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Alopecia - scaring & non-scaring type.

This document discusses hair science and the classification of alopecia. It begins by covering hair anatomy and the hair cycle process. It then classifies different types of alopecia as either noncicatricial (non-scarring) or cicatricial (scarring). One type covered in detail is alopecia areata, which is described as a chronic inflammatory disorder characterized by patchy hair loss without scalp atrophy. The etiology, clinical features, investigations, histopathology and prognosis of alopecia areata are summarized.

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Swetha Saravanan 1
CONTENT  Hair Science  Classification Of ALOPECIA  Hair Loss: Examination and Investigation  Management 2
Hair Science 3
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 4
Anatomy  The Anagen hair follicle is divided into: Upper Segment 1. Infundibulum 2. Isthmus Lower Segment 1. Stem 2. Bulb 5
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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 8
Follicular Papilla  Varies according to the phase of hair cycle.  Composed - specialized fibroblast like cells embedded in extracellular matrix.  Contains a loop of capillary blood vessels.  Volume of dermal papilla maybe responsible for controlling size of hair follicle. 9
Hair Shaft  3 layers : Medulla Cortex Hair Cuticle Medulla 1. Maybe continuous, interrupted or absent. 2. Contains few layers of rounded cells containing glycogen. 10
Cortex 1. Forms bulk of the hair shaft. 2. Consists of numerous layers of flattened elongated cells packed together. Hair Cuticle 1. 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. 11
Inner Root Sheath 1. 3 layers : Cuticle Huxley’s layer Henle’s layer 2. At the Isthmus the IRS disintegrates Outer Root Sheath 1. 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
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Ultra structure of Hair  Hard keratin with high sulfur content.  High sulfur content - extraordinary tensile strength.  S-H linkages of cysteine at the bulb are converted to S-S linkages of cysteine higher up. 14
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. 15
Hair Cycle Hair growth occurs in 3 stages : Anagen Catagen Telogen 16
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19 Anagen • Period of active hair growth. • Duration of this phase resp. for final 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 of epithelial cells in Dermal papilla.
 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. 20
 The melanocytes become active adding colour to 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 ). 21
22 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 follicle becomes thickened to form “glassy membrane”.  Base of the follicle along with dermal papilla moves upwards to lie below the level of Arrector muscle attachment. 23
24 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 25
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- telogen effluvium 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
Exogeneous Anabolic Steroids Accelerate androgenetic alopecia : Aggravate hirsutism β Adrenergic antagonist Causes telogen effluvium Cyclosporin Hypertrichosis Estrogen Prolong duration of anagen stage Finasteride Blocks 5 α Reductase type II Minoxidil Induces and prolongs anagen stage & Vellus  terminal hair OCP Cessation may cause telogen effluvium Phenytoin Hypertrichosis Retinoids Premature onset of catagen stage 27
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 28
Role of Growth Factors & Cytokines in Hair Follicle Development,Hair growth & Hair Cycle Activity EGF 1. Delays follicular development 2. Retards hair growth & cycling 3. Induces follicle regression & catagen–like changes in vitro 4. Stimulates elongation of hair. TGFα 1. Controls normal positional development of hair follicle 2. Retards hair growth in vitro in mice aFGF & bFGF 1. Responsible for formation & maintenance of perifollicular blood vessel 2. Important for skin appendage morphogenesis & their formation FGF4 1. Necessary for follicular development & epithelial regeneration. FGF5 1. Hair elongation inhibitor 2. Initiates transition from anagen to catagen phase 29
VEGF 1. Responsible for maintenance of the perifollicular capillaries in anagen TGFβ -1,2,3 1. Inhibits follicular development 2. 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 neurons 2. 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 31
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. 32
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. 33
Noncicatricial Alopecia Physiological 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 Bacterial Dermatophytosis Viral Chemical injury Caustics Cutaneous diseases DLE, FLP,pseudopelade Destructive neoplasms & granulomas Psychogenic conditions Neurotic excoriating tactile injury to skin 35
Miscellaneous Androgenetic alopecia(common baldness) Congenital alopecia Hair shaft abnormalities: monolothix, pili annulati, wooly hair 36
 Tricotillomania 37
 Moth –eaten appearance -Syphilis 38
 FLP 39
 Folliculitis 40
 DLE 41
Alopecia Areata Syn. Pelade, Area Celsi  Chronic inflammatory dermatologic disorder characterized by patchy loss of hair without atrophy  Described by Cornelius Celsus (AD 14-37)  Term was coined by Sauvages in 1760 42
Etiology  Genetic factors(10- 20%), positive family history  Autoimmunity  Stress  Diet  Infectious agent  Vaccination 43
 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. 44
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 45
 White hair- relatively spared, hence patients with canitis, 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 ,when the hair is bent inwards). 46
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Nail changes  Nail dystrophy  Pitting  Transverse /longitudinal rows  Beau’s lines  Onychorrhexis-nail plate split  Nail loss total 53
