• Alopecia: absence of hair from areas where it normally grows
    • Anagen phase: growing hairs, 90% scalp hair follicles at any time, lasts 2 to 6 years
    • Catagen phase: regression of follicle, <1% follicles, lasts 3 weeks
    • Telogen phase: Resting phase lasts 2 to 3 months; 50 to 150 telogen hairs shed per day.
  • Classified as scarring (cicatricial), nonscarring, or structural
  • Scarring (cicatricial) alopecia
    • Inflammatory disorders leading to permanent hair loss and follicle destruction
    • Includes lymphocytic, neutrophilic, and mixed subtypes
  • Nonscarring alopecia
    • Lack of inflammation, no destruction of follicle
    • Includes focal, patterned, and diffuse hair loss such as androgenic alopecia, alopecia areata (AA), telogen effluvium, anagen effluvium, syphilitic hair loss
  • Structural hair disorders
    • Brittle or fragile hair from abnormal hair formation or external insult


  • Androgenic alopecia: onset in males between 20 and 25 years of age; onset in females prior to 40 years of age, affecting as many as 70% of women >65 years of age
  • AA: onset usually prior to 30 years of age; men and women are equally affected; well-documented genetic predisposition

Incidence greatest in Caucasians, followed by Asians, African Americans, and Native Americans; in females, 13% premenopausal, with as many as 70% females >65 years of age

  • Androgenic alopecia: in males, 30% Caucasian by 30 years of age, 50% by 50 years of age, and 80% by 70 years of age
  • AA: 1/1,000 with lifetime risk of 1–2%
  • Scarring alopecia: rare, 3–7% of all hair disorder patients

Etiology and Pathophysiology

  • Scarring (cicatricial) alopecia
    • Slick smooth scalp without follicles evident
    • Inflammatory disorders leading to permanent destruction of the follicle; it is not known what causes inflammation to develop.
    • Three major subtypes based on type of inflammation: lymphocytic, neutrophilic, and mixed
    • Primary scarring includes discoid lupus, lichen planopilaris, dissecting cellulitis of scalp, primary fibrosing, among others.
    • Secondary scarring from infection, neoplasm, radiation, surgery, and other physical trauma, including tinea capitis
    • Central centrifugal cicatricial alopecia most common form of scarring hair loss in African American women; etiology unknown but likely secondary to hair care practices
  • Nonscarring alopecia
    • Focal alopecia
    • AA
      • Patchy hair loss, usually autoimmune in etiology, T cell–mediated inflammation resulting in premature transition to catagen then telogen phases
      • May occur with hair loss in other areas of the body (alopecia totalis [entire scalp]), alopecia universalis (rapid loss of all body hair)
      • Nail disease frequently seen
      • High psychiatric comorbidity (1)
    • Alopecia syphilitica: “moth-eaten” appearance, secondary syphilis
    • Postoperative, pressure-induced alopecia: from long periods of pressure on one area of scalp
    • Temporal triangular alopecia: congenital patch of hair loss in temporal area, unilateral or bilateral
    • Traction alopecia: patchy, due to physical stressor of braids, ponytails, hair weaves
  • Pattern hair loss
    • Androgenic alopecia: hair transitions from terminal to vellus hairs
    • Male pattern hair loss: androgen-mediated hair loss in specific distribution; bitemporal, vertex occurs where androgen sensitive hairs are located on scalp. This is a predominantly hereditary condition (2).
      • Increased androgen receptors, increased 5-α reductase leads to increased testosterone conversion in follicle to dihydrotestosterone (DHT). This leads to decreased follicle size and vellus hair (2).
      • Norwood Hamilton classification type I to VII
      • Female pattern hair loss: thinning on frontal and vertex areas (Ludwig classification, grade I to III). Females with low levels of aromatase have more testosterone available for conversion to DHT (3). This carries an unclear inheritance pattern (2).
      • Polycystic ovarian syndrome, adrenal hyperplasia, and pituitary hyperplasia all lead to androgen changes and can result in alopecia.
    • Drugs (testosterone, progesterone, danazol, adrenocorticosteroids, anabolic steroids)
  • Trichotillomania: intentional pulling of hair from scalp; may present in variety of patterns
  • Diffuse alopecia
    • Telogen effluvium: sudden shift of many follicles from anagen to telogen phase resulting in decreased hair density but not bald areas
      • May follow major stressors, including childbirth, injury, illness; occurs 2 to 3 months after event
      • Can be chronic with ongoing illness, including SLE, renal failure, IBS, HIV, thyroid disease, pituitary dysfunction
      • Adding or changing medications (oral contraceptives, anticoagulants, anticonvulsants, SSRIs, retinoids, β-blockers, ACE inhibitors, colchicine, cholesterol-lowering medications, etc.)
      • Malnutrition from malabsorption, eating disorders; poor diet can contribute.
    • Anagen effluvium
      • Interruption of the anagen phase without transition to telogen phase; days to weeks after inciting event
      • Chemotherapy is most common trigger.
      • Radiation, poisoning, and medications can also trigger.
  • Structural hair disorders
    • Multiple inherited hair disorders including Menkes disease, monilethrix, and so forth. These result in the formation of abnormal hairs that are weakened.
    • May also result from chemical or heat damaging from hair processing treatments

