Am J Clin Dermatol
DOI 10.1007/s40257-017-0297-6
REVIEW ARTICLE
Alopecia Areata of the Beard: A Review of the Literature
Jessica Cervantes1 • Raymond M. Fertig1 • Austin Maddy1 • Antonella Tosti1
Ó Springer International Publishing Switzerland 2017
Abstract Alopecia areata (AA) is a T-cell mediated
autoimmune disorder in which inflammatory cells attack
the hair follicle, resulting in round, well-circumscribed
patches of noncicatricial hair loss in normal appearing skin.
AA affecting the beard area is well known and is referred
to as AA of the beard (BAA) or AA barbae when
involvement is limited exclusively to the beard. BAA has
been documented in a select number of studies. We review
the literature and discuss the clinical features, epidemiol-
ogy, diagnosis, and treatment of BAA. Clinical presenta-
tion of BAA can vary and manifest as single small areas of
hair loss, multiple small or large simultaneous focuses, or
total hair loss. Most patients are middle-aged males with
focal patches of round or oval hair loss, mostly localized
along the jawline. Patches are characteristically well cir-
cumscribed and smooth with white hair present at the
periphery. Dermoscopic features of BAA include yellow
dots, broken hair, and short vellus hairs. BAA may be
associated with other autoimmune disorders, including
atopic dermatitis, vitiligo, and psoriasis. Many treatment
modalities are available for BAA, and selection of a ther-
apy depends on several factors, including disease activity,
extent of area affected, duration of disease, and age of the
patient. Topical corticosteroids are most commonly used as
initial treatment, followed by intralesional steroids. Other
therapeutic modalities are discussed.
& Jessica Cervantes
J.Cervantes1@umiami.edu
1
Department of Dermatology and Cutaneous Surgery,
University of Miami Miller School of Medicine, 1475 NW
12th Ave., Miami, FL 33136, USA
Key Points
Alopecia areata (AA) is an autoimmune disorder in
which inflammatory cells attack the hair follicles,
including those on the beard.
Adequate understanding of disease epidemiology,
pathogenesis, and treatment of AA of the beard are
lacking.
1 Introduction
Alopecia areata (AA) is an autoimmune disorder in which
inflammatory cells attack the hair follicle. T-cell mediated
destruction of hair follicles results in round, well-circum-
scribed patches of noncicatricial hair loss in normal
appearing skin [1]. There are several variants of alopecia,
including involvement of the entire scalp (AA totalis) and
involvement of the entire body (AA universalis) [2].
AA affecting the beard area is well known and is
referred to as AA of the beard (BAA) or AA barbae when
involvement is limited exclusively to the beard. It is
characterized by well-demarcated, smooth-surfaced pat-
ches of hair loss on the beard of male patients [3]. We
review the literature and discuss the clinical features, epi-
demiology, etiology, diagnosis, and treatment of BAA.
2 Materials and Methods
We performed a MEDLINE search, without language or
publishing data restrictions, to identify cases described in
the literature. The following MEDLINE search terms were

