Hair Loss and its Management in Children

Vibhu Mendiratta, Masarat Jabeen

Expert Rev Dermatol. 2011;6(6):581-590.

Abstract and Introduction

Abstract

Hair loss in children can cause psychological stress to the parent and patient alike. Alopecia can be
classified into congenital and acquired. Commonly encountered causes of pediatric alopecia (tinea
capitis, alopecia areata, traction alopecia and trichotillomania) are reversible if diagnosed early. Special
note should be made of the extent and type of alopecia (scarring or nonscarring), any hair shaft
anomalies and signs of inflammation. Diagnostic evaluation includes a bewildering array of age-old
simple bedside tests (e.g., potassium hydroxide preparation) to state-of-the art accurate instruments
(e.g., trichoscan). Systemic antifungal therapy is required for tinea capitis. Topical and systemic
immunomodulators are currently being employed for treating alopecia areata. A holistic approach would
include not just therapeutic intervention but also an active search for associated nutritional deficits,
underlying psychosocial disturbances and behavioral problems, the latter two requiring counseling and
behavior therapy. Children with permanent hair loss can be offered surgical hair transplantation or
camouflage devices, such as wigs.
Introduction

Though losing hair is not usually health threatening, it can scar a young child's vulnerable self esteem by
causing immense psychological and emotional stress; not just to the patient, but also to the concerned
parents and siblings. Thus, management of hair disorders can be quite a daunting task for the attending
physician and mandates a holistic approach to the patient. Nevertheless, an organized diagnostic and
management strategy can turn this challenging task into an interesting and fruitful exercise.
To fully understand hair loss in childhood, a basic knowledge of normal hair growth is necessary. The
normal hair cycle is divided into four phases: the active growth anagen phase, followed by a brief
catagen phase, the resting telogen phase and finally the shedding exogen phase. [1] Typically, 8595% of
hairs are in the anagen phase, which lasts approximately 3 years. Less than 1% of hairs are in catagen,
the transitional phase, which lasts from a few days to weeks. The telogen phase (which accounts for 5
15% of hairs and lasts about 3 months) ends when the new anagen hair emerges from the follicle.
For the classification of pathological hair loss in children, two major groups should be differentiated:
congenital and acquired hair loss.[2,3] This distinction is the first step in diagnosis ( & Figure 1).
Pathological hair loss, although rare in the first year of life, may be a symptom of an underlying
congenital syndrome or clue to an underlying metabolic disorder which may have a bearing on the
mental and physical development of a child.[46]
Box 1. Age-wise distribution of common causes of alopecia.

Preschool

Genotrichosis

Congenital aplasia cutis

Alopecia areata

Occipital alopecia

School going

Tinea capitis

Alopecia areata

Trichotillomania

Telogen effluvium

Traction alopecia

Adolescents

Telogen effluvium

Alopecia areata

Androgenetic alopecia

Hair cosmetic-induced alopecia

Triangular alopecia

Figure 1.

Approach to common causes of pediatric alopecia.

Hair loss on the scalp can also be classified as focal or diffuse (). Focal hair loss is secondary to an
underlying disorder that may cause nonscarring or scarring alopecia. [3]
Box 2. Classification of pediatric alopecia.

Diffuse alopecia

Isolated hair shaft anomalies presenting with hair breakage (in some cases with
associated defects):
o

Trichorrhexis nodosa

Monilethirix

Pseudomonilethrix

Pili torti

Genetic syndromes with hair shaft anomalies:

o

Netherton's syndrome

Menkes syndrome

Trichothiodystrophy

Ectodermal dysplasia

Arginosuccinicaciduria

Congenital hypotrichosis and atrichia with papular lesions (can be associated with
syndromes)

Production decline:
o

Patterned hair loss

Alopecia due to abnormal hair cycling:

o

Anagen loss:

Anagen effluvium

Loose anagen syndrome

Telogen loss:

Telogen effluvium

Focal alopecia

Scarring:
o

Trauma

Aplasia cutis

Nevoid condition

Syndromic associations

Folliculitis decalvans

DLE, LPP

Postinfections (e.g., kerion)

Nonscarring:
o

Alopecia areata

Tinea capitis

Traction alopecia

Trichotillomania

DLE: Discoid lupus erythematosus; LPP: Lichen planopilaris.

Patient's personal and family history, a thorough clinical examination, as well as general and specific
diagnostic procedures aid in correct diagnosis and early treatment. [3]
The key points in a patient's history are:

Age of onset of the patient: congenital or acquired;

Onset of hair loss: sudden or insidious;

Extent of alopecia: localized or diffuse;

Subsequent development of the disease and associated symptoms;

Physical and mental development (may be affected as a part of a genotrichosis);

Psychological problems of the child;

Obvious physical or emotional triggers in the previous 25 months, and any accompanying
complaints (e.g., fatigue, weight changes, and nail or skin abnormalities);

Past medical history including chronic illnesses, surgeries, medication, autoimmune,

dermatologic and psychiatric disorders (e.g., anxiety and obsessivecompulsive tendencies);

Family history of alopecia, autoimmune disease, dermatologic or psychiatric disorders;

Hair grooming practices (chemicals, tight braiding).

Examination should have the following components:

Sparsing of hair (hypotrichosis) or loss of hair (alopecia);

Thorough examination of scalp as well as the other hair-bearing areas of the body, especially
loss of axillary and pubic hair, eyelashes, eyebrows and body hair;

Type of alopecia: localized or diffuse, scarring or nonscarring;

Any hair shaft anomalies, hair quality, color, roughness and tendency to breakage, 'exclamationpoint' hairs;

Presence of erythema, edema, papules, pustules, scaling, atrophy, telangiectasias, follicular

hyperkeratosis, ulceration and scarring;

Hair pull test:

o

Approximately 20 hairs are grasped and firmly tugged away from the scalp;

The number of extracted hairs is counted;

>10% of grasped hairs or two hairs suggests positive pull test and active hair shedding.

The skin, nails, oral or genital mucous membranes (e.g., for evidence of associated dermatoses,
such as lichen planus);

Thorough clinical examination of the entire head and body is necessary in order to evaluate
impaired vision, defective hearing, dysmorphic features, clues to autoimmune or metabolic
diseases, or ectodermal anomalies.

