Hair and Nail Disorders

Digital Lecture Series : Chapter 24

Col. Manas Chatterjee

Senior Adviser, Professor and Head

Maj. Shekhar Neema

Graded Specialist and Asst Professor
Department of Dermatology, Command Hospital (EC), Kolkata
 CONTENTS

HAIR NAIL
 Structure  Structure
 Function  Function
 Alopecia  Nail changes in systemic diseases
 Excessive hair growth  Nail changes due to drugs
 Hair pigmentation  Common diseases of nail
 Hair cosmetics  Basic procedures

 MCQs
 Photoquiz
 Structure of hair

Types of hair :

 Lanugo (seen in utero)

 Vellus

 Terminal

Hair is a keratinized product of hair follicle.

It is present all over skin except on vermillion of lips, palms, soles and skin
of nail folds.
 Functions of hair

 Concerned with sexual and social communication

 Protective role eg. nasal and eyelash hair

 Sensory function: touch sensation

 Hair Cycle

 Hair follicles undergo a repetitive sequence of growth and rest called

the hair cycle.
 Anagen is period of active hair growth. Duration of this phase
decides the length of hair. In humans, it is maximum on scalp.
 Catagen is the regressive phase in which the follicular activity
declines and ceases.
 Telogen is the resting phase in which hair stays till the beginning of
next anagen phase.
 Disorders of hair

Disorders of hair can either be due to :

 Loss of hair from hair bearing areas (alopecia)

 Excessive hair

• Androgen dependent hair patterns of typically terminal hair (hirsutism)

• Patterns of increased hair growth other than in androgenic distribution

(hypertrichosis)
 Alopecia

 Classification:

 Non-cicatricial: preservation of follicles on clinical and histologic

examination. Common causes are alopecia areata, androgenetic
alopecia, female patterned hair loss and telogen effluvium.

 Cicatricial (scarring): destruction of follicles due to conditions eg:

trauma, infections, cutaneous lupus erythematosus, lichen planus. It
is irreversible.

There can be either diffuse or localised (patterned / non-patterned ) hair

loss.
 Alopecia areata

 Chronic inflammatory disease probably due to a T-cell mediated

response in genetically predisposed individuals. Environmental
factors may trigger the condition.

 Affects any hair bearing area; can be localized, extensive or diffuse.

The involvement of all scalp hair is alopecia totalis and
all body hair is alopecia universalis.

 May be associated with atopy, Down’s syndrome, vitiligo, pernicious

anemia, myxoedema, diabetes or hypertension in the family.
 Alopecia Areata

 The affected area shows total hair loss without any inflammation;
sometimes with short, easily extractable ‘exclamation-mark’ hair at
margin.

 Grey hair spared (going white overnight).

 Regrowth either spontaneous or following treatment; at first fine and

unpigmented but later resumes normal colour and calibre.

 Nail pitting, onycholysis may be associated.

 Alopecia Areata

Localised Non Scarring Alopecia : Alopecia Areata

 Differential diagnosis

 Tinea capitis

 Trichotillomania

 Secondary syphilis

 Androgenetic alopecia
 Treatment

 Majority of cases have spontaneous regrowth of hair without any

treatment.

 Steroids (usually topical or intralesional)

 Topical minoxidil

 Topical anthralin, phenol

 Topical immunotherapy: Dinitrochlorobenzene (DNCB), squaric acid

dibutyl ester (SADBE), diphencyprone (DPCP)

 Immunomodulators : Cyclosporin

 Photochemotherapy
 Prognosis

Majority will get complete regrowth sometimes without treatment in

1 year. A small percentage end up with severe chronic form.

 Poor prognostic indicators :

Onset in childhood, atopy, positive family history, extensive

involvement , nail dystrophy, other auto-immune conditions.
 Androgenetic alopecia (AGA)

 Most common cause of hair loss.

 Male patterned baldness(MPB) : 50% men affected by the age of 50

years.

 Female patterned hair loss(FPHL): 20-50% women affected by age of

50 years.

 Most likely inherited as autosomal dominant/ polygenic trait from

either parent; more from father.
 Pathogenesis

 Hormonal factors - 5 alfa reductase changes testosterone to

dihydrotestosterone (5-DHT).

 5 DHT facilitates miniaturization of hair.

 Aromatase in contrast inhibits process of miniaturization.

 Androgen receptors may be increased or may be hyper-responsive in

areas affected by AGA.
 Clinical features

 Pigmented terminal hairs are progressively replaced by finer, short

and virtually non-pigmented hairs.

