Alopecia - scaring & non-scaring type.

Swetha Saravanan

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CONTENT

Hair Science

Classification Of ALOPECIA

Hair Loss: Examination and Investigation

Management

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Hair Science

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Hair is a cutaneous appendage originally

evolved in mammals as a protective coat.

It is simple in structure, but has important

functions in social functioning

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Anatomy

The Anagen hair follicle is divided into:

Upper Segment

1. Infundibulum

2. Isthmus

Lower Segment

1. Stem

2. Bulb

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Adamson’s Fringe Upper part of the bulb.

Keratogenous zone.

Divided into 6 layers:

1. Medulla

2. Cortex

3. Hair cuticle

4. Cuticle of inner sheath

5. Huxley’s layer

6. Henle’s layer

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Follicular Papilla Varies according to the phase of hair cycle.

Composed - specialized fibroblast like cellsembedded in extracellular matrix.

Contains a loop of capillary blood vessels.

Volume of dermal papilla maybe responsible for

controlling size of hair follicle.

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Hair Shaft 3 layers :

MedullaCortexHair Cuticle

Medulla 1. Maybe continuous, interrupted or absent.

2. Contains few layers of rounded cells containing glycogen.

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Cortex1. Forms bulk of the hair shaft.

2. Consists of numerous layers of flattened elongated cells packed together.

Hair Cuticle1. Consists of 5 – 10 layers of flattened cells arranged in

overlapping “roof – tile” pattern.

2. The upwards pointing edges of the hair cuticle interlock with the downwards pointing edges of cuticle of inner sheath.

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Inner Root Sheath1. 3 layers :

Cuticle

Huxley’s layer

Henle’s layer

2. At the Isthmus the IRS disintegrates

Outer Root Sheath1. Most peripheral part of hair follicle.

2. Keratinize at the level of Isthmus.

3. Occasionally “companion layer” maybe seen in

between IRS and ORS.12

Ultra structure of Hair Hard keratin with high

sulfur content.

High sulfur content -extraordinary tensile strength.

S-H linkages of cysteine atthe bulb are converted toS-S linkages of cysteinehigher up.

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Functions of Hair Tactile perception

Protection of scalp from sunlight and trauma.

Protection of eyes from foreign bodies, sunlight & sweat

Screening nasal passages.

Reduce friction in intertriginous areas.

Disseminates apocrine odor

Contributes to psychological perception of beauty & attractiveness.

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Hair Cycle

Hair growth occurs in 3 stages : Anagen

Catagen

Telogen

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Anagen• Period of active hair growth.

• Duration of this phase resp. forfinal length of the hair.

• Usually lasts for 2 – 6 years. • Duration of Anagen genetically

determined.• About 85% of all hairs are in

this phase at any time.

• Onset of mitotic activity ofepithelial cells in Dermalpapilla.

Lower part of follicle elongates downwards along a preformed dermal tract ( stele ).

Dermal papilla expands .

A network of capillary blood vessels develop around the lengthening follicle.

Epithelial cells in the hair bulb undergo vigorous proliferative activity.

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The melanocytes become active adding colourto this newly forming hair.

Anagen consists of 6 substages.

Differences in the length of hair is due to variable duration of the last stage ( VI ).

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Catagen• Short transition stage that

occurs at the end of the anagen phase.

• Signals the end of active growth of hair.

• Usually lasts about 2 – 3 weeks.

• At the end of Anagen, epithelial

division declines and ceases.

• Proximal end of the hair shaft

keratinizes to form a club

shaped structure.

Lower part of the follicle involutes by

apoptosis.

Basement membrane surrounding the folliclebecomes thickened to form “glassy membrane”.

Base of the follicle along with dermal papillamoves upwards to lie below the level of

Arrector muscle attachment.

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Telogen• Resting phase of the hair

follicle.• Usually lasts for about 3

months.

• About 10 – 15% of all hairs

are in this phase at any time.• Quiscient period between

completion of follicular regression and onset of next anagen phase.

• Resting club hair lies within an epithelial sac.

