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HAIR
PROF. IHAB YOUNIS
Hair Anatomy
The hair follicle can be divided into 3 regions:
I-The lower segment (bulb and suprabulb): extends from the base of the follicle to the insertion of the erector
pili muscle.
II-The middle segment (isthmus): extends from the insertion of the erector pili to the entrance of the sebceous
gland duct.
III -The upper segment (infundibulum):extends from the entrance of the sebaceous gland duct to the
follicular orifice.
A hair consists of:
I-The bulb includes:
1-The papilla protrudes into the hair bulb and is responsible for instigating and directing hair growth.
2-The hair matrix surrounds the papilla. It consists of epithelial cells often interspersed with melanocytes.
The hair matrix epithelium is one of the fastest growing cell populations in the body. Matrix is composed of:
A-Inner root sheath
It coats and supports the hair shaft up to the level of the isthmus, at which it breaks down and exfoliates.
B-The outer root sheath
It covers the inner root sheath as it extends upward from the matrix cells at the lower end of the hair bulb to
the entrance of the sebaceous gland duct .
II-Hair shaft: Consists of 3 layers:
1-Cuticle: The outermost layer & consists of overlapping cells.
2-Cortex:The middle layer &constitutes the bulk of the hair and consists of cells that keratinize gradually as
they move upward from the hair matrix.
3-Medulla:The innermost layer is often completely absent in many cases.
The hair growth cycle
The hair growth cycle has three different phases:
Phase 1 – Anagen (85-90% of body hair)
•During the anagen phase, hair cells grow rapidly, producing the hair shaft from the follicle, which itself
grows deeper into the scalp. The length of anagen phase determines the maximum length of hair.
•Anagen hair bulbs are located in the subcutaneous fat.
•Phase 2 – Catagen (10-14% of body hair)
•It is the transitional or regressive phase. Essentially, it is when the hair stops growing and follicle shrinks
and part of it starts to die.
•Catagen bulbs are in the dermis.
•Phase 3 – Telogen (1-2% of body hair)
•It is the final resting stage.
•When the old hair is in this phase, the hair follicle becomes active again and a new hair in the anagen phase
develops, forcing the old telogen hair out. This is when we notice hairs in the bath or in brush, about100
scalp hairs are shed daily.
•Telogen bulbs are in the mid-to-upper dermis.
Duration of different phases of hair growth cycle
Telogen
Catagen
Anagen
2-3 years
3 months
2-3 weeks
Scalp
Other areas 4-7 months up to 9 months 3-4 weeks
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•At any particular time, not all human hair follicles in any given anatomical location are in identical growth
stages; some are in the anagen, while others are in the telogen or catagen .This phenomenon is referred to as
the mosaic pattern and is in contrast to some animals whose follicular units all are synchronized .This
explains some animals' ability to shed winter coats when the ambient temperature becomes warm, while
humans do not go bald during the follicular rest period.
•Scalp hair grows at an average rate of 0.4 mm/day, roughly 1 cm/month.
•It takes about 3 years for hair to reach the shoulders.
•Hair that is level with the waist is around five years old.
•Hair long enough to sit on, maybe as much as 12 years old.
Hormonal effects on hair growth cycle
•A loss of hairs at about two to three times the normal rate gives rise to a transient alopecia about 4-6 months
after parturition. At this time, the proportion of hairs in telogen can be as much as 15% whereas in late
pregnancy it may be less than 5%.
•This suggests that the passage of follicles into catagen, followed by shedding of club hairs, is slowed down
by pregnancy, but occurs precipitously after parturition when hormonal conditions are altered, particularly by
a rapid fall in estrogen.
•The effect of androgen will be discussed later.
Types of hair
•Lanugo hair:fine, soft, unmedullated and usually unpigmented hairs found on the fetus. They are normally
shed before birth and replaced by vellus hair by 36-40 weeks gestation.
•Postnatal hair may be divided into two kinds:
1-vellus, which is soft, unmedullated, occasionally pigmented and seldom more than 2cm long found on
children and women faces and the scalp of bald men.
2-terminal hair, which is longer, coarser, and often medullated and pigmented and found on scalp, eyebrows
and eyelashes and sexual hair.
Effect of age
•The first recognizable pubic hair appears at an average age of 13.4 years for boys and at 11.7 years for girls.
•Axillary and facial hair first appears about 2 years after the start of pubic hair growth.
The trichogram
•50 to 100 hairs are plucked from different parts of the scalp using a clamp with rubber tipped ends.
•The hairs are then examined under a microscope in order to determine which percentage of the hairs are in
each of the three phases of the hair growth cycle.
