INTRODUCTION — Androgenetic alopecia is the most common type of hair loss in men. The condition is characterized by the progressive loss of terminal hairs on the scalp in a characteristic distribution. The anterior scalp, mid scalp, temporal scalp, and vertex of the scalp are typical sites of involvement (picture 1A-D). "Male balding" and "male pattern hair loss" are additional terms used to refer to this condition.
The pathogenesis, clinical features, and diagnosis of androgenetic alopecia in men will be reviewed here. The treatment of androgenetic alopecia, androgenetic alopecia in women, and the general approach to the evaluation and diagnosis of hair loss are discussed separately.
●(See "Treatment of androgenetic alopecia in men".)
●(See "Female pattern hair loss (androgenetic alopecia in females): Management".)
●(See "Evaluation and diagnosis of hair loss".)
EPIDEMIOLOGY — Male androgenetic alopecia is a common postpubertal disorder that occurs worldwide and exhibits increasing prevalence with age. Prevalence estimates from studies in different countries suggest differences in prevalence based upon race or ethnicity; however, wide variation in study methods have made comparisons of prevalence estimates difficult [1-7].
For example, a study in the United States found at least moderate androgenetic alopecia (Hamilton-Norwood III or above (figure 1)) in 48 percent of 266 healthy men (ages 18 to 49 years), including 16 percent of men between the ages of 18 and 29 years and 53 percent of men between the ages of 40 and 49 years [6]. Prevalences of androgenetic alopecia appeared to be lower in a Korean study that involved examination of men visiting a hospital for regular health examinations. The Korean study found androgenetic alopecia (Hamilton-Norwood III or above) in only 14 percent of 5531 men (ages 20 and older), increasing from 2 percent among individuals aged 20 to 29 years to 11 percent among individuals aged 40 to 49 years [1]. The prevalence of androgenetic alopecia in the pediatric population (children and adolescents under 18) is not well studied.
PATHOGENESIS — Androgenetic alopecia is considered an androgen-dependent trait that requires a genetic predisposition. The interaction of these factors and other mechanisms that remain to be elucidated contributes to follicular miniaturization (the transition of larger, terminal hair fibers to small vellus hair fibers) in susceptible scalp areas. (See 'Androgens' below and 'Genetics' below and 'Follicular miniaturization' below and 'Other factors' below.)
Androgens — Consistent with a critical role for androgens, male androgenetic alopecia typically develops after puberty, a phase associated with a dramatic increase in androgen production. In addition, men with androgen insensitivity syndrome do not develop the condition [8]. (See "Pathogenesis and clinical features of disorders of androgen action", section on 'Complete androgen insensitivity (CAIS)'.)
Dihydrotestosterone (DHT) is the key androgen involved in the induction and promotion of male androgenetic alopecia [9]. DHT is a potent metabolite of testosterone and, compared with testosterone, has greater affinity for the androgen receptor.
The 5-alpha-reductase enzyme mediates the conversion of testosterone to DHT and exists in two isoforms in scalp hair follicles: type 1 and type 2. Although both isoforms have a role in androgenetic alopecia, the role of the type 2 isoform is greater. The type 2 isoform is located in the outer root sheath of hair follicles as well as the epididymis, vas deferens, seminal vesicles, and prostate. The type 1 isoform is located in sebaceous glands, epidermal and follicular keratinocytes, dermal papillae cells, and sweat glands.
The importance of 5-alpha-reductase is supported by the absence of androgenetic alopecia in men with mutations in the 5-alpha-reductase type 2 gene [10]. In addition, inhibitors of 5-alpha-reductase (eg, finasteride, dutasteride) are effective therapies for androgenetic alopecia. (See "Steroid 5-alpha-reductase 2 deficiency" and "Treatment of androgenetic alopecia in men".)
Intrinsic differences in hormone metabolism and hormone receptors may also contribute to androgenetic alopecia. Young men with androgenetic alopecia have higher levels of cellular 5-alpha-reductase and a higher quantity of androgen receptors in the balding scalp than in the nonbalding scalp [11]. In addition, production rates of DHT are higher in men with androgenetic alopecia than in men without the condition [12]. Although plasma testosterone concentrations are similar in balding and nonbalding men [13], elevated levels of unbound testosterone (the active fraction of testosterone) have been detected in some men with androgenetic alopecia [14,15].