Types of HAIR

Lanugo (wool like)

Fine, soft, unmedullated, unpigmented

Vellus Hair ( ≤0.03 mm )

Soft, unmedullated, pigmented

Terminal Hair ( ≥0.06 mm )

Coarse, medullated, pigmented

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Modulators of Hair Follicle Cycling in Humans

MODULATOR ACTION

Endogeneous

Androgens Promote miniaturization of follicles & shorten duration of the anagen stage in androgen sensitive areas of scalp;Enlarge follicles in androgen- dependent areas during adolescent

Estrogens Prolong anagen stage;Post partum reduction in estrogen- telogeneffluvium

Growth hormone Acts synergistically with androgen in adolescence

Prolactin Can induce hirsutism

Thyroxine Low levels can cause telogen effluvim;High levels may have similar effect 26

ExogeneousAnabolic Steroids Accelerate androgenetic alopecia :

Aggravate hirsutism

β Adrenergicantagonist

Causes telogen effluvium

Cyclosporin Hypertrichosis

Estrogen Prolong duration of anagen stage

Finasteride Blocks 5 α Reductase type II

Minoxidil Induces and prolongs anagen stage & Vellusterminal hair

OCP Cessation may cause telogen effluvium

Phenytoin Hypertrichosis

Retinoids Premature onset of catagen stage27

Rate of Hair Growth :

Part of the Body Rate of Growth

Scalp 0.45mm/day

Beard 0.35mm/day

Extremities 0.25mm/day

Forehead(vellus hair) 0.03mm/day

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Role of Growth Factors & Cytokines in Hair FollicleDevelopment,Hair growth & Hair Cycle Activity

EGF 1. Delays follicular development2. Retards hair growth & cycling3. Induces follicle regression & catagen–like changes in vitro4. Stimulates elongation of hair.

TGFα 1. Controls normal positional development of hair follicle2. Retards hair growth in vitro in mice

aFGF &

bFGF

1. Responsible for formation & maintenance of perifollicularblood vessel

2. Important for skin appendage morphogenesis & theirformation

FGF4 1. Necessary for follicular development & epithelialregeneration.

FGF5 1. Hair elongation inhibitor2. Initiates transition from anagen to catagen phase 29

VEGF 1. Responsible for maintenance of theperifollicular capillaries in anagen

TGFβ -1,2,3 1. Inhibits follicular development2. Gene over expression in epidermis marked

reduction of epidermal & follicular proliferation& dec. number of follicles in mice

BMP-2, BMP-4 1. Necessary for epithelial regeneration

NBFβ 1. Probably trophic functions for neurons2. Probably responsible for maintenance of

perifollicular nerves in anagen

TNFα 1. Responsible for induction of apoptosis

PDGF-A,B 1. Important in follicular development &vasculogenesis

2. Stimulates hair canal development 30

Classification of ALOPECIA

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Alopecia is defined as “ absence or loss of hair”.

It’s a chronic disorder secondary to the disease of

either the hair follicle, hair shaft or the scalp.

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Pseudoalopecia is defined as acute or chronic breakage

of hair due to congenital or acquired hair shaft

abnormalities secondary to trauma or chemicals.

Its characterized clinically by unintended short hair.

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Noncicatricial AlopeciaPhysiological Alopecia of infants, post-partum alopecia

Alopecia areata

Telogen effluvium

Infections Dermatophytosis, bacterial & spirochaetal infections

Chemicals & drugs: Thallium/Heparin/cancer chemotherapy/hypervitaminosis A

Physical trauma(self induced)

Trichotillomania, scratching of neurodermatitis

Endocrinopathy Hypo/ hyperthyroid, hypo/hyperparathyroid

Physical agents Mild trauma, epilating dose of radiotherapy, short term hair traction

Systemic agents SLE, dermatomyositis, sarcoidosis, Langerhan’s cell histocytosis, amylodosis 34

Cicatricial Alopecia

Physical trauma Long term traction of hair, x-ray overdose burn

Infections BacterialDermatophytosisViral

Chemical injury Caustics

Cutaneous diseases DLE, FLP,pseudopelade

Destructive neoplasms & granulomas

Psychogenic conditions Neurotic excoriating tactile injury to skin

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Miscellaneous

Androgenetic alopecia(common baldness)

Congenital alopecia

Hair shaft abnormalities: monolothix, pili annulati, wooly hair

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Tricotillomania 37

Moth –eaten appearance -Syphilis 38

FLP 39

Folliculitis 40

DLE 41

Alopecia AreataSyn. Pelade, Area Celsi

Chronic inflammatory dermatologic disordercharacterized by patchy loss of hair without

atrophy

Described by Cornelius Celsus (AD 14-37)

Term was coined by Sauvages in 1760

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Etiology Genetic factors(10- 20%), positive family history

