SEMINAR ON ALOPECIA

Chairperson : 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. Speakers :

Date & Time

5th April, 2005 at 2.00 pm.

Department of Dermatology, MMCH. & Renata Limited

Organized by :

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. Outer root sheath.

Mesodermal origin :

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

Higher incidence of alopecia areata in patients of1. Atopic dermatitis. 2. Autoimmune disease * SLE * Thyroiditis. * Myasthenia gravis. * Vitiligo. 3. Lichen planus. 4. Down syndrome.

ASSOCIATED DISEASE

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 markerEarly 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 : sites : Twenties or early thirties. 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

patternof

diffuse
density

and
and

reduction

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. II. Short anagen- by drugs, fever, physiological stress. Prolonged anagen- Pregnancy. follicle.

III. Conversion of telogen follicle to anagen

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