•Anagen hair usually have living cells on the root end, and the the root sheath around the lower hair fiber.
•Catagen hairs fibers have a tapered end.
•Telogen hairs have a club end and they do not have any living cells attached to the root.
•In order to determine at what rate baldness will progress, the proportion of anagen hairs is compared to the
proportion of catagen and telogen hairs
• As a (very) rough guide, a 10% telogen frequency is excellent and over 35% is a potential problem
•By repeating the trichogram over a time period, a hair loss condition can be followed. Equally, if a
treatment is being used, the effects of the treatment in terms of changing the frequency of telogen hairs, can
be measured
•Because the hair for examination is plucked out, the trichogram is not popular with most patients
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•In addition, the trichogram is becoming less popular with dermatologists because it is time consuming
Effect of Season on Hair growth cycle
• Scalp: Hair loss reaches a peak around August/September and is least in March where 90 % of follicles
are in anagen.
 Beared and Thigh: Growth is maximal in July and is lowest in January, probably reflecting changes in
circulating androgens.
I-EXCESSIVE HAIRINESS
Hirsuitism
Definition
•It the excessive growth of terminal hair in locations where hair growth in women usually is minimal or
absent as the face, chest, and areolae.
•It is different from hypertrichosis which refers to excess hair (terminal or vellus) in areas that are not
predominantly androgen dependent.
Etiology
•Hirsutism is common and is estimated to occur in 1 in 20 women of reproductive age in the United States
•The age of onset of hirsutism depends on its cause.
Causes
I-Endocrine-related causes
II-Idiopathic
III-Drug-related causes
IV-Familial hirsutism
V-Other causes
I-Endocrine-related causes
A-Ovarian causes
1-Polycystic ovary syndrome(PCOS)
•It is the most common cause of androgen excess and hirsutism.
•Virilization is minimal, and hirsutism is often prominent.
•Characteristic features include menstrual irregularities, dysmenorrhea, obesity & occasionally glucose
intolerance.
•Cutaneous manifestations of androgen excess may occur e.g. recalcitrant acne, acanthosis nigricans, and
alopecia on the crown area of the scalp.
2-Ovarian tumors
•Luteoma of pregnancy.
•Arrhenoblastomas.
•Leydig cell tumors.
•Hilar cell tumors.
•Thecal cell tumors.
B-Adrenal causes
1-Congenital Adrenal Hyperplasia
•In children may cause hirsutism. These children may be born with ambiguous genitalia, symptoms of salt
wasting, and failure to thrive. Additionally, they may develop masculine features
•Adult patients have clinical features that resemble PCOS
2-Cushing syndrome
•It is a noncongenital form of adrenal hyperplasia characterized by an excess of adrenal cortisol production
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•The excessive growth is predominantly vellus (non–androgen dependent) hair
II-Idiopathic
•Such patients have normal menses, normal-sized ovaries, no evidence of adrenal or ovarian tumors or
dysfunction, and no significant elevations of plasma testosterone or androstenedione.
• One theory suggests that many of these women may have mild or early PCOS and androgen levels in the
upper-normal ranges.
•The underlying mechanism in these patients may be an increase in androgen sensitivity or in 5-alphareductase activity in the skin.
III-Drug-related causes
•Some drugs can induce hirsutism by their inherent androgenic effects e.g. testosterone, danazol, and
anabolic steroids.
•Drugs such as phenytoin, minoxidil, cyclosporine, streptomycin, psoralen, penicillamine, and high-dose
corticosteroids can cause hirsutism. The exact mode of action of these drugs on hair follicles is not known,
but it is not androgenic.
IV-Familial hirsutism
•It is not associated with androgen excess.
•It is both typical and natural in certain populations, such as in some women some women of the
Mediterranean or Middle East.
•It is found most commonly in southern European and South Asian countries, in which it is considered to be
a normal trait.
•It is uncommon in sub-Saharan and American blacks and is observed least commonly in East Asians and
Native Americans.
V-Other causes
•Less common but potentially serious disorders that may be associated with hirsutism include anorexia
nervosa, acromegaly, hypothyroidism, hyperprolactinemia, and porphyria.
Clinically
The onset of hirsutism can take one of several forms:
•In familial hirsutism, it often appears during puberty.
•In patients with PCOS and CAH it usually develops gradually.
•Hirsutism appears abruptly when an androgen-secreting tumor arises.
•The initial task in the evaluation of hirsutism via the physical examination is to quantitate the disorder. This
task requires that terminal hair, which depends on androgen, be differentiated from vellus hair, which is
androgen-independent.
