Alopecia areata

Chronic

inflammatory disease involving

the hair follicles and sometimes the nails
T cell mediated autoimmune mechanism
occurring in genetically predisposed
individuals
Environmental factors may be triggering
the disease

Aetiology
Genetic

factors
Positive family history in 10-20%
Inheritance appears to be multifactorial
Association found with HLA-DR4,DR11
and DQ3
Polymorphisms in IL1RN and TNF alpha
gene have been reported

Frequency of AA is increased in Downs

syndrome (8.8%)
Increased association with autoimmune
polyglandular syndrome type I (30%)
Some studies suggest that AA has an
earlier age of onset in atopic patients but
this has been disputed in a study from
India

 Autoimmunity

AA is associated with other autoimmune

diseases like myxoedema and
pernicious anaemia
AA pts have an increased frequency of
circulating organ specific and non-organ
specific autoantibodies and non specific
abnormalities in T cell no. and function

Autoantibodies to various antigens of

hair follicle tissue have been found
AA is considered to be a T cell mediated
disease

 Environmental

factors
That AA may be caused by infection
directly or a remote focus cannot be
ruled out
Most frequently implicated factor is
psychological stress

Pathogenesis
Perifollicular

and intrafollicular T
lymphocyte infiltrate of hair bulb of
anagen follicles at margins of expanding
patches of AA
Infiltrate not seen around the isthmus as
in scarring alopecias hence follicles are
not destroyed in AA
Normal numbers of follicles with
increased no. in telogen

 Initial

event is precipitation of anagen follicles

into telogen
Anchoring of the hair within the follicle is
defective
Follicles are unable to develop beyond Anagen
3-4 and enter prematurely to telogen
Such repeated cycles occur till disease activity
subsides and then follicles are able to
progress further to anagen

 In

long standing disease, there may be a

decline in follicle density due to fibrosis
of perifollicular conn. tissues
Sparing of white hair seen sometimes in
AA has raised the possibility of it being a
disease of hair bulb melanocytes

Clinical features
Peak

age of onset b/w 2nd and 4th

decades
Initial lesion is a circumscribed, totally
bald, smooth patch
Short, easily extractable broken hairs,
known as exclamation mark hairs are
often seen at the margins in active
disease

 New

patches may appear in a cyclical fashion

after 3-6 weeks
Diffuse hair loss may also occur
Regrowth is at first fine and unpigmented but
the hairs regain their colour
Beard, eyebrows and eyelashes hair may be
lost
Alopecia totalis and universalis can occur
Ophiasis is extension of alopecia along the
scalp margins

 Relative

sparing of non-pigmented or
white hair
Hairs recover their pigmentation but if
they do not, concurrent vitiligo should be
considered
AA causes fine stippled pitting of the
nails classically but some cases also
show trachyonychia or a non specific
atrophic dystrophy

Differential diagnosis
In

children, tinea capitis and

trichotillomania are the main D/D
Early stages of scarring alopecia
Other causes of diffuse alopecia like
SLE and secondary syphilis

Prognosis
Potential

for regrowth is maintained for many

years and is possibly lifelong
New patches may develop as recovery occurs
elsewhere
In alopecia totalis and universalis,
spontaneous recovery is an exception
34-50% recover in one year and 14-25%
progress to totalis or universalis
Prognosis is poor if childhood onset or
ophiasis is present or long standing alopecia

Management
No

treatment can alter the course of the

disease
High rate of spontaneous remission (80%) in
patchy alopecia
Reassurance may be provided in such
patients
Corticosteroids
1. Intralesional depot CS
- For patchy alopecia

For maintaining regrowth of eyebrows in

alopecia universalis
Hydrocortisone acetate (25mg/ml) and
triamcinolone acetonide (5-10mg/ml)
Localized atrophy occurs but is
temporary and recovers in a few months
2. Potent topical CS not much role
side effect - folliculitis