used: ‘‘alopecia areata AND beard,’’ ‘‘alopecia AND
beard,’’ ‘‘alopecia areata of the beard,’’ and ‘‘alopecia
areata barbae.’’ We included case reports, case series,
review articles, and clinical trials that specifically men-
tioned the beard. After the initial search, we reviewed the
bibliographies of all manuscripts to discover any cases not
uncovered in our initial MEDLINE search. We also
reviewed the major hair textbooks (Table 1).
3 Results
Throughout the literature, reports on BAA are scarce. Here,
we present available information on clinical features, epi-
demiology, etiology, diagnosis, and treatment of BAA.
3.1 Clinical Features
Although AA can affect any hair-bearing region of the
body, the scalp is the most commonly affected area (90%)
[3]. The beard, accounting for *28% of cases, is the
second most commonly affected location [2]. The inci-
dence of BAA has been documented in a select number of
studies. A hospital-based observational study of 290 adults
in Sri Lanka [4] revealed that beard involvement was
exclusively seen in 20.5% of patients, and 8.7% of patients
had multiple sites involved. However, in those of Turkish
descent, the beard/mustache has actually been reported to
be the most regularly affected area in males when com-
pared with individual areas of the scalp (occipital, vertex,
parietal, temporal, and frontal), eyebrows and eyelashes.
Kavak et al. [5] examined 539 Turkish patients with AA
and noticed that 27.6% of males (92/333) had alopecic
patches in the beard. However, no data on exclusive beard
involvement were reported. Furthermore, as addressed by
the authors, this finding might be attributed to referral bias,
as beard involvement may cause more distress for men than
scalp involvement, thereby leading to more clinical con-
sultations and skewed incidence data.
Clinical presentation of BAA varies and can manifest as
either single small areas of hair loss, multiple small or large
simultaneous focuses, or total hair loss. Most patients are
middle-aged males with focal patches of round or oval hair
loss, mostly localized along the jawline [1]. Patches are
characteristically well circumscribed and smooth; the
presence of white hair at the periphery is also typical
(Fig 1a). However, in some patients, BAA presents with
diffuse thinning without well-defined patches (Fig 1b). In
dark-haired men, patches are quite conspicuous and easily
noticeable [6]. Pain and pruritus are uncommon findings.
Furthermore, nail findings, which are frequently seen in
patients with AA [7, 8], are not routinely present in BAA.
J. Cervantes et al.
Although AA can solely involve the beard (as in AA
barbae), it often presents concomitantly with alopecic
patches in other hair-bearing regions. In a retrospective
multicenter review, Saceda-Corralo et al. [3] observed that,
of 55 patients diagnosed with BAA, 45.5% (25/55)
developed alopecia of the scalp during follow-up; most
(52%; 13/25) had fewer than five concomitant alopecic
patches on the scalp, 28% (7/25) had multifocal AA of five
or more patches, 12% (3/25) presented with AA totalis, and
8% (2/25) presented with AA universalis. In 10.9% of
patients with BAA, AA was also documented to affect
other hair-bearing areas such as the eyebrows and arms.
Furthermore, in cases with subsequent scalp involvement,
80% of patients developed scalp lesions within the first
12.4 months, with an average time of 9.9 months and a
range of 2–40 months post BAA onset.
AA, whether confined to the beard or not, is a chroni-
cally relapsing inflammatory condition. In the study led by
Saceda-Corralo et al. [3], the majority of patients (74.5%)
experienced only one episode of BAA, and the remaining
25.5% had more than two episodes of BAA (six patients
experienced two episodes, four patients experienced three
episodes, and four patients had four or more episodes)
during a follow-up period of 12 months.
3.2 Epidemiology
With a lifelong prevalence of 1–2%, AA is the third most
common type of hair loss following androgenetic alopecia
and telogen effluvium [2, 3]. The mean age of onset for AA
is 40 years, yet a wide range of ages at onset is more often
observed in BAA. Saceda-Corralo et al. [3] documented a
mean age of 39.1 years with a range of 20–74 and mean
age of onset of 34.5 with a range 18–73 in the 55 patients
with BAA studied.
AA is associated with a 16% increased risk of other
autoimmune disorders [8]. Atopic dermatitis (14.5%),
vitiligo (3.6%), and psoriasis (3.6%) were the most fre-
quent autoimmune skin disorders observed by Saceda-
Corralo et al. [3], while Crohn’s disease (5.4%), asthma
(3.6%), and hyperparathyroidism (1.8%) were other com-
mon autoimmune comorbidities present in patients with
BAA. Similarly, thyroid disease was present at a higher
frequency in patients with BAA than in the general popu-
lation [3]. Sredoja Tisma et al. [9] presented a case of a
56-year-old man presenting with hemochromatosis and
BAA. Richmond et al. [10] published a case of a 40-year-
old White male with BAA in conjunction with primary
cutaneous follicle center lymphoma (CFCL) of the face and
scalp. A 43-year-old man with an 8-month history of AA of
the scalp and beard and Helicobacter pylori infection had
evidence of hair regrowth in both the scalp and beard after
eradication of the infection [11].
Table 1 Overview of studies analyzing clinical features, epidemiology, diagnosis and treatment of alopecia areata of the beard
Study Sample size Age/average age Other locations involved (% of pts) Disease characteristics of the beard Tx (% of pts) and response to and relapse Follow- Family Associated
(n with beard (range), y [average rate on tx up time history autoimmune
involvement) disease duration] of AA disorders