•The most widely accepted method of quantitation uses the Ferriman and Gallwey scale. In this approach,
hair growth is judged in each of 11 androgen-sensitive areas which are:
o(1) the upper lip, (2) chin, (3) chest, (4) leg, (5) thigh, (6) upper arm, (7) forearm, (8) upper back, (9) lower
back, (10), upper abdomen, and (11) lower abdomen
oThe grade for each area ranges from 0 (no terminal hair) to 4 (frankly virile)
oA woman with a score of 8 or higher is considered to have hirsutism. The total score correlates roughly
with the elevation of androgen levels
In women with moderate-to-severe hirsutism (score >15), seek additional signs of hyperandrogenism,
including (1) temporal hair recession, (2) oily skin, (3) masculine voice, (4) well-developed musculature, (5)
enlargement of the clitoris (>35 mm2 in surface area), (6) irregular menses, and (7) psychological changes
(e.g. heightened libido, aggressiveness).
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Investigations
•Testosterone serum level: Start with total testosterone and if it is normal, measure the free serum level
because hyperandrogenism decreases SHBG, so the biologically active free testosterone may be elevated
even if the total level is normal.
•No direct correlation exists between the levels of testosterone and the degree of hirsutism, because hirsutism
is caused by the action of dihydrotestosterone, which is the more potent testosterone metabolite.
•In most patients in whom the total testosterone level is greater than 200 ng/dL (>100 ng/dL in
postmenopausal women), a tumor workup is indicated. This workup includes a pelvic examination and
ultrasound imaging, which usually are adequate to diagnose PCOS. If the test results are negative, an adrenal
CT scan is performed.
•Early morning testing is advised to measure testosterone levels.
•Testosterone levels vary during the different phases of the menstrual cycle by approximately 25%.
•Dehydroepiandrosterone sulfate (DHEAS): Because testosterone can originate in either the adrenal cortex or
the ovary, an elevated testosterone level does not indicate the gland of origin. Accordingly, measurement of
elevated plasma levels of DHEAS, an androgen synthesized almost exclusively by the adrenal cortex, can
indicate excess adrenal function. Elevations in both testosterone and DHEAS suggest an adrenal origin,
whereas an isolated testosterone elevation indicates an ovarian source.
•If a woman shows severe or rapidly progressive hirsutism or she shows signs or symptoms of virilism do:
1-Serum androstenedione: A level greater than100 ng/dL suggests the presence of an ovarian or adrenal
neoplasm.
2-LH&FSH:Often, in women with PCOS, LH levels are elevated and FSH levels are depressed.
Treatment
Weight loss should be encouraged for obese patients, because obesity increases SHBG levels leading to a
decrease in free testosterone and decreases insulin resistance and the levels of serum luteinizing hormones.
I-Methods of eliminating hair :
1- Shaving: It is the easiest and safest method. No evidence suggests that shaving increases the rate or
coarseness of subsequent hair growth but It is often unacceptable to some women as being too 'masculine‘.
2- Chemical depilatories (e.g., Calcium thioglycolate) available in foam, cream, liquid and aerosol
forms.They produce results similar to shaving, but skin irritation is common.
3- Bleaching the hair with H2O2: This is an easy measure but bleached hair can look very obvious against
dark skin and skin irritation may occur.
4-Plucking: It is widely performed, but the act of plucking not only removes the hair shaft but also stimulates
the root into the anagen leading to a brief delay till the shaft grows again.
5-Waxing: It is performed by the application of a sheet of soft wax onto the skin and, as soon as it has
hardened with the hair shafts embedded, it is abruptly peeled off the skin, removing all the shafts. This is a
painful method and is often complicated by folliculitis (depilation dermatitis). Certain natural sugars, long
used in parts of the Middle East, are becoming popular in place of waxes as they appear to depilate as
effectively, but with less trauma
6-Threading: It is a method used in some Arab countries, is a technique in which cotton threads are used to
pull out hairs by their roots. Home epilating devices that remove hair by an electrical rotary method are
available. Both methods may produce traumatic folliculitis(depilation dermatitis)
7-Eflornithine (Vaniqa cream) :
•Recently approved by the FDA
•Acts as a hair growth inhibitor
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•Reportedly takes up to 2 months to work in approximately 30% of patients
•A thin film is applied bid to areas of hair growth
8-Electrolysis( destruction of hair follicle by an electrically heated needle introduced in it) :It is the only
permanent method for removal of hair. However, it is costly and time consuming, and largely has been
supplanted by use of laser techniques.
9- Laser hair removal:Several lasers exist:
•Pulsed diode lasers are generally less expensive and more reliable than other laser sources for hair removal.
