ALOPECIA
ALOPECIA
ALOPECIA
Palms Clitoris
Soles Prepuce
Ectodermal origin-
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
C. Hair breakage-
i. 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. Mixed-
i. 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 abnormality-
i. Hair breakage.
ii. Unruly hair.
Diffuse Hair Loss (Contd.)
• 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 Infections
Inflammation agents
Release of cytokines
Attack on
melanogically active anagen fallicle
(incomplete revcovery).
!
CLINICAL FEATURE (CONTD.)
• Few resting hairs may be found within the patches.
2. Trichotilomania.
3. Secondary syphilis
5. Alopecia neoplastica.
• 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
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 tree pattern”- diffuse and
progressive reduction of 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.)
• Hirsutism.
• Menstrual irregularities.
androgen hypersensitivity.
TREATMENT
1. Topical Minoxidil (2% & 5%)
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