Diagnostic Procedures
When tinea capitis is suspected:

Fungal culture by scraping the affected areas with a blunt scalpel, a sterile brush or moistened
gauze to gather affected hairs;

Woods lamp examination: as screening to detect flourescing species, such as Microsporum;

A potassium hydroxide preparation (to reveal hyphae): a scalp scraping or plucked hairs from
the affected area.

When alopecia areata is suspected:

Thyroid function

When telogen effluvium is suspected:

Hair pull test (already described);

If there is no obvious trigger of telogen effluvium tests include:

o

Sedimentation rate, complete blood count;

Serum ferritin;

Antinuclear antibody;

Thyroid function test;

Serology for syphilis.

When scarring alopecias are suspected:

4-mm punch scalp biopsy

When hereditary hair shaft disorders are suspected:

Serum biochemistry: for metabolic disorders;

To analyze hair structure:

Hair mount examination by light and polarizing microscopy;

Scanning or transmission electron microscopy, or both.

To analyze biochemical composition of affected hair.

o

Amino acid analysis by chromatography, spectroscopy (cysteine and sulfur content);

Keratin analysis.

Newer techniques:[714]

Videodermoscopy: the magnified images of hair follicle are useful for the differential diagnosis
between cicatricial and noncicatricial alopecia and between alopecia areata and trichotillomania;

Trichoscan: it is an automated software program for the accurate analysis of hair growth and
useful in monitoring the response to treatment;

Contrast-enhanced phototrichogram: a technique used to analyze hair growth activity using

photographic records and a scalp immersion proxigraphy method.

Frequent causes of alopecia encountered in general practice are discussed below.

Focal Noncicatricial Alopecia (Acquired)

Tinea Capitis

Tinea capitis is the commonest cause of patchy hair loss in children in the developing world owing to
poor socioeconomic conditions.[15] It is an infection of the scalp and associated hair, caused by
dermatophytes (generaTrichophyton and Microsporum except Trichophyton concenticum). The most
common cause is Trichophyton tonsuransin the USA and UK and Microsporum canis in the rest of the
world.[16,17] A clinician should be aware of its variable morphological presentations such as circular patches
of alopecia and marked scaling (grey patch type), black dots indicating broken hair (black dot type),
diffuse widespread scaling (seborrheic type), boggy nodules studded with pustules (kerion type) and
yellow crusts (scutula) that surround hair follicles with a peculiar musky odour (favus type caused
by Trichophyton schoenleinii).
Tinea capitis, once proven by culture or potassium hydroxide, requires systemic treatment. Flouroscence
by woods lamp is only displayed by a few species, so it is not a very sensitive tool in detection of tinea
capitis. Treatment is outlined in .[1821]
Table 1. Treatment options for tinea capitis.

Pharmacologic
agent

Regimen

The only oral US FDA approved treatment

Griseofulvin

Dose: 2025 mg/kg (micronized) or 15 mg/kg (ultramicronized) taken

with a fatty meal for 68 weeks

Itraconazole

5 mg/kg/day in 68 weeks

Fluconazole

6 mg/kg for 20 days or weekly pulse of 8 mg/kg for 816 weeks

Dose: 36 mg/kg for 48 weeks

Terbenafine

A RCT comparison of 4 weeks of terbinafine with 8 weeks of griseofulvin

showed no statistically significant difference overall. However, a
subgroup of Trichophyton responded better to terbenafine
and Microsporum audouinii responded better to griseofulvin

Adjuncts:
Topical selenium
sulphide shampoo
Zinc pyrithone
shampoo

Use by patients as well as all household members reduces transmission

Ketoconazole
shampoo
Povidone Iodine
shampoo
RCT: Randomized controlled trial.

Alopecia Areata

Alopecia areata (AA) is a chronic, organ-specific autoimmune disease, mediated by autoreactive T cells,
which affects hair follicles and sometimes the nails. Evidence of the autoimmune nature includes
reported associations between AA and other autoimmune disorders (e.g., Hashimoto thyroiditis) and,
histopathologically, the presence of lymphocytes around the hair bulb in a pattern resembling a swarm of
bees.[2223]
The characteristic lesion of AA is commonly an oval, totally bald, smooth patch involving the scalp or any
hair-bearing area on the body. A characteristic feature of an AA patch is 'exclamation-mark' hairs (broken,
short hairs that taper proximally) that may be present at its margin. The clinical presentation of AA is
subcategorized according to pattern or extent of the hair loss. It can be classified according to pattern as
classical patchy AA (most common), reticulated pattern of AA, ophiasis band like AA (hair loss in the
parietal temporo-occipital scalp) and sisaphio (a band of hair loss in the frontal parieto-temporal scalp).
[24]
If categorized according to extent of involvement, the following forms may be seen: alopecia areata
with partial loss of scalp hair; alopecia totalis (100% loss of scalp hair) and alopecia universalis (100%
loss of hair on the scalp and body).[22]
Indicators of a poor prognosis are the presence of other immune diseases, atopy, family history of AA,
young age at onset, nail dystrophy, extensive hair loss and ophiasis pattern. [23]
In the majority of patients, hair regrows entirely within 1 year without treatment. Because of the chance
for spontaneous resolution, it is often reasonable to do watchful waiting and reassurance initially. Should
the alopecia continue to worsen or persist, a therapy can be considered. It is helpful to get the patient
involved in a support group and/or counseling from the very first visit. The treatment of alopecia depends
on the extent of involvement and the age of the patient. In localized involvement, commonly used agents
include topical and intralesional corticosteroids, topical anthralin and minoxidil. In widespread
involvement, contact sensitization (e.g., diphenylcyclopropenone) and oral immunosuppressives are
usually resorted to.
Various treatment options are discussed in .[22,2552]
Table 2. Treatment options for alopecia areata.

