1. health and fitness
2. disease

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
INTRODUCTION
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 outer-
root 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.
•
5R has two Isozyme, 5R1 and 5R2
•
5R1 ubiquitously distributed in skin
particularly in sebaceous gland.
•
5R2 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.
•
“Professor’s 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-β hygroxylase.
3-β 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