American Journal of Clinical Dermatology

https://doi.org/10.1007/s40257-019-00479-x

REVIEW ARTICLE

Female Androgenetic Alopecia: An Update on Diagnosis

and Management
Michela Starace1 · Gloria Orlando2 · Aurora Alessandrini1 · Bianca Maria Piraccini1

© Springer Nature Switzerland AG 2019

Abstract
Female androgenetic alopecia (FAGA) is a common cause of non-scarring alopecia in women. The onset may be at any
age following puberty and the frequency increases with age. Clinically, it shows a diffuse hair thinning over the central
scalp, while the frontal hairline is usually retained. FAGA can have a significant psychological impact, leading to anxiety
and depression. For this reason, early diagnosis is very important to stop the progression of the disease. The sex hormonal
milieu is the main pathogenetic mechanism studied in FAGA. The role of androgens is not clearly defined and only one-third
of women with FAGA show abnormal androgen levels. Endocrinological diseases with hyperandrogenism associated with
FAGA comprise polycystic ovarian syndrome (PCOS), hyperprolactinemia, adrenal hyperplasia and, rarely, ovarian and
adrenal tumours. Usually the diagnosis of FAGA is made clinically. A complete clinical examination and a blood examina-
tion can reveal other signs of hyperandrogenism. Trichoscopy shows the typical hair miniaturization. A scalp biopsy can be
useful when the clinical evaluation does not provide a definitive diagnosis or when cicatricial alopecias with hair loss in the
distribution of FAGA or alopecia areata are suspected. FAGA is a slowly progressive disease. The goal of therapy is to stop
the progression and to induce a cosmetically acceptable hair regrowth. The most important drugs are topical minoxidil and
oral anti-androgens. The purpose of this review is to provide an update on FAGA and to create a guideline on diagnosis and
management of this frequent hair disease, not always easily recognizable from cicatricial alopecias with a similar distribution.

1 Introduction ‘Androgenetic alopecia’ (AGA) is used to refer to this

Female androgenetic alopecia (FAGA) is a common cause
of non-scarring alopecia in women [1]. Clinically it shows
a diffuse hair thinning over the central scalp, while the
frontal hairline is usually retained. It is typified by a pro-
gressive follicular miniaturization and an increased telo-
gen phase. Several studies have reported a reduced qual-
ity of life in women with FAGA. Indeed it can have a
significant psychological impact, leading to anxiety and
depression [2].
Michela Starace and Gloria Orlando equally contributed to this
article.
* Bianca Maria Piraccini
biancamaria.piraccini@unibo.it
1
Division of Dermatology, Department of Experimental,
Diagnostic and Specialty Medicine, University of Bologna,
V. Massarenti 1, 40138 Bologna, Italy
2 is characterized by a permanent progressive recession of the
Unit of Dermatology, Department of Medicine‑DIMED,
University of Padova, Padua, Italy
form of hair loss both in men and women, where ‘andro’
signifies a hormonal aetiology and ‘genetic’ refers to the
hereditary contribution. Some years ago, the term ‘female
pattern hair loss’ (FPHL) was introduced for this condition
in women [3]. Later it was clarified that FPHL refers to
all diseases with hair loss in a typical FAGA distribution.
Recently, cicatricial alopecias with hair loss in the dis-
tribution of typical FAGA have been reported. Fibrosing
alopecia in pattern distribution (FAPD) presents as a central
scarring hair loss with perifollicular erythema and follicular
hyperkeratosis and histological features of lichen planopila-
ris (LPP) and AGA [4]. Cicatricial pattern hair loss (CPHL)
is characterized by histological features similar to FAPD and
‘pencil–eraser-sized’ areas of focal atrichia, lacking the clin-
ical inflammatory signs seen in FAPD [5]. A common form
of cicatricial alopecia seen in African American women,
central centrifugal cicatricial alopecia (CCCA), appears in
the same area of the scalp as FAGA and is also characterized
by a perifollicular lymphocytic infiltrate [5]. Frontal fibros-
ing alopecia (FFA) is histologically similar to FAPD but it