Treatment

Advantages

Disadvantages

Nonsystemic therapy
Easy to apply at home
Topical corticosteroids

Can be used for large

areas

Poor data to support efficacy

Potential for skin atrophy

Painless
Intralesional corticosteroids

Can quickly regrow hair

Painful

Fairly reliable efficacy

Useful for only limited areas

Potential for skin atrophy

Multiple sittings required

Good evidence for
efficacy
Contact sensitization (e.g., with
Painless
squaric acid)
Can be used for large
areas
Anthralin

Good response in
majority cases

Topical irritants (e.g.,

capsaicin)

Potential for itchy reaction

Not an approved medication
High relapse rate
Pruritus can be troublesome
Long response time
Pruritus can be troublesome

Baxarotene

26% hair regrowth

reported

Dermal irritation

Prostaglandin analogue
(latanoprost, bimatoprost)

Well tolerated

Poor results in RCTs

Minoxidil

Nonirritant

Variable results

Nonirritant
Calcineurin inhibitors

Poor results
Easy to use

Laser (excimer, pulse infrared

diode)

Excellent results
reported

Expensive

No side effects reported

Fractional photothermolysis
laser

Single case report

Complete regrowth
reported after multiple
sessions

Expensive option

Systemic therapy

Systemic corticosteroids

Can be used for large

areas

Potential for serious adverse

effects
High relapse rate
High relapse rate

PUVA

Response rate >50%

Cumulative radiation exposure

Methotrexate

Response rates >60%

Side effect profile

Sulfasalazine

Relatively safe

Response rate <30%

IVIG

Safe in pregnancy

Expensive
Scanty data

Biologicals (alefacept,
adalimumab, etanercept,
efalizumab)

Poor response
Expensive
Side effect profile

Ciclosporin

Useful in widespread
cases

Infrared irradiation

Some success reported

Few reports showed

development of alopecia areata
while on ciclosporin
Confirmatory larger RCTs
required

IVIG: Intravenous immunoglobulin; PUVA: Psoralen plus UVA; RCT: Randomized controlled trial.
Trichotillomania

Sometimes preferentially referred to as trichotillosis (as the suffix mania can connote insanity)
trichotillomania refers to compulsive habit or desire to pull out the hair.[5355] The clinical manifestation is
usually quite distinctive, with a confluence of twisted and broken off hairs within an otherwise normal area
of the scalp. Counselling, psychotropic drugs such as clomipramine or sertraline, N-acetyl cysteine and
behavior modification techniques (e.g., habit-reversal therapy) are effective treatment options. [5662] As
glutamatergic dysfunction has been implicated in the pathogenesis of obsessivecompulsive disorder; Nacetylcysteine, a glutamate modulator, is a novel therapeutic agent found to be effective in
trichotillomania.
Traction Alopecia

Traction alopecia is caused by prolonged traction of scalp hair by use of hair styles, such as tight braids
and high pony tails, among others. Though usually the alopecia is reversible, if the traction is continued
over years, mechanical damage to hair follicles may result in permanent hair loss. [63,64] Cessation of the
offending hair practice is the treatment.
Syphilitic Alopecia

It may be the first sign of syphilis and can present as typical motheaten alopecia, generalized thinning of
the hair or may mimic alopecia areata. A high index of suspicion is required to diagnose this entity,
especially in sexually active adolescents.[65]

Focal Cicatricial Alopecia (Acquired)

Cicatricial alopecia damages hair follicles without regrowth. Stem cell failure at the base of the follicles
inhibits follicular recovery from the telogen phase, thus leading to an irreversible loss of hair. Common
causes of acquired focal cicatricial alopecia in the pediatric population are discussed below.
Lichen Planopilaris

Although predominantly a disease of adults, children can rarely be affected. Clinical hallmarks of active
disease include perifollicular violaceous papules and follicular hyperkeratosis. Histopathology
demonstrates the diagnostic features of lichenoid interface alteration. Limited disease is managed with
topicalor intralesional steroids. For those with rapidly progressive or extensive lesions, steroids, retinoids
or antimalarials are considered.[6669]

Linear Scleroderma

Most often seen in the first decade of life, linear scleroderma can present on the frontal scalp extending
to the forehead (en coup de sabre) as a linear shiny plaque with binding down of skin. It may be
associated with underlying bony, eye and CNS defects and requires a complete radiological work up to
exclude associated abnormalities. Histopathology reveals increased collagen in dermis with reduced
pilosebaceous appendages. Early diagnosis is important to halt the active inflammatory phase by
instituting treatment in the form of immunomodulators, such as steroids and hydroxychloroquine. [70]

Focal Cicatricial Alopecia (Congenital)

Common causes of congenital focal cicatricial alopecia are discussed below.
Temporal (Congenital) Triangular Alopecia

It presents as well-circumscribed triangular or ovoid patch of alopecia that involves the temporal region.
[71]
Vellus hair is present in the affected area. There is no effective treatment.
Aplasia Cutis Congenita

Aplasia cutis congenita constitutes a group of disorders that present at birth with eroded areas in the
scalp or body with or without other developmental anomalies.[72,73] The scalp erosions are characterized
by absence of a part of skin which heals spontaneously over a period of time and manifests as a patch of
cicatricial alopecia.
Nevus Sebaceous

Nevus sebaceous of Jadassohn is a common clinical entity which belongs to the group of epidermal nevi,
usually manifesting early in life in the form of an orange, waxy hairless circumscribed plaque most
commonly localized on the head and neck area.[74] It may be part of epidermal nevus syndrome in
association with other development anomalies. Excision is recommended in view of potential to develop
cutaneous malignancies.
Keratosis Follicularis Spinulosa Decalvans

Inherited as X-linked disease, keratosis follicularis spinulosa decalvans is characterized by widespread

follicular hyperkeratosis followed by atrophy, cicatricial alopecia of the scalp and photophobia. Topical
and intra-lesional corticosteroids and oral retinoids have been used with usually unsatisfactory results. [75]

Diffuse Alopecia (Congenital)

Common causes of congenital diffuse alopecia are discussed below.
Congenital Hypotrichosis & Atrichia

Hereditary simple hypotrichosis is a rare group of familial nonscarring hypotrichosis and atrichias without
associated internal abnormalities. Most of them are inherited in an autosomal dominant pattern. [7678]
Woolly Hair Hypotrichosis

It is characterized by tightly coiled, markedly curly and short hair. It may be associated with eye and teeth
defects, deafness, palmoplantar keratoderma and cardiac abnormalies (Naxos disease).