Genetics — Androgenetic alopecia is considered a heritable disorder [16], a concept supported by the results of familial studies [17-19]. A study of 572 men evaluated in a dermatology clinic for concerns unrelated to androgenetic alopecia found that young men with a balding father were more than five times more likely to have androgenetic alopecia than young men with fathers without the condition (relative risk 5.5, 95% CI 1.26-23.99) [18]. In addition, a study of approximately 500 monozygotic male twins and 400 dizygotic male twins between the ages of 25 and 36 attributed 80 percent of the variance in the extent of hair loss to genetic effects [19].
Multiple genetic susceptibility loci for androgenetic alopecia have been identified [20,21]. Examples include the androgen receptor (AR)/EDAR2 locus on the X chromosome [22], the PAX1/FOXA2 locus on chromosome 20p11 [23,24], and HDAC9 gene on chromosome 7p21.1 [16,25]. Chromosome 3q26 may also have a contributory role [26].
Follicular miniaturization — The perception of hair "loss" in androgenetic alopecia results from shortening of the anagen (growth) phase of hair follicles, rather than the complete cessation of hair growth in affected areas [27]. The shortened anagen phase leads to the production of shorter, thinner vellus hair shafts, a process called follicular miniaturization (picture 2). As additional follicles undergo miniaturization, hair coverage of the scalp progressively decreases. (See "Evaluation and diagnosis of hair loss", section on 'Hair biology'.)
Follicular miniaturization is caused by a hormonally mediated process at the level of the hair follicle dermal papilla [28]. At the cellular level, DHT binds to the androgen receptor, and the hormone-receptor complex then activates the genes responsible for the gradual transformation of large, terminal follicles to smaller follicles with a shortened anagen phase [29-32]. The precise mechanisms through which genetic variants contribute to the induction of follicular miniaturization remain unclear [33]. (See 'Genetics' above.)
The gradual transformation is associated with apoptosis of cells within the dermal papilla and a reduction in the overall size of the dermal papilla. This may be central to the miniaturization process given that the size of the dermal papilla correlates well with the caliber of the hair fiber produced.
Other factors — Although hormone-mediated pathogenic mechanisms have been an intensive focus of research, a variety of other pathogenic mechanisms may be relevant. These include Wnt signals, prostaglandin D2 signals, prostaglandin F2-alpha signals, and Janus kinase (JAK) signals, among others [34,35]. New treatments for androgenetic alopecia based upon targeting of these mechanisms are under investigation [36,37].
CLINICAL FEATURES — Androgenetic alopecia in men is characterized by varying degrees of hair follicle miniaturization and reduction in terminal hair density on the scalp in characteristic locations (picture 1A-D). The degree of scalp involvement may change over time as the condition progresses.
Some men with androgenetic alopecia may occasionally report symptoms such as itching, but it remains to be fully elucidated as to whether these symptoms are a bona fide feature of androgenetic alopecia and whether such symptoms correlate with the histologic findings of perifollicular inflammation that are known to characterize this hair loss condition. (See 'Histopathology' below.)
Many males with androgenetic alopecia who present with concerns about itching have identifiable reasons separate from the androgenetic alopecia itself, such as seborrheic dermatitis. Whether androgenetic alopecia itself has a symptomatic phase awaits further study.
Pattern and course — Signs of androgenetic alopecia may first appear during adolescence. Terminal hair loss typically begins in the temporal scalp, midfrontal scalp, or vertex area of the scalp (picture 1A-D). The severity of involvement of these areas is highly variable; in some men, the greatest degree of hair loss occurs at the vertex, and other men exhibit the most severe hair loss anteriorly. (See "Treatment of androgenetic alopecia in men", section on 'Surgery'.)
Androgenetic alopecia is a continuous process that progresses slowly over the course of many years. The two most common patterns for progression of hair loss are reviewed in this figure (figure 1). Hair loss occurs in waves of activity, with more rapid intervals of hair loss at certain times followed by periods of minimal activity.
Classification — The Hamilton-Norwood scale is commonly used to classify androgenetic alopecia, although other systems are also used [38]. The Hamilton-Norwood scale divides the clinical findings into seven stages and offers a visual depiction of the sequential stages of balding (figure 1). The scale also describes a less common type A variant of hair loss in which men demonstrate only the progressive movement of the anterior hairline posteriorly (figure 1) [39].
Not all men with androgenetic alopecia follow the hair loss patterns outlined by the Hamilton-Norwood scale. For example, 10 percent of men have a pattern that resembles female androgenetic alopecia (preservation of the frontal hairline and terminal hair loss in the central scalp) (picture 3) [40].