Autoimmunity

Stress

Diet

Infectious agent

Vaccination

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Genetic factors

1. MHC class I antigen HLA-DR4, DR 11 & DQ-3

2. DR4 & DR5 – ass. with severe type of AA.

3. TNF alpha has inhibitory effect on hair growth.

4. Chromosome 21

5. Atopy – early age onset & severe AA

Autoimmunity

1. Ass. – thyroid disease, anemia, DM, vitiligo, psoriasis.

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Clinical Features Smooth, localised, well demarcated patches

Progress circumferentially

Single / multiple

Scalp (90%), other regions also involved

Hairs are short, easily extractable broken ones,called “exclamation mark” seen at margins

1 – 5 % of AA AT – 2 yrs

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White hair- relatively spared, hence patients withcanitis, the onset of sudden diffuse A.A may result in hair

‘ going white’ over night.(canites subita)

Shuster described Coudability hairs ( a kink in the

normal looking hairs, 5-10mm above the surface ,whenthe hair is bent inwards).

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Nail changes Nail dystrophy

Pitting

Transverse /longitudinal rows

Beau’s lines

Onychorrhexis-nail plate split

Nail loss total

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Poor prognosis Atopy

Other immune disease

Family H/o AA

Excessive hair loss

Oophiasis pattern

Nail dystrophy

Poor patient compliance

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Investigations Hair – Pull test

Hair pluck test

Dermoscopy

SALT score ( severity of alopecia tool score)

Optical Coherence Tomography- detect hair shaft abnormalities.

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Histopathology Peribulbar and intrabulbar inflammatory infiltrate

concentrated in and around hair bulb giving “swarm

of bees” appearance.

Infiltrate mostly of T lymphocytes and macrophagespresent around the matrix and dermal papilla.

Miniaturization of hair follicles.

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CS’s 1. Hydrocortisone acetate 25mg/mL

2. Triamcinalone acetonide 5-10mg/mL

3. Accelerates regrowth

4. SE- Atrophy,pain,tingling - reversible

Anthralin1. .25%-.1% used

2. SE-irritation, scaling, folliculitis, stains

3. 1st line Rx in children

4. Growth occurs in 3mths

5. Total application time 6mths

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Alopecia totalis treated with topical immunotherapy (2,3-diphenylcyclopropenone): (A) before treatment; (B) unilateral hair regrowth after 15 weeks of unilateral treatment; (C) complete regrowth after 42 subsequent weeks of bilateral treatment. Courtesy of R Happle, University of Marburg, Marburg, Germany

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Telogen Effluvium

The term Telogen effluvium –first coined by Kligman.

Telogen hair- resting hairs with non pigmented club tip at

the proximal root & easily plucked from the scalp.

In this cond. premature covertion of anagen hair to

telogen hair takes place resulting in disproportionate

shedding & dec. in the total number of hair.

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EtiologyPhysiologic1. Physiologic effluvium of new born2. Postpartum effluvium3. Early changes of androgenic alopecia4. Injury/ stress5. High or prolonged fever6. Severe infection7. Severe chronic illness8. Severe psychologic stress9. Major sugery10. Hypothyroidism & other endocrinopathies11. Severe dieting or malnutrition

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Drugs and Toxins1. Antikeratinising agent ( etretinate)

2. Anticoagulants ( heparin)

3. Antithyroid agents

4. Alkylating agents

5. Anticonvulsants

6. Hormones

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Diagnosis Detailed patient history (drug/diet)

Complete blood count

TFT

Hair –pull test

Trichogram

ANA titre

Sr. Zinc levels

VDRL

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Treatment Normal hair growth occurs with time & resolution of

underlying causes.

No specific treatment – required

In case of no recovery – minoxidil can provide some benifits

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Androgenetic Alopecia Androgenic alopecia is hereditary thinning of the hair

caused due to androgens in genetically susceptible men

& women.

In males, male pattern hair loss / common baldness.

In females, female pattern hair loss.

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Clinical features MPHL- easily recognized

1. Described – Hamilton & Norwood

2. Thinning of hair in frontal & vertex area with progression of hair loss

3. Marginal parietal & occipital hair – retained.

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FPHL- differ from men.

1) Described by Ludwig

2) Diffuse thinning over the crown with no H/O shedding.

3) In women, hair thinning begins – frontal & later involve the entire scalp sparing the frontal hairline.

4) Hair density remains the same, hair no longer grows into its previous length.

