1. WEL COME TO
SEMINAR ON
ALOPECIA

2. SEMINAR ON ALOPECIA Chairperson : Dr. Shahab Uddin Ahmed Chowdhury.
Associate Professor & Head of the dept.
Department of Dermatology, MMC.
Speakers : Dr. Mohammad Shoeb Khan,
MD (Part-II)
&
Dr. Mohammed Saiful Islam Bhuiyan,
MD (Part-II), FCPS (Part-II)
Medical Officers,
Department of Dermatology, MMCH.
Date & Time : 5th April, 2005 at 2.00 pm.
Organized by : Department of Dermatology, MMCH.
Renata Limited

3. HAIR AND HAIR FOLLICLE

4. INTRODUCTION Hairs are keratinized elongated
structures derived from invaginations of
epidermis and project out from most of
the body surface.

5. AREAS WITHOUT HAIR: Palms Soles Lips Nipples Glans penis Clitoris
Prepuce
Labia minora
Inner surface of
labia majora

6. RACIAL PREVALENCE : Whites are hairiest. Asians are least hairy and
blacks fall in between.

7. TYPES OF HAIR Straight : Asians , whites. Spiral : Blacks, whites.
Morphologically :
Straight : Asians , whites.
Spiral : Blacks, whites.
Helical : Whites.
Wavy : Whites.

8. HAIR TYPES (Contd.) Fetal hair - Adult hair -
Lanugo hair : soft, fine, lightly pigmented hairs.
Adult hair -
Vellus hair : fine hairs cover most of the body
of youngsters and adults.
Terminal hair: long, coarse, pigmented hairs with
larger diameters.

9. NUMBER OF HAIRS Scalp : about 1,00,000 hairs.
Face : about 600 hairs /cm2.
Rest of the body : about 60 hairs/cm2.

10. LENGTH, WIDTH AND GROWTH RATE
Length : range from <1mm to > 1 meter.
Average uncut scalp hair : 25 – 100 cm.
(exceptionally 170 cm)
Width : from to 0.06mm.
Growth rate: about 1 cm/ month (terminal hair).

11. FUNCTIONS 1. Protects body surface from external injury.
2. Helps in sensory function.
Psycho – social importance.
Forensic importance.
i. Identification of race, sex, age and religion.
ii. Cause of death- can be determined.
iii. Time of death- can be determined.
5. Assist thermo- regulation: mainly in lower animals.

12. STRUCTURE OF HAIR AND HAIR FOLLICLE:

13. DEVELOPMENT OF HAIR Ectodermal origin-
1. Hair bud – develops from epidermis and penetrates the dermis.
2. Hair shaft – grows from cells in the centre of hair bud.

14. DEVELOPMENT OF HAIR (Contd.)
3. Inner root sheath – develops from cells in the
periphery of hair bud.
Mesodermal origin: Outer root sheath.
First hair come is lanugo hair at eyebrow and upper lip at twelve weeks of gestation.

15. DEVELOPMENT OF HAIR (Contd.)
3. Inner root sheath – develops from cells in the
periphery of hair bud.
Mesodermal origin : Outer root sheath.
First hair to come is lanugo hair at eyebrow and upper lip at weeks of gestation.

16. HAIR EMBRYOLOGY

17. HAIR CYCLE It is believed that each hair follicle goes
through hair cycle in a life time.
There are four phases-
Anagen : growing phase.
Catagen: involuting phase.
Telogen : resting phase.
Exogen : hair shedding phase.

18. ANAGEN (GROWING PHASE)
Last for about 1000 days.
Follicular cells grow, divide and become keratinized to form growing phase.
A darkly pigmented portion is evident just above the hair bulb.

19. CATAGEN (INVOLUTING PHASE)
Lasts for about 10 days.
Scalp hairs show a gradual thinning and decrease of the pigment.
Melanocytes cease producing melanin.
Matrix keratinocytes abruptly cease proliferating so that lower follicle involutes and regresses.

20. TELOGEN (RESTING PHASE)
Lasts for about 100 days.
Club-shaped proximal end shed from the follicle during telogen or subsequent anagen.
Growth of a new anagen hair leads to shedding of any remaining telogen hair.
But new hair does not “push out” the hair from the previous cycle.

21. EXOGEN (HAIR SHEDDING PHASE)
Recently added phase.
The term describes relationship between hair shaft and base of telogen follicle.
Hairs can be retained for more than one cycle.
Shedding phase is most likely independent of anagen and telogen.

