Last updated: August 8, 2023

Summarytoggle arrow icon

Alopecia is the loss of hair from any hair-bearing area of the body, but most often the scalp. It may be congenital or acquired, circumscribed or diffuse, and scarring or nonscarring. Androgenetic alopecia, a type of diffuse, nonscarring, acquired alopecia, is most common. Alopecia areata, an acquired, circumscribed, nonscarring alopecia, is the second most common type. Clinical diagnosis is usually possible. In ambiguous cases, diagnosis is aided by microscopic examination of the hair, trichogram, and scalp biopsy. Treatment depends on the type of alopecia and can include long-term (at least one year) use of topical minoxidil, corticosteroids (topical, intralesional, or oral), or antiandrogens. Surgery (hair transplant) or camouflaging techniques are used as ancillary treatments and/or when medical therapy is unsuccessful. The prognosis is variable and depends on the etiology and severity of hair loss.

Definitiontoggle arrow icon


Phases of hair growth [1]

Classificationtoggle arrow icon

Classification by etiology and pattern

Classification of alopecia by etiology and pattern [2][3][4][5]
Congenital Acquired
Diffuse alopecia
Circumscribed alopecia

Classification by presence of scarring [4]

Scarring (cicatricial) alopecia

  • Brocq pseudopelade [6]
    • Seen mainly in women 30–50 years of age
    • Irregular areas of irreversible hair loss, which become scarred areas at a later stage
  • Lichen planopilaris
  • Frontal fibrosing alopecia: a progressive form of frontotemporal hair loss associated with local scarring [7]
  • Central centrifugal cicatricial alopecia [7]
    • Alopecia that starts at the crown and spreads outwards
    • Occurs almost exclusively in Black women
  • Skin conditions causing scarring alopecia
  • Acquired scarring alopecia (e.g., via viral diseases, mycoses, burns, chemical burns)

Nonscarring alopecia

Diagnosticstoggle arrow icon

The diagnosis is often clear from the patient history and physical examination; however, there are several tests that help determine the type and etiology of alopecia.

Clinical evaluation [5]

Diagnostic studies [5][9][10]

Congenital alopeciastoggle arrow icon

Congenital diffuse alopecia [2]

  • Trichorrhexis nodosa: a hair shaft deformity characterized by the development of weak points in the shaft due to physical or chemical trauma or genetic predisposition
  • Pili torti: a condition in which the hair shaft is flattened and has multiple twists, resulting in fragile hair that breaks easily
  • Monilethrix (beaded hair): predominantly autosomal dominant disorder in which hair shafts break easily, resulting in a beaded appearance usually a few months after birth
  • Genetic syndromes: e.g., Menkes disease, Netherton syndrome

Congenital circumscribed alopecia

  • Temporal triangular alopecia [12]
    • A well-defined oval or triangular patch of alopecia in the temporal part of the scalp
    • Onset is often before adolescence.
    • Mimics alopecia areata and is differentiated from it by the absence of exclamation point hair
    • Treatment (if necessary): hair transplant or surgical excision for improved cosmesis
  • Nevus sebaceous [13][14]
    • A well-demarcated, hairless, velvety plaque that is typically orange or tan
    • At risk of malignant degeneration (e.g., basal cell carcinoma)
    • Treatment: surgical excision
  • Aplasia cutis congenita [15]
    • Intra-uterine developmental disruption of one/more layers of the scalp
    • A part of the scalp is missing at birth, which, on healing, causes a scarred, hairless patch
    • Treatment: depends on size, depth, location, and tissues involved

Acquired alopeciastoggle arrow icon

Telogen effluvium [5][16]

Anagen effluvium [5][17]

Traction alopecia [8][19]

  • Definition: hair loss due to chronic traction or tension on the hair follicles
  • Etiology: hairstyles involving tying the hair tightly
  • Clinical features: circumscribed hair loss at sites of traction, predominantly at the frontal and temporal scalp
  • Treatment
    • Remove the source of traction.
    • Potential additional treatments include topical and intralesional corticosteroids and topical minoxidil.

Androgenetic alopeciatoggle arrow icon

Definition [20]

A progressive, nonscarring alopecia that affects the regions of the scalp with the most androgen-sensitive hair follicles, resulting in a characteristic pattern of balding (bitemporal scalp in men and vertex and frontal scalp in women)

Epidemiology [5]

Etiology [20][21]

Pathophysiology [20]

Clinical features [22]

Diagnostics [22]

Differential diagnoses

Treatment [20][23]

Pharmacotherapy [5][24][25]

Minoxidil is a direct arteriolar vasodilator and can also be used to treat resistant hypertension. [29]

Nonpharmacological measures [24]

  • Camouflage: e.g., keratin fibers, hair dyes, toupées, wigs
  • Low-level laser therapy (LLLT): self-administered via combs or caps
  • Hair transplant surgery: Follicular units from the occipital scalp are extracted (either as small units or as a linear strip), divided into small units, and implanted into the bald areas. [23]