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Poor prognosis  Atopy  Other immune disease  Family H/o AA  Excessive hair loss  Oophiasis pattern  Nail dystrophy  Poor patient compliance 55
Investigations  Hair – Pull test  Hair pluck test  Dermoscopy  SALT score ( severity of alopecia tool score)  Optical Coherence Tomography- detect hair shaft abnormalities. 56
Histopathology  Peribulbar and intrabulbar inflammatory infiltrate concentrated in and around hair bulb giving “swarm of bees” appearance.  Infiltrate mostly of T lymphocytes and macrophages present around the matrix and dermal papilla.  Miniaturization of hair follicles. 57
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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  Anthralin 1. .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 62
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, Germany63
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. 64
Etiology Physiologic 1. Physiologic effluvium of new born 2. Postpartum effluvium 3. Early changes of androgenic alopecia 4. Injury/ stress 5. High or prolonged fever 6. Severe infection 7. Severe chronic illness 8. Severe psychologic stress 9. Major sugery 10. Hypothyroidism & other endocrinopathies 11. Severe dieting or malnutrition 65
Drugs and Toxins 1. Antikeratinising agent ( etretinate) 2. Anticoagulants ( heparin) 3. Antithyroid agents 4. Alkylating agents 5. Anticonvulsants 6. Hormones 66
Diagnosis  Detailed patient history (drug/diet)  Complete blood count  TFT  Hair –pull test  Trichogram  ANA titre  Sr. Zinc levels  VDRL 67
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 68
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. 69
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. 70
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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. 72
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Hair Loss Severity Classification  For MPHL, Norwood/ Hamilton scale  For FPHL, Ludwig’s classification scale 74
Pathology  l  Marked reduction in terminal hairs  Miniaturization of hair follicles  increase in secondary vellus hairs  Mild perifollicular infiltrate mostly lymphohistiocytic with or without concentric layers of perifollicular collagen deposition 75
Treatment 76
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Hair Loss: Examination & Investigation 78
Evaluation of Hair loss History & Examination 1. 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 products 79
Examination Physical appearance of hair and pattern of hair loss helps in diagnosis of possible etiology. 80
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 82
Noninvasive methods  Scalp score  Regional Hair pattern  Contrasting Felt examination  Daily hair Counts 83
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) 84
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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 86
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 87
Norwood-Hamilton scale of male pattern baldness 88
Ludwig scale for Women 89
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 90
 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. 91
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 to detect pathology. 92
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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 94
Hair Pull Test 95
 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 of alopecia areata 96
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 occipital region.  Alopecia - failure of development of new anagen hair rather than increased telogen hair ratio. In these patients hair pull test is normal. 97
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. 98
Trichogram (Hair Pluck Test) 99
The plucked hairs are arranged side by side on a glass slide and taped 100
Anagen hair - forcibly plucked terminal anagen hair showing the pigmented bulb with 'hockey-stick' appearance. 101
Telogen hair - forcibly plucked early telogen hair showing the hypopigmented, club-shaped cornified bulb with remanents of the cornified epithelial sac. 102
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. 103
Phototrichogram  Phototrichogram 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. 104
 These variables are: 1. Hair density 2. Hair thickness 3. Hair length 4. Linear growth rate. 105
 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 106
 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) 107
Invasive Methods Scalp Biopsy Indications: 1. Cicatricial alopecia 2. Undiagnosed - non-cicatricial alopecia Type: 1. Vertical 2. Horizontal 108
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 shaft 111
Medical Management of Androgenic Alopecia 112
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 114
 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. 115
Adverse Effects  Head ache  Mild irritant dermatitis  Occasional hirsutism 116
Finasteride  It’s a competent & specific inhibitor – type II 5α-reductase enzyme.  Prevents testosteroneDHT.  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. 117
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. 118
Adverse effects  Breast tenderness & enlargement  Hypersensitivity reactions- Pruritus, rash, urticaria , swelling of lips & face, testicular pain.  Erectile dysfunction.  Less libido. 119
Contraindications  In women- child bearing group & pregnant women  In children  In patients hypersensitive to drug. 120
Surgical Treatment  Hair transplantation  Hair weaving  Laser hair transplant  Follicular unit transplant 121
Reference  Text book on Alopecia – Dr Narendra G. Patwardhan  Rook’s text book of dermatology  Review article on Alopecia Areata - IJDVL 122
THANKYOU 123

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Alopecia - scaring & non-scaring type.