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Key Points 
Female androgenetic alopecia (FAGA) is the most com-
mon form of non-scarring alopecia in women, character-
ized by diffuse hair thinning over the central scalp.
Recently, cicatricial alopecias with hair loss in the distri-
bution of typical FAGA have been reported.
The diagnosis of FAGA is usually made clinically, but
blood examination is important to assess any associ-
ated diseases and trichoscopy is useful to follow up the
patient.
FAGA is a slowly progressive disease. The goal of
therapy is to stop the progression and to induce a cos-
metically acceptable hair regrowth.
fronto-temporal hairline; not a typical feature of FAGA, but
quite common in some forms of male AGA [5, 6].
In this context, FPHL has not been considered a dis-
ease but rather a phenotype of clinical presentations of
different disorders including some subtypes of cicatricial
alopecias [5].
The purpose of this review is to provide an update on
diagnosis and management of FAGA.
2 Epidemiology
The onset may be at any age following puberty and the
frequency increases with age [7, 8].
Although the real prevalence of FAGA is difficult to
determine due to the lack of universally accepted criteria
for the diagnosis, it is generally agreed that the frequency
of FAGA varies among different population groups.
In Caucasian women, the prevalence of FAGA increases
with age: from 3–12% during the third to fourth decade,
to 14–28% in postmenopausal women in their fifties and
29–56% in the population older than 70 years [9–11].
The prevalence of FAGA in Asian women has a similar
age-related trend, but it seems to be lower than in Cauca-
sian women.
A study conducted in 2001 with 4601 Korean women
showed an overall prevalence of 5.6% [12], the same rate
was observed in 2010 in a Chinese study involving 8446
women [13]. The largest study was conducted in 2013 in
Taiwan with 26,226 women and showed an overall preva-
lence of 11.8% [14]. There are no published data about the
prevalence of FAGA in the African population.
M. Starace et al.
3 Etiopathogenesis
Sex hormonal milieu is the main pathogenetic mechanism
studied in FAGA. Even though the relationship between
dihydrotestosterone (DHT) and male AGA has been con-
firmed [15], the role of androgens is not clearly defined in
FAGA. Indeed, only one-third of women with FAGA show
abnormal androgens levels [16].
An increased peripheral sensitivity to androgens has
been postulated to explain cases with normal levels of
androgens [17]. However, FAGA has also been described
in patients lacking androgen receptors, suggesting that an
androgen-independent mechanism could be involved [18].
Estrogen could have a protective role on human hair
growth, suggested by the increased prevalence of FAGA
following menopause, the prolongation of anagen during
pregnancy [19], the hair loss in women taking tamoxifen
or aromatase inhibitors for treatment of breast cancer [20]
and the documented complete hair regrowth in transsexual
individuals with AGA on estrogen [21, 22].
Recently, sequence variations in the androgen recep-
tor gene (AR) and estrogen receptor 2 gene (ESR2) have
been associated with susceptibility to FAGA [8]. However,
the association between FAGA and the aromatase gene
(CYP19A1) has not been confirmed [8]. No definitive fam-
ily inheritance has been identified.
Moreover, several data suggest that chronic inflam-
mation in the scalp may promote hair loss [23]. Histo-
logically, the miniaturization process is associated with
microinflammatory lymphocytic infiltrate in the peri-
infundibular region; and prostaglandin D2 (PG-D2), which
can inhibit hair growth in explanted human hair follicles
and in mice, is elevated in bald scalps, but this study is
confirmed only in men [24].
4 Clinical Presentation
FAGA is characterized by a progressive hair follicle minia-
turization with the conversion of terminal follicles in vellus-
like follicles, an increased telogen/anagen ratio and a short-
ened hair cycle. If untreated, it leads to a slow progressive
hair thinning of the scalp, though not to complete baldness,
as happens in males [16].
Three main patterns of FAGA presentation have been
described. Most frequently it shows a frontal hair thin-
ning accentuation resulting in the ‘Christmas tree’ pattern
(Olsen pattern) [25] (Fig. 1). The second most common
pattern is characterized by central scalp involvement with
the sparing of the frontal hairline (Ludwig pattern) [26]
(Fig. 2). Finally, in patients with significant androgeniza-
tion, bitemporal recession can be observed; rarely it could
Female Androgenetic Alopecia
Fig. 1  ‘Christmas tree’ pattern of female androgenetic alopecia
(FAGA), with frontal hair thinning accentuation
be associated with vertex thinning (Hamilton pattern) [27]
(Fig. 3).
However, severe FAGA often involves parietal and
occipital regions with diffuse hair thinning [28].
5 Associated Diseases
Many endocrinological diseases can be associated with
FAGA. Among them, the most frequently implicated in the
development of hyperandrogenism are polycystic ovarian
syndrome (PCOS), hyperprolactinemia, adrenal hyperpla-
sia and rarely, ovarian and adrenal tumours.
Moreover, FAGA have been linked to insulin resist-
ance, hypertension, diabetes mellitus and increased
Fig. 2  Typical female androgenetic alopecia (FAGA) presentation, with involvement of the central hairline at different degrees of severity (a–c)
Fig. 3  Hamilton pattern in female androgenetic alopecia (FAGA)
cardiovascular risk [29]. Higher aldosterone, C-protein,
D-dimers and insulin levels in women with FAGA could
explain this [30]. In female patients with early-onset
FAGA, some authors recommend ruling out the presence
of metabolic syndrome and/or cardiovascular disease [30].
6 Diagnosis
6.1 Medical History
Age of onset, duration and progression of the hair loss
should be investigated. In many cases, the family history
has a positive response, if it is negative, FAGA can’t be
excluded.
Patients should be asked about thinning and shedding.
Usually they describe a hair thinning on the central scalp
and complain about an increased visibility of the scalp
through the hair in this area. Patients should be investigated
for menarche, menstrual irregularities, menopause, amenor-
rhea, difficult in conceiving, signs of virilization (hirsutism,
deepening voice, clitoral enlargement) and acne. Closer