Alopecia areatatoggle arrow icon

Definition [30]

A nonscarring circumscribed alopecia that is characterized by well-demarcated patches of hair loss due to immune-mediated inflammation of hair follicles

Epidemiology [30]

  • Prevalence: ∼1 in 1000 people
  • Age of onset: mostly < 40 years
  • Sex: =


Clinical features [30][31]

  • Abrupt onset (within weeks)
  • Smooth, circular, well-defined patches of hair loss without scarring
  • Nail involvement (up to 40% of cases): nail pitting, onycholysis, Beau lines
  • Other autoimmune disorders may be present (e.g., vitiligo, autoimmune disorders of the thryoid).
  • Patterns of hair loss
    • Ophiasis: hair loss localized to the back and sides of the scalp
    • Sisiapho: sparing of the sides and back of the scalp
    • Extensive alopecia areata: hair loss affecting > 50% of the scalp
    • Alopecia universalis: All hair-bearing sites are affected (mimics telogen effluvium).
    • Alopecia totalis: complete baldness

Diagnostics [5]

Differential diagnosis [31]

Treatment [5][31][32]

Treatment is guided by the patient's age, disease duration, and disease extent. Options include:

Prognosis [19]

Referencestoggle arrow icon

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  2. Chien Yin GO, Siong-See JL, Wang ECE. Telogen Effluvium – a review of the science and current obstacles. J Dermatol Sci. 2021; 101 (3): p.156-163.doi: 10.1016/j.jdermsci.2021.01.007 . | Open in Read by QxMD
  3. Ghias MH, Amin BD, Kutner AJ. Albendazole-induced anagen effluvium. JAAD Case Rep. 2020; 6 (1): p.54-56.doi: 10.1016/j.jdcr.2019.08.010 . | Open in Read by QxMD
  4. Serrano-Falcón C, Fernández-Pugnaire MA, Serrano-Ortega S. Hair and Scalp Evaluation: The Trichogram. Actas Dermosifiliogr. 2013; 104 (10): p.867-876.doi: 10.1016/j.adengl.2013.03.009 . | Open in Read by QxMD
  5. Mounsey AL, Reed SW. Diagnosing and Treating Hair Loss. Am Fam Physician. 2009; 80 (4): p.356-362.
  6. Billero V, Miteva M. Traction alopecia: the root of the problem. Clin Cosmet Investig Dermatol. 2018; Volume 11: p.149-159.doi: 10.2147/ccid.s137296 . | Open in Read by QxMD
  7. Park AM, Khan S, Rawnsley J. Hair Biology. Facial Plast Surg Clin North Am. 2018; 26 (4): p.415-424.doi: 10.1016/j.fsc.2018.06.003 . | Open in Read by QxMD
  8. Singh G, Miteva M. Prognosis and Management of Congenital Hair Shaft Disorders with Fragility-Part I. Pediatr Dermatol. 2016; 33 (5): p.473-480.doi: 10.1111/pde.12894 . | Open in Read by QxMD
  9. Singh G, Miteva M. Prognosis and Management of Congenital Hair Shaft Disorders without Fragility-Part II. Pediatr Dermatol. 2016; 33 (5): p.481-487.doi: 10.1111/pde.12902 . | Open in Read by QxMD
  10. Stefanato CM. Histopathology of alopecia: a clinicopathological approach to diagnosis. Histopathology. 2010; 56 (1): p.24-38.doi: 10.1111/j.1365-2559.2009.03439.x . | Open in Read by QxMD
  11. Alzolibani AA, Kang H, Otberg N, Shapiro J. Pseudopelade of Brocq. Dermatol Ther. 2008; 21 (4): p.257-263.doi: 10.1111/j.1529-8019.2008.00207.x . | Open in Read by QxMD
  12. Jamerson TA, Aguh C. An Approach to Patients with Alopecia. Med Clin North Am. 2021; 105 (4): p.599-610.doi: 10.1016/j.mcna.2021.04.002 . | Open in Read by QxMD
  13. Mubki T, Rudnicka L, Olszewska M, Shapiro J. Evaluation and diagnosis of the hair loss patient: Part I. J Am Acad Dermatol. 2014; 71 (3): p.415.e1-415.e15.doi: 10.1016/j.jaad.2014.04.070 . | Open in Read by QxMD
  14. Mubki T, Rudnicka L, Olszewska M, Shapiro J. Evaluation and diagnosis of the hair loss patient: Part II. J Am Acad Dermatol. 2014; 71 (3): p.431.e1-431.e11.doi: 10.1016/j.jaad.2014.05.008 . | Open in Read by QxMD