22. PIGMENTATION OF HAIR Melanocytes are present in the bulb.
Hair color is determined by melanocytes.
Melanocytes are present in the bulb.
Melanocytes feed melanosomes mainly to
the medulla and cortex.
Melanocytic follicles produce melanin-
. eumelanin (dominant in brown-black hairs)
. phaeomelanin (dominant in red-blond hairs)

23. PIGMENTATION OF HAIR (Contd.)
Greying of hair – due to decreased
number and activities of melanocytes.
Vitiligo – due to destruction of
melanocytes.
Albinism – due to inactivity of

25. ALOPECIA Pathophysiology of hair loss :  Hair follicle.
Absence or loss of hair especially of the scalp.
Pathophysiology of hair loss :
1. Production failure –
 Failure to produce or continue to
 produce a normal hair follicle.
2. Aberration of –
 Normal hair cycle.
 Production of a normal hair shaft.
3. Destruction of –
 Hair follicle.

26. CLASSIFICATION OF ALOPECIA
FOCAL HAIR LOSS 
Non-Scarring:
A. Abnormality of cycling-
i. Alopecia areata.
ii. Syphilitic alopecia.
B. Production decline-
i. Androgenetic alopecia.
ii. Triangular alopecia.

27. FOCAL HAIR LOSS (Contd.)
C. Hair breakage-
i. Trichotillomania.
ii. Tinea capitis.
iii. Traction alopecia.
iv. Primary or acquired hair shaft abnormality.

28. SCARRING ALOPECIA ii. Lichen planopilaris.
Lymphocytic-
i. Chronic Cutaneous LE (DLE).
ii. Lichen planopilaris.
iii. Classic pseudopellade of Brocq.
iv. Alopecia mucinosa.
v. Central centrifugal cicatricial alopecia.
vi. Keratosis follicularis spinulosa decalvans.

29. SCARRING ALOPECIA (CONTD.)
B. Neutrophilic –
i. Folliculitis decalvans.
ii. Dissecting folliculitis/cellulitis.
C. Mixed-
i. Folliculitis (acne) keloidalis.
ii. Folliculitis (acne) necrotica.
iii. Erosive pustular dermatitis.

30. Diffuse Hair Loss  Abnormality of cycling – Hair shaft abnormality-
i. Alopecia areata.
ii. Telogen effluvium.
iii. Anagen effluvium.
iv. Loose anagen syndrome.
Hair shaft abnormality-
i. Hair breakage.
ii. Unruly hair.

31. Diffuse Hair Loss (Contd.)
C. Failure of follicle production-
i. Congenital universal atrichia.
ii. Alrichia with papular lesions.
iii. Hereditary vitamin-D- resistant
rickets.

32. ALOPECIA AREATA Definition:
Rapid and complete loss of hair in one or most often several round or oval patches, usually on the scalp, bearded area, eyebrows, eye lashes and less commonly on other hairy areas of the body.

33. ALOPECIA AREATA

34. ALOPECIA AREATA

35. ALOPECIA AREATA(Contd.)
Epidemiology:
Approximately 1.7% of the population will experience an episode of alopecia aerata during their life time.

36. ALOPECIA AREATA (Contd.)
Etiology
Exact cause is still unknown.
It is an autoimmune disease-
- Mediated by the cellular arm
(T- cell, macrophages ).
- Modified by genetic factors
(HLA-R4,DR11,DQ7)

37. ALOPECIA AREATA (Contd.)
-Triggered by environmental factors-
Trauma.
Neurogenic inflammation.
Infections agents.

38. ETIOPATHOGENESIS Trauma Neurogenic Inflammation Infections agents
Release of cytokines
Aberrant expression of MHC (due to failure of repression)
Aberrant expression of adhesion molecules

39. Haematopoietic cell migration (T-cell)
Production of follicular auto- antigen (Kerationcyte and melanocyte origin)
Attack on
melanogically active anagen fallicle
Follicular damage in anagen and rapid premature transformation to telogen.

40. FOUR DISTINCT STAGES OF ALOPECIA AREATA
i. Acute hair loss.
ii. Persistant (Chronic) baldness.
iii. Partial telogen to anagen conversion
(incomplete revcovery).
iv. Normal recovery.

41. CLINICAL FEATURE
Rapid and complete loss of hair in one or several patches.
Site – Scalp, bearded area, eyebrows, eye lashes and less commonly other areas of body.
Size – Patches of 1-5 cm in diameter.

42. CLINICAL FEATURE (CONTD.)
“Exclamation point” hair- at the periphery of hair loss, there are broken hairs, whose distal ends are broader than the proximal end. !