attention must be observed to drugs that can induce hyper-
androgenism such as anabolic-androgenic steroids, synthetic
proandrogens, progestins and antiepileptics. Other causes
of hair loss should be excluded such as iron deficiencies,
thyroid dysfunctions, medical treatment, infections, deficient
diet and rapid weight loss.
6.2 Physical Examination
It is useful to perform a complete clinical examination in
order to find other signs of hyperandrogenism, such as acne
and hirsutism. Hirsutism should be evaluated in locations
where typically women do not develop terminal hair (face,
abdomen, back and chest) and estimated with the Ferryman-
Gallwey scale (Fig. 4). In Caucasian woman, a score of 8 or
higher is indicative of hirsutism.
Impaired fertility, menstrual irregularities, amenorrhea,
hypertrichosis, hyperseborrhoea, obesity and severe acne
may be indicative of PCOS [1].
6.3 Scalp Examination
The diagnosis of FAGA is usually made clinically. A scalp
biopsy should be recommended for cases of uncertain
diagnosis but also for very young patients, patients with
diffuse FAGA and those who have suspicious clinical fea-
tures for the cicatricial forms. Since the occipital scalp is
not under androgen control and not involved in FAGA,
the best way to evaluate the hair thinning is by parting
hair vertically, both in the central and occipital scalp, and
comparing these two areas [25].
Several scales have been developed in order to evaluate
the severity of FAGA. Ludwig’s scale is divided into three
degrees, from a mild light thinning in the first degree,
to a complete absence of hair in the central scalp in the
third degree [31]. Savin’s scale quantifies eight stages of
Fig. 4  Clinical presentation of hirsutism on the face and the abdomen of a woman affected by female androgenetic alopecia (FAGA)
M. Starace et al.
increasing crown balding, and in addition there is a spe-
cial subcategory to detect frontal anterior recession [31].
Sinclair’s classification includes five colour photographs
of women’s scalps with the hair parted centrally; it is a
photographic measure of patients’ perception of the sever-
ity of their hair loss [31]. Olsen’s classification is similar
to Ludwig’s classification, but it underscores the accen-
tuation of fronto-vertical alopecia, with a triangular or
‘Christmas tree’ pattern [31].
6.3.1 Pull Test
Pull test could be positive in the central scalp and in the
initial phases of FAGA, showing telogen roots. It is usu-
ally negative in long-standing forms and the hair shedding
does not involve the scalp diffusely.
6.3.2 Trichoscopy
Trichoscopy is a non-invasive technique based on dermo-
scopic evaluation of the scalp, which allows a 10× magnifi-
cation. Recently, besides manual trichoscopy, videodermos-
copy has gained importance. It is a non-invasive diagnostic
tool, initially used to evaluate and monitor pigmented skin
lesions, that has proven to be useful in the scalp diseases. A
magnification ranging from 20× to 70× allows the in vivo
visualization of scalp epidermis, follicles, hair shafts and
vascular patterns. Moreover, images can be stored to get a
global photographic assessment that can be used in further
controls to evaluate the hair growth [32].
The main trichoscopical sign in FAGA is the presence of
hair diameter variability > 20% [33]. Moreover, it may show
yellow dots that are indicative of empty follicles, small areas
of focal atrichia and peripilar hyperpigmentation [34, 35].
Female Androgenetic Alopecia
Follicular ostia are usually preserved, helping in the differ-
ential diagnosis of scarring alopecia (Fig. 5).
In 2009, Rakowska et al. [36] proposed major and minor
dermoscopic criteria for the diagnosis of FAGA. Major cri-
teria include (1) more than four yellow dots in four images
in the frontal area; (2) lower average hair thickness in the
frontal area compared with the occipital area and (3) >10%
of thin hairs (< 0.03 mm) in the frontal area. Minor criteria
include (1) increased frontal to occipital ratio of single-hair
pilosebaceous units; (2) vellus hairs and (3) perifollicular
discoloration. The diagnosis of FAGA is made with the
presence of two major criteria or one major plus two minor
criteria.
6.3.3 Biopsy
It can be useful when the clinical evaluation does not provide
a definitive diagnosis, and cicatricial alopecias or alopecia
areata are suspected. From our experience, we recommend
the dermoscopy-guided biopsy of the scalp technique with
a 4-mm punch involving the dermis. Dermoscopy helps
select the most significant site to perform the biopsy, lead-
ing to a definitive pathological diagnosis in almost all cases.
In early stages of FAPD, for instance, dermoscopy identi-
fies even small areas of cicatricial alopecia and therefore it
allows a correct clinical-pathological diagnosis promptly. It
is best to avoid the bitemporal area as this region may have
miniaturized hairs in women without hair loss. Vertical and
horizontal sectioning should be evaluated [7, 37]. Horizontal
sections enable the evaluation of the number of hairs per
field of view. In FAGA, there is an increased number of min-
iaturized (vellus-like) hairs (Fig. 6). The ratio of terminal
to vellus-like hair follicles is typically < 3:1 in women with
this condition against > 7:1 in the normal scalp [38]. Other
typical histopathological features are an increase of telogen/
anagen ratio and an increased number of follicular stelae
Fig. 5  Trichoscopy of female androgenetic alopecia (FAGA): reduced
hair thickness with hair diameter variability, reduced number of hairs
with empty follicle (×20 magnification)
[7]. Low levels of mild perifollicular inflammation around
the upper portion of the hair follicle as well as perifollicular
fibrosis may be present.
6.3.4 Biochemical Examinations
A hyperandrogenic state should be considered in women
with FAGA associated with signs of androgen excess (e.g.
hirsutism, irregular menses, acne, hyperprolactinemia, acan-
thosis nigricans); while it is not indicated in all women with
FAGA [1]. Free androgen index test (FAI = total testosterone
[nmol L−1] × 100/sex hormone binding globulin [SHBG])
and prolactin as screening parameters for ovarian hyper-
androgenism and dehydroepiandrosterone sulfate (DHEA)
and 17-hydroxyprogesterone (17-OH-P) as screening param-
eters for androgen-producing tumours and adrenal congeni-
tal hyperplasia are recommended [39]. Note that testing of
androgen levels should be done during the follicular phase,
between the fourth and the seventh day of the cycle, and
that oral contraceptives should be discontinued for at least 2
months prior to this testing [40].
Ovarian and adrenal ultrasound could be prescribed to
rule out the presence of ovarian cysts and androgen-produc-
ing tumours or adrenal congenital hyperplasia [39]. Depend-
ing on the results, further investigations may be needed and
an interdisciplinary approach involving gynaecologists,
endocrinologists and dermatologists may be required [39].
Measurements of blood iron, ferritin, vitamin D, zinc and
thyroid profile may be useful to assess and treat other condi-
tions that may impact on hair regrowth in FAGA [1].
Fig. 6  Histopathology of female androgenetic alopecia (FAGA) with
increased number of miniaturized (vellus-like) hairs