•Q-switched YAG lasers work well in patients with darker skin.
•These lasers are ineffective for long-term hair removal. Most patients experience a two- to six-month
growth delay after a single treatment, and some have permanent hair removal after multiple treatments.
•Laser therapy works best on dark hair.
•Post-treatment hyperpigmentation may occur.
II-Systemic Therapy
A-Antiandrogens
Careful selection prior to initiating therapy is important because:
1- The effect on hair growth takes several months to become apparent and only partial improvement may be
expected Also, therapy may need to be taken indefinitely.
2-Antiandrogens feminize male fetuses and it is essential to prevent pregnancy.
3-They only have a suppressive, and not curative, effect that disappears a few months after stopping therapy.
4-The long-term safety of these drugs is unknown and tumors in laboratory animals have been reported.
Types:
•Cyproterone acetate (Diane Tab. Cypro-terone acetate 2mg+ ethinyl estradiol 0.035 mg ) :one tab/day for 21
days starting from the first day of menstruation. It inhibits androgen receptors.
•Spironolactone (Aldactone 50 mg tab):50 mg PO bid; may increase to 200 mg/d.It decreases testosterone
production in the adrenal gland by depleting microsomal cytochrome P450 and it is also a competitive
inhibitor of DHT-receptors.
•Finasteride (Proscar 5 mg Tab ):5 mg daily. It Inhibits 5 alfa reductase.
•Flutamide (Eulexin): 250 mg two to three times daily. It inhibits androgen receptors.
B-Oral contraceptives
Marvelon tab(150mgDesogestrel/30 micro gm Ethinylestradiol ): One tablet per day for 21 days, followed by
seven-day pill- free interval.
•Results show reductions in hair growth of 20-25% after 6-9 months' therapy, with a high degree of patient
satisfaction.
C-Corticosteroids
•Prednisone(Hostacorten 5 mg tab) 20 mg/day or Dexamethazone (Deltazone) 0.25-1 mg PO qd.
•Used in adrenal causes of hirsutism because of their feed-back inhibitory effect on ACTH.
Hypertrichosis
•It is excessive hair growth (density, length) beyond accepted limits of normal for age, race, sex in areas that
are not androgen-sensitive
Types
1-Hypertrichosis lanuginosa:
•Congenial:Overgrowth of silvery blonde to gray lanugo hair at birth or in early infancy.It is very rare (1 in
1 billion).
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•Acquired: In the milder forms hair is confined to the face, where it attracts attention by its appearance on
sites that normally are hairless(e.g. the nose and eyelids).
•It may ultimately involve the entire body, apart from the palms and soles.
•It always signals an underlying malignancy.
2-Universal hypertrichosis:
•Hair pattern is normal but in any site the hairs are larger and coarser than usual.
•Inheritance is determined by an autosomal dominant gene.
•Most often seen in dark-skinned Mediterranean and Middle Eastern subjects.
3-Nevoid hypertrichosis:
•Hair growth abnormal for the site and the age of the patient in its length, shaft diameter e.g. in melanocytic
nevi and Becker’s melanosis.
4-Drug induced:
•Minoxidil,Phenytoin, Cyclosporine, Psoralins,Topical steroids and Streptomycin.
5-Acquired circumscribed hypertrichosis:
•Occupational trauma e.g. circumscribed patches of hypertrichosis on the left shoulder in people frequently
carrying heavy objects.
•Iatrogenic:e.g. the sites of wart removal, sites of chronic eczema, under plaster casts
6-Medical conditions:
•Hypothyroidism:A profuse growth of hair on the back and the extensor aspects of the limbs.
•Malnutrition: Malabsorption states or in severe infections, may cause profuse generalized hypertrichosis in
children.
•Anorexia nervosa:An increased growth of fine, downy hair on face, trunk and arms.
•Dermatomyositis:Excessive hair growth has been noted mainly in children and principally on the forearms,
legs.
II-HAIR LOSS
Alopecia Areata
Etiology
•Prevalence in the general population is 0.1-0.2%.
•AA is responsible for 2% of patients seen by dermatologists.
•AA can occur at any age. As many as 44% of people with AA have onset at younger than 20 years. Onset in
patients older than 40 years is seen in fewer than 30% of patients.
•The cause of AA remains unknown but factors related to the cause may include:
Autoimmunity
•The most widely accepted hypothesis is that AA is a T-cell mediated autoimmune condition that is most
likely to occur in genetically predisposed individuals.
•Lesional biopsies of AA show a perifollicular lymphocytic infiltrate around anagen phase hair follicles. The
infiltrate consists mostly of T-helper cells and, to a lesser extent, T-suppressor cells.