Saceda- 55 (55) 39.1 (20–74) [NR] Scalp (45.5), eyebrow, arms (10.9) Multiple round or oval patches of Tx 1: topical steroids (32.4) 29.3 14.5% 10.9%
Corralo non-scarring hair loss Response to tx: 78.8% mo
et al. [3]
Relapse rate on tx: 23.5%
AEs: none
Alopecia Areata of the Beard

Tx 2: intralesional steroids (17.1)

Response to tx: 94.4%
Relapse rate on tx: 22.2%
AEs: skin atrophy
Tx 3: expectant attitude (16.2)
Response to tx: 59.4%
Relapse rate on tx: NA
AEs: none
Tx 4: topical MIN (15.2)
Response to tx: 62.5%
Relapse rate on tx: 12.5%
AEs: none
Tx 5: oral steroids (14.3)
Response to tx: 66.7%
Relapse rate on tx: 26.7%
AEs: high BP, myalgia, facial swelling
Tx 6: topical CNIs (4.8)
Response to tx: 20%
Relapse rate on tx: 20%
AEs: none
Emre et al. 4 (1) 38 [16 y] Occipital scalp (100) Multiple well-circumscribed, 1- to Tx: combination of topical corticosteroids, NR 100% 100%
[12] 4-cm oval/round, hairless patches intralesional TA injections (8 mg/ml),
cryotherapy, and MIN solution (2)
Response to tx: 100% partial response
Relapse rate on tx: NR; recurrence was
documented
AEs: NR
Eckert et al. 5 (1) 49 [1 mo to 19 y None Two patches, 20 9 20 cm and 70 9 Tx: non-ablative 1550 nm erbium glass 3y NR NR
[33] (range)] 50 cm fractional laser (Fraxel, 40 mJ, 8 passes, 3
sessions)
Response to tx: 50–75% at 1 mo for smaller
patch, [75% at 3 mo for larger patch
Relapse rate on tx: 0%
AEs: NR
Table 1 continued
Study Sample size Age/average age Other locations involved (% of pts) Disease characteristics of the beard Tx (% of pts) and response to and relapse Follow- Family Associated
(n with beard (range), y [average rate on tx up time history autoimmune
involvement) disease duration] of AA disorders

Ranawakaa 290 (49) 31 (18–65) [6 mo] Scalp (70.7), multiple sites (scalp, NR Tx 1: topical steroids (2.7) 5y 11% 12%
[4] beard, eyebrows, mustache; 8.7) Response to tx: NR
Relapse rate on tx: NR
AEs: NR
Tx 2: intralesional steroids (70)
Response to tx: NR
Relapse rate on tx: NR
AEs: atrophy, scarring
Tx 3: oral DEX mini pulse (28)
Response to tx: NR
Relapse rate on tx: NR
AEs: weight gain, increased urination,
dizziness
Tx 4: MIN lotion (14.5)
Response to tx: NR
Relapse rate on tx: NR
AEs: irritation
Khodaee [1] 1 44 [2] None One 1 9 1 cm, smooth focal patch Tx: NR 12 NR NR
Response to tx: NR
Relapse rate on tx: NR
AEs: NR
Sredoja 1 56 [2 mo] None One smooth, 2 cm normal-colored Tx: corticosteroid creams and emollients 6 wk 0% 100%
Tisma alopecic patch Response to tx: 100%
et al. [9]
Relapse rate on tx: 0%
AEs: NR
Campuzano- 1 43 [8 mo] Scalp (100) Patchy hair loss Tx: OME 20 mg bid, AMO 1000 mg bid, 44 wk NR NR
Maya [11] CLA 500 mg bid
Response to tx: 100% (starting at 4 wks with
complete hair regrowth by wk 16)
Relapse rate on tx: 0%
AEs: NR
Kavak et al.a 539 (92) 24 (2–75) [2 mo Occipital scalp (20), vertex (13.3), NR Tx: NR NR 24.1% NR
[5] (median)] parietal (11.8), temporal (8.7), frontal Response to tx: NR
(7.2), eyebrows, eyelashes (2.2)
Relapse rate on tx: NR
AEs: NR
Richmond 1 40 [NR] Scalp (100) Multiple well-circumscribed oval Tx: topical IMI and high-dose steroids 9 mo NR NR
et al.a [10] alopecia patches in beard and Response to tx: 100%
scalp with white hair regrowth
Relapse rate on tx: NR
AEs: NR
J. Cervantes et al.
Alopecia Areata of the Beard