  15. Vujovic A, Del Marmol V. The female pattern hair loss: review of etiopathogenesis and diagnosis.. Biomed Res Int. 2014; 2014: p.767628.doi: 10.1155/2014/767628 . | Open in Read by QxMD
  16. Lolli F, Pallotti F, Rossi A, et al. Androgenetic alopecia: a review. Endocrine. 2017; 57 (1): p.9-17.doi: 10.1007/s12020-017-1280-y . | Open in Read by QxMD
  17. Lause M, Kamboj A, Fernandez Faith E. Dermatologic manifestations of endocrine disorders. Transl Pediatr. 2017; 6 (4): p.300-312.doi: 10.21037/tp.2017.09.08 . | Open in Read by QxMD
  18. Olsen EA, Messenger AG, Shapiro J, et al. Evaluation and treatment of male and female pattern hair loss. J Am Acad Dermatol. 2005; 52 (2): p.301-311.doi: 10.1016/j.jaad.2004.04.008 . | Open in Read by QxMD
  19. Kanti V, Messenger A, Dobos G, et al. Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men - short version. J Eur Acad Dermatol & Venereol. 2017; 32 (1): p.11-22.doi: 10.1111/jdv.14624 . | Open in Read by QxMD
  20. Nestor MS, Ablon G, Gade A, Han H, Fischer DL. Treatment options for androgenetic alopecia: Efficacy, side effects, compliance, financial considerations, and ethics. J Cosmet Dermatol. 2021; 20 (12): p.3759-3781.doi: 10.1111/jocd.14537 . | Open in Read by QxMD
  21. Adil A, Godwin M. The effectiveness of treatments for androgenetic alopecia: A systematic review and meta-analysis. J Am Acad Dermatol. 2017; 77 (1): p.136-141.e5.doi: 10.1016/j.jaad.2017.02.054 . | Open in Read by QxMD
  22. Goren A, Naccarato T, Situm M, Kovacevic M, Lotti T, McCoy J. Mechanism of action of minoxidil in the treatment of androgenetic alopecia is likely mediated by mitochondrial adenosine triphosphate synthase-induced stem cell differentiation. J Biol Regul Homeost Agents. 2017; 31 (4): p.1049-1053.
  23. Dawber RP, Rundegren J. Hypertrichosis in females applying minoxidil topical solution and in normal controls. J Eur Acad Dermatol Venereol. 2003; 17 (3): p.271-5.doi: 10.1046/j.1468-3083.2003.00621.x . | Open in Read by QxMD
  24. van Zuuren EJ, Fedorowicz Z. Interventions for Female Pattern Hair Loss.. JAMA Dermatol. 2017; 153 (3): p.329-330.doi: 10.1001/jamadermatol.2016.5790 . | Open in Read by QxMD
  25. Sica DA. Minoxidil: an underused vasodilator for resistant or severe hypertension. J Clin Hypertens (Greenwich). 2004; 6 (5): p.283-7.doi: 10.1111/j.1524-6175.2004.03585.x . | Open in Read by QxMD
  26. Villasante Fricke AC, Miteva M. Epidemiology and burden of alopecia areata: a systematic review. Clin Cosmet Investig Dermatol. 2015; 8: p.397-403.doi: 10.2147/CCID.S53985 . | Open in Read by QxMD
  27. Harries MJ, Sun J, Paus R, King LE. Management of alopecia areata. BMJ. 2010; 341 (jul23 1): p.c3671-c3671.doi: 10.1136/bmj.c3671 . | Open in Read by QxMD
  28. Meah N, Wall D, York K, et al. The Alopecia Areata Consensus of Experts (ACE) study: Results of an international expert opinion on treatments for alopecia areata. J Am Acad Dermatol. 2020; 83 (1): p.123-130.doi: 10.1016/j.jaad.2020.03.004 . | Open in Read by QxMD
  29. Yin Li VC, Yesudian PD. Congenital triangular alopecia. In J Trichol. 2015; 7 (2): p.48-53.doi: 10.4103/0974-7753.160089 . | Open in Read by QxMD
  30. Moody MN, Landau JM, Goldberg LH. Nevus Sebaceous Revisited. Pediatr Dermatol. 2011; 29 (1): p.15-23.doi: 10.1111/j.1525-1470.2011.01562.x . | Open in Read by QxMD
  31. Patel P, Malik K, Khachemoune A. Sebaceus and Becker’s Nevus: Overview of Their Presentation, Pathogenesis, Associations, and Treatment. Am J Clin Dermatol. 2015; 16 (3): p.197-204.doi: 10.1007/s40257-015-0123-y . | Open in Read by QxMD
  32. Bharti G, Groves L, David LR, Sanger C, Argenta LC. Aplasia Cutis Congenita. J Craniofac Surg. 2011; 22 (1): p.159-165.doi: 10.1097/scs.0b013e3181f73937 . | Open in Read by QxMD

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