Transcript Scarring Alopecia.ppt

Scarring Alopecia
95 /10/3 ‫دوشنبه‬
‫باز اموزی پزشکان‬
Dr Gita Faghihi
Professor of Dermatology
Isfahan University of medical sciences.
Scalp hairs complete the body self-image
and patients with alopecia suffer from overt
disfiguration
Alopecia
None
Scarring
(Reversible)
Scarring
(Irreversible)
Non-scarring alopecias tend to
have preserved follicular ostia:
No clinically visible inflammation is noted in
most presentations
The term cicatricial or scarring alopecia :
potential of permanent destruction of the
hair follicle.
Clinically: there is effacement of follicular
orifices
Scarring alopecias have loss of
follicular ostia, or atrophy.
Clinical inflammation is frequently, but not
always, present.
 Histologic inflammation may be present.
 Ultimately, histologic confirmation is the
best method to confirm the presence of a
fibrosing/scarring process with loss of hair
follicles.

Dissecting Cellulites:
Synonyms:
 dissecting folliculitis
 most commonly begin on
the vertex
or/ occiput

Presents
as relatively painless, deep-seated, firm to
fluctuant nodules and abscesses.

The nodules and deep abscesses
commonly extend to form:
a complex pattern of interconnecting
sinuses and abscesses with purulent, or
hemopurulent material.
Pressure applied to one nodule or abscess: can
cause purulent exudate to emerge several
centimeters away.
 The epidermal surface overlying the sinuses and
nodules may or may not be erythematous and
scaly.
 Scattered superficial follicular pustules are
frequently present on the surface of the
nodules.
 Hypertrophic and keloidal scarring may occur in
affected areas.

Dissecting cellulitis of the scalp:
more common in young to middle-aged
black men.
 It may occur simultaneously with acne
conglobata and hidradenitis suppurativa.
This complex is known as the follicular
occlusion triad.

Treatment of Dissecting
Cellulities
 Initial
therapy : oral antibiotics
tetracycline (1 -2 g per day),
doxycycline (200 mg per day),
minocycline (50-200 mg per day).
 Combination antibiotic therapy
:cephalexin (1 g per day) and
rifampin (600 mg per day) has
been helpful.
Intralesional corticosteroid injections
(triamcinolone acetonide, 40 mg/mL) can
be helpful in noninfectious nodules and
sinuses.
 Oral corticosteroids tapered to low-dose
alternate-day usage may also be helpful.
 Isotretinoin (1 mg/kg per day) has been
effective in some reported cases.

Acne Keloidalis Nuchae
destructive pustulofollicular process
 occurs on the occipital scalp and
posterior neck
 primarily affects young black men.


begin as discrete follicular pustules and
papules

progress to form less discrete, large,
exophytic keloidal nodules and plaques
largely devoid of hair.
Pathogenesis and Etiology
 The

etiology : unknown
acne keloidalis nuchae : a variant of
acne vulgaris
 Bacteria
may be isolated.

Repetitive low-grade trauma

friction by football helmets, other headware,
and collars

Closed shaving of posterior scalp and neck hair
Treatment of Acne Keloidalis
Nuchae

Tetracycline, 1 g per day
Doxycycline 200mg/day
Minocycline 50-100mg/day
Erythromycin 1g per day

2. Topical antibiotics.


a. Erythromycin solution 2%
b. Clindamycin solution 1%




3. Tretinoin cream or gel 0.025%-0.1%
4. Benzoyl peroxide gel or lotion 5%-10%
5. Intralesional corticosteroid injections (triamcinolone acetonide, 340 mg/mL)
6. Surgical excision for large exophytic keloidal
Discoid Lupus Erythematosus
Discoid lupus erythematosus is a common
lesion
 typically found in young to middle-aged
adults
 2:1 female/male predominance.
 Age at onset : between 20-60 years


most commonly located on the
face, scalp, and inner ear
50% of patients with DLE have scalp
lesions
10% of patients: only scalp involvement
Patients with discoid lupus:
uncommonly progress to involvement with
systemic lupus erythematosus.
15% of patients with SLE may exhibit
DLE

Early lesions:
small erythematous papules or irregular
small, scaly plaques round to irregular
shaped atrophic, sclerotic plaques.

Thick,adherent scale frequently develops
that when removed reveals keratinous
plugs on its undersurface.
When DLE is active:
surrounding borders erythematous and
violaceous.
symptomatic including pruritus, burning
and pain.
 Both hyperpigmentation and
hypopigmentation is frequently seen.

DIF is positive for granular IgG but also
occasionally for IgM and IgA.
 Complement at DEJ is observed in 75%90% of cases.

The clinical diagnosis of DLE is usually
not difficult.
 The previously described clinical features
and distribution of lupus lesions are
usually quite characteristic.
 The presence of classic lesions at other
sites (ears, face, neck, chest, and arms)
can aid in the diagnosis.


A routine skin biopsy to confirm the clinical
diagnosis.


DIF in most cases is usually not necessary.

R/O SLE
relatively limited involvement:
Topical and intralesional corticosteroids
IL
triamcinolone acetonide, 3-10mg/mL:
into erythematous and violaceous
lesions
extensive scalp or cutaneous
involvement is present and is not
responding to local therapy:
consideration may be given to systemic
therapy.

Effective systemic medications :
oral prednisone and chloroquine
Lichen planopilaris:
The hair follicles are subsequently destroyed,
yielding atrophic,irregular, especially angular or
polygonal shaped patches of alopecia with
similar follicular papules at the periphery of the
patch of alopecia.
 In addition, similar spinous follicular papules as
well as more typical lichen planus lesions are
frequently present elsewhere on the body,
including mucous membranes and nails.


