Alopecia - scaring & non-scaring type.

1. Swetha Saravanan
1

2. CONTENT
 Hair Science
 Classification Of ALOPECIA
 Hair Loss: Examination and Investigation
 Management
2

3. Hair Science
3

4. 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

5. Anatomy
 The Anagen hair follicle is divided into:
Upper Segment
1. Infundibulum
2. Isthmus
Lower Segment
1. Stem
2. Bulb
5

6. 6

7. 7

8. 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

9. 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

10. 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

11. 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

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. 13

14. 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

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 growth occurs in 3 stages :
Anagen
Catagen
Telogen
16

17. 17

18. 18

19. 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.

20.  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

21.  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. 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.

23.  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. 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.

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 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

27. 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

28. 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

29. 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

30. 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

31. Classification of ALOPECIA
31

32. 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

33. 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

34. 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

35. 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

36. Miscellaneous
Androgenetic alopecia(common baldness)
Congenital alopecia
Hair shaft abnormalities: monolothix, pili annulati, wooly hair
36

37.  Tricotillomania 37

38.  Moth –eaten appearance -Syphilis 38

39.  FLP 39

40.  Folliculitis 40

41.  DLE 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. 47

48. 48

49. 49

50. 50

51. 51

52. 52

53. Nail changes
 Nail dystrophy
 Pitting
 Transverse /longitudinal rows
 Beau’s lines
 Onychorrhexis-nail plate split
 Nail loss total
53

54. 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 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

58. 58

59. 59

60. 60

61. 61

62.  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

63. 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

64. 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

65. 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

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 patient history (drug/diet)
 Complete blood count
 TFT
 Hair –pull test
 Trichogram
 ANA titre
 Sr. Zinc levels
 VDRL
67

68. 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

69. 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

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. 71

72.  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

73. 73

74. Hair Loss Severity Classification
 For MPHL, Norwood/ Hamilton scale
 For FPHL, Ludwig’s classification scale
74

75. 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

76. Treatment
76

77. 77

78. Hair Loss: Examination &
Investigation
78

79. 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

80. Examination
Physical appearance of hair and pattern of hair loss
helps in diagnosis of possible etiology.
80

81. 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

82. Blood Investigations
 Complete blood count
 VDRL
 Sr. iron
 Sr. ferritin
 Total iron binding capacity
 TFT
 Antinuclear factor –DLE
 Hormone levels
82

83. Noninvasive methods
 Scalp score
 Regional Hair pattern
 Contrasting Felt examination
 Daily hair Counts
83

84. 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

85. 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 of male
pattern baldness
88

89. Ludwig scale for Women
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- 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

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. 93

94. 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

95. Hair Pull Test
95

96.  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

97. 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

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. Trichogram (Hair Pluck Test)
99

100. The plucked hairs are 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 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

105.  These variables are:
1. Hair density
2. Hair thickness
3. Hair length
4. Linear growth rate.
105

106.  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

107.  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

108. Invasive Methods
Scalp Biopsy
Indications:
1. Cicatricial alopecia
2. Undiagnosed - non-cicatricial alopecia
Type:
1. Vertical
2. Horizontal
108

109. Terminal anagen hair-showing the 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. Medical Management of
Androgenic Alopecia
112

113. 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

114. Minoxidil
114

115.  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

116. Adverse Effects
 Head ache
 Mild irritant dermatitis
 Occasional hirsutism
116

117. 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

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
 Breast tenderness & enlargement
 Hypersensitivity reactions-
Pruritus, rash, urticaria , swelling of lips &
face, testicular pain.
 Erectile dysfunction.
 Less libido.
119

120. Contraindications
 In women- child bearing group & pregnant women
 In children
 In patients hypersensitive to drug.
120

121. Surgical Treatment
 Hair transplantation
 Hair weaving
 Laser hair transplant
 Follicular unit transplant
121

122. Reference
 Text book on Alopecia – Dr Narendra G. Patwardhan
 Rook’s text book of dermatology
 Review article on Alopecia Areata - IJDVL
122

123. THANKYOU
123