  • Family history of early patterned hair loss is common in androgenic alopecia, also in AA.
  • Rare structural hair disorders may be inherited.

Risk Factors

  • Genetic predisposition
  • Chronic illness including autoimmune disease, infections, cancer
  • Physiologic stress including pregnancy and childbirth
  • Poor nutrition
  • Medication, chemotherapy, radiation
  • Hair chemical treatments, braids, weaves/extensions

General Prevention

Minimize risk factors where possible.

Commonly Associated Conditions

  • See “Etiology and Pathophysiology.”
  • Vitiligo—4.1% patients with AA; may be the result of similar autoimmune pathways (4)



  • Description of hair loss problem: rate of loss, duration, location, degree of hair loss, other symptoms including pruritus, infection, hair care, and treatments
  • Medications
  • Medical illness including chronic disease, recent illness, surgeries, pregnancy, thyroid disorder, iron deficiency, poisonings, exposures
  • Psychological stress
  • Dietary history and weight changes
  • Family history of hair loss or autoimmune disorders

Physical Exam

  • Pattern of hair loss
    • Generalized, patterned, focal
    • Assess hair density, vellus versus terminal hairs, broken hair.
  • Scalp scaling, inflammation, papules, pustules
  • Presence of follicular ostia to determine class of alopecia
  • Hair pull test
    • Pinch 25 to 50 hairs between thumb and forefinger and exert slow, gentle traction while sliding fingers up.
      • Normal: 1 to 2 dislodge
      • Abnormal: ≥6 hairs dislodged
      • Broken hairs (structural disorder)
      • Broken-off hair at the borders patch that are easily removable (in AA)
  • Hair loss at other sites, nail disorders, skin changes
  • Clinical signs of thyroid disease, lupus, or other diseases
  • Clinical signs of virilization: acne, hirsutism, acanthosis nigricans, truncal obesity

Differential Diagnosis

Search for type of alopecia and then for reversible causes.

Diagnostic Tests & Interpretation

Initial Tests (lab, imaging)
  • No testing may be indicated depending on clinical appearance.
  • Nonandrogenic alopecia
    • TSH, CBC, ferritin
    • Consider: LFT, BMP, zinc, VDRL, ANA, prolactin all depending on clinical history and exam
  • Androgenic alopecia: especially in females
    • Consider free testosterone and dehydroepiandrosterone sulfate.

Diagnostic Procedures/Other
  • Light hair-pull test: Pull on 25 to 50 hairs; ≥6 hairs dislodged is consistent with shedding (effluvium, AA).
  • Direct microscopic exam of the hair shaft
    • Anagen hairs: elongated, distorted bulb with root sheath attached
    • Telogen hairs: rounded bulb, no root sheath
    • Exclamation point hairs: club-shaped root with thinner proximal shaft (AA)
    • Broken and distorted hairs may be associated with multiple hair dystrophies.
  • Biopsy: most important in scarring alopecia
  • Ultraviolet light fluorescence and potassium hydroxide prep (to rule out tinea capitis)