3. Long term oral CS

- 6 week tapering course of prednisolone starting at 40
mg/day
- treatment has to be continued to maintain growth and
response does not justify the risks
Contact immunotherapy
most effective and best documented treatment
Pt is sensitized to a potent allergen which is applied to
the scalp at weekly intervals to induce mild dermatitis

Allergens used are

dinitrochlorobenzene, squaric acid
dibutylester and diphenylcyclopropenone
Suggested m/a is that the allergen
competes for CD4 cells (antigenic
competition), local T suppressor cell
response and increased TGF beta which
suppresses the immune response

Treatment is discontinued if no response

after 6 months
ADR include occipital/cervical
lymphadenopathy, urticaria, severe
dermatitis, vitiligo and hyperpigmentation
Other therapies used include
photochemotherapy, minoxidil and
dithranol

Acquired cicatricial alopecia

Hair

follicle stem cells are located within the

outer root sheath (ORS)
Cicatricial alopecia is permanent areas of hair
loss due to destruction of hair follicles and
replacement by fibrous stellae
May result from primary disease of the follicles
or due to secondary factors

Causes of primary cicatricial

alopecia

1.

Inflammatory
Lymphocytic
CCLE
LPP
Graham-Little syndrome
Frontal fibrosing alopecia
Pseudopelade of Brocq
Alopecia mucinosa

Keratosis pilaris
Morphoea/scleroderma
2. Neutrophilic
Folliculitis decalvans
Dissecting cellulitis/folliculitis
3. Mixed
Acne keloidalis, acne necrotica
4. Non specific or end stage cicatricial alopecia

Causes of secondary cicatricial

alopecia
1.

2.

Traumatic
radiodermatitis, mechanical trauma,
postoperative, burns, dermatitis artefacta,
traction alopecia and hot comb alopecia
Sclerosing disorders
morphoea/scleroderma, lichen sclerosus,
chronic GVH

3. Granulomatous sarcoidosis, necrobiosis

lipoidica, infectious granulomas
4. Infectious
Bacterial folliculitis, carbuncle
Fungal kerion, favus
Viral shingles, varicella, HIV
Protozoal leishmaniasis, syphilis
Mycobacterial - TB

5. Neoplastic
Benign cylindroma, adnexal tumors
Malignant BCC, SCC, CTCL, secondary to
renal, breast, lung, GI malignancy, lymphoma,
leukemia
6. Developmental defects and hereditary
disorders aplasia cutis, epidermal naevi,
incontinentia pigmenti, porokeratosis of Mibelli,
icthyosis, EB

Non specific cicatricial alopecia

Idiopathic

non inflammatory irregular

permanent alopecia
Significant overlap with LPP
Histology shows non specific lymphocytic
infiltrate around follicular infundibulum and mid
follicle, follicles replaced by fibrous tracts at
edge of scarred patch. In areas of alopecia,
follicles are absent and epidermis is atrophic.
Dermis is sclerotic

 Initial

patch occurs over crown but can occur

anywhere
Oval patches which coalesce to form irregular
bald areas
No erythema and patches are smooth, shiny
and slightly depressed
Irregularly twisted hairs in patch as well as its
margins
Prognosis variable and unpredictable and no
effective management

 Lichen

planus
LPP, Graham-Little syndrome and frontal
fibrosing alopecia are 3 variants of cicatricial
alopecia resulting from LP
There may be only scalp involvement or
associated LP elsewhere
Drug induced LPP is not recognized

 Liquefaction

degeneration of basal cells,

colloid bodies and macrophages containing
pigment in dermis
Thickened horny and granular layer and
irregular acanthosis with a lymphocytic
infiltrate
Hairs may be replaced by keratin plugs and
follicles destroyed
Fibrin and IgM with complement in dermis and
BMZ on immunofluorescence

 C/f

scalp involvement is more common with

bullous or erosive form and LPP
Most pts are middle aged women
Initially violaceous papules, erythema and
scaling and later follicular plugs and smooth
and atrophic scarring
Twisted anagen hairs at the margins