•Depletion of these T-cell subtypes results in complete or partial regrowth of hair.
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•Using immunofluorescence,
antibodies to anagen phase hair follicles were found in as many as 90% of
patients with AA compared to fewer than 37% of control subjects.
• Whether these antibodies play a direct role in the pathogenesis or whether they are an epiphenomenon is
not known yet.
•Remission can be induced in AA by grafting affected areas onto immunosuppressed animals.
•Transfer of grafts from normal mice to AA-affected mice resulted in hair loss in the grafts.
• In conclusion, certain factors within the hair follicles, and possibly, in the surrounding milieu, trigger an
autoimmune reaction.
Genetics
•Many factors favor a genetic predisposition for AA.
•A positive family history for AA was found in 10-20% of patients compared to 1.7% in control subjects.
•HLA DQ3 was found in more than 80% of patients with AA.
Cytokines
•Interleukin 1 and tumor necrosis factor were shown to be potent inhibitors of hair growth in vitro.
Subsequent microscopic examination of these cultured hair follicles showed morphologic changes similar to
those seen in AA.
Clinically
•AA most often is asymptomatic, but some patients (14%) experience a burning sensation or pruritus in the
affected area.
•A single patch occurs in 80%,12.5% have 2 patches, and 7.7% have multiple patches. No correlation exists
between the number of patches at onset & subsequent severity.
•The skin of AA is smooth, slightly erythematous or normal-colored.
•Presence of exclamation point hairs (i.e. hairs tapered near its proximal end) is pathognomonic but is not
always found.
•Positive pull test at the periphery of a plaque usually indicates that the disease is active, and further hair
loss can be expected.
•AA affects the scalp in 66.8-95% of patients,however, the beard in 28%, eyebrows in 3.8%, and extremities
in 1.3% of patients. More than one area can be affected.
•In localized (<50% involvement) patchy AA; spontaneous regrowth occurs in most patients within a few
months, with or without treatment.
•In a study involving 736 patients, the relapse rate was 90% over 5 years.
•AA can be classified according to its pattern into:
o Localized and patchy.
o Reticular pattern: occurs when hair loss is more extensive and the patches coalesce.
o Ophiasis: hair loss localized to the sides and lower back of scalp.
o Sisaipho (ophiasis spelled backwards): occurs when hair loss spares the sides and backof the head.
o Alopecia totalis:100% hair loss on the scalp.
o Alopecia universalis: complete hair loss on all hair-bearing areas.
Nail involvement
•Occurs in 6.8-49.4% of patients and most commonly is seen in patients with severe forms
•Pitting is the most common finding
Associated conditions
•Atopic dermatitis is seen in 9-26% of patients& vitiligo in 2-3% of patients.
•Clinically evident thyroid disease was found in 0.85% of patients.
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•Collagen vascular diseases have been found in 0.6-2% of patients.
•AA is seen in 6-9% of patients with Down syndrome.
•Psychiatric diseases are seen in 17-22% of patients.
•Major stress factors (e.g. death in family) were reported in 12% of patients.
Treatment
I-Corticosteroids
A-Intralesional steroids:
•They are the first-line treatment in localized conditions.
•Triamcinolone acetonide (Kenacort A 40 mg) is used most commonly; concentrations vary from 5-10 mL.
•Less than 0.1 mL is injected per site, and injections are spread out to cover the affected areas
(approximately 1 cm between injection sites.
•Injections are administered intradermally using an insulin syringe(30-gauge needle).
•Injections are administered every 2-4weeks.
•Regrowth occurs in 92% of patients with patchy AA and 61% of patients with AT.
•Regrowth usually is seen within 4-6 weeks in responsive patients. Patients with rapidly progressive,
extensive, or long-standing AA respond poorly.
•Hair growth may persist for 6-9 months after a single injection.
•If no growth is present at 3 months, it is generally not worth continuing the procedure.
•Adverse effects mostly include pain during injection and minimal transient atrophy (10%). Atrophy takes
the form of a dent that usually returns to normal in 6 months.
B-Topical steroids:
• Their usefulness remains under debate.
• For children, topical corticosteroids may be the most practical alternative.
• Betamethasone dipropionate cream (Diprosone) induced regrowth in 61% of patients with localized lesions
•Clobetasol propionate(Dermovate) under occlusion induced regrowth in 28.5% of patients with AT/AU
after 6 months. Treatment must be continued for a minimum of 3 months before regrowth can be expected,
and maintenance therapy is necessary.