50% to 70% of patients with lichen
planopilaris :
have lichen planus elsewhere on the body.
The main symptom: pruritus.


initial perifollicular erythema the follicular
acuminate papules

smooth patches of hair loss, and in the scalp,
scarring alopecia is a common sequela.

End stage : a permanent loss of pilosebaceous
units and may clinically resemble pseudopelade.
Diagnosis of Lichen planopilaris:

The combination of follicular papules in an
area of alopecia and signs of lichen planus
elsewhere on the body is virtually
diagnostic of lichen planopilaris.
Chronic cutaneous lupus erythematosus is
generally not confused with lichen
planopilaris.
 Lesions of discoid lupus erythematosus
frequently exhibit follicular plugging and
follicular accentuation, but the
interfollicular skin is more inflamed and
sclerotic than in lichen planopilaris.


Course: can last several months to several
years.

Therapy : controlling perifollicular inflammation
and pruritus.
the most effective therapies in LPP.:
 High-potency topical corticosteroids and oral
corticosteroids


Oral corticosteroids (30 to 40 mg per day)
with subsequent taper have been reported
to be the most efficacious therapy for
controlling pruritus and hair loss.

Alopecia Mucinosa (Follicular Mucinosis)
Mucin deposition and subsequent degeneration
of hair follicles : patches and plaques of
alopecia.
 most commonly involves:
the face, scalp, and neck, but involvement of
extremities may also occur.
 Clinically detectable alopecia is most often
present in those lesions involving the scalp and
face.


have variable morphology ranging
from indurated, scaling, erythematous
plaques and nodules to noninflammatory
circular patches resembling alopecia
areata.

Age at onset ranges from 2 to 80 years.

Two clinically distinct groups of alopecia
mucinosa (follicular mucinosis) exist:
lymphoma associated and non-lymphoma
associated.

Mycosis fungoides is the most common
lymphoproliferative disorder associated
with alopecia mucinosa and follicular
mucinosis and usually occurs in patients
30 years of age and older.
The reported incidence of lymphoma in
alopecia mucinosa ranges from 9.4% to
60%.
 Close follow up of patients with repeated
biopsy is therefore required.

Non-lymphoma associated alopecia
mucinosa:
frequently occurs in children and young
adults and is usually self-limiting without
resultant permanent alopecia.
 In addition, Hodgkin's lymphoma may
rarely occur in association with childhood
alopecia mucinosa .

Treatment of alopecia
mucinosa:

Non-lymphoma associated :
Topical Coticosteroids
Intralesional Coticosteroids
lymphoma associated :
Treatment of lymphoma
Follicultis Decalvens
is a form of alopecia
(hair loss) that
involves scarring.
It is characterised by
redness and swelling
and pustules around
the hair follicle
(folliculitis) that leads
to destruction of the
follicle and
consequent
permanent hair loss.
Folliculitis decalvans
affects both men and women
and may start first during
adolescence or at any time in
adult life.
The exact cause is unknown.
In most cases Staphylococcus
aureus can be isolated from
the pustules but the role of
the bacteria is not clear.
What is the treatment of
folliculitis decalvans?




There is no permanent cure for the condition but it can
be controlled to some degree by using medications.
Oral antibiotics such as minocycline, tetracycline,
rifampicin, clindamycin, fusidic acid, ciprofloxacin and
dicloxacillin have all been tried with varying results from
patient to patient.
In some severe forms, addition of an oral corticosteroid
may be necessary.
Oral isotretinoin can result in long-term remissions in
some patients.
pseudopelade of Brocq
discrete asymptomatic areas
of scalp hair loss (most
commonly affecting the
vertex and parietal scalp).
 pseudopelade of Brocq is
slowly progressive.
 Disease progression in
pseudopelade eventually
ends spontaneously.

in the physical examination
to exclude evidence of other forms of scarring
alopecia.
 Most cases of pseudopelade of Brocq represent the
end stage of LPP, DLE, or folliculitis decalvans.
 Pseudopelade of Brocq is a diagnosis of exclusion.
 rare familial cases have been reported.

pseudopelade of Brocq

Oral steroid mini pulse (oral
dexamethasone/betamethasone 5 mg/day
on two consecutive days… every week)
has been successful.
Frontal Fibrosing Alopecia (FFA)

Band-like area of
hair loss along the
frontal hairline
and above the
ears

Loss of eyebrows

Lymphocyte
mediated
Central Centrifugal Cicatricial
Alopecia (CCCA)



Mainly seen in women of
African-descent
Lymphocyte mediated
Hair loss typically begins at
the vertex or mid-scalp and
extends outward in a
centrifugal manner. scalp
may appear shiny.
symptoms, tenderness, itch
and burning are common.
Treatment of central centrifugal
cicatricial alopecia





Potent topical steroids (or
intralesional steroids
tacrolimus ointment,
pimecrolimus cream
doxycycline 100 mg twice
daily,for several weeks to
months)
Hydroxychloroquine
Ciclosporin.
Hair transplantation

can be considered in individuals with wellcontrolled CCCA for at least one year.
However, graft survival is low.
surgical correction of alopecia

should not be performed if
the patient has any active
scalp disease or
inflammation

Recent advances in follicle
unit extraction (FUE) have
also led to improved
survival and more natural
outcomes in scarring
alopecia patients
‫تشخیص شما چیست‬
‫؟؟‬
Lichen planus
Frontal fibrosing alopecia
The end