  • 1.
  • 2.
    CONTENT  Hair Science Classification Of ALOPECIA  Hair Loss: Examination and Investigation  Management 2
  • 3.
  • 4.
    Hair is acutaneous appendage originally evolved in mammals as a protective coat. It is simple in structure, but has important functions in social functioning 4
  • 5.
    Anatomy  The Anagenhair follicle is divided into: Upper Segment 1. Infundibulum 2. Isthmus Lower Segment 1. Stem 2. Bulb 5
  • 6.
  • 7.
  • 8.
    Adamson’s Fringe  Upperpart 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 8
  • 9.
    Follicular Papilla  Variesaccording to the phase of hair cycle.  Composed - specialized fibroblast like cells embedded in extracellular matrix.  Contains a loop of capillary blood vessels.  Volume of dermal papilla maybe responsible for controlling size of hair follicle. 9
  • 10.
    Hair Shaft  3layers : Medulla Cortex Hair Cuticle Medulla 1. Maybe continuous, interrupted or absent. 2. Contains few layers of rounded cells containing glycogen. 10
  • 11.
    Cortex 1. Forms bulkof the hair shaft. 2. Consists of numerous layers of flattened elongated cells packed together. Hair Cuticle 1. 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. 11
  • 12.
    Inner Root Sheath 1.3 layers : Cuticle Huxley’s layer Henle’s layer 2. At the Isthmus the IRS disintegrates Outer Root Sheath 1. 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
  • 13.
  • 14.
    Ultra structure ofHair  Hard keratin with high sulfur content.  High sulfur content - extraordinary tensile strength.  S-H linkages of cysteine at the bulb are converted to S-S linkages of cysteine higher up. 14
  • 15.
    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. 15
  • 16.
    Hair Cycle Hair growthoccurs in 3 stages : Anagen Catagen Telogen 16
  • 17.
  • 18.
  • 19.
    19 Anagen • Period ofactive hair growth. • Duration of this phase resp. for final 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 of epithelial cells in Dermal papilla.
  • 20.
     Lower partof 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. 20
  • 21.
     The melanocytesbecome active adding colour to 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 ). 21
  • 22.
    22 Catagen • Short transitionstage 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.
  • 23.
     Lower partof the follicle involutes by apoptosis.  Basement membrane surrounding the follicle becomes thickened to form “glassy membrane”.  Base of the follicle along with dermal papilla moves upwards to lie below the level of Arrector muscle attachment. 23
  • 24.
    24 Telogen • Resting phaseof 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.
  • 25.
    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 25
  • 26.
    Modulators of HairFollicle 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- telogen effluvium 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
  • 27.
    Exogeneous Anabolic Steroids Accelerateandrogenetic alopecia : Aggravate hirsutism β Adrenergic antagonist Causes telogen effluvium Cyclosporin Hypertrichosis Estrogen Prolong duration of anagen stage Finasteride Blocks 5 α Reductase type II Minoxidil Induces and prolongs anagen stage & Vellus  terminal hair OCP Cessation may cause telogen effluvium Phenytoin Hypertrichosis Retinoids Premature onset of catagen stage 27
  • 28.
    Rate of HairGrowth : 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 28
  • 29.
    Role of GrowthFactors & Cytokines in Hair Follicle Development,Hair growth & Hair Cycle Activity EGF 1. Delays follicular development 2. Retards hair growth & cycling 3. Induces follicle regression & catagen–like changes in vitro 4. Stimulates elongation of hair. TGFα 1. Controls normal positional development of hair follicle 2. Retards hair growth in vitro in mice aFGF & bFGF 1. Responsible for formation & maintenance of perifollicular blood vessel 2. Important for skin appendage morphogenesis & their formation FGF4 1. Necessary for follicular development & epithelial regeneration. FGF5 1. Hair elongation inhibitor 2. Initiates transition from anagen to catagen phase 29
  • 30.
