Hair Examination and Hair Diseases

MUDr. M. Arenbergerová, PhD.

Hair is composed of strong structural protein called keratin. This is the same kind of protein that makes up the nails and the outer layer of skin.

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Each strand of hair consists of three layers.An innermost layer or medulla which is only present in large thick hairs. The middle layer known as the cortex. The cortex provides strength and both the color and the texture of hair. The outermost layer is known as the cuticle. The cuticle is thin and colorless and serves as a protector of the cortex.

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•Hair can absorb water, fluids or chemicals•Hair can be coated with different materials

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Dermal papilla

At the base of the hair follicle is the dermal papilla. The dermal papilla is feed by the bloodstream which carries nourishment to produce new hair. The dermal papilla is a structure very important to hairgrowth because it contains receptors for male hormones and androgens. Androgens regulate hairgrowth and in scalp hair Androgens may cause the hair follicle to get progressively smaller and the hairs to become finer in individuals who are genetically predisposed to this type of hair loss.

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Hair examination

•Medical history•Lost hair count•Traction test•Trichogramm (hair pluck test)•Mycological examination•Biopsy•Hormonal examination•Microscopic examination of hair structure•Digital Phototrichogramm

Hair

•Number of hairs: 100 000 – 150 000•Density: 175-300/cm²•Thickness: 0,1-0,25 mm•Hair growth: 0,35 mm/day (1 cm per month)•Hair lost: 25-100/den•Hair can grow: 12-84 cm in length•Hair growing: 90-95 %•Hair resting: 5-10 %

Hair cycle

Phase Duration Percent

anagen 2-6 years 80-90%

catagen 1-2 weeks 1-3%

telogen 2-4months 10-20%

Hormons Scalp hair Body hairs

androgens

estrogens

Hair cycle

Phase Duration Percent

anagen 2-6 years 80-90%

catagen 1-2 weeks 1-3%

telogen 2-4months 10-20%

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anagen catagen telogen

1-epidermis, 2-infundibulum, 3-sebaceous gland, 4-m. arrector pili,5-hair shaft, 6-hair matrix, 7-blood vessel, 8-dermal papilla

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Androgenetic alopecia (AGA)• Most frequent disease of hair follicle• 50 % men > 40 is affected with MAGA• 50 % women > 50 is affected with FAGA

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• Genetic disposition (polygenic inheritance x

• AD heredity?)

• Androgen level (1 % free androgen, 99 % bound to plasmatic proteins)

• Number of androgen receptors

• Age (higher age: physiologic lost of hair follicle density)

Androgenetic alopecia-ethiology

79 % SHBG

20 % albumin

0,5 % CBG50 % more androgen receptors than women

SHBG: sex hormone-binding globulin, CBG: steroid hormone receptors

Hair follicle-androgen metabolism

testosterone (T) dihydrotestosterone (DHT)

5 alpha-reductase

3x higher content of 5 alpha reductase

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3x higher content of 5 alpha- reductase

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Effect of androgens on hair follicles

• Binding of androgens to androgen receptors on follicle keratinocytes

• Active complex

• Active complex migrates to cell nucleus

• Modificated protein synthesis in cells

• Different dynamics of hair cycle in hair follicle

• Reduction of anagen phase

• Regressive metamorphosis

Regressive metamorphosis

Hair follicles sensitive to DHT begin to miniaturize, shortening the lifespan of each hair follicle affected. Eventually, these affected follicles stop producing cosmetically acceptable hair.

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Clinical image of MAGA

Hamilton-Norwood scale

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Klinický obraz FAGA

Ludwig scale

Slow recession in frontal region, distinct centre parting, front hairline is still present

FPHL - female pattern hair loss

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Vlasový cyklus u AGA

•Anagen 2-7 years•In MAGA anagen phase shortens from years to months•Telogen phase is expanding•Anagen/telogen ratio changes form 6 to 8 : 1 to abnormal ratio 0,1 to 3 : 1 •Finally the anagen phase is so short, that the hair doesn´t reach the skin surface - alopecia