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Hair Loss Severity Classification

For MPHL, Norwood/ Hamilton scale

For FPHL, Ludwig’s classification scale

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Pathology

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Marked reduction in terminal hairs

Miniaturization of hair follicles increase in secondary

vellus hairs

Mild perifollicular infiltrate mostly lymphohistiocyticwith or without concentric layers of perifollicularcollagen deposition

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Treatment

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Hair Loss: Examination &

Investigation

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Evaluation of Hair lossHistory & Examination1. Time period of hair loss(congenital, acquired)

2. Progression of hair loss

3. Any positive family history

4. H/o G.I dysfunction, thyroid gland dysfunction, psychological disorders

5. H/o any surgical intervention / chronic illness

6. All medications

7. In females, menstrual & obstetric history

8. Hair care routine/ hair products79

Examination

Physical appearance of hair and pattern of hair loss

helps in diagnosis of possible etiology.

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Disease Common pattern seen

Diseases with patterned loss

Androgenic alopecia Women – central thinning

Men -- ‘M’ shaped thinning

Syphilis ‘Moth eaten ‘ appearence

Trichotillomania Bizarre, incomplete thinning ,stubble

Diseases with diffuse hair loss

Alopecia universalis Body & scalp involved

Telogen effluvium alopecia totalis , chemotherapy or drug induced metabolic disorders

Diseases with focal loss

Alopecia areata Patchy hair loss

Tinea capitis Fragile & easily broken hair

Trichotillomania Patchy, incomplete thinning with stubble

Traction alopecia Frontal & temporal loss of hair

Cicatricial alopecia Presence of cellulitis or folliculitis81

Blood Investigations Complete blood count

VDRL

Sr. iron

Sr. ferritin

Total iron binding capacity

TFT

Antinuclear factor –DLE

Hormone levels

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Noninvasive methods

Scalp score

Regional Hair pattern

Contrasting Felt examination

Daily hair Counts

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Scalp Scores Global photographs

Head shots taken at a short distance away from the

patient who is seated in front of a plain cloth.

Standard global views- vertex, midline, frontal, temporal.

GB’s – taken before and at various stages of treatment

Rating – 7 point scale (-3 to +3)

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Macrophotographs – 4 times magnification

_ density & diameter of hair

Area 14mm x 13mm

Density graded 1 to 6

1- fewer than 4 hairs

6- more than 40 hairs

Diameter graded 1 -thin

2 -medium

3 -thick

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Regional Hair pattern

The pattern of hair loss in androgenic alopecia is well defined & distinct in both men and women.

Norwood – Hamilton scale - male

Ludwig scale - female

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Norwood-Hamilton scale of male pattern baldness

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Ludwig scale for Women

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Contrasting Felt Examination AIM- To see the short, miniature hairs of the scalp.

PROCEDURE- An index card with black felt glued on one side and white felt on the opposite side is used.

After parting in the hair, the index card is held along the scalp

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INFERENCE- Fine short

hairs with broken or tapered

distal tips project up along

the edge of the felt.

These miniature hairs –

in the androgen dependent areas both men & women.

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Daily Hair Counts Useful for quantitative assessment of the actual number of

hairs shed daily in patients with complaints of excessive

shedding.

Collect for 14 consecutive days

Average daily loss – 30-70 hairs /day.

If >70 hairs – microscopic examination is done todetect pathology.

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Semi-invasive methods Hair Pull Test

Hair Feathering Test

Trichogram( Hair Pluck Test)

Unit Area Trichogram

Phototrichogram & Videotrichogram

Digital Epiluminescence Microscopy

Global Photographs in Phototrichogram

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Hair Pull Test

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Telogen hair is easily extracted than anagen hair

PROCEDURE-

1. About 60 hairs- pulled with constant traction

2. Bulb of extracted hair is examined

3. The number of telogen hair is counted

4. Expressed as percentage of total hair pulled

Upto 7% - normal

>10% - effluvium

Telogen effluvium, anagen effluvium, loose anagen syndrome,early cases of patterned alopecia and the advancing edge ofalopecia areata

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Other drawbacks of this test: Washing hair before- may give false low No. of telogen hair.

Frequency of telogen shedding varies day to day.

Seasonal variation – inc. spring & autumn.

More in the frontal & vertex region compared to occipitalregion.

Alopecia - failure of development of new anagen hair ratherthan increased telogen hair ratio. In these patients hair pulltest is normal.

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Hair Feathering Test AIM- detecting abnormal hair fragility and hair shaft

breakage.

