Alopecia

ALOPECIA

• DR. MANAR GHANEM

Hair Structure [Anatomy of the Hair Follicle]

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Hairs are classified into three main types:

• Lanugo hairs: Fine long depigmented hairs covering the fetus, but shed about 1 month before birth.
2. Vellus hairs: Fine short unmedullated hairs, but coarses than lanugo hairs covering much of the body surface. They replace the lanugo hairs just before birth.

3. Terminal hairs: Long coarse medullated (pigmented) hairs seen, for example, in the scalp, and pubic region.
Classification of Hairs
Terminal hairs vellus (male pattern alopecia)


Vellus hairs terminal (hirsutisim)

Each follicle passes, independently of its neighbours, through regular cycles of growth and shedding. There are three phases of follicular activity:

• Anagen: The active phase of hair production.

lasts for 3-5 years. Account for 85% of scalp hair
• Catagen: A short phase of conversion from active growth to the resting phase. Growth stops, and the end of the hair becomes club-shaped. last about 3 weeks. Account 1-2 % of scalp hair.
• Telogen: A resting phase at the end of which the club hair is shed. last about 3 months. Account 14% of scalp hair.
The Hair Cycle

• The duration of each of these stages varies from region to region.

• The scalp contains an average of 100 000 hairs.
• As many as 100-150 hairs may be shed from the normal scalp every day as a normal consequence of cycling.
• Average scalp hair growth: 0.35 mm/day or ~ 1cm/month.
• Cutting or shaving the hair have no effect on hair growth.
• Female hair grows faster than male hair.

CLASSIFICATION OF ALOPECIA

• Localized A. is characterized by well-defined patchy areas of hair loss, while diffuse hair loss involves the whole scalp.
• Non-scarring A. has better prognosis than scarring A. as the hair usually grow again after a time because the hair roots are preserved.
• Hair loss in scarring A. is permanent [no hope for cure] due to damaged hair roots by the scarring process.

CAUSES OF LOCALIZED NON-SCARRING ALOPECIA

• Alopecia areata
• Androgenetic alopecia (Early stages)
• Tinea capitis (early treatment may prevent scarring)
• Pyogenic infections e.g. boils or folliculitis.
• Moth-eaten alopecia (Secondary syphilis)
• Traumatic alopecia:
• Trichotillomania [Hair pulling habit]
• Traction alopecia
• Neonatal frictional alopecia (Occipital)





Gray-patch tinea capitis presented as localized non scarring alopecia. [Alopecia, erythema and scaliness]

Traction alopecia

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Traumatic hair loss in a newborn “Frictional alopecia”

CAUSES OF LOCALIZED SCARRING ALOPECIA
• Physical injury e.g. trauma and burn
• Severe infections
• Fungal infections e.g. Kerion or Favus
• Bacterial infections e.g. Boils and Carbuncles
• Protozoal infestation (e.g. cut. leishmaniasis)
• Viral infection e.g. Herpes zoster
• Neoplasms: Cicatricial BCC, SCC, Metastatic Ca
• Lichen planus (Lichenplanopilaris)
• CTDs e.g. DLE and Morphea
• Folliculitis decalvans
• Sarcoidosis
• Iatrogenic (IL-CS injections)

Localized cicatricial alopecia (LP)

Localized scarring alopecia due to lichenplanopilaris

Localized scarring alopecia [DLE]

DLE

CAUSES OF DIFFUSE ALOPECIA

• Androgenitic alopecia
• Diffuse alopecia areata (A. totalis and A. universalis)
• Physiological (Neonatal alopecia)
• Anagen effluvium
• Telogen effluvium


Alopecia areata
AA is one of the commonest hair problems in dermatological daily practice. It affects about 1-2% of the patients seen at out-patient skin clinics.
It is an acquired idiopathic disorder characterized by well-defined, single or multiple, non-cicatrical patches of hair loss.
It may affect any age group, although more common in young people. Both sexes are equally affected.
AA can involve any hairy area in the body (scalp, eyebrows, eyelashes, moustache, beard, axillary hair, pubic hair, body “truncal” hair and hair of the extremities).
الحاصة البقعية ”داء الثعلب“

• Immunological factors: AA may be considered as an autoimmune disease for the following reasons:
• Association with other autoimmune disorders like vitiligo, atopic dermatitis, Hashimoto’s thyroiditis , Addison’s disease, DM, Pernicious anemia …..etc.
• Presence of circulating organ specific auto-antibodies e.g. anti-thyroid antibodies .
• Histologically, T lymphocytes around affected hair bulbs.
• Genetic factor: about 10-25% of cases may be familial.
• Psychological factor: Severe psychological upset probably acts as a precipitating or triggering factor.
Aetiology of AA

Patches of AA occur most commonly in the scalp and secondly in the beard area.

The skin in the involved area is normal i.e. no scarring, scaling or erythema.

Close examination of the alopecic patches may show the tendency of hair at the periphery of these patches to be thinner proximally and thicker distally and look like an exclamation mark [!]. Exclamation mark sign indicates active disease but not necessarily bad prognosis.


AA may involve the nails and up to 50% of patients may show fine pitting of the nails.
Clinical picture:

An exclamation-mark hair

Pathognomonic exclamation mark hairs seen around the edge of alopecic areas. They are broken off about 4mm from the scalp, and are narrowed and less pigmented proximally.

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Extensive AA

AA in the beard
A. universalis
Different severities of AA

The characteristic uninflamed patch of alopecia areata

AA: Single patch in the scalp of an adult person

Two patches of AA, the upper patch showing white hair at its periphery

The outcome is unpredictable.






In the first attack, regrowth is usual within a few
months.



Subsequent episodes tend to be more extensive & regrowth is slow.





Few patients loss all the scalp hair (alopecia totalis), or from the whole skin surface (alopecia universalis).