Ectodermal Dysplasias

These genodermatoses are characterized by absent or inadequate development of one or more of the
epidermal appendages namely hair, sweat glands, sebaceous glands, nails and teeth.
Genetic Syndromes With Hair Shaft Anomalies

Netherton Syndrome Netherton syndrome is a severe, autosomal recessive form of ichthyosis

associated with mutations in the SPINK5 gene with characteristic hair microscopy showing typical nodes
resembling bamboo joints. Other features include erythroderma, ichthyosis linearis circumflexa, failure to
thrive and atopic state.[7982]
Menkes Kinky Hair Syndrome Menkes kinky hair syndrome is an X-linked recessive disorder of copper
metabolism, characterized by microcephaly, pale skin, silvery brittle scalp hair and progressive
neurological deterioration.[8388]
Trichothiodystrophy Trichothiodystrophy is characterized by trichorrhexis-nodosa like hair fractures due
to a defect in synthesis of high-sulfur proteins. It can present as brittle hair, intellectual impairment,
decreased fertility, short stature (BIDS), ichthyosis and BIDS or photosensitivity and ichthyosis and BIDS.
Polarized microscopy reveals a characteristic tiger-tail pattern. [89]
Isolated Hair Shaft Anomalies

Trichorrhexis Nodosa In light microscopy, trichorrhexis nodosa, shows hair fracture with individual
cortical cells and their fragment splaying-out resembles two brushes whose ends are pushed together. [90
92]

Monilethirix Monilethirix is characterized by uniform elliptical nodes and intermittent constrictions

('internodes') along the hair shaft. Clinically it presents as scalp follicular keratosis and hypotrichosis. It
can rarely be associated with koilonychia, mental retardation or ectodermal defects. [93]
Pili Torti Pili torti consists of closely grouped twists of hair, occurring in groups of three to ten at irregular
intervals along the shaft.

Diffuse Alopecia (Acquired)

Common causes of acquired diffuse alopecia in the pediatric population are discussed below.
Alopecia Due to Abnormal Hair Cycling

Loose Anagen Syndrome Loose anagen syndrome is a disorder of anagen hair anchorage to the hair
follicle, characterized by the ability to easily and painlessly pull out large numbers of anagen hairs from
the scalp. Physical examination shows sparse growth of thin, fine hair and diffuse or patchy alopecia
without inflammation or scarring. Trichogram demonstrates 98100% of plucked hairs to be anagen
hairs. Light microscopy may reveal ruffling of the cuticle adjacent to the anagen bulb giving a 'floppy
sock' appearance. In most patients the condition improves spontaneously.[9496]
Telogen Effluvium

Telogen effluvium refers to an abnormality of the normal hair cycle leading to excessive loss of telogen
hair. Frequent triggers include physiologic effluvium of the newborn, febrile illnesses, catabolic illnesses,
such as malignancies, hypothyroidism, medications (e.g., retinoids and valproate), stress, surgery, caloric

or protein deprivation and chronic iron deficiency. Assuming there is no intervening pathological process,
the loss is usually replaced in 612 months. Treatment revolves around addressing the underlying cause.
[97,98]

Anagen Effluvium

Anagen effluvium is the abrupt loss of 8090% of hair, which occurs when the anagen phase is
interrupted. Radiotherapy to the head, systemic chemotherapy especially alkylating agents (e.g.,
cyclophosphamide) and exposure to toxic agents are usually the inciting events. These agents disrupt
the anagen cycle and cause varying degrees of hair follicle dystrophy. Replacement with a normal pelage
usually occurs rapidly after discontinuation of chemotherapy, but radiotherapy can cause permanent
scarring alopecia.[99103]

Decline in Hair Production

Androgenetic Alopecia

Androgenetic alopecia encompasses male pattern hair loss and female pattern hair loss and is identified
as the most frequent cause of hair loss in adolescents (male:female ratio of 2:1). It is usually due to
action of dihydrotestosterone on a genetically susceptible hair follicle leading to progressive hair
miniaturization. In adolescent girls the most common patterns of hair loss are centrifugal loss at the
crown and the frontal accentuation or 'christmas tree' pattern. In adolescent boys it commonly manifests
as bitemporal recession and thinning in the frontal and vertex. Although the pathogenesis remains
speculative, endocrine evaluation and a strict follow-up are recommended in prepubertal patients with
androgenetic alopecia. Topical minoxidil and finasteride (only in male patients) is effective. [102]

Expert Commentary
Diagnosing a given case of childhood alopecia is not just crucial for preventing irreversible hair loss, but
may also turn out to be the necessary clue to an otherwise unfathomable multisystem illness or an
explanation for an unexplained developmental delay. The most frequent causes of childhood alopecia
(tinea capitis, alopecia areata, traction alopecia and trichotillomania) are usually reversible if detected
early. The evaluation of a child with scalp hair loss should always include a detailed history, physical
examination and microscopic examination of the hair. A thorough examination of scalp, skin, mucosa,
teeth, nails and relevant systemic examination can be helpful in clinching accurate diagnosis. Newer
techniques, such as videodermoscopy, trichoscan and contrast-enhanced phototrichogram aid in solving
clinical dilemmas.
Congenital alopecia remains a largely neglected area with not many treatment options. There is a well
perceived need for hair clinics dedicated solely to the study of disorders causing hair loss. Newer
therapeutic armentatorium for alopecia areata, such as baxarotene, lasers (excimer, pulse infrared diode,
fractional photothermolysis) and infrared irradiation has been found to be useful while biologicals and
prostaglandin analogues (latanoprost, bimatoprost) has been found to be ineffective. N-acetylcysteine
has been found useful in trichotillomania. Counseling and support groups can be invaluable to reduce
psychological sequelae. Promising modalities for scarring alopecias are alginate gel implantation with
microencapsulation of hair follicle stem cell and dermal papilla cells.