7 Differential Diagnosis
Multiple hair disorders may be present with clinical fea-
tures that resemble FAGA. Moreover, FAGA can coexist
with other disorders. The main differential diagnoses include
telogen effluvium (TE), diffuse or incognita areata alopecia
(AA) and cicatricial alopecias that can be present in a FAGA
distribution.
7.1 Telogen Effluvium
TE is caused by the early entry of anagen hair into the tel-
ogen phase, leading to increased shedding. It is typically
subsequent to a stressful event (emotional difficulties, preg-
nancy, recent surgery, viral infections), or caused by drugs,
malnutrition or endocrine disorders. In the acute form, hair
loss is evident 2–3 months following the trigger event, and
full regrowth is seen after 6–12 months; whereas chronic TE
can persists for 6 months or more.
Although it may be most evident in the temporal area,
the hair loss occurs in all areas of the scalp [41]. A hair
pull test often demonstrates increased shedding of telogen
hairs. There are no specific trichoscopic signs to detect
(Fig. 7). Of note, an episode of acute TE can reveal under-
lying FAGA [42].
7.2 Diffuse and Incognita Alopecia Areata
Diffuse and incognita AA are autoimmune disorders histo-
logically characterized by infiltration of ­Th1 cells around
and within the hair follicles. They lack the characteristic
patches of classical AA and instead demonstrate wide-
spread scalp hair thinning [43]. Due to the preferential
loss of pigmented hairs, adult patients may complain of
rapid greying of the hair. Pull test is usually positive.
Fig. 7  In telogen effluvium, all of the scalp can be affected (a) but the disease is more evident in the temporal area (b)
M. Starace et al.
Trichoscopy shows diffuse yellow dots, black dots and
dystrophic hair. A biopsy is useful to confirm the diag-
nosis (Fig. 8).
7.3 Cicatricial Alopecias with a Female Pattern
Distribution
7.3.1 Fibrosing Alopecia in Pattern Distribution (FAPD)
In 2000, Zinkernagel and Truëb described 19 patients
aged from 35 to 74 years—15 women and 4 men—with a
form of progressive scarring alopecia limited to the area
of FAGA and named FAPD [4]. FAPD is usually presented
with diffuse hair thinning on the central scalp associated
with itching [4]. Trichoscopy shows perifollicular ery-
thema, follicular keratosis and loss of follicular orifices
limited to the involved area (Fig. 9). Histology shows hair
follicle miniaturization and a lichenoid inflammatory infil-
trate with perifollicular lamellar fibrosis targeting the isth-
mus and the infundibular region, indistinguishable from
LPP. Since its first description, several cases of FAPD have
been reported [44–46].
7.3.2 Cicatricial Pattern Hair Loss (CPHL)
In 2005, Olsen coined the term CPHL to describe a form
of cicatricial alopecia in a case of FPHL, lacking the peri-
follicular erythema and follicular hyperkeratosis seen in
FAPD [5]. Typically, it affects women over 40 years and
the specific trichoscopical sign is the presence of small
“pencil–eraser-sized” areas of focal atrichia [5] (Fig. 10).
Histological examination shows perifollicular lymphocytic
infiltrate surrounding the isthmus, sebaceous gland loss and
concentric lamellar fibrosis [5, 47].
Female Androgenetic Alopecia
Fig. 8  Diffuse areata alopecia (AA) is characterized by a diffuse hair thinning (a)  and trichoscopy shows diffuse yellow dots with dystrophic
hair (b) (×20 magnification)
Fig. 9  a Clinically evident hair thinning and mild erythema in the
crown area in a subject with fibrosing alopecia in pattern distribution
(FAPD). b Trichoscopy shows peripilar casts, perifollicular erythema
7.3.3 Central Centrifugal Cicatricial Alopecia (CCCA)
CCCA is a lymphocytic cicatricial alopecia presenting pri-
marily in African Americans in the second or third dec-
ade of life [48]. Clinically it begins in the central midline
scalp and slowly progresses centrifugally. In the advanced
stages the affected scalp is smooth and shiny and there is
progressive loss of follicular ostia. Itching and pain can be
associated.
Olsen has hypothesized that these women may have
underlying FAGA that becomes inflammatory with the use
of some hair care practices, such as hot combs, relaxers and
occlusive ointment, leading to a cicatricial type of hair loss
[49, 50].
and hyperkeratosis. Miniaturized hair and diameter variability are
lacking (×20 magnification)
Trichoscopy shows peripilar white/grey halos, a honey-
comb pigmented network, point–point white dots, white
patches and variability in the hair shafts. Inflammatory
signs, such as perifollicular erythema and follicular kerato-
sis, can be present [5] (Fig. 11).
7.3.4 Frontal Fibrosing Alopecia (FFA)
FFA, first described by Kossard in 1994 [6], is permanent
cicatricial alopecia of unknown etiology. Hormonal milieu,
genetic predisposition, environmental factors and autoim-
munity have been supposed to be involved [51]. It affects
mainly middle-aged post-menopausal women, although
it has been reported both in males and in premenopausal
women [52]. The incidence of the disease is increasing in
Europe, the United States and Asia.
 M. Starace et al.

