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]
Overview
Since alopecia ha many different causes, the pathophysiologic mechanism for its development varies according to the cause.
Pathophysiology
Alopecia Areata
- The exact pathogenesis of alopecia areata is not fully understood.
- It has been theorized that T-cell-mediated autoimmunity must be involved in its development.
- The hair follicle typically has low levels of major histocompatibility complex expression, which provides protection from the immune system. It is believed that in alopecia Areata that protection is lost, resulting in a CD8+ T lymphocyte attack to the bulb of the hair, generating an inflammatory infiltrate in the [[peribulbar[[ region of the hair follicle.[1][2]
- Genes involved in the pathogenesis of alopecia areata include MCHR2 and MCHR2-AS1 which are related to the MHC pathway (melanin concentrating hormone).[3]
- There is an association of alopecia Areata with other autoimmune diseases such as vitiligo, autoimmune thyroid disease, celiac disease, systemic erythematous, chronic atrophic gastritis which further reinforces its relationship with autoimmunity.[4]
Telogen effluvium
- Telogen effluvium is not a disease per se, but it is a common cause of hair loss due to a triggering event that increases the number of hair follicles that are in the catagen or telogen phase (shedding and resting phase) of the hair development cycle.
- It is of non-scarring type.
- There are many different events that can act as triggers for this condition, such as febrile diseases (malaria, HIV, tuberculosis), drugs (oral contraceptives, anticonvulsants, beta blockers, captopril antithyroid drugs and hypolipidemic drugs), thyroid diseases, organ dysfunction, nutritional (iron or zinc deficiency) or local factors such as hair dye.[5]
- Telogen hairs are usually at least at 25% for the diagnosis of telogen effluvium to be made.[6]
Traumatic alopecia
- Usually seen on children that pull their hair, same mechanism as traction alopecia.
- May be associated with trichotillomania - a psychiatric condition in which the patient repeatedly pulls their hair.[7]
Androgenetic alopecia
- In androgenetic alopecia there is a 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
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- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
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IF the disease has a known genetic component:
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
IF certain pathology findings are characteristic of the disease:
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Genetics
- Some diseases are genetic, and have particular inheritance patterns, and express different phenotypes.
- The effect that genetics may have on the pathophysiology of a disease can be described in this section.
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- [Disease name] is transmitted in [mode of genetic transmission] pattern.
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Associated Conditions
- Conditions associated with the disease can be detailed in this section.
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- Condition 1: A brief explanation of the condition and its association with the disease
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Histopathology
In androgenetic alopecia, there are miniaturized hair follicles with an increase in the telogen-to-anagen ratio without inflammatory reaction. In anagen effluvium, there is a decrease in anagen hair without any inflammatory response. Finally, in alopecia mucinosa, there is an infiltrate of the epidermis, dermis, and peribulbar lymphocytic infiltrate mainly anaplastic cells. In patients with alopecia areata, there is a peribulbar lymphocytic infiltrate with a decrease in the ratio of anagen to telogen hair. Telogen effluvium is characterized by an increase in the number of catagen hair. In tinea capitis, there is evidence of fungal infection as under a microscope along with a neutrophilic infiltrate.
References
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ "StatPearls". 2020. PMID 28613598.
- ↑ "StatPearls". 2020. PMID 30844205.
- ↑ 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.