•The most common adverse effect is local folliculitis, which appears after a few weeks of
treatment,telangiectasias and local atrophy. No systemic adverse effects have been reported.
C-Systemic steroids
•Prednisolone 40 mg was used for 3 days, then the dose was reduced by 5 mg every 3 days until the patient is
tapered off the drug
•Although the initial regrowth appears promising, the prednisone dose necessary to maintain cosmetic
growth usually must be high enough that adverse effects are inevitable, and most patients relapse after
therapy is discontinued
II-Topical immunotherapy
•It is the induction of an allergic contact dermatitis by topical application of potent contact allergens e.g.
squaric acid dibutylester (SADBE) and diphencyprone (DPCP).
•Topical immunotherapy has been used for almost 20 years with no serious adverse effects reported.
However,FDA does not approve the use of DPCP, but approves SADBE provided that it will be administered
in a physician's office.
•These therapies are generally reserved for patients older than 10 years of age and for those with greater than
50% of the scalp involved.
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•Treatment is provided weekly.
•The patient first is sensitized directly on the scalp with a 2% concentration on a small area (2 cm).
•The following week, a low concentration (0.0001%) is applied.
•The concentration is increased slowly every week as needed until a mild tolerable allergic contact dermatitis
is elicited.
•The response rate varied with the extent of the alopecia: Cosmetically acceptable regrowth was seen in
17.4% of patients with AT/AU, 60.3% in patients with 75-99% hair loss, 88.1% in patients with 50-74% hair
loss, and 100% regrowth in those with 25-49% hair loss.
•A lag period of 3 months was usually present between the onset of therapy and the beginning of regrowth.
•The relapse rate after reaching significant regrowth was 62.6%.
•Adverse effects include pruritus, blistering, secondary infection, urticaria and cervical lymphadenopathy.
Vitiligo has developed on the application site in 6.7-7.5% of patients.
III-PUVA
•Both systemic and topical PUVA therapies have been used.
•Regrowth occurs after 20-40 treatments.
•The success rate to be at best 6.3% for partial AA and 12.5% for AT and AU. PUVA generally is not an
effective long-term treatment for AA.
IV-Minoxidil
•Used in patients with extensive disease(50-99% hair loss).
•The 5% solution appears to be more effective.
•Initial regrowth can be seen within 12 weeks, but continued application is needed to achieve cosmetically
acceptable regrowth.
•Response rates vary from 8-45%.
•It is of little benefit in patients with AT/AU.
Androgenetic Alopecia
Etiology
•Inheritance may be determined by a number of genes.
•The AR gene provides instructions for making androgen receptors.
•Variations in the AR gene lead to increased activity of androgen receptors in hair follicles leading to
increased activity of DHT.
•DHT attacks hair follicles on the head and destroy them.
•Not all women with pattern hair loss have proven androgen-dependence.
•The majority of women with pattern hair loss have no increase in serum androgens, no other
signs/symptoms of androgen hypersensitivity, and do not respond to androgen inhibition with reversal of hair
loss.
•Women with profound hyperandrogenemia, which is usually due to a tumor related or PCOS, may develop
severe diffuse central scalp hair loss.
•It is an extremely common disorder that affects roughly 50% of men and perhaps as many women older
than 40 years.
•In premenopausal women 13% have some evidence of androgenetic alopecia. After the age of 40 years it
may affect around 50%.
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•However, the incidence increases
greatly in women following menopause, it may affect 75% of women
older than 65 years.
Clinically
I- Males:
•There is gradual replacement of terminal hair by smaller hairs.
•It occurs a characteristic pattern, which spares the posterior and lateral scalp margins, even in the most
advanced cases, and even in old age.
•The Hamilton pattern shows a sequence starting by bitemporal recession followed by balding of the vertex.
•Variations in the pattern are governed at least in part by genetic factors.
•The rate of progression is probably determined by heredity.
II- Females:
•The most frequent presentation in women is a diffuse alopecia over the crown. This produces a gradual
thinning of the hair rather than an area of marked baldness.
•Unlike men, the frontal hairline is often preserved in women with this disorder.
•Hair patterns of the classical 'male type' shown by Hamilton occur with increasing frequency after the
menopause.
Treatment
I- Medical treatment
1- Minoxidil(Hair back,Performa,Hair gain spray)
•Mode of action is essentially unknown, minoxidil appears to cause vasodilatationion. Vasodilation
lengthens the duration of the anagen. Regrowth is more pronounced at the vertex than in the frontal areas and
is not noted for at least 4 months.
•The medication should be applied to the scalp twice a day, with the earliest clinical response seen at 4 to 6
months and generally a maximum response at 1 year.