HISTOPATHOLOGY — Androgenetic alopecia has distinct histopathologic findings that can be identified on scalp specimens sectioned horizontally or vertically:
●Horizontal sections – The histologic features of androgenetic alopecia are more readily seen in horizontal sections. Depending on the severity of the clinical findings, there is a variable mixture of terminal, vellus, and vellus-like hair follicles in the dermis. The vellus and vellus-like hairs are less than 0.03 mm in diameter [41]. Terminal hairs (greater than 0.06 mm) are seen in the reticular dermis.
The ratios of anagen to telogen (A:T) hair follicles and terminal to vellus (T:V) hair follicles are altered in androgenetic alopecia and can be readily evaluated with horizontal sections. In the course of androgenetic alopecia, the A:T ratio is reduced from 12:1 to less than 5:1. The T:V ratio is progressively reduced as miniaturization progresses [42]. For example, with further progression of the condition, the T:V ratio may slowly approach 1:1, and then the ratio is reversed, with T:V ratios of 1:2 or less and conversion from terminal to vellus hairs becomes complete. These alterations in the T:V ratio can be extremely helpful in the diagnosis of androgenetic alopecia.
●Vertical sections – Vertical sections show terminal hair follicles rooted in the subcutaneous and reticular dermis and vellus hair follicles located more superficially in the papillary dermis. Vertical columns of connective tissue, known as follicular stelae or follicular streamers, can be seen [43,44]. The follicular stelae that originate in the deep dermis and underlie vellus hairs in the more superficial dermis may represent connective tissue that previously surrounded terminal hair follicles prior to miniaturization [42].
Inflammation is not uncommon in histologic specimens from androgenetic alopecia despite the fact that it is classified as a noninflammatory form of hair loss. In one retrospective study that included 53 female and 5 male patients with androgenic alopecia, perifollicular inflammation was found in 88 percent of biopsies [45]. Inflammation was found in the isthmus and infundibulum, although the inflammation at the level of the isthmus was more common. Inflammation was typically mild, although moderate and severe inflammation at the level of the isthmus was not uncommon.
The inflammation in androgenetic alopecia differs significantly from the intense peribulbar inflammation that is typically found in alopecia areata. The precise role of the inflammatory response seems unclear, although its presence early in the course of androgenetic alopecia and around miniaturized hairs has led some authors to postulate it may contribute to miniaturization, perifollicular fibrosis [46], and fibrosis [47].
Mild, perifollicular fibrosis is an additional feature that may be detected [43]. Although perifollicular fibrosis as well as peri-isthmal/infundibular inflammation can be seen in scarring alopecias, such as lichen planopilaris, the scarring alopecias typically show loss/reduction of sebaceous glands and often lichenoid-type changes in the outer root sheath that are not present in androgenetic alopecia [48].
The presence of inflammation or fibrosis may have prognostic significance in androgenetic alopecia. In a study of male patients with androgenetic alopecia treated with topical minoxidil, 55 percent of 22 men with inflammation or fibrosis responded to minoxidil compared with 77 percent of 22 men without histopathologic evidence for inflammation or fibrosis [43]. Further studies are necessary to confirm this finding.
ASSOCIATED DISORDERS — Androgenetic alopecia may have negative psychosocial effects and has been linked to other disorders, such as cardiovascular disease and prostate cancer.
Psychosocial effects — The psychosocial impact of androgenetic alopecia on men varies. Overall, the impact tends to be less than for women with female pattern hair loss. However, men may experience stress and psychologic distress related to hair loss, reduced quality of life, and infrequently, related body dysmorphic disorder [49]. (See "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis", section on 'Psychosocial dysfunction' and "Body dysmorphic disorder: Clinical features".)
Cardiovascular disease — Multiple studies have investigated the relationship between androgenetic alopecia and cardiovascular disease or risk factors for cardiovascular disease, including studies that have identified elevated rates of cardiovascular disease in patients with vertex hair loss [50,51], vertex and frontal hair loss [52], early-onset hair loss [53], and rapidly progressive hair loss [53]. In addition, increased risks for hypertension [54], excess weight [55], abnormal lipids [56], insulin resistance [57], carotid atheromatosis [58], and death from diabetes or heart disease [59] have been reported in this population. Studies investigating an association between androgenetic alopecia and the metabolic syndrome have yielded conflicting findings [58,60-62].
Distinct guidelines for the detection and prevention of cardiovascular disease in individuals with androgenetic alopecia have not been established. (See "Metabolic syndrome (insulin resistance syndrome or syndrome X)".)