Fig. 10  a Hair thinning of the central scalp in a patient with cicatricial pattern hair loss (CPHL). b Trichoscopy shows fibrotic areas and loss of
follicular ostia, absence of diameter variability and perifollicular erythema and hyperkeratosis (20× magnification)

Fig. 11  Typical case of central centrifugal cicatricial alopecia (CCCA): clinical presentation (a) and trichoscopy (b) (×20 magnification)

FFA is considered a clinical variant of LPP lacking the
well defined areas of alopecia typical of LPP. Clinically, it
is characterized by a progressive recession of the fronto-
temporal hairline, similar to some forms of male AGA.
However, this pattern has rarely been described in FAGA
as well [5].
Loss of eyebrows, eyelashes and peripheral body hair
is often associated with FFA. Eyebrow alopecia could be
the initial manifestation of the disease [53]. Non-inflam-
matory facial papules are reported in about one third of
all cases [53]. Up to 90% of patients report subjective
symptoms in the affected area, such as itching and tricho-
dynia [53]. The association with FAGA is often reported.
The pull test can show dystrophic anagen roots, but
it is usually negative. Trichoscopy shows perifollicular
erythema, follicular hyperkeratosis, white patches and
absence of follicular ostia in the fronto-temporal hairline
(Fig. 12). ‘Lonely hair’ could be seen in the scarring area.
Histology shows a typical lichenoid perifollicular lym-
phocytic infiltrate associated with perifollicular lamellar
fibrosis involving predominantly the vellus hair follicles.
The main features of FAGA and cicatricial alopecias
with a female pattern distribution are listed in Table 1.
8 Treatments
FAGA is a slowly progressive disease [1]. The goal of
therapy is to stop the progression and to induce a cos-
metically acceptable hair regrowth [32]. It is essential
to discuss with the patient the therapeutic options, their
costs and side effects, the importance of the use of and
adherence to treatments, always remembering to set real-
istic expectations. An objective method to evaluate hair
regrowth is the global photographic assessment, which is
Female Androgenetic Alopecia

Fig. 12  A case of frontal fibrosing alopecia (FFA) with eyebrow involvement (a): at trichoscopy, perifollicular erythema and hyperkeratosis with
absence of follicular ostia is evident (b) (×20 magnification)

Table 1  Main features of FAGA and cicatricial alopecias with a female pattern distribution
FAGA​ FAPD CPHL CCCA​ FFA

Clinical features Onset after puberty Mostly targets post- Onset after the fourth Targets almost Mostly targets post-
menopausal women decade exclusively African menopausal women
American women
Mostly involves the Involvement of the Involvement of the Begins in the central Progressive recession
central scalp central scalp central scalp scalp and progresses of the fronto-tempo-
centrifugally ral hairline
Slowly progressive Cicatricial hair loss Cicatricial hair loss Cicatricial hair loss Cicatricial hair loss
hair thinning
Widened central part- Clinically evident ‘Pencil–eraser-sized’ Clinically evident Itching and trichodynia
ing line erythema areas of focal inflammation may
atrichia be present
Trichoscopic features Hair diameter vari- Follicular erythema Absence of follicular Peripilar white/grey Follicular erythema
ability > 20% erythema halos
Yellow dots indicative Perifollicular hyper- Absence of perifolli- Honeycomb pig- Perifollicular hyper-
of empty follicles keratosis cular hyperkeratosis mented network keratosis
Follicular ostia usu- Loss of follicular ostia Loss of follicular ostia Point–point white dots Loss of follicular ostia
ally preserved
Peripilar hyperpig- White fibrotic patches White fibrotic patches White fibrotic patches White fibrotic patches
mentation
Histological features T:V reduced (< 3:1) Lichenoid infiltrate of Lichenoid infiltrate of Perifollicular lympho- Lichenoid infiltrate of
hair follicles hair follicles cytic infiltrate hair follicles
Telogen:anagen Concentric perifol- Concentric perifol- Concentric perifol- Concentric perifollicu-
increased licular lamellar licular lamellar licular lamellar lar lamellar fibrosis
fibrosis fibrosis fibrosis
Increased number of Lymphocytic interface Lymphocytic interface Sebaceous glands loss Sebaceous glands loss
follicular stelae dermatitis dermatitis
Mild perifollicular Sebaceous glands loss Sebaceous glands loss Premature disintegra-
inflammation/fibro- tion of internal root
sis may be present sheath

CCCA​ central centrifugal cicatricial alopecia, CPHL cicatricial pattern hair loss, FAGA​female androgenetic alopecia, FAPD fibrosing alopecia
in pattern distribution, FFA frontal fibrosing alopecia, T:V terminal to vellus-like hair follicles ratio

