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Hair Examination and Hair Diseases MUDr. M. Arenbergerová, PhD.
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PICTURE 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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PICTURE
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PICTURE
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PICTURE 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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PICTURE Hair can absorb water, fluids or chemicals
Hair can be coated with different materials PICTURE
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PICTURE 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
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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: /den Hair can grow: cm in length Hair growing: % Hair resting: %
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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
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PICTURE Hair cycle Phase Duration Percent anagen 2-6 years 80-90%
catagen 1-2 weeks 1-3% telogen 2-4months 10-20% PICTURE
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PICTURE 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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PICTURE
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PICTURE
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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 PICTURE
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Androgenetic alopecia-ethiology
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) 79 % SHBG 20 % albumin 0,5 % CBG 50 % more androgen receptors than women SHBG: sex hormone-binding globulin, CBG: steroid hormone receptors
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Hair follicle-androgen metabolism
5 alpha-reductase testosterone (T) dihydrotestosterone (DHT) 3x higher content of 5 alpha reductase
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PICTURE
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3x higher content of 5 alpha- reductase PICTURE
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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
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PICTURE 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 PICTURE Hamilton-Norwood scale
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PICTURE Klinický obraz FAGA
Slow recession in frontal region, distinct centre parting, front hairline is still present Ludwig scale FPHL - female pattern hair loss
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PICTURE
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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
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Follicle miniaturization
Change of follicle structure: follicle miniaturization Terminal hair becomes thin, short, velus-like
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Diagnostics Traction test +/- Trichogram, fototrichogram
Histological examination Hormonal examination man: T, DHT, SHBG woman: T, DHT, SHBG, prolactin, follicle stimulating hormone (FSH), dihydroepiandrosterone (DHEA), dihydroepiandrosterone-sulphate (DHEAS), +/-cortisol. Examination: day of menstruation cycle, min. 3 month after stop of contraceptives
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Diagnostics-women Family history Gynecological history
Pharmacological history Examination: Signs of hirsutism, acne, hypetrichosis, seborrhea tumors, hormonal syndromes SAHA syndrome (female hyperandrogen syndrome): seborrhea acne hirsutism alopecia AGA (mamle type of AGA)
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Diferential diagnostics of AGA
PICTURE Acute telogen effluvium
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PICTURE
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PICTURE Alopecia areata
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Alopecia universalis PICTURE
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PICTURE alopecia areata in a child
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PICTURE Scarring alopecia
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PICTURE Diffuse effluvium
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Trichogram Preparation 5 days NOT wash hair, NO hair cosmetics
Hair collection Diffuse effluvium frontal and occipital part Androgenetic alopecia Alopecia areata spot-edge and opposite site
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Collection Forceps Ca. 50 hairs Epilation Method Microscopic examination of hair bulb and hair shaft Slide- turpentine-cover slip After 24 h microscopic examination (HP 25 x)
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PICTURE Trichogram anagen hair 80% dysplastic anagen hair up to 30%
medulla cortex PICTURE anagen hair 80% dysplastic anagen hair up to 30% catagen hair 1-3% telogen hair 20% dystrofic hair up to 2%
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PICTURE Hair structural defect normal hair pilus anulatus monil-
ethrix pilus tortus 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
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PICTURE Trichotillomania
Trichotillomania: obscessive pulling out of own hair.
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PICTURE
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PICTURE
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Alopecia areata Autoimunne disease Polygenic inheritance
Focus: chronic infection More frequent in chromosomal defects (chromosome 21) metabolic x emotional influence?
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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
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Alopecia areata PICTURE
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Alopecia areata PICTURE Peribulbar T- lymphocyte infiltration
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Clinical picture Bald spots (spot baldness) Not painful
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
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PICTURE Nails in Alopecia areata
Onychodystrophy - trachyonychia, koilonychia, leukonychia, pitting
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Alopecia areata multilocularis
PICTURE
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Alopecia areata-ophiatic type
PICTURE
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PICTURE
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PICTURE Syphilitic Alopecia
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PICTURE Scarring Alopecia
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PICTURE 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.
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Therapy PICTURE
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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
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after PICTURE before
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after PICTURE before
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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
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Digital phototrichogram
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Digital phototrichogram
camera extension spot 1 cm2
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Digital phototrichogram
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Digital phototrichogram
Epilation: 2 mm
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Digital phototrichogram
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Digital phototrichogram
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