    VEGF 1. Responsiblefor maintenance of the perifollicular capillaries in anagen TGFβ -1,2,3 1. Inhibits follicular development 2. 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 neurons 2. 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
  • 31.
  • 32.
    Alopecia is definedas “ absence or loss of hair”. It’s a chronic disorder secondary to the disease of either the hair follicle, hair shaft or the scalp. 32
  • 33.
    Pseudoalopecia is definedas 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. 33
  • 34.
    Noncicatricial Alopecia Physiological Alopeciaof 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
  • 35.
    Cicatricial Alopecia Physical traumaLong term traction of hair, x-ray overdose burn Infections Bacterial Dermatophytosis Viral Chemical injury Caustics Cutaneous diseases DLE, FLP,pseudopelade Destructive neoplasms & granulomas Psychogenic conditions Neurotic excoriating tactile injury to skin 35
  • 36.
    Miscellaneous Androgenetic alopecia(common baldness) Congenitalalopecia Hair shaft abnormalities: monolothix, pili annulati, wooly hair 36
  • 37.
  • 38.
     Moth –eatenappearance -Syphilis 38
  • 39.
  • 40.
  • 41.
  • 42.
    Alopecia Areata Syn. Pelade,Area Celsi  Chronic inflammatory dermatologic disorder characterized by patchy loss of hair without atrophy  Described by Cornelius Celsus (AD 14-37)  Term was coined by Sauvages in 1760 42
  • 43.
    Etiology  Genetic factors(10-20%), positive family history  Autoimmunity  Stress  Diet  Infectious agent  Vaccination 43
  • 44.
     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. 44
  • 45.
    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 45
  • 46.
     White hair-relatively spared, hence patients with canitis, 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 ,when the hair is bent inwards). 46
  • 47.
  • 48.
  • 49.
  • 50.
  • 51.
  • 52.
  • 53.
    Nail changes  Naildystrophy  Pitting  Transverse /longitudinal rows  Beau’s lines  Onychorrhexis-nail plate split  Nail loss total 53
  • 54.
  • 55.
    Poor prognosis  Atopy Other immune disease  Family H/o AA  Excessive hair loss  Oophiasis pattern  Nail dystrophy  Poor patient compliance 55
  • 56.
    Investigations  Hair –Pull test  Hair pluck test  Dermoscopy  SALT score ( severity of alopecia tool score)  Optical Coherence Tomography- detect hair shaft abnormalities. 56
  • 57.
    Histopathology  Peribulbar andintrabulbar inflammatory infiltrate concentrated in and around hair bulb giving “swarm of bees” appearance.  Infiltrate mostly of T lymphocytes and macrophages present around the matrix and dermal papilla.  Miniaturization of hair follicles. 57
  • 58.
  • 59.
  • 60.
  • 61.
  • 62.
     CS’s 1. Hydrocortisoneacetate 25mg/mL 2. Triamcinalone acetonide 5-10mg/mL 3. Accelerates regrowth 4. SE- Atrophy,pain,tingling - reversible  Anthralin 1. .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 62
  • 63.
    Alopecia totalis treatedwith 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, Germany63
  • 64.
    Telogen Effluvium  Theterm 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. 64
  • 65.
    Etiology Physiologic 1. Physiologic effluviumof new born 2. Postpartum effluvium 3. Early changes of androgenic alopecia 4. Injury/ stress 5. High or prolonged fever 6. Severe infection 7. Severe chronic illness 8. Severe psychologic stress 9. Major sugery 10. Hypothyroidism & other endocrinopathies 11. Severe dieting or malnutrition 65
  • 66.
    Drugs and Toxins 1.Antikeratinising agent ( etretinate) 2. Anticoagulants ( heparin) 3. Antithyroid agents 4. Alkylating agents 5. Anticonvulsants 6. Hormones 66
  • 67.
    Diagnosis  Detailed patienthistory (drug/diet)  Complete blood count  TFT  Hair –pull test  Trichogram  ANA titre  Sr. Zinc levels  VDRL 67
  • 68.
    Treatment  Normal hairgrowth occurs with time & resolution of underlying causes.  No specific treatment – required  In case of no recovery – minoxidil can provide some benifits 68
  • 69.
    Androgenetic Alopecia  Androgenicalopecia 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. 69
  • 70.
    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. 70
  • 71.
  • 72.
     FPHL- differfrom 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. 72
  • 73.
  • 74.