General Measures

  • Consider potential harms and benefits to the patient prior to treatment. Many will gain an improved quality of life that is of benefit (2)[A].
  • Stop any possible medication causes if possible; this will often resolve telogen effluvium (5)[C].
  • Treat underlying medical causes (e.g., thyroid disorder, syphilis).
  • Traction alopecia: Change hair care practices; education
  • Trichotillomania: often requires psychological intervention to induce behavior change


  • Nonscarring
  • Androgenic alopecia: Treatment must be continued indefinitely; can use in combination
    • Minoxidil (Rogaine): 2% topical solution (1 mL BID) for women, 5% topical solution (1 mL BID) or foam (daily) for men; works in 60% of cases (3)[A]
      • Unclear mechanism of action; appears to prolong anagen phase
      • Adverse effects: skin irritation, hypertrichosis of face/hands, tachycardia; category C in pregnancy (3)[A]
    • Finasteride (Propecia): 1 mg/day for men and women (off-label) (6)[A]; 30–50% improvement in males, poor data in females (2)[A]
      • 5-α reductase inhibitor, reduces DHT in system, increases total and anagen hairs, slows transition of terminal to vellus hairs
      • Works best on vertex, least in anterior, temporal areas
      • Adverse effects: loss of libido, gynecomastia, depression. Caution in liver disease; absolutely no use or contact during pregnancy, category X, reliable contraception required in female use (6)[A]
    • Spironolactone (Aldactone): 100 to 200 mg/day (off-label) (3)[C]
      • Aldosterone antagonist, antiandrogen; blocks the effect of androgens, decreasing testosterone production
      • Adverse effects: dose dependent, hyperkalemia, menstrual irregularity, fatigue; category D in pregnancy
    • Ketoconazole: decreases DHT levels at follicle, works best with minoxidil in female androgenic alopecia (6)[A]
    • Combination: Finasteride + minoxidil has superior efficacy to monotherapy (2)[A].
  • AA: no FDA-approved treatment; high rate of spontaneous remission in patchy AA. Treatments all focus on symptom management rather than etiology.
  • Intralesional steroids
    • Triamcinolone: 2.5 to 5.0 mg/mL (3)[C]
      • First line if <50% scalp involved
      • Inject 0.1 mL into deep dermal layer at 0.5 to 1.0 cm intervals with 1/2 in 30-gauge needle, every 4 to 6 weeks; maximum 20 mg per session (1)[C]
      • Adverse effects: local burning, pruritus, skin atrophy
    • Topical steroids: very limited evidence for efficacy
    • Betamethasone: 0.1% foam shows limited hair regrowth (1)[C].
      • Adverse effects: folliculitis, high relapse rate after discontinuation
    • Systemic glucocorticoids: Use in extensive, multifocal AA; may induce regrowth but requires long-term monthly treatment to maintain growth (1)[B]
      • Adverse effects: hyperglycemia, adrenal insufficiency, osteoporosis, cataracts, obesity
      • Psychiatric: SSRIs, psychiatric care, support groups
    • PUVA light therapy + prednisone: moderate effectiveness in diffuse AA
    • Tinea capitis: See “Tinea (Capitis, Corporis, Cruris).”

Surgery/Other Procedures

  • Hair transplantation
  • Wigs, hairpieces, extensions
  • Surgical: graft transplantation, flap transplantation, or excision of the scarred area; used primarily in scarring alopecia
  • Platelet-rich plasma: has been shown to restore dormant hair follicles and stimulate new hair growth
  • Laser therapies to promote growth: lacks evidence

Complementary and Alternative Medicine

  • Many herbal medications are available; no clear evidence at this time
  • Volumizing shampoos can help remaining hair look fuller.

Ongoing Care


If nutritional deficit noted, supplementation may be necessary.

Patient Education

National Alopecia Areata Foundation:


  • Androgenic alopecia: Prognosis depends on response to treatment.
  • AA: often regrows within 1 year even without treatment. Recurrence common. 10% have severe, chronic form; poor prognosis more likely with long duration, extensive hair loss, autoimmune disease, nail involvement, and young age
  • Telogen effluvium: maximum shedding 3 months after the inciting event and recovery following correction of the cause. Usually subsides in 3 to 6 months but takes 12 to 18 months for cosmetically significant regrowth; rarely, permanent hair loss, usually with long-term illness
  • Anagen effluvium: Shedding begins days to a few weeks after the inciting event, with recovery following correction of the cause; rarely, permanent hair loss
  • Traction alopecia: excellent prognosis with behavior modification
  • Cicatricial alopecia: hair follicles permanently damaged; prognosis depends on type of alopecia and available treatments.
  • Tinea capitis: excellent prognosis with treatment