 In

frontal fibrosing alopecia, there is frontal

recession with loss of folicular orifices and
perifollicularerythema and hyperkeratosis at
the margins
Occurs in postmenopausal women and the
frontal hairline recedes in a straight line rather
than bitemporally
In Graham-Little syndrome, there is
progressive cicatricial alopecia of scalp, loss of
pubic and axillary hair without scarring and
keratosis pilaris (lichen spinulosus) over trunk,
limbs and occasionally the eyebrows and face

 Management

Short course of systemic steroids

I/L steroids in active inflammatory stage
HCQ and acitretin have some role
Ciclosporin and thalidomide have been
reported as useful in Graham-Little syndrome

DLE
Inflammation

of infundibular region containing

the stem cells is believed to cause the scarring
alopecia
Scarring alopecia occurs in 20% of men and
50% of women with DLE
Areas of erythema and scaling with follicular
plugging
ANA positive in 35% of cases and IgM, IgG
and complement in BMZ
Potent topical and I/L CS, and systemic
prednisolone may halt the disease progression

 Antimalarials

form the mainstay of cases

refractory to steroids and produce a remission
in 3 months in majority of cases
Early treatment can produce a regrowth of hair
Acitretin, ciclosporin, cyclophosphamide,
thalidomide and MTX can be used in refractory
cases

Pseudopelade of Brocq
Idiopathic,

chronic, slowly progressive, patchy

cicatricial alopecia due to atrophic folliculitis
There is no evidence of inflammation
In early lesions , light lymphocytic infiltrate
may be present around the upper 2/3 of the
hair follicle. Follicles and sebaceous glands
are destroyed
In later lesions a thin atrophic epidermis with a
sclerotic dermis and fibrotic streams called as
fibrotic ghosts are seen extending into the
subcutis

 Elastic

fibres are seen around the lower third

of follicle in Pseudopelade of Brocq with acidalcohol-orcein stain which are absent in other
scarring alopecias
C/f
Women over 40 years are commonly affected
Asymptomatic and discovered by chance
Remains confined to the scalp initially on the
vertex

 Small

and round or oval smooth, soft and

depressed patches
If process is active, hairs at margins are easily
extracted
It is a slow process and can burn out
spontaneously
Direct immunofluorescence is negative or only
weak IgM on sun-exposed skin
The diagnostic criteria have been given by
Braun-Falco et al.

 Management

Irreversible
Does not respond to topical or intralesional CS
If no active inflammatory changes, autografting
from unaffected to scarred scalp or surgical
expansion techniques may be considered

 Follicular

degeneration syndrome
also called as hot comb alopecia
Cicatricial alopecia starts as a patch over the
vertex and spreads in a centrifugal pattern.
Similar to female pattern hair loss
Middle aged black females who chemically
straighten their hair
No treatment available

Folliculitis decalvans and tufted

folliculitis
Clinically

evident persistent chronic folliculitis

which leads to progressive scarring
An abnormal host response to S. aureus is
proposed which may be due to defective CMI
Histology reveals follicular abscesses, foreign
body granulomas and eventually extensive
fibrosis

 Men

are affected from their adolescence and

women in their thirties
Round patches of alopecia surrounded by
crusting and follicular pustules which appear in
successive crops and destroy the follicles
Tufted folliculitis is a variant where
circumscribed areas of scalp inflammation
heal with scarring char. by tufts of upto 15
hairs emerging from a single orifice

 The

tufts consist of a central anagen hair

surrounded by telogen hairs arising from
individual follicles and converging towards a
common dilated follicular infundibulum
Tufting is due to emergence of hairs from
beneath the free edge of the scales
It should be differentiated from fungal kerion

Treatment
Prolonged

courses of flucloxacillin to eradicate

S.aureus but relapses occur
Topical clindamycin for localized areas
Tetracyclines are also effective
Rifampicin in a dosage of 300 mg bd induces
prolonged remission
Should be given in combination with
ciprofloxacin, doxycycline, clarithromycin to
prevent emergence of resistant organisms
Tufting may be reduced by tar shampoos and
keratolytics