a standardized and reproducible method to estimate the
severity of the disease in each patient [32].
8.1 Minoxidil
8.1.1 Topical Minoxidil
Topical minoxidil is the first-line treatment for FAGA
approved by the US FDA. Its efficacy has been proved in
double-blind placebo-controlled trials [54–56]. Minoxidil
is a potassium channel blocker originally used as an oral
hypotensive, whose peculiar side effect was an increase
in hair regrowth. Topical minoxidil is available in 2%
and 5% solutions and in a 5% foam. The precise mecha-
nism of action is not yet known; some hypotheses include
enhanced vasodilatation and proliferative, anti-androgenic
and anti-inflammatory effects [57]. The final result is to
prolong the anagen phase of the hair follicle and induce an
enlargement of miniaturized follicles, obtaining the con-
version of miniaturized hair follicles to terminal hair folli-
cles [55]. Minoxdil 2% solution applied twice daily shows
similar efficacy to minoxidil 5% solution or foam applied
once daily [56]. Topical minoxidil should be applied as
1 mL of solution with a pipette directly on the dry scalp.
It doesn’t need massage and it is advisable to apply it 2 h
before bed to allow adequate time for drying and to avoid
it spreading on the face during sleep. Its efficacy could
be observed after 6–12 months of treatment [32]. If suc-
cessful, it should be continued indefinitely. Its withdrawal
will lead to a TE because of the simultaneous transition to
hair telogen with a minoxidil-dependent prolonged ana-
gen phase. Patients should be informed about a transitory
increase in telogen hair shedding during the first months of
treatment [55]. The most disturbing side effect in women is
hypertrichosis [54]. It can be the result of the personal sen-
sitivity, or, more often, due to incorrect application with
local spreading. Irritant or allergic contact dermatitis may
occur, commonly related to the solution vehicle propylene
glycol [32]. If patch testing confirms a contact dermatitis,
a switch can be made to 5% foam—that doesn’t contain
propylene glycol—or to oral minoxidil.
8.1.2 Oral Minoxidil
Patients are considered eligible for oral minoxidil if their
hair loss does not respond to topical minoxidil or if they
don’t tolerate it [58]. Oral minoxidil is used at much lower
doses than those used to treat high blood pressure; indeed,
doses range from 0.25 to 2.5 mg/day [58]. It can cause a sig-
nificant reduction in blood pressure if it is given with other
anti-hypertensive treatments. Other side effects include fluid
retention and hypertrichosis.
M. Starace et al.
8.2 Hormone‑Modulating Treatments
The hormone-modulating treatments used for FAGA include
antiandrogen receptor antagonists, which avoid testosterone
and DHT binding to their receptor, and real antiandrogens,
which alter androgen levels at the hair follicle.
It must be remembered that 5-α-reductase inhibitors or
antiandrogens are forbidden in pregnant women. Abnormali-
ties of external male genitalia, namely feminization of the
male foetus, were reported in animal studies. Strict contra-
ception should be used during and for at least 30 days after
discontinuation of these drugs [1].
They are mainly prescribed off-label for the treatment of
FAGA and their use is still contested. Indeed, several studies
including a metanalysis did NOT evidence any improvement
with either antiandrogens or 5-alfa-reductase inhibitors [59].
Due to their teratogen potential, many antiandrogen stud-
ies have been conducted in post-menopausal women. More
studies are needed to assess the real potential of antiandro-
gens in different ages and biochemical situations. Their
administration is advisable, in association with Minoxidil,
in cases of poor response to the latter or in patients with
hyperandrogenism [1].
8.2.1 Finasteride
Finasteride is a 5-α-reductase type II inhibitor that blocks
the conversion of testosterone in DHT, stopping hair loss
and increasing hair growth [60]. Finasteride is approved by
the US FDA for the treatment of benign prostatic hypertro-
phy and male AGA; it is used off-label for the treatment of
FAGA.
A study including 137 post-menopausal women with
normal androgen levels and treated with 1 mg of finasteride
for 12 months did not show significant improvements [61].
However, finasteride has shown its effectiveness both in
normo-androgenic and in hyperandrogenic patients in some
studies utilizing higher doses (2.5–5 mg per day) [62–65].
In our clinical practice, we usually prescribe 2.5–5 mg
daily. It requires at least 6–12 months of treatment to achieve
hair regrowth. Responding patients need to continue the
treatment to maintain obtained results [32].
Besides the teratogenic effect, finasteride has been asso-
ciated with estrogen-mediated malignancies such as breast
cancer, because it can generate estrogen excess [66]. There-
fore, finasteride should not be prescribed if the patient has a
family history of breast cancer.
It is generally well tolerated; side effects include head-
aches, depression, nausea, hot flushes and decreased libido
[60, 67].
Female Androgenetic Alopecia
8.2.2 Dutasteride
Dutasteride is an inhibitor of 5-α-reductase types I and II.