•Continuing topical treatment with the drug is necessary indefinitely because discontinuation of treatment
produces a rapid reversion to the pretreatment balding pattern.
•Patients who respond best are those who have a recent onset of androgenetic alopecia and small areas of
hair loss.
•About 20 to 25 % of patients will have notable clinical regrowth, although most patients will experience at
least a stabilization of loss.
•A 48-week study compared the 2 strengths in men and found that 45% more regrowth occurred with the
5% compared with the 2% solution.
•In general, women respond better to topical minoxidil than men. The increase in effectiveness of the 5%
solution was not evident for women. In addition, the occurrence of facial hair growth appears to be increased
with the use of the 5% solution.
2-Fenistride(Nopecia 1 mg cap)
•It is a 5 alpha-reductase type 2 inhibitor.
•Dose : 1 mg PO once daily.
•It can be used only in men because it can produce ambiguous genitalia in a developing male fetus.
•It has been shown to diminish the progression of androgenetic alopecia and, in many patients, it has
stimulated hair regrowth.
•Sexual adverse events occurred in 1.8 % of those on the drug versus 1.3 % of those on placebo.
3-Dutastride
 It inhibits both type 1 and 2 of 5-alpha reductase .
 The most common adverse reaction was impotence (1%).
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 The FDA has not given approval for using dutasteride to treat male pattern hair loss.
II- Surgery
•Micrografts produce a natural-looking frontal hair line.
•Rotation flaps from the parietal to the frontal area may give a better appearance.
•Reduction of the bald area by removal of an ellipse from the vault may cover the top of the head by
stretching the remaining parietal scalp.
•Expansion techniques have been used successfully.
Telogen effluvium
•It is the shedding of hair, due to premature entry
of anagen follicles into telogen, a process which may be a
response of the follicles to many different types of stress.
•The emerging hairs help to force the resting hairs out of the follicle. The interval between the inciting event
in telogen effluvium and the onset of shedding corresponds to the length of the telogen phase (average 3 mo).
Etiology
•Acute illness such as febrile illness, severe infection, major surgery and severe trauma.
•Chronic illness such as malignancy, and any chronic debilitating illness, such as systemic lupus
erythematosus, end-stage renal disease, or liver disease.
•Hormonal changes such as pregnancy and delivery (can affect both mother and child), hypothyroidism, and
discontinuation of estrogen-containing medications.
•Changes in diet like crash dieting, anorexia, low protein intake, and chronic iron deficiency.
•Heavy metals such as selenium, arsenic, and thallium.
•Medications, of which the most frequently cited are beta-blockers, anticoagulants, retinoids (including
excess vitamin A), carbamazepine, and immunizations.
•Allergic contact dermatitis of the scalp.
•This condition is quite common.
•Because hormonal changes in the postpartum period are a common cause of telogen effluvium, women may
have a greater tendency to experience this condition. In addition, women tend to find the hair shedding more
troublesome than men do; thus, more women seek medical attention for the condition. Chronic telogen
effluvium has been reported mainly in women.
Clinically
•Patients complain of falling out of hair at an increased rate. Occasionally, they note that the remaining hair
feels less dense.
•Telogen effluvium can be acute or chronic.
•In both forms hair is lost diffusely from the entire scalp but complete alopecia is not seen.
•Acute telogen effluvium is defined as hair shedding lasting less than 6 months. Patients complain of
relatively sudden onset of hair loss. Careful questioning usually reveals a metabolic or physiologic stress 1-6
months before the start of the hair shedding.
•Chronic telogen effluvium is hair shedding lasting longer than 6 months. The onset is often insidious, and it
may be difficult to identify an inciting event. Because of the duration of the hair shedding, patients are more
likely to complain of decreased scalp hair density, or they may note that their hair appears thin and lifeless.
Investigations
•In active telogen effluvium, the gentle hair pull test will yield at least 4 hairs with each pull. If the patient's
active shedding has ceased, the hair pull will be normal.
•The trichogram: If greater than 25% of extracted hairs are in telogen, the diagnosis is confirmed.
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•Scalp biopsy is the most useful test to confirm the diagnosis, although this is seldom necessary if the history
is characteristic and a gentle hair pull produces numerous telogen hairs.
•If a patient is unwilling to undergo a scalp biopsy but would like confirmation of the diagnosis, serial hair
collections may be obtained:
-The patient should be instructed to collect all hairs shed in a 24- hour period.This process should be
repeated every week or every other week, for a total of 3 or 4 collections.
- Collections totaling 100 hairs or more in a given 24-hour period are indicative of ongoing telogen
effluvium. If the collections are performed over several weeks while the telogen effluvium is resolving,
the number of hairs collected each time should decrease. This finding can be very comforting to the
patient.