Dissecting cellulitis of the scalp

Perifolliculitis

of the scalp, deep and superficial

abscesses in the dermis, sinus tract formation
and extensive scarring
No specific organism is isolated
Associated with hidradenitis suppurativa, acne
conglobata, pilonidal sinus and
spondyloarthropathy
Occurs predominantly in black males b/w ages
of 18 and 40 years

 Painful,

firm, skin coloured nodules near

vertex which later become soft and fluctuant
Nodules coalesce to form tubular ridges with
an irregular cerebriform pattern
Thin blood stained pus exudes from crusted
sinuses
Hair is lost from the summits of inflammatory
lesions and retained in valleys
Fatal SCC may develop after many years

 Histology

shows perifolliculitis with destruction

of pilosebaceous follicles and other cutaneous
appendages

Treatment

Isotretinoin (1mg/kg/day), in combination with

prednisolone and erythromycin daily may
induce remission and significant hair regrowth
in areas not irreversibly damaged

 Antibiotics

are stopped after 4 weeks and

steroids are tapered off
Isotretinoin is continued for 6 months and
reintroduced if relapse occurs
In recalcitrant cases, widespread excision and
grafting may be done
Laser assisted hair removal may cause
improvement

 In

cicatricial pemphigoid, scalp involvement

occurs in 10% of cases
Oval atrophic glazed and yellowish patches
may be seen in scalp in necrobiosis lipoidica
often with conspicuous telangiectases
Cutaneous sarcoidosis and granuloma
annulare may produce atrophic scarring of the
scalp

Artefactual alopecia
Cosmetic

alopecia
Hair loss occurs due to structural damage to
hair shaft leading to excessive weathering and
breakage
Hair loss occurs due to injury to hair follicles
by prolonged traction from hair styling

 Traction

alopecia begins in the temporal

regions and in front of and above the ears
Use of rollers and ponytail styles may induce
alopecia in frontal and temporal regions
Tight braiding, twisting of hairs in Sikh turbans
and tight scarves can induce alopecia

 Halo

scalp ring temporary or permanent,

scalp hair loss by prolonged pressure on
vertex by uterine cervix during or prior to
delivery
Prolonged pelvic operations in Trendelenburg
position may cause alopecia due to pressure
ischaemia
Chronic radiodermatitis produced by radiation
therapy of malignant tumour of scalp may
cause alopecia

Trichotillomania
A psychiatric

disorder with dermatological

expression charac. by a compulsive habit of
pulling out the hair
In infants and young children, it is a habit akin
to thumb-sucking and nail biting
Slightly more common in boys and resolves
spontaneously or with minimal treatment
In older children and adults, it is a chronic
psychiatric problem

 This

form occurs predominantly in females

with F:M ratio of 7:1
It is considered to be the result of many
disorders like OCD, personality disorders,
body dysmorphophobic disorders, MR and
psychosis
Histology shows numerous empty canals.
Intraepithelial and perifollicular haemorrhages
and intrafollicular pigment casts. Many follicles
are in catagen with very few or none in telogen

 C/F

Hair is plucked from one frontoparietal region

Bizarre or angular patch of hair loss with
twisted and broken hairs at various distances
from scalp
A uniform coarse stubble may be formed in
adults but hair is not lost completely
Eyebrows, eyelashes, beard and rarely mons
pubis and perianal region may be affected
Trichobezoar is a rare accompaniment

 Tinea

capitis or alopecia areata should be

excluded

Treatment

Clomipramine, fluoxetine and neuroleptic

agents are reported to be useful
Psychotherapy

Pityriasis amiantacea
Inflammatory

scaling reaction of scalp often

without evident cause
Psoriasis and seborhoeic dermatitis are
associated
Occurs at an average age of 25 years
Masses of adherent silvery scales, overlapping
like the tiles of a roof, adhere to the scalp
attach in layers to hair shafts
Some hair loss occurs which regrows but
scarring alopecia has been reported