 MPHL: pattern of progression is uniform; starts as frontoparietal

recession and involves the entire scalp sparing the occipital fringe;
graded into 8 stages by Hamilton.

 FPHL : widened central parting earliest sign; progresses through 3

stages of Ludwig.
Male Pattern Alopecia
Female Pattern Alopecia
 Androgenetic Alopecia

Patterned Non scarring alopecia : Androgenetic Alopecia

 Female Pattern Hair Loss

Patterned Non scarring alopecia

 Treatment

 Medical :

• Topical Minoxidil (2 to 10%)

• Oral Finasteride (1 mg or less)

 Surgical :

• Follicular unit transplant/extraction

• Scalp reduction

 Cosmetic cover :

• Wigs, hair bonding, hair weaving

 Telogen effluvium (TE)

 Sudden significant hair loss 2-3 months after an offending insult where hair
follicles are pushed prematurely from anagen to telogen phase.

 Offending insults : fever, post partum, crash dieting, hypoproteinemia, iron

deficiency, major surgeries, prolonged anaesthesia, hypo and
hyperthyroidism, major internal disease, acute psychologic stress and
medication.
 Trichotillomania

 Psychiatric disorder in which there is a compulsive habit of pulling out

the hair.

 Bizarre pattern of hair loss in which hair is twisted and broken at

various distances from clinically normal scalp

 Management : may vary from identification of stressful episode with

accompanying support, parent education, support of psychologist and
psychiatrist, drug therapy (antidepressants etc.)
Trichotillomania
 Alopecia due to tinea capitis

 Seen essentially in pre-pubertal age group

 It is patchy, incomplete and is due to breakage of hair shaft invaded
by dermatophytes.
 It is fully reversible except in cases of inflammatory involvement due
to species of dermatophytes derived from animals/soil or if
inflammatory process destroys the hair follicles
 Cicatricial alopecia

 Seen as an area of thin, shiny, dry and depressed skin with

telangiectasia; absence of follicular openings.
 Could be developmental / hereditary, traumatic, secondary to tinea
capitis, discoid lupus erythematosus, herpes zoster, bacterial
infections, neoplastic disorders, cicatricial pemphigoid, pseudopelade
of Brocq
 Treatment: Excision and primary closure for small patches,
autografting and scalp expansion, cosmetic camouflage for large
patches.
Scarring Alopecia
 Excessive hair

 Growth of hair that in any given site is coarser, longer or more

profuse than is normal for the age, sex and race.
 Hirsutism : androgen dependent hair patterns of typically terminal
hair.
 Hypertrichosis : patterns of increased hair growth involving non-
androgen dependent follicles.
 Hirsutism

 Growth in females of coarse terminal hair in adult male pattern of

distribution i.e. face, chest, upper back.
 Androgen dependent.
 Idiopathic or due to hyperplasia / tumors involving ovaries, adrenal
cortex or pituitary.
 May be due to drugs, reduced plasma sex hormone binding globulin,
increased androgen receptor or 5 alfa reductase activity in skin.
 Other causes : HAIR-AN and SAHA syndromes.
 Approach to a hirsute patient

 Enquire about the pattern of hirsutism, alopecia, features of

virilisation.
 Probe into the menstrual history, family history and intake of drugs
such as glucocorticoids, anabolic steroids.
 Systemic examination: Deepening of voice, muscle bulk, loss of body
contours, hypertension, striae distensae and clitoromegaly.
 Cutaneous examination: Associated acne, acanthosis nigricans,
androgenetic alopecia.
 Investigate to rule out hormonal aberrations like polycystic ovarian
disease or androgen secreting tumors.
 Treatment

 Cosmetic : depilatory creams, plucking, bleaching, electrolysis,

eflornithine.
 Lasers : Long pulse Nd:YAG, intense pulse light, diode, alexandrite.
 Hormonal correction : any tumors have to be removed.
 Drugs : cyproterone acetate, finasteride, flutamide, spironolactone,
leuprolide, ketoconazole, medroxyprogesterone acetate.
 Hair pigmentation and cosmetics

 Canities : greying of hair with age.

