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SEMINAR ON ALOPECIA

Chairperson

Speakers

Date & Time

Organized by :

Dr. Shahab Uddin Ahmed Chowdhury.


Associate Professor & Head of the dept.
Department of Dermatology, MMC.
Dr. Mohammad Shoeb Khan,
MD (Part-II)
&
Dr. Mohammed Saiful Islam Bhuiyan,
MD (Part-II), FCPS (Part-II)
Medical Officers,
Department of Dermatology, MMCH.
5th April, 2005 at 2.00 pm.
Department of Dermatology, MMCH.
&
Renata Limited

HAIR AND HAIR FOLLICLE

INTRODUCTIO
N

Hairs are keratinized elongated

structures derived from invaginations of


epidermis and project out from most of
the body surface.

AREAS WITHOUT HAIR:


Palms
Soles
Lips
Nipples
Glans penis

Clitoris
Prepuce
Labia minora
Inner surface of
labia majora

RACIAL PREVALENCE :
Whites are hairiest.
Asians are least hairy and
blacks fall in between.

TYPES OF HAIR
Morphologically :
Straight :
Spiral :
Helical :
Wavy :

Asians , whites.
Blacks, whites.
Whites.
Whites.

HAIR TYPES (Contd.)


Fetal hair Lanugo hair : soft, fine, lightly pigmented hairs.

Adult hair Vellus hair : fine hairs cover most of the body
of youngsters and adults.
Terminal hair: long, coarse, pigmented hairs with
larger diameters.

NUMBER OF HAIRS
Scalp : about 1,00,000 hairs.
Face : about 600 hairs /cm2.
Rest of the body : about 60 hairs/cm2.

LENGTH, WIDTH AND GROWTH RATE


Length : range from <1mm to > 1 meter.
Average uncut scalp hair : 25 100 cm.
(exceptionally 170 cm)
Width : from 0.005 to 0.06mm.
Growth rate: about 1 cm/ month (terminal hair).

FUNCTIONS
1. Protects body surface from external injury.
2. Helps in sensory function.
3. Psycho social importance.
4. Forensic importance.
i. Identification of race, sex, age and religion.
ii. Cause of death- can be determined.
iii. Time of death- can be determined.
5. Assist thermo- regulation: mainly in lower animals.

STRUCTURE OF HAIR AND HAIR FOLLICLE:

DEVELOPMENT OF HAIR
Ectodermal origin1.

Hair bud develops from epidermis and


penetrates the dermis.

2.

Hair shaft grows from cells in the


centre of hair bud.

DEVELOPMENT OF HAIR (Contd.)


3.

Inner root sheath develops from cells in the


periphery of hair bud.

Mesodermal origin: Outer root sheath.

First hair come is lanugo hair at eyebrow and


upper lip at twelve
weeks

of gestation.

DEVELOPMENT OF HAIR (Contd.)


3.

Inner root sheath develops from cells in the


periphery of hair bud.

Mesodermal origin :

Outer root sheath.

First hair to come is lanugo hair at eyebrow


and upper lip at 12
weeks of gestation.

HAIR EMBRYOLOGY

HAIR CYCLE
It is believed that each hair follicle goes
through 10-20 hair cycle in a life time.
There are four phases1. Anagen : growing phase.
2. Catagen: involuting phase.
3. Telogen : resting phase.
4. Exogen : hair shedding phase.

ANAGEN (GROWING PHASE)


Last for about 1000 days.
Follicular cells grow, divide and become

keratinized to form growing phase.


A darkly pigmented portion is evident just

above the hair bulb.

CATAGEN (INVOLUTING PHASE)


Lasts for about 10 days.
Scalp hairs show a gradual thinning and
decrease of the pigment.
Melanocytes cease producing melanin.
Matrix

keratinocytes

abruptly

cease

proliferating so that lower follicle involutes


and regresses.

TELOGEN (RESTING PHASE)

Lasts for about 100 days.

Club-shaped proximal end shed from the


follicle during telogen or subsequent anagen.

Growth of a new anagen hair leads to


shedding of any remaining telogen hair.

But new hair does not push out the hair from
the previous cycle.

EXOGEN (HAIR SHEDDING PHASE)


Recently added phase.
The term describes relationship between hair
shaft and base of telogen follicle.
Hairs can be retained for more than one
cycle.
Shedding phase is most likely independent of
anagen and telogen.

PIGMENTATION OF HAIR
Hair color is determined by melanocytes.

Melanocytes are present in the bulb.