AE adverse effects, AMO amoxicillin, bid twice daily, BP blood pressure, CLA clarithromycin, CNIs calcineurin inhibitors, DEX dexamethasone, IMI imiquimod, MA methylaminolevulinic acid, MIN minoxidil, mo months,
autoimmune
Associated

disorders

NR
Family
history
of AA

NR
Follow-
up time

8 mo
Tx: MA PTD (red light, 630 nm, 37 J/cm2
Tx (% of pts) and response to and relapse

Response to tx: 100% (after 4 sessions)

Relapse rate on tx: NR
AEs: erythema
for 7.5 min)
rate on tx

NA not applicable, NR not reported, OME omeprazole, PTD photodynamic therapy, TA triamcinolone acetonide, tx treatment, wk week, y year
Disease characteristics of the beard

Fig. 1 Gross findings of alopecia areata of the beard: physical

NR

examination reveals a a hairless patch on the right jawline extending

to the neck. The patch is smooth with white hair at the periphery.
b Some patients may present with diffuse thinning without well-
Other locations involved (% of pts)

defined patches

3.3 Etiology
Study reports findings of alopecia areata that are not specific to the beard area

Genetic and familial studies specifically on BAA are

scarcely reported in the literature. Saceda-Corralo et al. [3]
documented positive family history in 14.5% of patients
None

with BAA. Emre et al. [12] presented a case series of four

family members simultaneously affected with AA, in
which the 38-year-old father had a 16-year history of
(range), y [average
disease duration]
Age/average age

recurrent AA of the scalp and beard, and other family

26 [14 mo]

members had the scalp, eyebrows and eyelashes affected.

All patients studied also had multiple psychological dis-
turbances [12].
(n with beard
involvement)

3.4 Diagnosis
Sample size
Table 1 continued

6 (1)

For the majority of BAA cases, clinical examination is

sufficient for diagnosis. Smooth, discrete areas of hair loss
et al.a [32]
Fernandez-