    Hair Loss SeverityClassification  For MPHL, Norwood/ Hamilton scale  For FPHL, Ludwig’s classification scale 74
  • 75.
    Pathology  l  Markedreduction in terminal hairs  Miniaturization of hair follicles  increase in secondary vellus hairs  Mild perifollicular infiltrate mostly lymphohistiocytic with or without concentric layers of perifollicular collagen deposition 75
  • 76.
  • 77.
  • 78.
    Hair Loss: Examination& Investigation 78
  • 79.
    Evaluation of Hairloss History & Examination 1. 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 products 79
  • 80.
    Examination Physical appearance ofhair and pattern of hair loss helps in diagnosis of possible etiology. 80
  • 81.
    Disease Common patternseen 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
  • 82.
    Blood Investigations  Completeblood count  VDRL  Sr. iron  Sr. ferritin  Total iron binding capacity  TFT  Antinuclear factor –DLE  Hormone levels 82
  • 83.
    Noninvasive methods  Scalpscore  Regional Hair pattern  Contrasting Felt examination  Daily hair Counts 83
  • 84.
    Scalp Scores  Globalphotographs 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) 84
  • 85.
  • 86.
     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 86
  • 87.
    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 87
  • 88.
    Norwood-Hamilton scale ofmale pattern baldness 88
  • 89.
  • 90.
    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 90
  • 91.
     INFERENCE- Fineshort 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. 91
  • 92.
    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 to detect pathology. 92
  • 93.
  • 94.
    Semi-invasive methods  HairPull Test  Hair Feathering Test  Trichogram( Hair Pluck Test)  Unit Area Trichogram  Phototrichogram & Videotrichogram  Digital Epiluminescence Microscopy  Global Photographs in Phototrichogram 94
  • 95.
  • 96.
     Telogen hairis 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 of alopecia areata 96
  • 97.
    Other drawbacks ofthis 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 occipital region.  Alopecia - failure of development of new anagen hair rather than increased telogen hair ratio. In these patients hair pull test is normal. 97
  • 98.
    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. 98
  • 99.
  • 100.
    The plucked hairsare arranged side by side on a glass slide and taped 100
  • 101.
    Anagen hair -forcibly plucked terminal anagen hair showing the pigmented bulb with 'hockey-stick' appearance. 101
  • 102.
    Telogen hair -forcibly plucked early telogen hair showing the hypopigmented, club-shaped cornified bulb with remanents of the cornified epithelial sac. 102
  • 103.
    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. 103
  • 104.
    Phototrichogram  Phototrichogram wasintroduced by Saitoh in 1970  Technique that allows in vivo study of physiology of the hair cycle and measurement of various hair growth variables. 104
  • 105.
     These variablesare: 1. Hair density 2. Hair thickness 3. Hair length 4. Linear growth rate. 105
  • 106.
     PROCEDURE- Day 0t(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 106
  • 107.
     INFERENCE- 1. Hairvariables 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) 107
  • 108.
    Invasive Methods Scalp Biopsy Indications: 1.Cicatricial alopecia 2. Undiagnosed - non-cicatricial alopecia Type: 1. Vertical 2. Horizontal 108
  • 109.
    Terminal anagen hair-showingthe IRS and the ORS109
  • 110.
    AGA Male scalp-follicular unit with three vellus hairs ; one terminal and one secondary hair germ 110
  • 111.
    Vellus hair –IRS thicker than the hair shaft 111
  • 112.
  • 113.
    Treatment options forAGA 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
  • 114.
  • 115.
     Main actionsof 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. 115
  • 116.
    Adverse Effects  Headache  Mild irritant dermatitis  Occasional hirsutism 116
  • 117.
    Finasteride  It’s acompetent & specific inhibitor – type II 5α-reductase enzyme.  Prevents testosteroneDHT.  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. 117
  • 118.
    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. 118
  • 119.
    Adverse effects  Breasttenderness & enlargement  Hypersensitivity reactions- Pruritus, rash, urticaria , swelling of lips & face, testicular pain.  Erectile dysfunction.  Less libido. 119
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    Contraindications  In women-child bearing group & pregnant women  In children  In patients hypersensitive to drug. 120
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    Surgical Treatment  Hairtransplantation  Hair weaving  Laser hair transplant  Follicular unit transplant 121
  • 122.
    Reference  Text bookon Alopecia – Dr Narendra G. Patwardhan  Rook’s text book of dermatology  Review article on Alopecia Areata - IJDVL 122
  • 123.