Melanocytes feed melanosomes mainly to
the medulla and cortex.
Melanocytic follicles produce melanin. eumelanin (dominant in brown-black hairs)
. phaeomelanin (dominant in red-blond hairs)

PIGMENTATION OF HAIR (Contd.)

Greying of hair due to decreased


number and activities of melanocytes.

Vitiligo due to destruction of


melanocytes.
Albinism due to inactivity of
melanocytes.

ALOPECIA

Absence or loss of hair especially of the scalp.

Pathophysiology of hair loss :


1. Production failure
Failure to produce or continue to
produce a normal hair follicle.
2. Aberration of
Normal hair cycle.
Production of a normal hair shaft.
3. Destruction of
Hair follicle.

CLASSIFICATION OF ALOPECIA
1. FOCAL HAIR LOSS
Non-Scarring:

A. Abnormality of cyclingi. Alopecia areata.


ii. Syphilitic alopecia.

B. Production declinei. Androgenetic alopecia.


ii. Triangular alopecia.

FOCAL HAIR LOSS (Contd.)


C. Hair breakagei. Trichotillomania.
ii. Tinea capitis.
iii. Traction alopecia.
iv. Primary or acquired hair shaft abnormality.

SCARRING ALOPECIA
A. Lymphocytic-

i. Chronic Cutaneous LE (DLE).


ii. Lichen planopilaris.
iii. Classic pseudopellade of Brocq.
iv. Alopecia mucinosa.
v. Central centrifugal cicatricial alopecia.
vi. Keratosis follicularis spinulosa
decalvans.

SCARRING ALOPECIA (CONTD.)


B. Neutrophilic
i. Folliculitis decalvans.
ii. Dissecting folliculitis/cellulitis.
C. Mixedi. Folliculitis (acne) keloidalis.
ii. Folliculitis (acne) necrotica.
iii. Erosive pustular dermatitis.

Diffuse Hair Loss


A.

Abnormality of cycling
i. Alopecia areata.
ii. Telogen effluvium.
iii. Anagen effluvium.
iv. Loose anagen syndrome.

B.

Hair shaft abnormalityi. Hair breakage.


ii. Unruly hair.

Diffuse Hair Loss (Contd.)

C. Failure of follicle productioni. Congenital universal atrichia.


ii. Alrichia with papular lesions.
iii. Hereditary vitamin-D- resistant
rickets.

ALOPECIA AREATA
Definition:
Rapid and complete loss of hair in one or
most often several round or oval patches,
usually on the scalp, bearded area,
eyebrows, eye lashes and less commonly on
other hairy areas of the body.

ALOPECIA AREATA

ALOPECIA AREATA

ALOPECIA AREATA(Contd.)
Epidemiology:
Approximately 1.7% of the population will
experience an episode of alopecia aerata
during their life time.

ALOPECIA AREATA (Contd.)


Etiology

Exact cause is still unknown.


It is an autoimmune disease- Mediated by the cellular arm
(T- cell, macrophages ).
- Modified by genetic factors
(HLA-R4,DR11,DQ7)

ALOPECIA AREATA (Contd.)


-Triggered by environmental factors Trauma.
Neurogenic inflammation.
Infections agents.

ETIOPATHOGENESIS
Trauma

Neurogenic
Inflammation

Infections
agents

Release of cytokines
Aberrant expression of MHC (due to
failure of repression)
Aberrant expression of adhesion
molecules

Haematopoietic cell migration (T-cell)


Production of follicular auto- antigen
(Kerationcyte and melanocyte origin)
Attack on
melanogically active anagen fallicle
Follicular damage in anagen and rapid
premature transformation to telogen.

FOUR DISTINCT STAGES OF


ALOPECIA AREATA
i. Acute hair loss.

ii. Persistant (Chronic) baldness.


iii. Partial telogen to anagen conversion
(incomplete revcovery).
iv. Normal recovery.

CLINICAL FEATURE
Rapid and complete loss of hair in one
or several patches.
Site Scalp, bearded area, eyebrows,
eye lashes and less commonly other
areas of body.
Size Patches of 1-5 cm in diameter.

CLINICAL FEATURE (CONTD.)


Exclamation point hair- at the periphery of

hair loss, there are broken hairs, whose distal


ends are broader than the proximal end.

CLINICAL FEATURE (CONTD.)


Few resting hairs may be found within the patches.
Going gray overnight- a mysterious phenomenon
is observed in fulminant alopecia areata.
In about 10% cases of long standing extensive
alopecia areata, some nail changes develop.