PROCEDURE-

1. Distal 2 to 3cm – hairs in involved areas – grasped &

pulled.

2. Grasped hair - checked for broken fragments

3. Microscopic examination- confirms nature of hair

shaft defect & type of fracture.

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Trichogram (Hair Pluck Test)

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The plucked hairs are arranged side by side on a glass slide and taped

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Anagen hair - forcibly

plucked terminal anagenhair showing the pigmented

bulb with 'hockey-stick'appearance.

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Telogen hair - forcibly plucked

early telogen hair showing the

hypopigmented, club-shaped

cornified bulb with remanents of the cornifiedepithelial sac.

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Unit Area Trichogram In a marked out area (30mm2) – hair is epilated- the

proportion of various type of hair is counted.

A/T ratio, shaft diameter, density.

Av. diameter – healthy hair- ≥ 80μ𝑚.

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PhototrichogramPhototrichogram was introduced by Saitoh in

1970

Technique that allows in vivo study of physiology of the hair cycle and measurement of various hair

growth variables.

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These variables are:

1. Hair density

2. Hair thickness

3. Hair length

4. Linear growth rate.

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PROCEDURE-

Day 0 t(0) -Clipping the hair short (1mm) in a marked

area.

Photograph is taken- high magnification

Day 2 (t2)

After 48 h, the second photograph was taken

Patient advised – not to wash hair

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INFERENCE-

1. Hair variables at Day 0

Density of hair in the specified area

Length of hairs (L1)

2. Hair variables at Day 2

The length of hairs (L2)

Hair growth in mm/day, (L2-L1)/2

Number of hairs showing hair growth.(Anagen hairs)

Number of hairs not grown. (Telogen hairs)

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Invasive MethodsScalp Biopsy

Indications:

1. Cicatricial alopecia

2. Undiagnosed - non-cicatricial alopecia

Type:

1. Vertical

2. Horizontal

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Terminal anagen hair-showing the IRS and the ORS109

AGA Male scalp- follicular unit with three vellus hairs ; one terminal and one secondary hair germ 110

Vellus hair – IRS thicker than the hair shaft111

Medical Management of

Androgenic Alopecia

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Treatment options for AGA in Men

Hormone modifiers

Androgen blockade

1. 5 α- reductase inhibitors (finasteride)

2. Androgen-receptor inhibitors(Spironolactone,cyproterone acetate)

Estrogen -mediated

1. Hormone replacement

2. Oral contraceptives

Biologic response modifiers

1. Minoxidil

2. Tretinoin 113

Minoxidil

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Main actions of Minoxidil on the hair follicle;

1. Inc. in the proportion of hair - anagen phase by promoting premature entry of the hair follicle into the anagen phase

2. Prolongs the length of anagen phase

3. Dec. the no. of follicles – telogen phase

4. Inc. – hair follicle size & hair diameter

On topical application- rapid inc. of hair growth is seen as soon as

6 to 8 weeks & max. effect at 12 to 16 weeks.

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Adverse Effects

Head ache

Mild irritant dermatitis

Occasional hirsutism

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Finasteride It’s a competent & specific inhibitor – type II 5α-reductase

enzyme.

Prevents testosteroneDHT.

65% bioavaiability.

90% of circulating drug bound to plasma protein.

Crosses the BBB.

Metabolized in liver, via cytochrome P450 enzyme.

Metabolites formed in liver –excreted in faeces with 40%in urine.

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Indications & Dosage Androgenic alopecia with mild to moderate hair loss

of vertex & ant. mid scalp area.

Its effectiveness in bitemporal recession has not been

established.

Recommended dosage- 1mg orally OD daily use ≥3 months.

Withdrawal of drug – revesal effect in 12 months.

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Adverse effectsBreast tenderness & enlargement

Hypersensitivity reactions-

Pruritus, rash, urticaria , swelling of lips &

face, testicular pain.

Erectile dysfunction.

Less libido.

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Contraindications In women- child bearing group & pregnant women

In children

In patients hypersensitive to drug.

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Surgical Treatment Hair transplantation

Hair weaving

Laser hair transplant

Follicular unit transplant

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Reference Text book on Alopecia – Dr Narendra G. Patwardhan

Rook’s text book of dermatology

Review article on Alopecia Areata - IJDVL

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THANKYOU

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Alopecia - scaring & non-scaring type.

Health & Medicine

Transcript of Alopecia - scaring & non-scaring type.