Clinical Dermatology Review

: 2022  |  Volume : 6  |  Issue : 2  |  Page : 69--74

Pathogenesis of androgenetic alopecia

Ajithkumar Kidangazhiathmana1, Parvathy Santhosh2,  
1 Department of Dermatology, Government Medical College, Thrissur, Kerala, India
2 Department of Dermatology, Malabar Medical College Hospital and Research Centre, Kozhikode, Kerala, India

Correspondence Address:
Ajithkumar Kidangazhiathmana
Department of Dermatology, Government Medical College, Kottayam, Kerala


The pathogenesis of androgenetic alopecia (AGA) is a complex interplay of genetic, hormonal, and environmental factors. In scalp follicles of susceptible individuals, androgens promote miniaturization of hair and shorten hair growth in the anagen stage, ultimately leading to AGA. The major circulating androgen, testosterone, is converted to the more potent androgen dihydrotestosterone by the enzyme 5α-reductase (5αR). Androgen receptors (ARs) and 5αR are significantly more in balding scalp hair follicles than those from nonbalding follicles. Genetic predisposition plays a crucial role in AGA. Various genetic loci including AR gene and the ectodysplasin A2 receptor (EDA2R) (AR/EDA2R locus in Xq11-q12) have been strongly implicated. The basic pathology of AGA is progressive miniaturization of the terminal hair follicles and eventual conversion of terminal hair to vellus hair. The duration of the anagen phase diminishes progressively with each cycle, while the length of telogen phase remains constant or may be prolonged. This eventually results in a reduction of the anagen to telogen ratio. With each successive shortening of hair cycle, the length of each hair shaft is reduced, and it becomes too short for the growing hair to attain even the minimum length required to reach the skin surface, resulting in an empty follicular pore. Hair follicle miniaturization leads to conversion of terminal hairs into secondary vellus hairs. Although many mechanisms have been proposed, the actual mechanism of hair miniaturization has not yet been fully elucidated. This article attempts to collate the existing information regarding the pathogenesis of AGA.

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Kidangazhiathmana A, Santhosh P. Pathogenesis of androgenetic alopecia.Clin Dermatol Rev 2022;6:69-74

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Kidangazhiathmana A, Santhosh P. Pathogenesis of androgenetic alopecia. Clin Dermatol Rev [serial online] 2022 [cited 2023 Jan 31 ];6:69-74
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The pathogenesis of androgenetic alopecia (AGA) is a complex interplay of genetic, hormonal, and environmental factors. The underlying molecular mechanisms are yet to be elucidated fully.[1] In this article, we aim to provide a comprehensive account of what is known till date about the pathomechanisms of AGA.

 Role of Androgens

Hamilton's work in 1951 attempting to elucidate the complex roles of androgens, genetics, and age in AGA, was the first of its kind. He observed that men castrated before puberty did not develop AGA, and that it is possible to induce AGA in castrated men by injecting testosterone. This established that androgens were prerequisites for the development of common baldness.[2] Since then, extensive research has been carried out in this front.

Role of androgens in hair growth

The effect of androgens on human hair growth varies, depending on body site. In androgen-dependent areas (beard, axillary, and pubic hair), androgens stimulate the growth of terminal hair in puberty, but, in scalp follicles of susceptible individuals, they promote miniaturization of hair and shorten hair growth in the anagen stage, ultimately leading to AGA. This reciprocal effect is termed “androgen paradox”.[3],[4],[5] The differential gene expression and response to androgens may be responsible for this variability of responses.[6]

Androgen metabolism

The effect of androgens on hair follicles depends on local bioavailability rather than circulating levels. Skin is a peripheral organ of androgen metabolism. Sebocytes synthesize testosterone from adrenal precursors and are also capable of inactivating them, thus playing a major role in androgen homeostasis.[7] Keratinocytes, too, are responsible for androgen degradation. The major circulating androgen, testosterone, reaches the skin through capillary blood. Testosterone is converted to the more potent androgen dihydrotestosterone (DHT) by the enzyme 5α-reductase (5αR). Dehydroepiandrosterone (DHEA), DHEA-S, and androstenedione, which are the “weak” androgens' are converted to testosterone and DHT, the more potent androgens, in sebocytes, sweat glands, and dermal papilla cells (DPCs).[8] Androgen metabolism in the skin is summarized in [Figure 1].{Figure 1}

