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.
• Genes involved in the pathogenesis of alopecia areata include MCHR2 and MCHR2-AS1 which are related to the MHC pathway (melanin concentrating hormone).
• 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.

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 non-scarring, meaning that it is not definitive.
• 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.
• Telogen hairs are usually at least at 25% for the diagnosis of telogen effluvium to be made.

Template Sentences

IF the pathogenesis of the disease is unclear:

• It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].

IF the disease is infectious…

• …and the route of transmission is known:
  • [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
  • Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.

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.

Template sentences

• [Disease name] is transmitted in [mode of genetic transmission] pattern.
• Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].

Associated Conditions

• Conditions associated with the disease can be detailed in this section.

Template sentences

• The most important conditions/diseases associated with [disease name] include:
  • Condition 1: A brief explanation of the condition and its association with the disease
  • Condition 2: A brief explanation of the condition and its association with the disease

For an example of an associated conditions sub-section of pathophysiology, click here.

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.