The hair lost in AA may become grey-white in color on regrowth especially on spontaneous regrowth i.e. without treatment.






AA usually dose not affect grey hair (only pigmented hair is involved by AA).

Course

White hair
Post A.A.

• Unusually widespread alopecia especially alopecia totalis and alopecia universalis.

• Early onset of the disease i.e. onset before puberty.
• Multiplicity of the patches.
• Chronicity (Recurrent cases).
• Presence of nail changes.
• Involvement of the scalp margin (Ophiasis),especially at the nape of the neck.
• Familial AA [Positive F.H of AA].
• Association with atopy or Down’s syndrome.
Bad Prognostic Pointers (Signs) in AA

Bad Prognostic signs

Differential diagnosis
• Tinea capitis.
2. Traction alopecia.

3. Trichotilomania

4. Secondary syphilis.

5. DLE (DISCOID LUPUS ERYTHEMATOSUS )

6. Lichen planus

Management of AA

• Reassurance (not contagious with high rate of spontaneous recovery). The aim of therapy is to facilitate recovery.
• Topical irritants to stimulate hair growth such as dithranol (0.1–0.25% ), Garlic, Plant extracts ….etc. are often used but with limited success.
• Topical minoxidil 5% solution.
• Topical corticosteroids.
• Intralesional steroids (triamcenolone 5-10 mg/ml)
• PUVA may be considered in resistant cases unresponsive to other therapies and in extensive cases like A. totalis and universalis.
• Immunomodulators e.g. Oral zinc sulfate
• Wigs may be necessary for extensive cases.


Trichotillomania
• Trichotillomania ( Hair-pulling habit ) is a discomfort habit in children like nail-biting and lip-licking. It is a type of traumatic localized non-scarring alopecia not uncommonly seen in children and occurs more in girls than in boys.
• Affected individuals may have obsessive compulsive neurosis.
• The usual involved sites are the sides of the scalp or the fronto-vertical area.
• The hairs in the affected area are usually broken at different lengths from the scalp surface which is a characteristic feature of trichotillomania.

Trichotillomania

Diagnosis
can usually be made on the history.
The patches are irregular in outline and hair loss is never complete.

Management includes

-reassurance, explanation to the parents or the patient that it is due to the habit of hair pulling,
- tranquilizers may be given and referral to psychiatrist may be necessary in some cases.
Trichotillomania


Traction alopecia
• Hair can be pulled out by many methods:
hot combing, tight hairstyle & using hair rollers.
• Hair being lost in area of maximal tension.
• Marginal alopecia is a common pattern, in which hair loss occur around the edge of the scalp (at the sides or at the front).
• The bald area show short broken hairs, folliculitis & sometime scarring.

• Traction

Male pattern alopecia

• Its a physiological reaction induced by androgen in genetically predisposed men.
• Its inheritance is polygenic.
• Thinning of hair begin between 12 - 40 years.
• About 50% of the population develop this condition before the age of 50.
• Its due to progressive shortening of successive anagen cycles.

Hamilton scale for grading male pattern hair loss.

Male-pattern hair loss in a man

1. Topical minoxidil 2%, 5%.

2. Oral fenisteride 1mg, 5mg.
3. Hair transplant.
4. Scalp reduction & flap.

Treatment:

Female pattern alopecia

In females, normal androgen level causes baldness only in strongly predisposed women (less predisposed women need high androgen level to produce baldness). The female hormone, estrogen, may have protective role in preventing common baldness.

It affect females in their 20s or 30s.

There is gradual loss of hair on the central scalp, with retention of the normal hair line without fronto-temporal recession.

Differ from male pattern baldness:

• In females, diffuse thinning of the fronto-vertical hair with preservation of the frontal line.
There may be a moderate loss of hair on the crown,
but this rarely progresses to total or near baldness
as in men.

2. Male pattern baldness can begin at puberty where

as female pattern baldness begins around thirty,
& it gets worse with menopause.

Ludwig scale for grading female pattern hair loss

Pattern of hair loss in women with androgenetic alopecia

Male
Female

Telogen Effluvium

• Premature termination of anagen & high number of normal hairs enter the resting telogen phase.
• Usually no more than 50% of the hair is affected.
• The follicle is not diseased, scarring & inflammation are absent.
• Resting hairs on the scalp remain about 100 days before
• they lost, so telogen hair loss should occurs approximately
• 3 months after the event.
• The hair loss begins abruptly & last about 4 weeks.
• Full recovery can be expected.
•

Causes of telogen effluvium:

Can be triggered by any severe illness or condition. The most common causes are:

• Parturition (Postpartum telogen effluvium)

• Fever (Post febrile telogen effluvium): may be caused by any febrile illness.
• Severe dieting: Kwashiorkor, starvation diet, and inappropriate weight reduction programs.
• Severe stress (major surgery, hemorrhage, car accident, severe psychological upset …..etc.)
• Hypothyroidism
• Renal dialysis
• Drugs (Drug-induced telogen effluvium): the most common ones are: Bromocreptine, Captopril, Coumarin anticoagulants, Carbamazepine, etc…

Post febrile telogen effluvium

There is no specific therapy for telogen effluvium but the patients can be reassured that their hair fall will be temporary and hair will grow again after few months.
Treatment

Anagen Effluvium

Abrupt loss of hair from follicles that are in their growing phase.

The only hair left are those in the telogen phase.

The rapidly dividing cells of the matrix & cortex are affected.

90% of the scalp hairs are in anagen phase, so a large number of hair can be affected.

• With cessation of drug therapy, anagen follicles resume their normal activity within a few weeks; the process is entirely reversible.
Causes:
1. Chemotherapy.
2. Radiotherapy.
3. Poisoning: arsenic, lithium….





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