The enzyme 5αR has 2 isoforms-Type 1 and Type 2, encoded by steroid-5αR 1 and 2 (SRDA1 and SRDA2) genes, respectively. The Type 1 isoform is the one that exists in androgen-independent organs such as liver and brain, while Type 2 is expressed in androgen-dependent organs including epididymis and prostate.[1],[8] The Type 1 isozyme is composed of 259 amino acids and is located in skin mainly in sebocytes, but also in epidermal and follicular keratinocytes, DPCs, sweat glands and fibroblasts. It was previously thought that 5aR1 may be dominant in hair follicles, but a recent study detected activity of both 5aR1 and 5aR2 in microdissected hair follicles. It has been found that 5αR activity is higher in balding hair follicles than occipital hair follicles from both men and women. At the mRNA level, 5aR2 mRNA is higher in DPCs from AGA and beard, than in those from the occipital scalp, while 5aR1 is equally expressed in all scalp sites. It has also been demonstrated that women and men have higher levels of receptors and 5αR Type I and II in frontal hair follicles compared to occipital follicles, whereas higher levels of aromatase are present in their occipital follicles.[3],[9],[10],[11]

Androgen receptors

All androgen-dependent hair follicles require androgen receptors (ARs) to respond.[12] The AR is a 110-kDa ligand-inducible nuclear receptor that binds to an androgen response element and thus regulates the expression of target genes. Cutaneous ARs are located in epidermal and follicular keratinocytes, sebocytes, sweat gland cells, DPCs, dermal fibroblasts, endothelial cells, and genital melanocytes.[13],[14]

ARs are significantly more in DPCs from balding scalp hair follicles than those from nonbalding follicles.[15] DNA methylation of the AR promoter region is increased in hair follicles of the occipital scalp, compared with those from the vertex scalp with AGA. Increased AR methylation, results in reduced AR expression, which may be protective for occipital hairs from miniaturization and hair loss.[16]

 Genetic Basis of Androgenetic Alopecia

Genetic predisposition plays a crucial role in AGA. Although it was previously suggested that AGA has an autosomal dominant inheritance, it has subsequently been established that the inheritance follows a polygenic model.[17],[18]

Genome-wide association studies have recently identified strong association signals for AGA in the X chromosome. AR gene and the ectodysplasin A2 receptor (AR/EDA2R locus in Xq11-q12) have been strongly implicated.[19] Various AR polymorphism and AR restriction sites have been investigated.[20] A specific AR gene polymorphism termed StuI polymorphism has been found to be linearly related to AR activity, and associated with AGA risk. The AR-E211 A allele has been found to be associated with a lower risk of alopecia, while theEDA2R gene variation causes susceptibility to AGA.[21],[22],[23]

Heilmann et al., who suggested a polygenic component to AGA, identified four risk loci located in 2q35, 3q25.1, 5q33.3, and 12p12.1. The strongest association signal was observed in the locus 2q35, which contains the WNT10A gene. The WNT10A gene is expressed in the bulge region of hair follicle during the anagen phase of the hair growth cycle and has been shown to have a genotypic effect on hair follicle expression.[19] Several other genetic loci linked to AGA have been identified, including 1p36.22, 2q37, 7p21.1, 7q11.22, 17q21.31, 18q21.1, 20p11, and 3q26 and also a polymorphism in the APCDD1 gene, a WNT signalling inhibitor located in 18p11.2.[24],[25],[26],[27] The identification of autosomal loci for AGA susceptibility suggests that androgen-independent pathways are also involved in AGA pathogenesis.[28]

Recent studies have demonstrated no involvement of the well-established locus on chromosome 20p11 in female pattern hair loss (FPHL), but suggested that the locus on X-chromosome containing the AR gene and the EDA2R gene might be specifically involved in the pathogenesis of early-onset FPHL.[29] Another genome-wide association study has suggested that the aromatase gene (CYP19A1) may contribute to FPHL.[30]

 Pathogenic Mechanisms

The pathogenesis of AGA involves two main components: (a) Hair follicle miniaturization, and (b) changes to the hair cycle. The basic pathology of AGA is progressive miniaturization of the terminal hair follicles and eventual conversion of terminal hair to vellus hair. Although many mechanisms have been proposed, the actual mechanism of hair miniaturization has not yet been fully elucidated.