Follicle miniaturization

•Change of follicle structure: follicle miniaturization

•Terminal hair becomes thin, short, velus-like

Diagnostics

•Traction test +/-•Trichogram, fototrichogram•Histological examination•Hormonal examination

man: T, DHT, SHBGwoman: T, DHT, SHBG, prolactin, follicle stimulating hormone (FSH), dihydroepiandrosterone (DHEA), dihydroepiandrosterone-sulphate (DHEAS), +/-cortisol. Examination: 3.-5. day of menstruation cycle, min. 3 month after stop of contraceptives

Diagnostics-women

•Family history•Gynecological history•Pharmacological history

•Examination:

Signs of hirsutism, acne, hypetrichosis, seborrheatumors, hormonal syndromes

SAHA syndrome (female hyperandrogen syndrome):•seborrhea•acne•hirsutism•alopecia AGA (mamle type of AGA)

Diferential diagnostics of AGA

•Acute telogen effluvium PICTURE

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Alopecia areata

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Alopecia universalis

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alopecia areata in a child

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Scarringalopecia

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Diffuse effluvium

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Trichogram

Preparation 5 days NOT wash hair, NO hair cosmetics

Hair collectionDiffuse effluvium frontal and occipital partAndrogenetic alopecia

Alopecia areata spot-edge and opposite site

Collection •Forceps•Ca. 50 hairs •Epilation

MethodMicroscopic examination of hair bulb and hair shaft

•Slide- turpentine-cover slip•After 24 h microscopic examination (HP 25 x)

Trichogram

medulla

cortex

anagen hair80%

dysplastic anagen hairup to 30%

catagen hair1-3%

telogen hair20%

dystrofichairup to 2%

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Hair structural defect

normal hair

pilus anulatus

monil-ethrix

pilustortus

trichor-rhexis trichoptilosis

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Trichorrhexis nodosa

Symptoms of TN include:hair that breaks easily, patches of hair loss or extremely short hair, thickened or thinned areas along the hair shaft,chronically split ends with whitish discoloration.hair straightening, overheating by a hair dryer, frequent swimming in chlorinated water

Trichotillomania

Trichotillomania: obscessive pulling out of own hair.

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Alopecia areata• Autoimunne disease• Polygenic inheritance• Focus: chronic infection• More frequent in chromosomal defects (chromosome

21)• metabolic x emotional influence?

Pathogenesis

• Cell lymphocyte cluster around affected anagen follicles, causing inflammation

• Relase of cytotoxic substances• Apoptosis of hair follicle keratinocytes• Toxic disruption of hair follicle• Telogen phase prolongation• Exclamation mark (!) type of hair

Alopecia areata

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Alopecia areata

Peribulbar T- lymphocyte infiltration

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Clinical picture• Bald spots (spot baldness)

alopecia areata monolocularis alopecia areata multilocularis alopecia areata barbae alopecia totalis alopecia universalis

• Not painful

• Fall out over a short period of time

• Frequent association with asthma bronchiale, atopic dermatitis, hypothyroidism

Nails in Alopecia areata

Onychodystrophy - trachyonychia, koilonychia, leukonychia, pitting

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Alopecia areata multilocularis

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Alopecia areata-ophiatic type

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Syphilitic Alopecia

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Scarring Alopecia

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Aplasia Cutis Congenita

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Trichoscopy

• trichoscopy shows regularly distributed "yellow dots" (hyperkeratotic plugs), small exclamation-mark hairs, and "black dots" (destroyed hairs in the hair follicle opening)

Trichoscopy is method of dermoscopy for visualization of scalp at 10 to 70-fold magnification.

Therapy

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Therapy

•Spontaneous regression•Corticosteroids•Immunosupressants•Diphenylcyclopropenone (diphencyprone)

Diphencyprone •Acts as a local irritant, triggering a local sensitization •Triggers an immune response that opposes the action of the autoreactive cells that otherwise cause hair loss •Regrowth of 40% pts. at 6 months, being sustained in two thirds of these after a 12-month-follow up-period

before

after

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before

after

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Phototrichogram

Phototrichogram

• Non-invasive method

• 2 pictures of a certain spot at the scalp

• Time span (24-72 h)

• Comparison of pictures with digital software

• Anagen hair grow

Digital phototrichogram

camera extension spot 1 cm2

Digital phototrichogram

Digital phototrichogram

Epilation: 2 mm

Digital phototrichogram

Digital phototrichogram

Digital phototrichogram