is highly suggestive of AA. Bald patches are circular or

Guarino

coin shaped, with smooth underlying skin that may be

Study

slightly red. Further diagnostic processes include

a

trichoscopy and histology. Dermoscopic features of scalp
AA include yellow dots, exclamation mark hairs, circle
hairs, short vellus hairs that might be clustered, black dots,
coudability hairs, and broken hairs [13]. There are cur-
rently no studies on trichoscopy of the beard area; from the
authors’ experience, exclamation mark hairs are rarely seen
as patients usually shave to make the disease less notice-
able. The most common findings include yellow dots,
broken hair, and short vellus hairs (Fig. 2). Pathologic
findings of scalp AA include peribulbar lymphocytic
inflammatory infiltrates surrounding anagen follicles
(‘‘swarms of bees’’), follicular edema and miniaturization,
cellular necrosis, microvesiculation, and pigment inconti-
nence in the hair bulb [14]. Histopathological studies of
AA on the beard area are lacking.
Differential diagnosis for patients presenting with hair
loss on the beard can include trichotillomania, Brocq
pseudopelade, tinea barbae, lichen planopilaris, and frontal
fibrosing alopecia. Trichotillomania is an impulse control
disorder in which hair loss results from a patient’s repeti-
tive self-pulling of hair. Although men typically pull hair
from the stomach/back, 10% have been reported to target
the beard [15]. Brocq pseudopelade is a cicatricial alopecia
that results in smooth skin-colored alopecic patches. The
scalp is the primary location, but involvement of the beard
area has also been documented [16]. Tinea barbae is a
trichophytosis involving the beard and mustache areas of
the face, most commonly caused by Trichophyton verru-
cosum and Trichophyton mentagrophytes. The inflamma-
tory response around the hair follicle results in hair dropout
[17]. Lichen planopilaris and frontal fibrosing alopecia,
which are primary lymphocytic cicatricial alopecias, may
affect the beard and cause permanent hair loss [18].
Fig. 2 Dermoscopic findings of alopecia areata of the beard:
dermoscopy shows yellow dots, broken hairs, and short vellus hairs.
Exclamation mark hairs, although characteristic of alopecia areata,
are rarely seen in alopecia areata of the beard
J. Cervantes et al.
3.5 Treatment
Many treatment modalities are available for AA, and
selection of a therapy depends on several factors, including
disease activity, extent of area affected, duration of disease,
and age of the patient [19]. Currently, no guidelines are
established for specific therapeutic approaches for BAA
[20, 21]. Furthermore, no randomized controlled trials in
the treatment of BAA have been undertaken. Most treat-
ments discussed are based on clinical experience and
uncontrolled case series.
The first therapeutic approach in BAA should involve
local therapies. According to Saceda-Corralo et al. [3],
topical corticosteroids are most commonly used as initial
treatment, followed by intralesional steroids. Highly potent
topical steroids such as desoximetasone cream and clobe-
tasol propionate foam might not be the best option for long-
term use in this area, as evidence for the effectiveness is
limited, even for the scalp [20]. A common side effect of
topical steroid use is folliculitis [20].
There is much greater evidence showing that corticos-
teroids injected intralesionally stimulates hair growth
[20, 22]. A meta-analysis of 12 studies reported intrale-
sional triamcinolone acetonide as the most effective treat-
ment in patients with limited AA and shorter duration of
disease [23]. According to the British Association of Der-
matologists’ guidelines, monthly injections of triamci-
nolone acetonide is most suitable for treating patchy hair
loss of limited extent and for cosmetically sensitive sites
[20]. A dosage of 2.5 mg/ml should be used when injecting
the face [21]. Corticosteroids should be injected just
beneath the dermis in the upper subcutis. An injection of
0.05–0.1 ml will produce a tuft of hair growth of about
0.5 cm in diameter. Side effects from repeated intralesional
steroid injections include pain and skin atrophy at injection
sites [20].
Although minoxidil is highly effective in the treatment
of androgenetic alopecia, its effect in patients with AA
remains unclear. Minoxidil (5%, twice daily) may help hair
regrowth in some patients with BAA. One study compared
the effectiveness of 5 and 1% minoxidil in patients with
AA and reported more frequent regrowth of hair in those
using 5% minoxidil, although few observed cosmetically
worthwhile results [24].
Topical immunotherapies such as 2,3-diphenylcyclo-
propenone (DPCP) have also been shown to be effective in
the treatment of AA in 50–60% of patients [21]. When
using DPCP, the skin is sensitized using a 2% solution
followed by weekly applications of the lowest concentra-
tion that will cause mild irritation 24–36 h after application
[25]. Once the appropriate concentration for the patient is
established, therapy is continued weekly. If the patient does