43. EXCLAMATION MARK HAIRS

44. CLINICAL FEATURE (CONTD.)
Few resting hairs may be found within the patches.
“Going gray overnight”- a mysterious phenomenon is observed in fulminant alopecia areata.
In about 10% cases of long standing extensive alopecia areata, some nail changes develop.

45. EXTENSIVE PATCHY ALOPECIA AREATA.

46. DIFFUSE PATTERN OF HAIR LOSS IN ALOPECIA AREATA

47. CLINICAL FEATURE (CONTD.)
“Alopecia totalis” – Total loss of scalp hair.
“Alopecia universalis” – Loss of entire body hair including scalp hair.
“Ophiasis” – Loss of hair confluent along the temporal and occipital scalp.
“Sisaipho”- Loss of hair of entire scalp except temporal and occipital area.

48. ALOPECIA UNIVERSALIS

49. ALOPECIA TOTALIS

50. OPHIASIS PATERN OF ALOPECIA AREATA

51. ASSOCIATED DISEASE Higher incidence of alopecia areata in patients of-
1. Atopic dermatitis.
2. Autoimmune disease –
* SLE
* Thyroiditis.
* Myasthenia gravis.
* Vitiligo.
3. Lichen planus.
4. Down syndrome.

52. HISTOLOGY
Peribulbar, Perivascular and outer- root sheath infiltration with T-cells and macrophages.
The follicular size are diminished and identified in more superficial dermis.

53. DIFFERENTIAL DIAGNOSIS
1. Tinea capitis.
2. Trichotilomania.
3. Secondary syphilis
4. Congenital triangular alopecia.
5. Alopecia neoplastica.
6. Early lupus erythematosus.

54. TREATMENT Spontaneous recovery is extremely common
for patchy alopecia areata.
For localized patchy alopecia areata- • Steroid- both local (intralesional and
topical) and systemic (in short course).

55. TREATMENT (CONTD.)
- High potent topical steroid used as first line therapy.
- Intralesional steroid given at 4-6 weeks interval.
- Systemic steroid (Short course, <8 weeks) alone or in conjunction with topical steroid.

56. TREATMENT (CONTD.) If lack of response after several months therapy-
Topical 1% Anthralin cream - applied for minutes and then shampooed off the treated side.
5% topical minoxidil – as a single agent or as an adjuvant with topical Anthralin.
PUVA.

57. TREATMENT (CONTD.) Contact sensitizer – - Squaric acid dibutyle ester,
- Diphencyprone,
- Dinitrochlorobenzene.
Psychological support.
In extensive scalp hair loss- cosmetically expectable alternatives.

58. HEALED ALOPICIA UNIVERSALIS AFTER PUVA THERAPY

59. PROGNOSIS Poor prognostic marker- - Early onset (Prepubertal)
- Extensive involvement.
- Prolong duration (>5years)
- Ophiasis.

60. ANDROGENETIC ALOPICIA

61. ANDROGENETIC ALOPICIA

62. ANDROGENETIC ALOPECIA
Synonyms : Male Pattern alopecia,
Male pattern baldness,
Common baldness
Secretarial alopecia.
Definition : It is a very common, potentially
reversible scalp hair loss that generally spares
parietal and occipital areas (Hippocratic
wreath) of the scalp.

63. ANDROGENETIC ALOPECIA (Contd.)
Age : Twenties or early thirties.
sites : Chiefly vertex and frontotemporal
regions.
Etiopathogenesis:
Exact mechanism is still unknown.
Hereditary (Probably autosomal dominant) &
Androgen (specifically dihydrotestesterone)

64. ETIOPATHOGENESIS (Contd.)
Testesterone 5R Dihydrotesterone.
5R has two Isozyme, 5R1 and 5R2
5R1 ubiquitously distributed in skin particularly in sebaceous gland.
5R2 is found in outer root sheath and dermal papillae.

65. ANDROGEN Androgen - androgen receptor complex in cytoplasm
transformation of receptor to expose DNA binding domain
binds to androgen response element of DNA
Transcription and translation
certain effector protein,

66. ETIOPATHOGENESIS (Contd.)
EFFECTS
- Shortening of anagen and
lengthening of telogen
- Follicle become short and sclerosis of dermis and miniaturization or reduction of hair present.

67. CLINICAL FEATURE Hair loss starts any time after puberty
“Whisker hairs” – first sign of impending male pattern alopecia, appear at the temple.
“Professor’s angle” – anterior hair line recedes backward on each side.
Eventually entire top of the scalp become devoid of hair.