EXTENSIVE PATCHY ALOPECIA AREATA.

DIFFUSE PATTERN OF HAIR LOSS IN ALOPECIA AREATA

CLINICAL FEATURE (CONTD.)


Alopecia totalis Total loss of scalp hair.
Alopecia universalis Loss of entire body

hair including scalp hair.


Ophiasis Loss of hair confluent along the

temporal and occipital scalp.


Sisaipho- Loss of hair of entire scalp except

temporal and occipital area.

ALOPECIA UNIVERSALIS

ALOPECIA TOTALIS

OPHIASIS PATERN OF ALOPECIA AREATA

ASSOCIATED DISEASE

Higher incidence of alopecia areata in


patients of1. Atopic dermatitis.
2. Autoimmune disease
* SLE
* Thyroiditis.
*
Myasthenia
gravis.
*
Vitiligo.
3. Lichen planus.
4. Down syndrome.

HISTOLOGY
Peribulbar, Perivascular and outerroot sheath infiltration with T-cells and
macrophages.
The follicular size are diminished and
identified in more superficial dermis.

DIFFERENTIAL DIAGNOSIS
1. Tinea capitis.
2. Trichotilomania.
3. Secondary syphilis
4. Congenital triangular alopecia.
5. Alopecia neoplastica.
6. Early lupus erythematosus.

TREATMENT
Spontaneous recovery is extremely common
for patchy alopecia areata.
For localized patchy alopecia areata

Steroid- both local (intralesional and


topical) and systemic (in short course).

TREATMENT (CONTD.)
- High potent topical steroid used as first
line therapy.
- Intralesional steroid given at 4-6 weeks
interval.
- Systemic steroid (Short course, <8 weeks)
alone or in conjunction with topical steroid.

TREATMENT (CONTD.)
If lack of response after several months therapy Topical 1% Anthralin cream - applied for 15-20
minutes and then shampooed off the treated side.
5% topical minoxidil as a single agent or as an
adjuvant with topical Anthralin.
PUVA.

TREATMENT (CONTD.)
Contact sensitizer
- Squaric acid dibutyle ester,
- Diphencyprone,
- Dinitrochlorobenzene.
Psychological support.
In extensive scalp hair loss- cosmetically
expectable alternatives.

HEALED ALOPICIA UNIVERSALIS


AFTER PUVA THERAPY

PROGNOSIS
Poor prognostic marker-

Early onset (Prepubertal)

Extensive involvement.

Prolong duration (>5years)

Ophiasis.

ANDROGENETIC ALOPICIA

ANDROGENETIC ALOPICIA

ANDROGENETIC ALOPECIA
Synonyms :

Male Pattern alopecia,


Male pattern baldness,
Common baldness
Secretarial alopecia.
Definition :
It is a very common, potentially
reversible scalp hair loss that generally spares
parietal and occipital areas (Hippocratic
wreath) of the scalp.

ANDROGENETIC ALOPECIA (Contd.)


Age :

Twenties or early thirties.

sites :

Chiefly vertex and frontotemporal


regions.

Etiopathogenesis:

Exact mechanism is still unknown.

Hereditary (Probably autosomal dominant) &


Androgen (specifically dihydrotestesterone)

ETIOPATHOGENESIS (Contd.)
Testesterone

5 R

Dihydrotesterone.

5R has two Isozyme, 5R1 and 5R2

5R1 ubiquitously distributed in skin


particularly in sebaceous gland.

5R2 is found in outer root sheath and


dermal papillae.

ANDROGEN
Androgen - androgen receptor complex in cytoplasm
transformation of receptor to expose DNA binding domain

binds to androgen response element of DNA


Transcription and translation
certain effector protein,

ETIOPATHOGENESIS (Contd.)
EFFECTS
- Shortening of anagen and
lengthening of telogen
- Follicle become short and sclerosis of
dermis and miniaturization or reduction
of hair present.

CLINICAL FEATURE

Hair loss starts any time after puberty


Whisker hairs first sign of impending
male pattern alopecia, appear at the
temple.

Professors angle anterior hair line


recedes backward on each side.

Eventually entire top of the scalp become


devoid of hair.

PATTERN OF HAIR LOSS

Androgenetic alopecia in women


Etiology :
i. Genetic Predisposition,
ii. Androgen excess,
Ovarian cause- Polycystic ovarian syndrome,
- Other ovarian tumor,
. Unilateral benign
microadenoma.
. Leydig cell tumor
. Hilar cell tumor.

