease causing sudden, well-circumscribed round patches of hair loss at any age, while androgenetic alopecia is a genetically driven, slowly progressive patterned thinning linked to androgen sensitivity, typically affecting the crown and temples in men and the central scalp in women. Areata can remit or relapse unpredictably, whereas androgenetic alopecia follows a steady, progressive course without treatment.
Key drugs
Related conditions and differentials
Sources and further reading
StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: L65.9
Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.