Hair follicles consist of mesenchymal and ectodermal components. The ectodermal part consists of an invagination of the epidermis into the dermis and subcutaneous fat. The hair bulb contains the hair matrix, which produces the hair shaft. The mesenchymal component is the dermal papilla, a small collection of specialized fibroblasts that is totally surrounded by the hair bulb.[31] The dermal papilla, located in the middle of the hair bulb at the follicle base, regulates the various aspects of the epithelial follicle and determines the type of hair produced.[32],[33] What initiates these processes is still not clear. An abrupt reduction in the cells of hair papilla is suggested by Whiting as the initial event in hair miniaturization.[34] A different process has been proposed by Guarrera and Rebora who suggested that an accelerated mitotic process in the hair matrix leads to decreased time for differentiation, increased telogen shedding, and increased and prolonged lag phase.[35]

 Hair Cycle Dynamics

Normally human hair is replaced cyclically. The four phases of hair growth include cyclic phases of growth (anagen), involution (catagen), resting (telogen), and shedding (exogen).[36] The anagen phase lasts for 3–5 years, and catagen lasts for a few weeks. The period of hair follicle quiescence (telogen) that follows, lasts approximately 3 months.[37] Hair follicle regeneration occurs in approximately the 1st week of anagen, and once regenerated, the anagen phase continues until the hair reaches its final length.

Hair cycle is controlled by a number of molecular signals including growth factors, nuclear receptors, cytokines, and intracellular signaling pathways. Growth factors such as insulin-like growth factor-1, hepatocyte growth factor, keratinocyte growth factor, and vascular endothelial growth factor promote the anagen phase of the hair cycle. Similarly, transforming growth factor-beta, interleukin 1-alpha, and tumor necrosis factor-alpha promote the onset of catagen.[37]

Hair cycle dynamics in androgenetic alopecia

The changes in hair cycle dynamics (shortening of anagen and an increase in telogen duration) are the most important component of the pathogenesis of AGA. When women with FPHL are compared to controls, the reduction in total hair density due to the increase in empty follicles is about five times greater than the increase in vellus hairs due to miniaturization.

In AGA, the duration of the anagen phase diminishes progressively with each cycle, while the length of telogen phase remains constant or may be prolonged. This eventually results in a reduction of the anagen to telogen ratio.[38] Thus, with each successive shortening of hair cycle, the length of each hair shaft is reduced, and it becomes too short for the growing hair to attain even the minimum length required to reach the skin surface, resulting in an empty follicular pore. This substage of the telogen phase that is prolonged in AGA is kenogen, the phase that follows exogen and produces empty follicles. In kenogen, the hair follicle rests physiologically. This phase last longer in AGA leaving a higher percentage of empty hair follicles contributing to balding.[39] The reduction in total hair count is presumed to reflect the increased proportion of hairs in kenogen.[31],[40],[41]

 Hair Follicle Miniaturization

Hair follicle miniaturization is the histological hallmark of AGA.[42]

The dermal papilla is principal in the maintenance and control of hair growth and is likely to be the target of androgen-mediated events leading to follicle miniaturization and alterations in hair cycle.[43],[44]

Hair follicle miniaturization leads to conversion of terminal hairs into secondary vellus hairs. Miniaturization occurs initially in the secondary follicles, leading to the reduction in hair density that precedes visible baldness.[42] Baldness ensues when all of the hairs within a follicular unit (FU) are miniaturized.