ETIOLOGY (CONTD.)
Adrenal cause
- Congenital adrenal hyperplasia (androgenital
syndrome) due to deficiency of
21 hydroxylase (most common)
11- hygroxylase.
3- hydroxysteroid dehydrogenase.
- Tumor
Adrenal adenoma
Carcinoma.

CLINICAL FEATURE
Pattern of hair loss :
Christmas
progressive

tree

pattern-

reduction

of

diffuse

and

density

and

diameter of hairs in the mid scalp.

Maintenance of frontal hair lines with only


slight recession.

ANDROGENETIC ALOPECIA IN WOMEN

CLINICAL FEATURE (CONTD.)


Other evidence of androgen excess:
Acne.
Hirsutism.
Menstrual irregularities.
Majority of women with pattern hair loss
have
No increased serum androgen,
No other sign symptom of
androgen hypersensitivity.

TREATMENT
1. Topical Minoxidil (2% & 5%)

-non specific hair growth promoter


affecting anagen induction.
- M/A is not clear, its ca channel
opener activity is important.
2. Systemic Finesteride (1mg daily).

TREATMENT (CONTD.)
3. In women spironolactone ( >100
mg daily).
- Flutamide (250-500
mg bid or tid).
- Cyproterone actate.
4. Surgical treatment- Micrograft &
minigraft from non-androgen
dependent site (occiput).

TELOGEN EFFLUVIUM
It is a reaction pattern to a variety of
physical and mental stressors represents
a precipitous shift of a percentage of
anagen hairs to telogen.

Causes of Telogen Effluvium


Endocrine
- Hypo- or hyperthyroidism.
- Postpartum.
- Peri- or postmenopausal state.
Nutritional
- Biotin deficiency.
- Caloric deprivation.
- Essential fatty acid deficiency.
- Iron deficiency.
- Protein deprivation.
- Zinc deficiency.

Causes of Telogen Effluvium

(Contd.)
Drugs
Angiotensin-converting enzyme inhibitors.
Anticoagulants.
Antimitotic agents.
Benzimidazoles.
Beta blockers.
Interferon
Lithium

Causes of Telogen Effluvium (Contd.)


-

Oral contraceptives.
Retinoids.
Vitamin A excess.

Physical stress
-

Anemia
Surgery.
Systemic illness.

Psychological stress

Events related to pathogenesis of


telogen effluvium
I.

Short anagen- by drugs, fever, physiological


stress.

II.

Prolonged anagen- Pregnancy.

III. Conversion of telogen follicle to anagen


follicle.

Pathology
1. > 12% to 15% of terminal follicles are in
telogen.
2. Follicle itself is not diseased.
3. No inflammation or dystrophic changes.

CLINICAL PRESENTATION

Lots of hairs coming out by the roots


complained by patient.
Diffuse hair loss with clinically perceptible
thinning of hairs usually 3-5 weeks of
inciting signal and shedding continue for
about 3-4 month after removal of inciting
cause.
150 to > 400 hair loss daily.
Hair density may take 6-12 months to
return to base line.
Pull test.
Clip test.

TREATMENT
No specific therapy.
In majority cases hair will grow spontaneously
within few month after removing inciting cause.
In some patients with chronic telogen effluvium- 5% minoxidil solution, 70% success in
man .
- For Premenopausal women, 5% minoxidil
solution + cyproterone acitate 50 mg from
day 5 to 15 of menstrual cycle taken
together with ethynnyl estradiol (0.035
mg/day).

TREATMENT (CONTD.)
For post menopausal women,
- Cyproterone acetate 50 mg/day.
- Spironolactone (50- 100 mg/day) or flutamide
125- 250 mg/ day alternative to cyproterone
acetate.

TRICHTILLOMANIA

A neurotic practice of plucking or breaking


hair from scalp or eyelash resulting usually
localized or

widespread areas of alopecia

contains hairs of varying length.

Mostly girls under age of 10 years.

Disturbed mother- child relationship.

TRICHOTILOMANIA

TRICHOTILOMANIA IN A WOMEN

ALOPECIA SYPHILITICA
Typical motheaten appeorance on the occipital
scalp or generalized thinning of hairs or both.
Eyebrows, eyelash and body hairs also
involved.
It may be one or sole cutaneus manifestation of
secondary syphilis.
Treatment of syphilis may reverse the hair loss.

ALOPICIA OF SECONDARY SYPHILIS

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