Prostate cancer — Studies evaluating the relationship between androgenetic alopecia in men and prostate cancer have yielded varied results [14,63-69]. A systematic review and meta-analysis of seven case-control studies (4078 cases and 4916 controls) that used a standardized tool to classify androgenetic alopecia found an association between vertex pattern hair loss in androgenetic alopecia and increased risk for prostate cancer (pooled odds ratio [OR] 1.25, 95% CI 1.09-1.44) but did not find an association between any pattern of androgenetic alopecia and the disease [70]. A subsequent systematic review and meta-analysis that included both case-control and cohort studies yielded similar findings [71].
An analysis of data from the National Health and Nutrition Examination Survey Epidemiologic Follow-up Study on 4316 men 25 to 74 years of age followed up from between 1971 and 1974 to 2011 found that androgenetic alopecia was associated with a 56 percent increased risk of death from prostate cancer (hazard ratio [HR] 1.56, 95% CI 1.02-2.37) [72].
Further confirmation is needed before a recommendation for the use of androgenetic alopecia in screening decisions for prostate cancer.
Other — An 18-year prospective study including over 30,000 male participants in the Health Professionals Follow-up Study found a modest increase in the risk of colon cancer for men with frontal-only baldness and frontal-plus-mild-vertex baldness compared with men without baldness (HR 1.29, 95% CI 1.03-1.62; and HR 1.31, 95% CI 1.01-1.70, respectively) [73]. Additional studies are needed to confirm this association.
DIAGNOSIS — The diagnosis of androgenetic alopecia in males is usually straightforward and can be made through obtaining a history and performing an examination of the hair and scalp. Slow, progressive, asymptomatic hair loss with evidence of follicular miniaturization on the temporal, frontal, and/or vertex regions of the scalp supports a diagnosis of androgenetic alopecia. Other patterns of hair loss or diffuse hair loss should raise suspicion for alternative diagnoses. (See "Evaluation and diagnosis of hair loss", section on 'Nonscarring alopecia'.)
History — The patient history should include an assessment of the progression, distribution, and extent of hair loss, as well as associated symptoms and family history. Men with androgenetic alopecia typically describe slow, progressive hair loss without associated symptoms. A family history of similar hair loss is common.
Rapid hair loss or hair loss accompanied by itching, burning, or scalp tenderness suggests an alternative or coexisting diagnosis. In particular, rapid hair loss related to telogen effluvium may unmask previously unnoticed androgenetic alopecia. (See "Telogen effluvium".)
The approach to the patient interview for hair loss is reviewed in detail separately. (See "Evaluation and diagnosis of hair loss", section on 'Patient interview'.)
Physical examination — The physical examination should include careful examination of the scalp and hair. (See "Evaluation and diagnosis of hair loss", section on 'Physical examination'.)
Follicular miniaturization in a distribution consistent with androgenetic alopecia essentially confirms the diagnosis (picture 1A-D). Examination of the caliber of hair fibers against a paper that is a color that contrasts with the hair facilitates visualization of miniaturized hairs.
Examination with a dermatoscope is also helpful for identification of miniaturized hairs and diagnosis (picture 2) [74]. Dermoscopic features of androgenetic alopecia include hair diameter diversity, perifollicular pigmentation/peripilar signs, and yellow dots (table 1) [74,75]. Focal atrichia (small areas with a complete absence of hair) may also be seen. (See "Overview of dermoscopy of the hair and scalp".)
Patients with clinical findings of androgenetic alopecia who report rapid hair loss should undergo a hair pull test to assess for coexisting active telogen effluvium. (See "Evaluation and diagnosis of hair loss", section on 'Hair pull test' and "Telogen effluvium".)
Scalp biopsy — Histopathologic examination is not usually necessary for diagnosis. However, androgenetic alopecia has distinctive histologic features, and biopsies can be used to confirm the diagnosis in the infrequent cases in which the diagnosis is uncertain [43,76]. (See 'Histopathology' above.)
A 4 mm punch biopsy is the preferred procedure for obtaining a tissue specimen for diagnosis. Many clinicians obtain two biopsies, one for horizontal (transverse) sectioning and one for vertical sectioning. Horizontal sectioning of the tissue specimen allows for visualization of more follicles and tends to yield more useful results than vertical sectioning [43]. Some pathology laboratories will process a single 4 mm punch specimen into vertical and horizontal sections (HoVert technique) [77,78]. (See 'Histopathology' above and "Skin biopsy techniques", section on 'Biopsy techniques'.)