The process of follicular miniaturization which occurs in AGA does not simultaneously affect all follicles within a FU and this leads to diffuse thinning of hair in the initial days of AGA. Secondary follicles are affected initially and primary follicles are miniaturized last.[43] The follicular miniaturization does not occur in step-wise fashion as was once believed. It occurs abruptly between anagen cycles and not within the anagen phase. The finding that the cross-sectional area of individual hair shafts remains constant throughout fully developed anagen, indicating that the hair follicle, and its dermal papilla, remains the same size, supports this.

It is thought that the disruption of movement of cells between the dermal papilla and dermal sheath in AGA causes a loss of cells from the dermal sheath, and then, the dermal papilla that leads to hair follicle miniaturization.[45]

The size of the dermal papilla determines the size of the hair bulb and ultimately the hair shaft produced.[46] A greater than ten-fold reduction in overall cell numbers in dermal papilla is likely to account for the decrease in hair follicular size. The mechanism by which this decrease occurs is unexplained and may be the result of apoptotic cell death, decreased keratinocyte proliferation, cell displacement with loss of cellular adhesion leading to dermal papilla fibroblasts dropping off into the dermis, or migration of cells in dermal papilla into the dermal sheath associated with the outer root sheath of the hair follicle.[47]

Cells from the dermal papilla and dermal sheath have the capability to undergo both smooth muscle and adipose differentiation in vitro. There might be contribution from cells from the follicle mesenchyme toward the maintenance of the arrector pili. The loss of a progenitor cell population that maintains both the arrector pili and the dermal papilla might cause the muscle degeneration seen in AGA. Furthermore, possibly the loss attachment between bulge stem cell and arrector pili might explain why AGA is irreversible unlike alopecia areata.[32],[45]

 Pathology of Androgenetic Alopecia

When there is doubt about the diagnosis, 4 mm punch vertex scalp biopsies are the ideal specimens suggested. Horizontal scalp biopsies have more diagnostic information than vertical biopsies as scalp hairs are best seen on horizontal scalp biopsy. Triple horizontal biopsies have showed 98% diagnostic accuracy compared with 79% in a single biopsy in female AGA.[48]

FUs consist of a primary follicle from which rise an arrector pili muscle, a sebaceous gland, and multiple secondary follicles distal to the arrector pili. Hairs from secondary follicles commonly emerge from a single infundibulum. Only scalp hair FUs give rise to secondary hairs.

The earliest change in AGA is focal basophilic degeneration of the connective tissue sheath of the lower one-third of anagen follicles. Progressive miniaturization of anagen hair leads to hairs of different sizes in cross section (anisotrichosis). In very advanced stages of this process the vellus follicles disappear, leaving thin hyaline strands in the dermis. Progressive fibroplasias of the perifollicular sheath are part of this process. Transverse sections of hair show decreased hair diameter of individual hairs and an increased number of telogen hairs.

The prime feature found in scalp biopsies is the reduction in the terminal anagen hair count due to the replacement of terminal hairs with secondary pseudo-vellus hairs, and residual angiofibrotic tracts.[49] There is a change in the ratio of terminal to vellus hairs from >6:1 to <4:1. Furthermore, the anagen to telogen hair ratio reduces from 12:1 to 5:1.[50],[51]

In the connective tissue beneath the vellus follicles, small elastin bodies (Arão–Perkins bodies) which indicate sites of the papillae can be seen. These elastin bodies can be stained with the acid orcein method, but not the Verhoeff elastic stain. Erector pili muscles diminish in size and are seen attached to remnants of follicles. The number of sebaceous glands are generally decreased though some studies show increase in size, number, and lobulation of sebaceous glands.[52]

Perivascular infiltration of lymphocytes and mast cells and mild vasodilatation seen in AGA is referred to as microinflammation.[52]

A rare inflammatory variant of AGA shows infrabulbar and peri-isthmic inflammation. Distinguishing chronic telogen effluvium from AGA may be difficult histopathologically.[52]


To summarize, the pathogenesis of AGA [Figure 2] is a combination of genetic and hormonal factors leading to miniaturization of hair and shortening of anagen and an increase in telogen duration. More studies are underway to further elucidate this complex process, which leads to clinical androgen tic alopecia.{Figure 2}

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The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


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