68. PATTERN OF HAIR LOSS

69. Androgenetic alopecia in women
Etiology :
Genetic Predisposition,
Androgen excess,
Ovarian cause-
- Polycystic ovarian syndrome,
- Other ovarian tumor,
. Unilateral benign
microadenoma.
. Leydig cell tumor
. Hilar cell tumor.

70. ETIOLOGY (CONTD.) Adrenal cause
- Congenital adrenal hyperplasia (androgenital
syndrome) due to deficiency of –
21 hydroxylase (most common)
11-β hygroxylase.
3-β hydroxysteroid dehydrogenase.
- Tumor
Adrenal adenoma
Carcinoma.

71. CLINICAL FEATURE Pattern of hair loss :
“Christmas tree pattern”- diffuse and progressive reduction of density and diameter of hairs in the mid scalp.
Maintenance of frontal hair lines with only slight recession.

72. ANDROGENETIC ALOPECIA IN WOMEN

74. CLINICAL FEATURE (CONTD.)
Other evidence of androgen excess:
Acne.
Hirsutism.
Menstrual irregularities.
Majority of women with pattern hair loss have
No increased serum androgen,
No other sign symptom of
androgen hypersensitivity.

75. TREATMENT
1. Topical Minoxidil (2% & 5%)
-non specific hair growth promoter affecting anagen induction.
- M/A is not clear, its ca channel opener activity is important.
2. Systemic Finesteride (1mg daily).

76. TREATMENT (CONTD.) 3. In women – spironolactone ( >100 mg daily).
- Flutamide ( mg bid or tid).
- Cyproterone actate.
4. Surgical treatment- Micrograft & minigraft from non-androgen dependent site (occiput).

77. TELOGEN EFFLUVIUM It is a reaction pattern to a variety of
physical and mental stressors represents
a precipitous shift of a percentage of
anagen hairs to telogen.

78. Causes of Telogen Effluvium
Endocrine
- Hypo- or hyperthyroidism.
- Postpartum.
- Peri- or postmenopausal state.
Nutritional
- Biotin deficiency.
- Caloric deprivation.
- Essential fatty acid deficiency.
- Iron deficiency.
- Protein deprivation.
- Zinc deficiency.

79. Causes of Telogen Effluvium (Contd.)
Drugs
Angiotensin-converting enzyme inhibitors.
Anticoagulants.
Antimitotic agents.
Benzimidazoles.
Beta blockers.
Interferon
Lithium

80. Causes of Telogen Effluvium (Contd.)
Oral contraceptives.
Retinoids.
Vitamin A excess.
Physical stress
Anemia
Surgery.
Systemic illness.
Psychological stress

81. Events related to pathogenesis of telogen effluvium
Short anagen- by drugs, fever, physiological stress.
Prolonged anagen- Pregnancy.
Conversion of telogen follicle to anagen follicle.

82. Pathology > 12% to 15% of terminal follicles are in telogen.
Follicle itself is not diseased.
No inflammation or dystrophic changes.

83. CLINICAL PRESENTATION
“Lots of hairs coming out by the roots” complained by patient.
Diffuse hair loss with clinically perceptible thinning of hairs usually 3-5 weeks of inciting signal and shedding continue for about 3-4 month after removal of inciting cause.
150 to > 400 hair loss daily.
Hair density may take 6-12 months to return to base line.
Pull test.
Clip test.

84. TREATMENT No specific therapy.
In majority cases hair will grow spontaneously within few month after removing inciting cause.
In some patients with chronic telogen effluvium-
- 5% minoxidil solution, 70% success in
man .
- For Premenopausal women, 5% minoxidil
solution + cyproterone acitate 50 mg from
day 5 to 15 of menstrual cycle taken together with ethynnyl estradiol (0.035
mg/day).

85. TREATMENT (CONTD.)
For post menopausal women,
- Cyproterone acetate 50 mg/day.
- Spironolactone ( mg/day) or flutamide mg/ day alternative to cyproterone acetate.

86. TRICHTILLOMANIA
A neurotic practice of plucking or breaking hair from scalp or eyelash resulting usually localized or widespread areas of alopecia contains hairs of varying length.
Mostly girls under age of 10 years.
Disturbed mother- child relationship.

87. TRICHOTILOMANIA

88. TRICHOTILOMANIA IN A WOMEN

89. ALOPECIA SYPHILITICA
Typical motheaten appeorance on the occipital scalp or generalized thinning of hairs or both.
Eyebrows, eyelash and body hairs also involved.
It may be one or sole cutaneus manifestation of secondary syphilis.
Treatment of syphilis may reverse the hair loss.

90. ALOPICIA OF SECONDARY SYPHILIS