DIFFERENTIAL DIAGNOSIS — Hair loss related to androgenetic alopecia should be distinguished from other causes of nondiffuse hair loss, such as hairline maturation, alopecia areata, traction alopecia, cicatricial alopecias, and trichotillomania. Given its frequent occurrence, androgenetic alopecia may also coexist with these and other hair and scalp diseases:
●Hairline maturation – Slight recession of the hairline is a normal, hormonally mediated occurrence that typically begins in early adulthood. In men, this involves up to two centimeters of posterior recession of the leading edge of the hairline from its childhood position [79]. Minor temporal recession also occurs, further contributing to a change in the shape of the hairline. The limited extent of hairline recession contrasts with the more extensive recession and vertex involvement that occurs in androgenetic alopecia.
●Alopecia areata – Alopecia areata is an immune-mediated form of nonscarring hair loss. Alopecia areata most often manifests as sudden hair loss in circular, discrete areas but may also present with larger patches of alopecia or loss of all scalp hair (picture 4). In particular, the rare sisaipho (ophiasis inversus) pattern, which involves loss of hair on the frontal, temporal, and parietal scalp, may be mistaken for androgenetic alopecia (picture 5). In contrast to the slow, progressive course of androgenic alopecia, hair loss in alopecia areata tends to be rapid. A scalp biopsy is useful for distinguishing challenging cases. (See "Alopecia areata: Clinical manifestations and diagnosis".)
●Traction alopecia – Traction alopecia is a type of hair loss that results from prolonged or repetitive tension on hair. The location of hair loss correlates with the site of traction. The frontal and temporal scalp are the most common affected areas (picture 6). A history of a traction-inducing hairstyle and hair loss in the correlating distribution supports the diagnosis. If the diagnosis remains uncertain, a biopsy can be helpful. (See "Traction alopecia".)
●Cicatricial (scarring) alopecias – Patches of scarring hair loss or frontal hairline recession from cicatricial alopecias may be confused with androgenetic alopecia, particularly when clinical signs of inflammation are minimal or resolved (picture 7A-C). However, unlike androgenetic alopecia, close examination of the involved scalp will reveal findings consistent with scarring (absence of follicular ostia and vellus hairs). In addition, a history of inflammatory signs or symptoms (eg, pruritus, pain, inflamed papules, pustules) in the affected area is often present in cicatricial alopecias. When necessary, a scalp biopsy can distinguish androgenetic alopecia from cicatricial alopecia. (See "Evaluation and diagnosis of hair loss", section on 'Cicatricial alopecia'.)
●Trichotillomania – Trichotillomania is a psychiatric disorder characterized by recurrent hair pulling. Patients often present with bizarrely shaped patches of alopecia and hair shafts of different lengths due to multiple episodes of hair puling. The diagnosis usually can be made based upon the patient history. A scalp biopsy can help to confirm the diagnosis in challenging cases. (See "Skin picking (excoriation) disorder and related disorders", section on 'Trichotillomania'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Alopecia".)
INFORMATION FOR PATIENTS — Educational materials on this topic are available for patients (see "Patient education: Androgenetic alopecia in men and women (Beyond the Basics)"). We encourage you to print or e-mail this topic review, or to refer patients to our public web site, www.uptodate.com/patients, which includes this and other topics.
SUMMARY AND RECOMMENDATIONS
●Overview – Androgenetic alopecia is a common condition in postpubertal males that is characterized by the loss of terminal hairs in select areas on the scalp. (See 'Epidemiology' above.)
●Pathogenesis – Hormonal, genetic, and other factors contribute to the development of male androgenetic alopecia. The effects of dihydrotestosterone on susceptible follicles contributes to follicular miniaturization, which manifests clinically as the replacement of terminal hairs by short, thin (vellus) hairs. (See 'Pathogenesis' above.)
●Clinical features – The appearance of male androgenetic alopecia varies among individuals. The temporal, anterior, mid scalp, and/or vertex areas of the scalp are typically affected (picture 1A-D). The occipital scalp is usually spared. The loss of terminal hairs slowly progresses over the course of years. (See 'Clinical features' above.)
●Diagnosis – The diagnosis of androgenetic alopecia is usually made clinically and is based upon the detection of slow, progressive hair loss and follicular miniaturization in a distribution consistent with androgenetic alopecia. For the infrequent cases in which the diagnosis is uncertain, a biopsy can be used to confirm the diagnosis. (See 'Diagnosis' above.)
●Associated disorders – Some men with androgenetic alopecia may experience negative psychosocial effects. Androgenetic alopecia has also been associated with other disorders, such as cardiovascular disease and prostate cancer. (See 'Associated disorders' above.)