Treatment
Tar

or salicylic acid ointments are used

Preparation is left on the scalp for several
hours and then washed off
Scales may be gently removed using a metaltoothed comb
An antidandruff or tar shampoo may be
needed to maintain remission
Potent topical CS lotions may be beneficial in
some cases

Atrichia congenita
Usually

autosomal recessive as an isolated

defect
Hair follicles are absent in adult life and
sebaceous glands are smaller
Scalp hair is normal at birth but is shed
between 1st and 6th months, after which no
further growth occurs
Few straggling pubic and axillary hairs and
scanty eyebrows and eyelashes may be
present

 Atrichia

congenita may be associated with

progeria, hidrotic ectodermal dysplasia,
Moynahans syndrome

Circumscribed alopecia of
congenital origin
Epidermal

naevi present as warty or smooth

but slightly indurated plaques
Non cicatricial alopecia may develop around
melanocytic naevi
Aplasia of all layers of skin
Circumscribed non cicatricial alopecia occurs
due to hypoplasia or aplasia of a group of
follicles and includes vertical, sutural and
triangular alopecia

Trichogram
The

trichogram is a standardized lightmicroscopic investigation of the hair-roots from

the epilated hair.
This method enables the investigator to decide
on the activity of the hair loss at the time of the
investigation.
It is able to establish the ratio of growing
(anagen) and resting (telogen) hair, as well as
hair at the regression phase

Before performing a trichogram, for eight weeks,

the patient should not use any hair cosmetics
such as colorations, permanent waves or an
electric curling comb
Five days prior to examination, the hair should
not be washed, otherwise the rate of telogen
will be falsified

 50

100 epilated hairs from the frontal and

occipital scalp are necessary
They are embedded in a special medium or
fixed with a tesa-film strip onto an object slide

Trichoscan
A modification of the classic Trichogram
Shaving an area of scalp that is
approximately 1.8cm squared. Hair is not
completely shaved to the scalp, but only
enough to leave short hair shafts visible
After 3 days, die is applied to the shaved
area using a wooden spatula and left in
place for 10 to 12 minutes

 A video

image is taken at a magnification of 20

times
Using the logic that anagen hairs grow 0.3mm
per day, and telogen hairs do not grow, the
trichoscan software analyzes the image and
determines the anagen
Simple, fast and photographic processing,
painlessness of the procedure and the
reproducibility of the results

Surgical restoration
Scalp

flaps: This hair restoration surgery

technique involves the moving of tissue from
one area of the scalp to another, such as a
strip of scalp from the hair bearing temple
moved forward to the bald frontal hairline.
Scalp reduction: A hair restoration surgery
technique where baldness is reduced by
cutting out a segment of bald scalp skin.

Hair follicle transplant

The

graft in this case consists of a single

follicular unit as it exists in nature with
adjoining sebaceous glands, the surrounding
adventitial sheath and the supportive nerve
and blood tissue
In the Direct Hair Implant technique,the
follicular units are instead directly extracted
one-by-one using custom-made, precise
micro-surgical tools less than a millimeter in
diameter.

Laser Hair Transplant

It

used laser beam to vaporize a narrow slot in

the scalp for the implanting hair graft
The laser hair restoration technique always
leaves surface change and scarring
High energy laser beams may damage hairs
existing near the implant site because of
burning of the surrounding tissue

 The

high energy of laser beam leads to the

closing of the blood vessels
Blood supply is very crucial for nourishing the
grafts after they are transplanted
Laser assisted transplants either are not able
to grow or heal more slowly and have
unpredictable growth due to impaired blood
flow

 Destroys

the collagen and weakens the elastic

support around the newly transplanted grafts
Also increases the clot around the graft which,
in turn, decreases oxygen perfusion and
retards healing

Thank You