It has demonstrated more efficacy than finasteride in male
patients with AGA [68]. It is approved for benign prostatic
hypertrophy, while it is used off label for male AGA and
FAGA [60]. It has been reported to successfully treat FAGA
at doses that range from 0.25 to 0.5 mg/day [69]. It is well
tolerated but due to its long half-life, women of childbearing
potential should continue to use effective contraception for
at least 6 months post-discontinuation [1].
8.2.3 Spironolactone
Spironolactone is a potassium-sparing diuretic primarily
used for the treatment of hypertension, hyperaldosteronism
and heart failure. It is also approved for the treatment of
hirsutism [60]. The mechanisms of action of spironolactone
are complex, since they are mediated not only by the direct
antagonist of aldosterone on androgen receptors, but also
indirectly through the reduction of hyperandrogenism and
systemic inflammation [70]. This molecule partially inhibits
ovarian and adrenal steroidogenesis, blocks 5-α-reductase
and 17-hydroxysteroid dehydrogenase at the ovarian and
adrenal level, activates aromatase and increases SHBG [70].
The initial dose is usually 50 mg per day for 1 month, then
100–200 mg/day thereafter. It should be continued for at
least 6–9 months to assess its efficacy. There are limited
data about the efficacy of spironolactone in FAGA. A study
included 80 women aged between 12 and 79 years with
FAGA receiving a minimum of 12 months of oral antian-
drogen therapy. Forty women received spironolactone 200
mg daily and 40 women received cyproterone acetate (50 mg
daily if post-menopausal or 100 mg for 10 days per month
if premenopausal). There were no significant differences in
the results between spironolactone and cyproterone acetate.
Thirty-five (44%) women had hair regrowth, 35 (44%) had
no clear change in hair density before and after treatment
and 10 (12%) experienced continuing hair loss during the
treatment period. In conclusion, 88% of women receiving
oral antiandrogens can experience a halt of progression of
their FAGA, or even a clinical improvement [71].
Spironolactone is generally well tolerated and its side
effects include headaches, decreased libido, menstrual
irregularities, orthostatic hypotension, breast tenderness and
hyperkalaemia. However, some studies have evidenced that
patients younger than 50 years without renal diseases have
no risk of hyperkalaemia, thus monitoring is not required
[72].
In women who complain of orthostatic hypotension,
it can be useful to take some pastilles of pure liquorice
because liquorice can reduce the side effects related to the
diuretic activity of spironolactone. In cases of intermenstrual
bleeding, the addition of 2.5 mg nomegestrol for 4–5 days
from the 14th day of the menstrual cycle can block the
bleeding and, after some cycles of treatment, the bleeding
could disappear [70].
Spironolactone is a valid alternative to finasteride in
patients that show FAGA associated with hirsutism or acne
[73].
8.2.4 Cyproterone Acetate
Cyproterone acetate (CPA) is an antiandrogen that acts by
blocking androgen receptors and decreasing testosterone
levels by suppressing luteinizing hormone and follicle-
stimulating hormone release. It is approved in Europe and
Canada to treat hirsutism, acne and female alopecia, but
it is not approved in the United States [60]. As mentioned
above, its efficacy is similar to spironolactone [71]. In a
1-year trial, CPA was compared with minoxidil 2% in 66
women with FAGA. While minoxidil showed an improve-
ment, statistically significant hair regrowth did not occur
in the CPA group [74]. However, even if not statistically
significant, women with irregular menstrual cycles seem
to respond better than those with regular menstrual cycles.
CPA is generally prescribed in combination with an estrogen
in oral contraceptive pills. The suggested regimens for the
treatment of FAGA in premenopausal women are 100 mg/
day on days 5–15 of the menstrual cycle alongside ethinyl
estradiol 50 µg on days 5–25, or 50 mg/day on days 1–10
and ethinyl estradiol 35 µg on days 1–21. Postmenopausal
women may be treated with 50 mg daily.
Side effects include menstrual cycle irregularities, weight
gain, breast tenderness, reduced libido, depression and nau-
sea. Moreover, it should not be prescribed to patients with
liver diseases. There is an increased risk of venous thrombo-
embolism in patients taking oral contraceptives containing
estrogen, which can then be enhanced in patients taking CPA
contraceptives [32].
8.2.5 Flutamide
Flutamide antagonises the receptor to which testosterone
and DHT bind. US FDA approved it for the treatment of
prostate cancer [60].
Flutamide is usually administered at doses that range
from 62.5 to 250 mg daily for FAGA.
Although it has shown to be more efficient than finas-
teride and spironolactone in FAGA [75], it is not habitually
prescribed due to the risk of hepatotoxicity, which can lead,
in rare cases, to hepatic failure. Physicians who prescribe
flutamide should monitor serum transaminase at baseline,
monthly for the first 4 months and periodically thereafter
[60]. Flutamide should not be prescribed in patients with

