Alopecia androgenetica

Last Updated: 2025-08-21

Author(s): Navarini A., Huber S.

ICD11: L64

Hippocrates (alopecia hippocratica)

Androgenetic effluvium/alopecia, alopecia oleosa, alopecia seborrhoica, calvities hippocratica, female/male baldness, female pattern alopecia, androgenetic alopecia (AGA), pattern baldness, common balding, hereditary balding/thinning

Polygenic hair loss characterized by progressive miniaturization of the hair follicles and reduced hair density in the androgen-sensitive areas of the scalp.

  • Androgenetic alopecia is the most common form of hair loss in men and women. 
  • The prevalence rate in men in their 30s, 40s, and 50s in the Caucasian population is approximately 30%, 40%, and 50%, respectively.
  • The overall prevalence among adult women is 32.3%, with prevalence increasing with age: from 8% in the 20–29 age group to 68% in women aged 60–75 (Müller Ramos et al., 2023).
  • Caucasians are most affected, while people of Asian, Native American, or African American descent are less affected.
     

The classification is based on gender.

 

Norwood–Hamilton scale (1951/1975) (men) (Bouhanna et al., 2000)

  • Stage I: Normal hair growth
  • Stage II: Receding hairline
  • Stage III: Tonsure-like, occipital-parietal hair thinning, hair bridge still present
  • Stage IV: Almost complete hair loss in the parietal area, with a lateral and posterior hair rim remaining
  • Stage V: Thin, ring-shaped, occipital and parietal residual hair

 

Ludwig scale (1977) (women) (Bouhanna et al., 2000):

  • Stage I: Incipient hair thinning in the parting region, only noticeable when parting the hair
  • Stage II: Clearly visible hair thinning in the parting area, the frontal hairline is becoming visible
  • Stage III: Pronounced baldness in the frontoparietal region, existing frontal hairline

 

Basic and specific classification (2007) (universal for women and men) (Lee et al., 2007)

  • There are four basic types (L, M, C, U) and two specific types (V, F). Each type is divided into three or four sub-types depending on severity. The basic types describe the shape of the front hairline. The specific types refer to the hair density of the frontal and vertex regions. The final hair loss type is determined by combining a basic type with a specific type (if applicable) (Lee et al., 2007).

  • The interaction of genetic, hormonal, and metabolic factors as well as microinflammation is crucial for the development of androgenetic alopecia.
  • Susceptibility to androgenetic alopecia is mainly influenced by hereditary factors. 
  • Androgenetic alopecia follows a polygenic model, largely consisting of gene polymorphisms of the androgen receptor (AR) genes on the Xq12 chromosome, accompanied by increased receptor activity in the hair follicles after binding of dihydrotestosterone. 
  • The mutated androgen receptors in the hair follicles bind to dihydrotestosterone and initiate an enhanced signaling cascade that leads to a shortening of the anagen phase and, as a result, to thinner and shorter hair, in the sense of a miniaturization of the hair follicles. The terminal hairs are replaced by vellus hairs.
  • Occipital hair is less sensitive due to its androgen receptor methylation. 
  • In women, it rarely occurs secondarily to other underlying diseases (e.g., polycystic ovary syndrome) that lead to elevated peripheral androgen levels.
     

  • Hair loss can begin as early as puberty. 
  • Seasonal exacerbation is often observed in spring and fall. 
  • The pattern of hair loss varies between the sexes. In men, the frontotemporal region and the parting are mainly affected. In female androgenetic alopecia, the parting is primarily affected, with the front hairline remaining unaffected. 
     

  • The diagnosis is made clinically. Pull tests, dermatoscopy, and trichograms are useful. A scalp biopsy may also be performed if necessary. 
  • Macroscopically, hair thinning is found in the androgen-sensitive areas of the scalp. 
  • The hair pull test should be performed both frontally and occipitally. In androgenetic alopecia, the pull test is only positive frontally and not occipitally, in contrast to telogen effluvium. 
  • Reflected light microscopy reveals anisotrichosis >20% in the androgen-sensitive areas. 
  • Diagnostic features of androgenetic alopecia in the trichogram include increased hair shaft diameter diversity, shortening of the hair, dystrophic hair, and an increased telogen hair rate. 
  • Any substrate deficiency (e.g., ferritin, zinc, vitamin D, vitamin B12, folic acid) that may promote effluvium should always be ruled out. 
  • Hormone tests are generally not indicated in men.
  • In women, if there are corresponding anamnestic indications of hyperandrogenemia (including hirsutism, pronounced acne, seborrhea, irregular menstrual cycles, infertility, clitoral hypertrophy, metabolic syndrome, known PCOS) or hyperprolactinemia (including galactorrhea), an endocrinological evaluation (referral to a specialist (endocrinology/gynecology)) is recommended.

Histologically, there is typically an increase in vellus hair with perifollicular inflammation and fibrosis and a slightly elevated telogen/anagen ratio.

Due to the association between androgenetic alopecia and ischemic heart disease or metabolic syndrome, patients with AGA should also be examined for dyslipidemia and other cardiovascular risk factors.

It is essential to start treatment as early as possible.

The severity of androgenetic alopecia increases with age.

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