Alopecia pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: José Eduardo Riceto Loyola Junior, M.D.[2]


Since alopecia has many different causes, the pathophysiologic mechanism for its development varies widely according to the cause. Alopecia areata, for example, is related with CD8+ T-cell autoimmunity, while androgenetic alopecia is related with androgen hormones effects' on the hair follicle which leads to its miniaturization and hair loss. Tinea capitis on the other hand is an infectious disease that can damage the hair follicle and lead to definitive hair loss.


The most common causes for alopecia and its pathophysiology mechanism are briefly discussed below:

Alopecia Areata

Alopecia areata - from

Telogen effluvium

Traumatic alopecia

  • Usually seen on children that pull their hair, the same mechanism as traction alopecia.
  • May be associated with trichotillomania - a psychiatric condition in which the patient repeatedly pulls their hair.[7]

Androgenetic alopecia

Androgenetic alopecia - from
  • In androgenetic alopecia there is marked miniaturization of the hair follicle and disruption of the hair cycle.
  • It is thought that in androgenetic alopecia the hair loss is the result of the shortening of the anagen phases of hair development and enlongation of the telogen phase that gradually takes place until the hair eventually doesn't even leave the skin surface.[8]
  • The is also an increase in the period from the hair shedding to its regrowth.[8]
  • The miniaturization affects the hair follicle globally, including the dermal papilla which is essential for its maintenance.[8]
  • It is mediated by the presence of androgens, which is further reinforced by the fact that eunuchs do not bald.
  • The molecular mechanism of action for the androgens such as testosterone and 5α-dihydrotestosterone (DHT) to act on the hair follicle is not fully understood.
  • It is theorized that some genes that regulate the follicle cycling may be regulated by the presence of androgens and that the expression of such genes are related to the concentrations of androgen and androgen receptors in the follicle.[8]
  • It is also theorized through observation of families with androgenetic alopecia that these genes related to the disease may act in an autosomal dominant manner in men and autosomal recessive manner in women, though there is strong evidence for a polygenic mode of inheritance.
  • Finasteride is used to treat androgenetic alopecia being a potent 5-alpha-reductase type-2 inhibitor, inhibiting the conversion of testosterone to DHT.

Tinea capitis

Tinea capitis - from
  • Tinea capitais is caused by dermatophyte species that are able to invade keratinized tissues like the hair.
  • It is usually transmitted via direct contact with organisms from other humans, animals, soil, or fomites.
  • The dermatophyte infects the hair and grows towards the stratum corneum. It then affects the hair which becomes brittle and break.[9]
  • It may present with black dots, which is the non-inflammatory form of the disease, causing fracture of the hair. It also may present with intense inflammation which leads to follicular destruction, and may complicate with kerion, an abscess in the scalp, or favus, another inflammatory form in which there is a honeycomb destruction of the hair shaft. Both are severe forms of the disease.[9]

Anagen Effluvium

  • Anagen effluvium occurs mostly due to chemotherapy.
  • Chemotherapeutic agents cause cessation of the hair growth during anagen phase, due to disruption of the cell cycle caused by the medication.[9]


  1. Paus R, Ito N, Takigawa M, Ito T (2003). "The hair follicle and immune privilege". J Investig Dermatol Symp Proc. 8 (2): 188–94. doi:10.1046/j.1087-0024.2003.00807.x. PMID 14582671.
  2. Paus R, Bertolini M (2013). "The role of hair follicle immune privilege collapse in alopecia areata: status and perspectives". J Investig Dermatol Symp Proc. 16 (1): S25–7. doi:10.1038/jidsymp.2013.7. PMID 24326544.
  3. Fischer J, Degenhardt F, Hofmann A, Redler S, Basmanav FB, Heilmann-Heimbach S; et al. (2017). "Genomewide analysis of copy number variants in alopecia areata in a Central European cohort reveals association with MCHR2". Exp Dermatol. 26 (6): 536–541. doi:10.1111/exd.13123. PMID 27306922.
  4. Trüeb RM, Dias MFRG (2018). "Alopecia Areata: a Comprehensive Review of Pathogenesis and Management". Clin Rev Allergy Immunol. 54 (1): 68–87. doi:10.1007/s12016-017-8620-9. PMID 28717940.
  5. Malkud S (2015). "Telogen Effluvium: A Review". J Clin Diagn Res. 9 (9): WE01–3. doi:10.7860/JCDR/2015/15219.6492. PMC 4606321. PMID 26500992.
  6. "StatPearls". 2020. PMID 28613598.
  7. "StatPearls". 2020. PMID 30844205.
  8. 8.0 8.1 8.2 8.3 Ellis JA, Sinclair R, Harrap SB (2002). "Androgenetic alopecia: pathogenesis and potential for therapy". Expert Rev Mol Med. 4 (22): 1–11. doi:10.1017/S1462399402005112. PMID 14585162.
  9. 9.0 9.1 9.2 "StatPearls". 2020. PMID 30725594.