not develop an allergic response to DPCP, squaric acid
Alopecia Areata of the Beard
dibutylester (SADBE) can be used [26]. Side effects of
topical immunotherapy include occipital and/or cervical
lymphadenopathy and severe dermatitis [20]. No studies
have been published on the efficacy and safety of topical
immunotherapy on the beard area. In the authors’ experi-
ence, treatment is usually well tolerated, but efficacy is
lower than in the scalp.
Systemic corticosteroids have also been used in the
treatment of AA. One study reported 30–47% of patients
with AA treated with a 6-week course of oral prednisolone
showed more than 25% hair regrowth [27]. Several studies
have also reported using high-dose pulsed corticosteroids
to achieve a cosmetically worthwhile response in about
60% of patients [20, 28, 29]. However, the side effects of
systemic corticosteroids means their use, especially for
BAA, is not well supported.
The 308-nm excimer laser is another treatment option
that offers high doses of long-wave monochromatic ultra-
violet B (UVB) radiation. It has been shown to be effective
in inducing hair regrowth in solitary lesions in patients with
AA [30]. One study found the excimer laser to be effective
in four of ten lesions of patchy AA involving the beard area
[31]. Another study in Spain observed complete regrowth
of hair in a patient with BAA after four sessions of pho-
todynamic therapy, whereas those with AA of the scalp did
not achieve complete hair regrowth [32]. In a similar
manner, non-ablative 1550 nm erbium glass fractional
laser was recently documented to induce full beard
regrowth in BAA. A patient in his late 40s presented to the
dermatology clinic with complaints of new alopecic pat-
ches on the beard every month without any apparent trig-
gers. After 3 months of treatment, consisting of three
sessions of Fraxel laser at a fluence of 40 mJ/cm2, density
of 6–8, and eight passes, investigators documented [75%
hair regrowth as early as 1 month after the final session. No
side effects were noted [33].
Narrowband UVB phototherapy has shown excellent
treatment response in 20% of patients who present with
extensive AA. However, this was demonstrated in a ret-
rospective, uncontrolled study in which most patients were
also receiving systemic corticosteroids [34]. UVB light
treatment has resulted in complete hair and beard regrowth,
as documented by Krook [35] and by Sinclair et al. [36],
although hair loss may recur following discontinuation of
treatment. Psoralen and ultraviolet A (PUVA) is another
possible treatment option for AA [20, 21, 37]; however, no
data are available on the efficacy of PUVA on the beard.
Natural home remedies have also been discussed as
possible therapeutic options for BAA; however, no evi-
dence exists to support their efficacy. The herbs burdock,
sage, and rosemary have been speculated to stimulate hair
follicles and encourage hair growth. Aloe vera, onion juice,
jojoba, castor oil, coconut oil, and almond oil, among
others, have likewise been associated with acceleration of
hair growth in BAA. Spontaneous remission of alopecic
patches on the beard is common, especially in patients with
limited patchy hair loss of short duration. As such, leaving
BAA alone without treatment is also a possible option [38].
Data on the incidence of spontaneous regrowth in the beard
have not been reported.
4 Conclusion
Although BAA and AA barbae are frequent clinical pre-
sentations of AA, adequate understanding of disease epi-
demiology, pathogenesis, and treatment is lacking. This
review discusses our current understanding of BAA in
terms of clinical presentation, epidemiology, etiology,
diagnosis, and treatment.
Although BAA is typically considered a cosmetic ail-
ment, a high prevalence of anxiety and depressive symptoms
have been reported in affected patients [22, 23]. BAA may
cause psychological distress for men, as there is no easy or
reasonable way to cover up the patches, whereas AA of the
scalp can possibly be covered or concealed under long hair. It
is also possible that the pathogenesis of BAA may differ from
that of AA as some men present only with patches in the
beard, whereas others progress to scalp involvement. Further
investigational studies of patients presenting with BAA as
the first or only clinical feature of alopecia are necessary to
better appreciate the nature of this disease.
Compliance with Ethical Standards
Conflict of interest Jessica Cervantes, Raymond Fertig, Austin
Maddy, and Antonella Tosti have no conflicts of interest and no
commercial associations with any product or device described in the
article. Dr. Antonella Tosti has served as a consultant for P&G and
DS Laboratories; as Principal Investigator for Incyte and Pfizer; has
received author royalties from Taylor & Francis; is the Editor in chief
for Karger Publishers; and is on the scientific board for the National
Alopecia Areata Foundation.
Funding No funding was received for this manuscript.
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