Five-year View

Recent advances in epithelial stem cell biology have led to successful isolation of hair follicle stem cells,
which creates the opportunity to bioengineer hair follicles for the treatment of hair loss.
Utilizing effectiveness of alginate gel in cell implantation, microencapsulation of the hair follicle stem cells
and dermal papilla cells can be implanted into the bald scalp of the patient. As both follicle stem cells and
dermal papilla cells have strong proliferative capacity, the patient's own cells could be expanded
considerably in vitro.[103105] A genome-wide association study, which implicates T-cell and natural killer cell
activation pathways, has opened the window for new approaches in future clinical trials of alopecia
areata. Future treatment approaches for alopecia areata include use of drugs that block the NKGDactivating ligand and NKG2D receptor interaction, halt activated T cells, or modification of the
inflammatory cytokine network (e.g., anti-CD25, anti-CTLA-4, Jak 1/2 inhibitor, anti-NKG2D, Syk
inhibitor).[26]
Congenital alopecias remain a domain of orphan diseases with little to offer in terms of treatment except
camouflage and wigs. Research to refine knowledge of genes controlling the differentiation of hair
follicles is likely to develop treatment breakthroughs, such as gene therapy.

Sidebar
Key Issues

Acknowledging patients' concerns and having an empathetic approach to hair loss goes a long
way. Patients often appreciate a supportive diagnostic and therapeutic approach.

Although alopecia has myriad causes, a careful study of history, close attention to the
appearance of the hair loss and a few simple tests can quickly narrow the potential diagnoses.

Scarring alopecias, although rare, are considered true trichologic emergencies as hair loss can
be irreversible if prompt appropriate therapy is not instituted.

Focal alopecia is more likely to be acquired than diffuse alopecia.

Frequent causes of nonscarring focal alopecia are usually treatable (tinea capitis, alopecia
areata, traction alopecia and trichotillomania).

Evaluation of alopecia in infants should include recording of family history to exclude genetic
disorders and examination of teeth, nails, skeletal system and the eyes, along with a thorough
systemic examination.

Androgenetic alopecia can be the presenting sign of an underlying endocrine disorder in preadolescents.

Offering psychosocial support and nonpharmacologic techniques to help the child appear more
like their peers should be part of care.

References

1.

Tiede S, Kloepper JE, Bodo E et al. Hair follicle stem cells: walking the maze. Eur. J. Cell
Biol. 86(7), 355376 (2007).

2.

Tosti A, Gray J. Assessment of hair and scalp disorders. J. Investig. Dermatol. Symp.
Proc. 12(2), 2327 (2007).

3.

Hillmann K, Blume-Peytavi U. Diagnosis of hair disorders. Semin. Cutan. Med. Surg. 28(1), 33
38 (2009).

4.

Olszewska M, Warszawik O, Rakowska A, Sowiska M, Rudnicka L. Methods of hair loss

evaluation in patients with endocrine disorders. Endokrynol. Pol. 61(4), 406411 (2010).

5.

Bennssar A, Ferrando J, Grimalt R. Congenital atrichia and hypotrichosis. World J.

Pediatr. 7(2), 111117 (2011).
Comprehensive evaluation of myriad causes of neonatal alopecia detailing the work-up and
available management options.

6.

Tielsch Goddard A. Hair loss in an adolescent. J. Pediatr. Health Care 25(4), 261265 (2011).
Excellent review outlining the approach to alopecia in the adolescent population, delving into
pharmacologic as well as nonpharmacologic treatment options and outlining the importance of
psychological support to the vulnerable adolescent patient.

7.

Gassmueller J, Rowold E, Frase T et al. Validation of TrichoScan technology as a fullyautomated tool for evaluation of hair growth parameters. Eur. J. Dermatol. 19(3), 224231
(2009).

8.

Dhurat R, Saraogi P. Hair evaluation methods: merits and demerits. Int. J. Trichology 1(2), 108
119 (2009).

9.

Van Neste D, Leroy T, Conil S. Exogen hair characterization in human scalp. Skin Res.
Technol. 13(4), 436443 (2007).

10. Hughes R, Chiaverini C, Bahadoran P, Lacour JP. Corkscrew hair: a new dermoscopic sign for
diagnosis of tinea capitis in black children. Arch. Dermatol. 147(3), 355356 (2011).
11. Iorizzo M, Pazzaglia M, Starace M, Militello G, Tosti A. Videodermoscopy: a useful tool for
diagnosing congenital triangular alopecia. Pediatr. Dermatol. 25(6), 652654 (2008).
12. Wallace MP, de Berker DA. Hair diagnoses and signs: the use of dermatoscopy. Clin. Exp.
Dermatol. 35(1), 4146 (2010).
Good evaluation of the utility of a new diagnostic aid and its advantages and limitations.
13. Rudnicka L, Olszewska M, Rakowska A, Kowalska-Oledzka E, Slowinska M. Trichoscopy: a new
method for diagnosing hair loss. J. Drugs Dermatol. 7(7), 651654 (2008).
14. Tonci RJ, Lipozenci J, Pastar Z.Videodermoscopy in the evaluation of hair and scalp
disorders. Acta Dermatovenerol. Croat. 15(2), 116118 (2007).
15. Ali S, Graham TA, Forgie SE. The assessment and management of tinea capitis in
children. Pediatr. Emerg. Care 23(9), 662665 (2007).

 Overview of diagnosis and treatment strategies of tinea capitis.