 Premature canities : onset of greying before 20 years in Caucasians
and 30 years in Africans.
 Poliosis : localised patch of grey hair; congenital and acquired.
 Hair cosmetics : shampoos, conditioners, hair dyes and bleaches.
Nails
 Functions of nails

 Help to grasp and manipulate objects

 Help in ‘pincer grip’

 Protect terminal phalanx and fingertip

 Serve an aesthetic and cosmetic purpose

 Nail changes in systemic diseases

 Clubbing
 Koilonychia
 Beau’s lines
 Subungual hematoma / Splinter hemorrhages
 Color changes of nails
 Periungual / subungual tumors
 Clubbing

3 major categories :
 Idiopathic
 Hereditary - congenital
 Acquired :

80% cases associated with

respiratory ailments, 10-15%
with cardiovascular and the rest
with various extrathoracic
diseases like Inflammatory bowel
disease.
 Koilonychia (spoon nails)

3 types :
 Idiopathic
 Hereditary
 Acquired :

Trauma, dermatologic diseases,

Raynaud’s phenomenon, iron
deficiency (not the most
common cause)
 Beau’s lines

 Transverse depression across nail

plate.
 Caused by serious systemic
illness, drug reaction, bullous
dermatoses, severe psychologic
stress, local trauma, eczemas,
idiopathic.
 Nail changes due to systemic drugs

 Asymptomatic growth rate change and pigmentation abnormalities are the

most common changes.

 Other changes: Transient shedding, photo-onycholysis, brittle nails, Beau’s

lines, permanent nail deformities.

 Common drugs : Antibiotics like tetracycline, cephalosporins;

fluoroquinolones, antimalarials, retinoids, psoralens, chemotherapeutic
drugs.
 Common skin conditions with nail changes

 Psoriasis

 Lichen planus

 Fungal infections

 Bacterial infections

 Viral infections

 Ingrown nails (trauma induced)

 Eczemas
 Nail psoriasis

 Seen in up to 50% of patients with psoriasis

 May be the first manifestation of psoriasis

 Seen in several nails; both finger and toe nails may be affected

 Diagnostic signs include extensive irregular pitting, oil drop sign and
onycholysis with erythematous borders.

 Other abnormalities often seen are nail thickening, subungual

hyperkeratosis, nail crumbling etc.
Nail psoriasis
 Nail Lichen planus

 Nail abnormalities evident in 10% cases with skin / mucosal lichen

planus

 Also occurs in absence of skin / mucosal involvement

 Thinning and longitudinal ridging / fisssuring of nail plate, pterygium

formation, subungual hyperkeratosis

 Permanent destruction may occur

Lichen planus
 Onychomycosis

 Involvement of one / few nails

 Examination of skin may give a clue

 Four patterns of onychomycosis

• Distal and lateral subungual onychomycosis (DLSO)

• Proximal subungual onychomycosis (PSO)

• White superficial onychomycosis (WSO)

• Total dystrophic onychomycosis (TDO)

 Onychomycosis : causes

 Caused by dermatophytes, candida and moulds.

 Is known to affect >10% of population in western world.

 Predisposing factors : occlusive footwear, diabetes mellitus,

hyperhidrosis, immunosuppression, trauma, poor peripheral
circulation.

 Most common pathogens are Trichophyton rubrum, Trichophyton

mentagrophytes and candida species.
Onychomycosis : see one hand involvement
 Ingrown nail

 Common condition due to

piercing of nail plate into lateral
nail fold
 Improper trimming of nails and
tight, ill-fitting footwear
 Great toe nail most commonly
involved
 Causes inflammation, pain and
sometimes formation of extra
granulation tissue
 Colour changes in nails

Leuconychia Nail hyperpigmentation

 Useful investigations

 KOH mount

 Mycologic culture

 Nail clipping

 Biopsy-nail plate/nail bed

 Radiologic studies
 Therapeutic procedures

 Chemical nail avulsion using 40% urea

 Nail avulsion : partial and total

 Nail splinting

 Nail matrix injections

 Chemical / surgical matricectomy

 Electrosurgery / radiosurgery / cryotherapy, laser ablation of growths like

verrucae, myxoid cyst

 Surgical removal of growths like glomus tumor

 MCQ’s

Q.1) Which phase of hair cycle has maximum duration among the following?
A. Catagen
B. Telogen
C. Kenogen
D. Anagen

Q.2) Which of the following is not a poor prognostic marker in alopecia

areata?
E. Nail involvement
F. Oophiasis pattern
G. Solitary patch
H. Associated Autoimmune diseases
 MCQ’s

Q.3) Nail involvement is seen in what percentage of psoriasis patient?

A. 10 %
B. 50%
C. 20%
D. None

Q.4) What is the most common pattern of nail involvement in

onychomycosis?
E. Distal - lateral subungal onychomycosis (DLSO)
F. Proximal subungal onychomycosis (PSO)
G. Total dystrophic onychomycosis (TDO)
H. White superficial onychomycosis (WSO)
 Photo Quiz

Classify the type of alopecia and enumerate few causes

 Photo Quiz

Identify the nail disorder

Thank You!