Alopecia

Introduction
Hair

has no vital function in humans but

has important psychological functions

Types

of hair
Prenatal hair lanugo fine, soft
unmedullated and unpigmented hair
Postnatal hair It constitutes of terminal
and vellus hair

 Terminal

hair
Coarse, long, usually pigmented and
medullated
Limited to scalp, eyebrows and
eyelashes
Replaces vellus hair after puberty in
response to androgens
Vellus hair fine, soft, unmedullated and
occasionally pigmented hair

 Follicle

density is highest in the fetus

and gradually decreases with growth
due to increase in skin surface area
This decrease is less marked over the
head
Highest follicle density with lower visible
vellus hairs is over forehead and cheeks

Anatomy of hair follicle

Hair

is the keratinized product of the hair

follicle
The hair follicle is continuous with the
epidermis at the upper end and extends
into the dermis and even into subcut.
layer in case of longer follicles
Hair shaft is made up of outer cuticle,
cortex and a variable medulla

Hair cycle
A repetitive

sequence of growth and rest

Active hair growth is k/a anagen which
determines the final length of hair
80-90% of hair follicles on human scalp
are in anagen at any one time
In anagen epithelial cells overlying the
dermal papilla undergo mitosis

Hair cycle

 The

involutionary phase where growth

ceases is k/a catagen in which there is
follicular regression
The period between the completion of
this regression and the onset of next
anagen is k/a telogen
The club hair is shed through an active
process k/a exogen

Control of hair cycle

Primarily

by intrinsic mechanism within

individual follicles
Modulated by local and systemic factors
Synchronous hair cycling is lost with
increasing age in humans
Beyond neonatal period, hair follicles
cycle independently of their neighbours

 Scalp

hairs transplanted onto other sites

retain the cyclical behaviour of the donor
site
Epithelial cells in outer root sheath and
mesenchymal cells in dermal papilla are
thought to underlie intrinsic control of
hair cycle.

Androgens and hair growth

Facial,

trunk and extremity hair in male

and pubic and axillary hair in both sexes
is dependant on androgens from
testicular, adrenocortical and ovarian
sources
Growth hormone is necessary as a
synergistic factor
Androgens are necessary for balding of
the human scalp

alpha DHT mediates the effects of

testosterone on hair growth
Hair follicles possess 5 alpha reductase
activity
Possibly circulating DHT also contributes
to androgen effects on hair growth
The androgen receptor is a nuclear
hormone receptor and acts as a
transcription factor

 Androgens

induce changes in gene

expression in hair follicles
Hair follicles in occipital skin show little
or no response to androgens
Androgen responsiveness is determined
at the level of the follicle or its immediate
tissue env

 Dermal

papilla is considered to be the

primary target of androgen action
Dermal papillae express 5 alpha
reductase 2
Androgens may act on hair growth by
altering the no. of cells in the dermal
papillae and its ECM

Androgenetic alopecia
Occurs

in genetically predisposed
individuals
Androgen mediated conversion of
susceptible terminal hairs into vellus
hairs
Hamilton-Norwood grading scale is used
to diagnose and classify extent of hair
loss in clinical situations

 Ludwig

scale is widely used to classify

FPHL
The other scales used are Olsen scale,
Ebling Rook scale and Savin scale
Savin scale is same as Ludwig scale
except that it also measures overall
thinning of hair

Hamilton Norwood scale

Ludwig scale

 At

least 94% of adult men develop some

degree of frontoparietal recession after
puberty
This limited recession (stage I) does not
always progress and may be a
manifestation of sexual maturity
Early onset MPB progresses more
rapidly

 Female

pattern hair loss has a later age

onset
FPHL manifests as reduction in hair
volume over the crown with complete or
near complete preservation of the frontal
hairline
Christmas tree pattern with widening of
the central parting line in the mid frontal
scalp

 An

identical pattern of hair loss is also

seen in females without androgens
Thus other non androgen dependant
mechanisms can produce hair loss,
which mimics AGA
Minor bitemporal recession also occurs
in more than 25% of women in their 20s

Inheritance of AGA
Association

of MPB with a polymorphism

of androgen receptor gene on the X
chromosome
Necessary but not sufficient
Possible role for polymorphisms in both
androgen receptor gene and aromatase
gene in FPHL

Hormonal influences
Normal

male levels of androgen are

sufficient to make manifest the degree of
baldness determined genetically for the
individual
In women with strong genetic
predisposition, normal female androgen
levels can induce early baldness but in
others it will not occur unless androgen
levels are increased

 In

response to testosterone, anti TGFbeta 1 derived from the dermal papilla

cells is proposed to suppress hair growth
in AGA
Beard and pubic hair dermal papilla cells
have higher and occipital scalp follicles
have lower levels of androgen receptors

 In

AGA, duration of anagen decreases with

each hair cycle
Reduction of anagen : telogen ratio from 12:1
to 5:1
Terminal : vellus hair ratio is less than 4:1 in
AGA
Hair growth rate remains constant
Ultimately, anagen becomes so short that that
the growing hair fails to reach the skin surface
The latent phase is prolonged and thus hair
numbers are reduced