16. Mohrenschlager M, Seidl HP, Ring J, Abeck D. Pediatric tinea capitis: recognition and
management. Am. J. Clin. Dermatol. 6, 203213 (2005).
17. Seebacher C, Bouchara JP, Mignon B. Updates on the epidemiology of dermatophyte
infections.Mycopathologia 166(56), 335352 (2008).
18. Gupta AK, Cooper EA, Bowen JE. Meta-analysis: griseofulvin efficacy in the treatment of tinea
capitis. J. Drugs Dermatol. 7(4), 369372 (2008).
19. Ghannoum MA, Wraith LA, Cai B, Nyirady J, Isham N. Susceptibility of dermatophyte isolates
obtained from a large worldwide terbinafine tinea capitis clinical trial. Br. J. Dermatol. 159(3),
711713 (2008).
20. Elewski BE, Caceres HW, DeLeon L et al. Terbinafine hydrochloride oral granules versus oral
griseofulvin suspension in children with tinea capitis: results of two randomized, investigatorblinded, multicenter, international, controlled trials. J. Am. Acad. Dermatol. 59(1), 4154 (2008).
21. White JM, Higgins EM, Fuller LC. Screening for asymptomatic carriage of Trichophyton
tonsurans in household contacts of patients with tinea capitis: results of 209 patients from South
London. J. Eur. Acad. Dermatol. Venereol. 21(8), 10611064 (2007).
22. Wasserman D, Guzman-Sanchez DA, Scott K, McMichael A. Alopecia areata. Int. J.
Dermatol. 46(2), 121131 (2007).
23. Alkhalifah A, Alsantali A, Wang E, McElwee KJ, Shapiro J. Alopecia areata update: part I. Clinical
picture, histopathology, and pathogenesis. J. Am. Acad. Dermatol. 62(2), 177188 (2010).
In-depth review of recent advances in the knowledge of the aetiology and various
manifestations and associations of alopecia areata.
24. Kos L, Conlon J. An update on alopecia areata. Curr. Opin. Pediatr. 21(4), 475480 (2009).
Highlights important concepts for the general approach in the management of alopecia areata.
25. Mukherjee N, Burkhart CN, Morrell DS. Treatment of alopecia areata in children. Pediatr.
Ann. 38(7), 388395 (2009).
26. Hordinsky MK. Treatment of alopecia areata: 'what is new on the horizon?' Dermatol. Ther. 24,
364368 (2011).
Excellent review of upcoming new and promising modalities in alopecia areata.
27. Chang KH, Rojhirunsakool S, Goldberg LJ. Treatment of severe alopecia areata with
intralesional steroid injections. J. Drugs Dermatol. 8(10), 909912 (2009).
28. El-Zawahry BM, Bassiouny DA, Khella A, Zaki NS. Five-year experience in the treatment of
alopecia areata with DPC. J. Eur. Acad. Dermatol. Venereol. 24(3), 264269 (2010).

29. Pan Y, Rao NA. Alopecia areata during etanercept therapy. Ocul. Immunol. Inflamm. 17(2), 127
129 (2009).
30. Kirshen C, Kanigsberg N. Alopecia areata following adalimumab. J. Cutan. Med. Surg. 13(1),
4850 (2009).
31. Roseborough I, Lee H, Chwalek J, Stamper RL, Price VH. Lack of efficacy of topical latanoprost
and bimatoprost ophthalmic solutions in promoting eyelash growth in patients with alopecia
areata. J. Am. Acad. Dermatol. 60(4), 705706 (2009).
32. Kamel MM, Salem SA, Attia HH. Successful treatment of resistant alopecia areata with a
phototoxic dose of ultraviolet A after topical 8-methoxypsoralen application. Photodermatol.
Photoimmunol. Photomed. 27(1), 4550 (2011).
33. Ohtsuki A, Hasegawa T, Ikeda S. Treatment of alopecia areata with 308-nm excimer lamp. J.
Dermatol. 37(12), 10321035 (2010).
34. Pugashetti R, Koo J. Phototherapy in pediatric patients: choosing the appropriate treatment
option. Semin. Cutan. Med. Surg. 29(2), 115120 (2010).
35. Alkhalifah A, Alsantali A, Wang E, McElwee KJ, Shapiro J. Alopecia areata update: part II.
Treatment. J. Am. Acad. Dermatol. 62(2), 191202 (2010).
Detailed overview of topical and systemic therapeutic armamentarium including table
summaries of recommendations.
36. Lee JW, Yoo KH, Kim BJ, Kim MN. Photodynamic therapy with methyl 5-aminolevulinate acid
combined with microneedle treatment in patients with extensive alopecia areata. Clin. Exp.
Dermatol. 35(5), 548549 (2010).
37. Al-Mutairi N. 308-nm excimer laser for the treatment of alopecia areata in children. Pediatr.
Dermatol. 26(5), 547550 (2009).
38. Yoo KH, Kim MN, Kim BJ, Kim CW. Treatment of alopecia areata with fractional
photothermolysis laser. Int. J. Dermatol. 49(7), 845847 (2010).
39. Garg S, Messenger AG. Alopecia areata: evidence-based treatments. Semin. Cutan. Med.
Surg. 28(1), 1518 (2009).
40. Ito T, Aoshima M, Ito N, Uchiyama I, Sakamoto K, Kawamura T et al. Combination therapy with
oral PUVA and corticosteroid for recalcitrant alopecia areata. Arch. Dermatol. 301(5), 373380
(2009).
41. Mavilia L, Mori M, Rossi R, Campolmi P, Puglisi Guerra A, Lotti TG. 308 nm monochromatic
excimer light in dermatology: personal experience and review of the literature. Ital. Dermatol.
Venereol. 143(5), 329337 (2008).
42. Fernndez-Guarino M, Harto A, Garca-Morales I, Prez-Garca B, Arrazola JM, Jan P. Failure
to treat alopecia areata with photodynamic therapy. Clin. Exp. Dermatol. 33(5), 585587 (2008).