Additional Reading

Otberg N. Primary cicatricial alopecias. Dermatol Clin. 2013;31(1):155–166. [PMID:23159184]

See Also



  • L63.0 Alopecia (capitis) totalis
  • L63.1 Alopecia universalis
  • L63.9 Alopecia areata, unspecified
  • L64.0 Drug-induced androgenic alopecia
  • L64.8 Other androgenic alopecia
  • L64.9 Androgenic alopecia, unspecified
  • L65.0 Telogen effluvium
  • L65.9 Nonscarring hair loss, unspecified


  • 704.00 Alopecia, unspecified
  • 704.01 Alopecia areata
  • 704.02 Telogen effluvium
  • 704.09 Other alopecia


  • 19754005 Alopecia totalis
  • 238725004 non-scarring alopecia (disorder)
  • 39479004 Telogen effluvium (disorder)
  • 400088006 Scarring alopecia
  • 56317004 Alopecia (disorder)
  • 68225006 Alopecia areata (disorder)
  • 86166000 Alopecia universalis (disorder)
  • 87872006 Male pattern alopecia (disorder)

Clinical Pearls

  • History and physical are necessary in determining type of alopecia for appropriate treatment.
  • Treatment of underlying medical condition or removal of triggering medication will often resolve hair loss.
  • Educating the patient about the nature of the condition and expectations is key to care.
  • Alopecia can affect the psychological condition of the patient, and it may be necessary to address this in any type of hair loss.


Anastasia N. Gevas, DO
Kelli M. Gevas, MD


Figure 10-4
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Alopecia areata. Note black, flecklike "exclamation mark" hairs at the periphery.
Figure 10-5
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Alopecia areata. This man's alopecia areata is limited to his beard.
Figure 10-6
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Alopecia areata (alopecia universalis). This patient has lost most of her eyebrows, which she colors in with an eyebrow pencil. She also lacks eyelashes, pubic hair, axillary hair, and hair on her extremities.
Figure 10-7
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Alopecia areata (regrowing hair). In this patient with alopecia areata, clusters of hair regrew after intralesional triamcinolone acetonide injections. Some of the regrown hairs are white (vitiliginous).
Figure 10-8
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Trichotillomania. This condition is seen most often in young girls. Hairs tend to be broken at different lengths. The areas of alopecia are not completely devoid of hair.
Figure 10-11
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Traction alopecia. This woman's alopecia is the result of the use of tight curlers: Note the symmetric loss of hair in a frontotemporal distribution. Also note the "relaxed" curl that was chemically straightened.
Figure 10-12
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Traction alopecia. Note the fringe of residual hairs at the distal margin of alopecia. These hairs were too short to be "grabbed" by the hair curlers.


  1. Alkhalifah A. Alopecia areata update. Dermatol Clin. 2013;31(1):93–108.  [PMID:23159179]
  2. Blumeyer A, Tosti A, Messenger A, et al; for European Dermatology Forum. Evidence-based (S3) guideline for the treatment of androgenic alopecia in women and in men. J Dtsch Dermatol Ges. 2011;9(Suppl 6):S1–S57. [PMID:21980982]
  3. Rathnayake D, Sinclair R. Innovative use of spironolactone as an antiandrogen in the treatment of female pattern hair loss. Dermatol Clin. 2010;28(3):611–618.  [PMID:20510769]
  4. Kumar S, Mittal J, Mahajan B. Colocalization of vitiligo and alopecia areata: coincidence or consequence? Int J Trichology. 2013;5(1):50–52.  [PMID:23960402]
  5. Harrison S, Bergfeld W. Diffuse hair loss: its triggers and management. Cleve Clin J Med. 2009;76(6):361–367.  [PMID:19487557]
  6. Atanaskova Mesinkovska N, Bergfeld WF. Hair: what is new in diagnosis and management? Female pattern hair loss update: diagnosis and treatment. Dermatol Clin. 2013;31(1):119–127.  [PMID:23159181]

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