 Progressive

miniaturization of hair
follicles due to decrease in dermal
papilla size occurs in b/w hair cycles
In FPHL, this occurs rapidly, possibly in
the space of a single cycle
It leaves behind stellae as remnants also
k/a fibrous tracts or streamers

 Arao

Perkins body may be seen within

the stellae
They are a cluster of elastic fibres
With progressive shortening of hair,
multiple clumps may be seen like rungs
of a ladder
Inflammation and fibrosis account for
difficulty in reversing the miniaturization

 Principal

D/D of AGA in females is CTE

There is h/o diffuse hair shedding
without widening of the central parting
Commonly there is mild bitemporal
recession in CTE

Treatment
Proper

counselling about the need for

maintenance therapy
Medical Mx
Minoxidil used in conc of 2% in
women and 2 & 5% in men
- most effective in whom balding process
is at an early stage
- benefit most pronounced in 1 st 6 months

Probable M/a direct effects on keratinocyte

differentiation and proliferation within the hair
follicle, alteration of androgen metabolism and
improved vascularisation in dermal papilla
Side effects of minoxidil mild irritation and
hypertrichosis of temples
- Clinical regression occurs after 3 months of
stopping treatment
- To maintain beneficial effect, applications
must continue twice daily for rest of their lives

Other uses of minoxidil

1. Occassionally in alopecia areata
2. Alopecia caused by chemotherapy
3. Stimulation of growth in hair
transplants
4. Prevention of hair loss occurring as a
complication of cosmetic surgery

 Finasteride

Selective antagonist of 5 alpha

reductase II
Reduces DHT and limits follicular
miniaturization, encourages growth of
terminal hairs
Dosage 1 mg/day
Maximal follicles recruited by 1 year

Side effects are loss of libido, erectile

dysfunction
Finasteride is a teratogen but no
adverse pregnancy outcomes have been
reported
Has no effect on spermatogenesis or
semen production
Dutasteride combined type I and II
inhibitor used mainly in BPH

 Spironolactone,

cyproterone acetate and

flutamide are effective in arresting AGA
in women
Use of flutamide is limited due to rare
but potentially fatal hepatotoxicity

Telogen effluvium

1.

Premature termination of anagen

Five functional types
Immediate anagen release
Follicles are stimulated to leave anagen and
enter telogen prematurely
Increased hair shedding 2-3 months later
Common after severe illness or drug induced
hair loss

Reversal with resumption of the normal

cycle
2.Delayed anagen release
Postpartum hair loss or telogen
gravidarum
Seen after 2-3 months of childbirth
3.Short anagen syndrome idiopathic
shortening of anagen

4. Immediate telogen release

Shortening of normal telogen
Minoxidil can cause this
5. Delayed telogen release
Occurs after a prolonged telogen f/b transition
to anagen
Occurs in animals with synchronous hair
cycles during shedding of winter coats
May occur seasonally in some humans

Acute telogen effluvium

Occurs

2-3 months after high fever,

surgical trauma, sudden starvation or
haemorrhage, emotional stress
Telogen gravidarum or discontinuation of
OC pills
Daily losses from under 100 to over
1000
May be severe but never total
Spontaneous regrowth in 3-6 months

 Hair

pull test is positive but a ve test

dosent exclude it
Strongly positive for telogen hairs at the
vertex and scalp margins
Trichogram shows >25% telogen hairs

Chronic diffuse telogen hair loss

Due

to prolonged or repeated insults

Telogen hair shedding for >6 months
May be primary or secondary to other
causes
Thyroid disorders hair loss is
reversible except in long standing
hypothyroidism when hair follicles are
atrophied

 Profound

iron deficiency
Can be corrected by iron replacement
Hair follicles may temporarily fail to reenter anagen
Important d/d is AGA which is easier to
prevent progression than stimulating
regrowth in females
Punch biopsy can clarify the diagnosis

 Acrodermatitis

enteropathica and acquired

zinc deficiency due to long standing parenteral
nutrition
Diffuse hair loss with no other signs is never a
result of zinc deficiency
Crash dieting with severe protein-calorie
restriction, marasmus, hypoproteinemia,
pancreatic disease, EFA deficiency seen in
parenteral nutrition and hypervitaminosis A

 Liver

disorders and CRF can produce sparse

scalp hair
May be an early sign of Hodgkins disease
SLE and DM, secondary syphilis
Etretinate and acitretin commonly cause a
dose related hair loss but isotretinoin less
commonly causes it cause a telogen
anchorage defect and reduce duration of
anagen

Chronic telogen effluvium

Occurs

in middle aged women b/w 30-50

years of age
Idiopathic self limiting condition with
increased telogen hair shedding of
atleast 6 months duration
No widening of central parting and no
follicular miniaturization
It is believed to be related to shortening
of anagen

 Women

report ability to grow their hair very

long in childhood and report a high hair density
prior to hair loss
Hair pull test is positive over vertex and scalp
margins
Scalp biopsy taken from vertex differentiates it
from AGA
Histology in CTE is normal but anagen :
telogen ratio is 8:1 and terminal : vellus hair
ratio is normal

 Mainly

supportive treatment required

Hair growth recovers within 6 months
Iron supplements can be given
Minoxidil 2% is also used

Thank You