43. Rashidi T, Mahd AA. Treatment of persistent alopecia areata with sulfasalazine. Int. J.
Dermatol. 47(8), 850852 (2008).
44. Bakar O, Gurbuz OJ. Is there a role for sulfasalazine in the treatment of alopecia areata? Am.
Acad. Dermatol.57(4), 703706 (2007).
45. Kuldeep C, Singhal H, Khare AK, Mittal A, Gupta LK, Garg A. Randomized comparison of topical
betamethasone valerate foam, intralesional triamcinolone acetonide and tacrolimus ointment in
management of localized alopecia areata. Int. J. Trichology 3(1), 2024 (2011).
46. Ait Ourhroui M, Hassam B, Khoudri I. Treatment of alopecia areata with prednisone in a oncemonthly oral pulse. Ann. Dermatol. Venereol. 137(89), 514518 (2010).
47. Kang H, Wu W, Lo B et al. Hair follicles from alopecia areata patients exhibit alterations in
immune privilege associated gene expression in advance of hair loss. J. Invest.
Dermatol. 130(11), 25352537 (2010).
48. Das S, Ghorami RC, Chatterjee T, Banerjee G. Comparative assessment of topical steroids,
topical tretenoin (0.05%) and dithranol paste in alopecia areata. Indian J. Dermatol. 55(2), 148
149 (2010).
49. Efentaki P, Altenburg A, Haerting J, Zouboulis CC. Medium-dose prednisolone pulse therapy in
alopecia areata.Dermatoendocrinol. 1(6), 310313 (2009).
50. Tosti A, Duque-Estrada B. Treatment strategies for alopecia. Expert Opin. Pharmacother. 10(6),
10171026 (2009).
51. Chang KH, Rojhirunsakool S, Goldberg LJ. Treatment of severe alopecia areata with
intralesional steroid injections. J. Drugs Dermatol. 8(10), 909912 (2009).
52. Barak Y, Amiran MD, Fineberg E, Lang Y. Perforating eye injury caused by a Dermojet
syringe. Arch. Dermatol.145(8), 958960 (2009).
53. Flessner CA, Lochner C, Stein DJ, Woods DW, Franklin ME, Keuthen NJ. Age of onset of
trichotillomania symptoms: investigating clinical correlates. J. Nerv. Ment. Dis. 198(12), 896900
(2010).
54. Murphy C, Redenius R, O'Neill E, Zallek S. Sleep-isolated trichotillomania: a survey of
dermatologists. J. Clin. Sleep Med. 3(7), 719721 (2007).
55. Bloch MH, Landeros-Weisenberger A, Dombrowski P, Kelmendi B, Wegner R, Nudel J.
Systematic review: pharmacological and behavioral treatment for trichotillomania. Biol.
Psychiatry 62(8), 839846 (2007).
56. Rahman O, Toufexis M, Murphy TK, Storch EA. Behavioral treatment of trichotillomania and
trichophagia in a 29-month-old girl. Clin. Pediatr. (Phila.) 48, 951953 (2009).
57. Grant JE, Odlaug BL, Kim SW. N-acetylcysteine, a glutamate modulator, in the treatment of
trichotillomania: a double-blind, placebo-controlled study. Arch. Gen. Psychiatry 66(7), 756763
(2009).

58. Grant JE, Odlaug BL, Chamberlain SR, Kim SW. Dronabinol, a cannabinoid agonist, reduces
hair pulling in trichotillomania: a pilot study. Psychopharmacology (Berl.) doi:10.1007/s00213011-2347-8 (2011) (Epub ahead of print).
59. Grant JE, Odlaug BL. Update on pathological skin picking. Curr. Psychiatry Rep. 11(4), 283288
(2009).
60. Van Ameringen M, Mancini C, Patterson B, Bennett M, Oakman J. A randomized, double-blind,
placebo-controlled trial of olanzapine in the treatment of trichotillomania. J. Clin.
Psychiatry 71(10), 13361343 (2010).
61. Leombruni P, Gastaldi F. Oxcarbazepine for the treatment of trichotillomania. Clin.
Neuropharmacol. 33(2), 107108 (2010).
62. Franklin ME, Zagrabbe K, Benavides KL. Trichotillomania and its treatment: a review and
recommendations.Expert Rev. Neurother. 11(8), 11651174 (2011).
63. Khumalo NP, Ngwanya RM. Traction alopecia: 2% topical minoxidil shows promise. Report of
two cases. J. Eur. Acad. Dermatol. Venereol. 21(3), 433434 (2007).
64. Khumalo NP, Jessop S, Gumedze F, Ehrlich R. Determinants of marginal traction alopecia in
African girls and women. J. Am. Acad. Dermatol. 59(3), 432438 (2008).
65. Nam-Cha SH, Guhl G, Fernndez-Pea P, Fraga J. Alopecia syphilitica with detection
of Treponema pallidum in the hair follicle. J. Cutan. Pathol. 34(Suppl. 1), 3740 (2007).
66. Ochoa BE, King LE Jr, Price VH. Lichen planopilaris: annual incidence in four hair referral
centers in the United States. J. Am. Acad. Dermatol. 58(2), 352353 (2008).
67. Estrada BD, Tamler C, Sodre CT, Barcaui CB, Pereira FB. Dermoscopy patterns of cicatricial
alopecia resulting from discoid lupus erythematosus and lichen planopilaris. An. Bras.
Dermatol. 85(2), 179183 (2010).
68. Chiang C, Sah D, Cho BK, Ochoa BE, Price VH. Hydroxychloroquine and lichen planopilaris:
efficacy and introduction of Lichen Planopilaris Activity Index scoring system. J. Am. Acad.
Dermatol. 62(3), 387392 (2010).
69. Crisstomo MR, Crisstomo MC, Crisstomo MG, Gondim VJ, Benevides AN. Hair loss due to
lichen planopilaris after hair transplantation: a report of two cases and a literature review. An.
Bras. Dermatol. 86(2), 359362 (2011).
70. Tollefson MM, Witman PM. En coup de sabre morphea and Parry-Romberg syndrome: a
retrospective review of 54 patients. J. Am. Acad. Dermatol. 56(2), 257263 (2007).
71. Yamazaki M, Irisawa R, Tsuboi R. Temporal triangular alopecia and a review of 52 past cases. J.
Dermatol.37(4), 360362 (2010).
72. Bilginer B, Onal MB, Bahadir S, Akalan N. Aplasia cutis congenita of the scalp, skull and dura
associated with AdamsOliver syndrome. Turk. Neurosurg. 18(2), 191193 (2008).