impaired hepatic function at baseline. Other minor side
effects include decreased libido and hot flushes.
8.3 Other Treatments
8.3.1 Prostaglandin Analogues
Latanoprost and bimatoprost are anti-glaucoma drugs with
the well known side effects of eyelash growth caused by the
stimulation of the anagen phase, and periocular skin pig-
mentation. Topical latanoprost 0.1% led to increased hair
density in a small placebo-controlled trial including 16 male
patients [76], whereas bimatoprost 0.03% injections were
not effective in a case report of a post-menopausal woman
with FAGA [77]. Moreover, some studies link the inflam-
mation in the scalp to an increased level of PG-D2, with a
consequent miniaturization of hair follicles, and the topical
application of PG-D2 has been shown to inhibit hair growth
[24]. Actually, research is being carried out to verify if drugs
able to block the PG-D2 receptor (GPR44) could have a
potential application in patients with AGA.
8.3.2 Light Therapy
After the first published report of paradoxical hair growth in
patients treated with intense pulsed light (IPL) for removal
of unwanted hair, an interest has grown for the potential
effects and applications of low-level laser light therapy
(LLLT) to treat alopecia [78]. This phenomenon has been
called ‘paradoxical hypertrichosis’ and is widely acknowl-
edged to occur with an incidence rate ranging from 0.6 to
10% with low fluences of all laser types.
The mechanism of LLLT on hair growth is not yet known;
it is hypothesized that the light enhances mitochondrial res-
piratory activity and production of adenosine triphosphate
[79]. The treatment is usually performed at home and there
are many devices designed such as brushes, combs, hoods
and helmets.
The FDA has approved different LLLT devices for use
in AGA: for example, the HairMax LaserComb and the
TOPHAT 665. They are usually well tolerated; side effects
include scalp dryness, itching, tenderness and a warm sen-
sation. A recent paper compared the use of LLLT for adult
androgenetic alopecia with a review and meta-analysis of
randomized controlled studies [80].
The majority of studies found an overall improvement in
hair regrowth, thickness and patient satisfaction following
LLLT therapy. Further controlled randomized clinical stud-
ies are required to establish the efficacy of these devices
[81–83].
M. Starace et al.
8.3.3 Platelet‑Rich Plasma
Platelet-rich plasma (PRP) is obtained by centrifuging
patient’s own blood and concentrating the platelets. Platelets,
often with added growth factor, chemokines and cytokines,
are then injected in the affected areas [84].
PRP has begun to be used in many specialties, such as
orthopaedics, aesthetics and plastic surgery, because plate-
let activation promotes wound healing and induces tissue
regeneration, with the release of various growth factors and
cytokines such as platelet-derived growth factor, transform-
ing growth factor beta (TGF-β), vascular endothelial growth
factor, epidermal growth factor and insulin-like growth fac-
tor [85].
The efficacy of PRP during hair transplants has been eval-
uated, and a considerable improvement in the density and
regrowth of the transplanted hair follicles has been observed
after the growth factors’ stimulation [85].
The mechanisms of action on hair follicles are still under
debate. In vitro PRP induces the proliferation of dermal
papilla cells and prevents apoptosis by inducing an increase
in Akt and Bcl-2 expression. Furthermore, PRP contributes
to the formation of hair epithelium and stem cell differen-
tiation into hair follicle cells, thanks to an upregulation of
β-catenin, which is expressed in the bulge area of the follicle.
The increased expression of FGF-7 (fibroblast growth fac-
tor-7) determines an extended anagen phase of hair cycle.
Moreover, in androgenetic alopecia, PRP increases prolifera-
tion of bulge cells with release of Ki-67. Finally, thanks to
the suppression of inflammatory cytokines, PRP appears as
a potent anti-inflammatory agent [85].
According to recent studies, PRP proved to be a promis-
ing option for the treatment of FAGA [85–87]. A placebo-
controlled, randomized, half-head trial that included 12 men
and 13 women with AGA found a greater increase in hair
density in sites treated with PRP compared with control sites
6 months after the first of three monthly PRP treatments
[88].
Moreover, three studies assessing the efficacy of PRP in
female patients were included in the evidence-based evalu-
ation of the last European Guidelines for AGA [32, 89–91].
Based on these studies, it was concluded that there was
insufficient evidence to support the use of PRP in FAGA
[32].
Although studies may differ in methodology, patient
selection and treatment technique, regrowth rates have been
reported after five local treatments of 3 mL of PRP at 2- to
3-week intervals [92].
The main side effects of PRP include pain and transient
post-treatment oedema and tenderness, persistent tricho-
dynia, psoriasiform scalp reactions, telogen effluvium, sec-
ondary infections and scarring [32].
Female Androgenetic Alopecia
Even though further studies are needed to confirm its
efficacy and to define standardized protocols for treatments,
PRP can represent a viable option in patients in whom stand-
ard treatments do not produce satisfactory results [85].
8.3.4 Microneedling
Microneedling is a minimally invasive procedure that
involves the use of a skin roller with small needles that cause
minor skin injuries. It has become initially popular for the
management of acne scars and facial rejuvenation [92].
Recently, the use of microneedling has been investigated as
a potential therapeutic option for the treatment of hair disor-
ders due to its capacity to enhance growth factor production,
facilitate hair follicle development and cycling, amplify col-
lagen and elastin production and create microchannels that
allow transdermal delivery of medications, such as minoxidil
or PRP, through the stratum corneum [93].
In our experience, we recommend microneedling treat-
ment three times a month, for at least 6 months. For the pro-
cedure, the patients are anaesthetized with a local mixture
of lidocaine and prilocaine/tetracaine cream 1 h before the
procedure. Rolling is done with a dermaroller with a needle
length of 1.5 mm over affected areas until mild erythema and
point–point bleeding is noted. Patients are recommended to
resume the application of topical treatments after 24 h [93].
Microneedling is usually well tolerated. Reported side
effects are pain or discomfort at the site of treatment, bleed-
ing, infections and enlargement of the lateral cervical lymph
nodes [93].
There is evidence that this technique may be effective in
male AGA, based on the results of a 12‐week, randomized,
evaluator‐blinded study on 100 patients [94]. Single case
reports, case series, or small randomized controlled trials
have shown promising results in FAGA, suggesting the
effectiveness of microneedling in combination with other
validated treatments of AGA [93, 95, 96]. In particular, a
case series studying the association of microneedling with
topical minoxidil in FAGA showed that the frontal area, the
typical androgenetic affected area in females, has the most
improvement with the microneedling technique [93].
To date, it is considered a valid method to be paired with
the existing techniques [92]. Future large controlled clinical
trials exploring the utility of microneedling are imperative to
prove its validation as an evidence based therapeutic option.
8.3.5 Ketoconazole
Ketoconazole is an antifungal drug used to treat seborrheic
dermatitis. Oral administration has proven to be effective in
reversing the biochemical and clinical abnormalities of ovar-
ian hyperandrogenism. In FAGA, ketoconazole shampoo
has proved its utility, especially if used in combination with
other treatments [97]. This effect could be due to its anti-
inflammatory power, reducing Malassezia, and to its ability
to decrease DHT in the skin acting as an androgen receptor
antagonist [97]. It is recommended in women with FAGA
associated with seborrheic dermatitis or sebopsoriasis.
8.3.6 Topical Hormonal Treatments
The anti-androgen fluridil and the anti-estrogen fulvestrant
are not recommend for FAGA therapy [32].
8.4 Hair Transplant
Hair transplant is a valid option in patients who do not
achieve a cosmetically satisfying response to topical and
systemic agents [98]. It is a minimally invasive technique
in which hair follicles from the occipital area, called the
‘donor site’, are transplanted to the bald area. It is indicated
in women with a high hair density in the donor site and no
overlying diffuse TE. Final results can be assessed after 9–12
months. In many cases, multiple surgical sessions are needed
and the potential transplant failure should not be excluded
[32]. After the transplant, patients should continue previ-
ous treatment with minoxidil or antiandrogens. Side effects
include early temporary hair loss, pain and infections.
9 Conclusion
FAGA is a common form of non-scarring alopecia in
women. Clinically it is characterized by hair thinning in the
central scalp and histologically by miniaturization of hair
follicles and by an increased number of telogen hairs in the
involved area.
Recently, the following cicatricial alopecias with hair loss
in a FAGA distribution have been described: FAPD, CPHL,
CCCA and FFA. In order to rule out the presence of a cica-
tricial alopecia, trichoscopical examination should always
evaluate the frontal hairline and the crown area in patients
complaining of hair thinning, especially if associated with
itching or pain. In doubtful cases, a trichoscopy-guided
biopsy can be decisive.
The predilection of FAGA, FAPD, CPHL, CCCA and
FFA for postmenopausal women, the effectiveness of andro-
gen-modulating treatments and the histological finding of
perifollicular inflammation involving mainly the minia-
turized hair follicles suggest an overlap or a progression
between these diseases.
More studies are necessary to further elucidate the rela-
tionship between these diseases and therefore determine the
correct management and treatments.
 M. Starace et al.

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