73. Neri I, Savoia F, Giacomini F, Raone B, Aprile S, Patrizi A. Usefulness of dermatoscopy for the
early diagnosis of sebaceous naevus and differentiation from aplasia cutis congenita. Clin. Exp.
Dermatol. 34(5), 5052 (2009).
74. Hamm H, Hger PH. Skin tumors in childhood. Dtsch. Arztebl. Int. 108(20), 347353 (2011).
75. Berbert AL, Mantese SA, Rocha A, Cherin CP, Couto CM. Keratosis follicularis spinulosa
decalvans: case report. An. Bras. Dermatol. 85(4), 537540 (2010).
76. Thomas M, Daniel S. Atrichia congenita with papular lesions. Indian J. Dermatol. Venereol.
Leprol. 77(1), 7072 (2011).
77. Chabchoub I, Ayadi L, Mejdoub I et al. Alopecia, congenital ichthyosis, and growth delay, what is
the diagnosis?Arch. Pediatr. 17(12), 16851686 (2010).
78. Redler S, Kruse R, Eigelshoven et al. Marie Unna hereditary hypotrichosis: identification of
a U2HR mutation in the family from the original 1925 report. J. Am. Acad. Dermatol. 64(4), 45
50 (2011).
79. Halverstam CP, Vachharajani A, Mallory SB. Cushing syndrome from percutaneous absorption
of 1% hydrocortisone ointment in Netherton syndrome. Pediatr. Dermatol. 24(1), 4245 (2007).
80. Larregue M, Guillet G. [Collodion baby with neonatal signs of trichothiodystrophy misdiagnosed
as Netherton syndrome: reassessment of a previous diagnostic error]. Ann. Dermatol.
Venereol. 134(3), 245248 (2007).
81. Komatsu N, Saijoh K, Jayakumar A et al. Correlation between SPINK5 gene mutations and
clinical manifestations in Netherton syndrome patients. J. Invest. Dermatol. 128(5), 11481159
(2008).
82. Burk C, Hu S, Lee C, Connelly EA. Netherton syndrome and trichorrhexis invaginata a novel
diagnostic approach. Pediatr. Dermatol. 25(2), 287288 (2008).
83. Cosimo QC, Daniela L, Elsa B, Carlo DV, Giuseppe F. Kinky hair, kinky vessels, and bladder
diverticula in Menkes disease. J. Neuroimaging 21(2), 114116 (2011).
84. Price DJ, Ravindranath T, Kaler SG. Internal jugular phlebectasia in Menkes disease. Int. J.
Pediatr. Otorhinolaryngol. 71(7), 11451148 (2007).
85. Balestracci A, Caletti MG, Missoni M. A case of Menkes' disease with nephrocalcinosis and
chronic renal failure.Pediatr. Nephrol. 24(6), 12551256 (2009).
86. La Fontaine S, Mercer JF. Trafficking of the copper-ATPases, ATP7A and ATP7B: role in copper
homeostasis.Arch. Biochem. Biophys. 463(2), 149167 (2007).
87. Bertini I, Rosato A. Menkes disease. Cell Mol. Life Sci. 65(1), 8991 (2008).
88. Kaler SG, Holmes CS, Goldstein DS et al. Neonatal diagnosis and treatment of Menkes
disease. N. Engl. J. Med. 358(6), 605614 (2008).

89. Usuda T, Saijo M, Tanaka K, Sato N, Uchiyama M, Kobayashi T. A Japanese trichothiodystrophy

patient withXPD mutations. J. Hum. Genet. 56(1), 7779 (2011).
90. Miyamoto M, Tsuboi R, Oh-I T. Case of acquired trichorrhexis nodosa: scanning electron
microscopic observation. J. Dermatol. 36(2), 109110 (2009).
91. Fichtel JC, Richards JA, Davis LS. Trichorrhexis nodosa secondary to argininosuccinic
aciduria. Pediatr. Dermatol. 24(1), 2527 (2007).
92. Burkhart CG, Burkhart CN. Trichorrhexis nodosa revisited. Skinmed 6(2), 5758 (2007).
93. Singh G, Siddalingappa K, Nischal KC, Naik LC, Lokanatha K. Monilethrix in three
generations. Indian J. Dermatol. 53(2), 99100 (2008).
94. Dhurat RP, Deshpande DJ. Loose anagen hair syndrome. Int. J. Trichology 2(2), 96100 (2010).
95. Bolotin D, Ortel B, Stein SL. Poorly growing hair in a child. Skinmed 8(4), 246247 (2010).
96. Agusti-Mejias A, Lpez-Davia J, Garca R, Febrer I, Alegre de Miquel V. [Loose anagen hair
syndrome. Diagnostic use of the trichogram]. Ann. Pediatr. (Barc.) 73(5), 293295 (2010).
97. Mounsey AL, Reed SW. Diagnosing and treating hair loss. Am. Fam. Physician 80(4), 356362
(2009).
Example of an algorithmic approach to alopecia with a brief overview of common treatment
options.
98. Bedocs LA, Bruckner AL. Adolescent hair loss. Curr. Opin. Pediatr. 20(4), 431435 (2008).
99. Trueb RM. Chemotherapy-induced alopecia. Semin. Cutan. Med. Surg. 28(1), 1114 (2009).
100.
Tosti A, Pazzaglia M. Drug reactions affecting hair: diagnosis. Dermatol. Clin. 25(2),
223231 (2007).
101.
Miteva M, Misciali C, Fanti PA, Vincenzi C, Romanelli P, Tosti A. Permanent alopecia
after systemic chemotherapy: a clinicopathological study of 10 cases. Am. J.
Dermatopathol. 33(4), 345350 (2011).
102.
Gonzalez ME, Cantatore-Francis J, Orlow SJ. Androgenetic alopecia in the paediatric
population: a retrospective review of 57 patients. Br. J. Dermatol. 163(2), 378385 (2010).
103.
Zhao J, Liu LQ, Wang YJ et al. Treatment of alopecia by transplantation of hair follicle
stem cells and dermal papilla cells encapsulated in alginate gels. Med. Hypotheses 70(5), 1014
1016 (2008).
104.
Rose PT. The latest innovations in hair transplantation. Facial Plast. Surg. 27(4), 366
377 (2011).
Comprehensive update on the recent advances and techniques in hair transplantations.

105.
Garza LA, Yang CC, Zhao T et al. Bald scalp in men with androgenetic alopecia retains
hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells. J.
Clin. Invest. 121(2), 613622 (2011).

Papers of special note have been highlighted as:

of interest
of considerable interest

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a
financial interest in or financial conflict with the subject matter or materials discussed in the manuscript.
This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants
or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.
Expert Rev Dermatol. 2011;6(6):581-590. 2011 Expert Reviews Ltd.