Treatment
•Because acute telogen effluvium resolves spontaneously, treatment usually is limited to reassurance.
•While chronic telogen effluvium is less likely to resolve rapidly, reassurance is appropriate for these
patients. Often, the knowledge that the hair loss will not progress to baldness is comforting to the patient. The
patient should be encouraged to style the hair in a way, which masks any perceived defects in hair density.
•Any reversible cause of hair shedding, such as poor diet, iron deficiency, hypothyroidism, or medication
use, should be corrected.
•While topical minoxidil is not proven to promote recovery of hair in telogen effluvium, this medication has
a theoretical benefit and is well tolerated. Patients who are eager to play an active role in their treatment may
choose to use minoxidi
Traction alopecia
•It is a common cause of hair loss due to pulling forces exerted on the scalp hair.
•Hair loss is due to sustained traction which causes hair to loosen from its follicular roots and folliculitis and
atrophy.
•Three basic mechanisms of traction alopecia have been proposed:
1-Trichotillomania
2-Telogen conversion
3-Overprocessing
1-Trichotillomania
(Greek, hair-pulling madness)
•It is a compulsive habit that induces an individual to pluck hair repeatedly.
Etiology
•It occurs more than twice as frequently in females as in males, but below the age of 6 years boys outnumber
girls by 3:2.
•It is seven times more frequent in children than adults.
•Emotional deprivation in the maternal relationship may be important in initiating the habit.
Clinically
•In the younger patients, there is an ill-defined patch on which the hairs are twisted and broken at various
distances from the clinically normal scalp.
•The hair pulling tic develops gradually and unconsciously but is not usually denied by the patient.
•In the more severe form, the patient usually consistently denies touching his or her hair. The patient presents
with an extensive area of scalp on which the hair has been reduced to a coarse stubble uniformly 2.5-3mm
long. Most characteristically, the plucked area covers the entire scalp apart from the margin.
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Treatment
•Habit Reversal Training : patients are trained to recognize their impulse to pull and to redirect this impulse.
•Patients may be asked to record the date, time, location, and number of hairs pulled, as well what they are
thinking or feeling at the time. This can help the patient learn to identify situations where they commonly
pull out their hair and develop strategies for avoiding episodes.
•Treatment with Clomipramine(Anafranil), a tricyclic antidepressant, was shown to significantly improve
symptoms.
2-Telogen conversion
•It is the most common cause of traction alopecia.
•Excessive traction for prolonged periods (eg, cornrows , ponytails) leads to conversion of the anagen phase
to the telogen phase.
Clinically
•Patients usually complain of itching and dandruff.
• Marginal alopecia (alopecia linearis frontalis) results from the use of tight curlers, rollers during childhood.
•In this condition, the distribution of hair loss follows a characteristic pattern in the temporal scalp, starting
in the periauricular area and extending forward in a triangular manner.
•In chignon alopecia hair loss occurs in patients with a long history of pulling their hair into a bun.
•Similar to marginal alopecia, perifollicular erythema with occasional peripilar hair casts can be seen.
Treatment
•Immediately after traction alopecia is diagnosed, any practices that exert traction on the hair must be
discontinued. This leads to complete reversal of the hair loss and regrowth within several months.
•Topical or oral antibiotics may be prescribed to aid in the reduction of inflammation.
•When traction alopecia is detected later in its natural course, hair loss may be irreversible. Achieving
cosmetically acceptable correction of alopecia by means of surgical hair transplantation procedures (eg,
punch grafting, flap rotation) is possible.
3-Overprocessing
•Chemical treatment of hair with dyes, bleaches, or straighteners disrupts the keratin structure in a manner
that reduces its tensile strength.
•The hair becomes fragile and is unusually susceptible to breakage.
•Normal combing can lead to the sudden loss of hair en masse.
Cicatricial alopecia
•It is alopecia which accompanies or follows the destruction of hair follicles, whether by a disease affecting
the follicles themselves or by some process external to them.
Causes
1-Developmental defects and hereditary disorders e.g.
•Aplasia cutis which appears as parchment-like scars with alopecia.
•Epidermal nevus.
2-Physical injuries e.g.
•Mechanical trauma.
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•Burns.
3- infections
•Fungal e.g. Kerion.
•Bacterial e.g. folliculitis and furuncles.
•Protozoal e.g.leishmaniasis.
•Viral e.g. herpes zoster.
4-Tumours e.g. BCC and SCC
5-Dermatoses of uncertain etiology e.g.
•Graham-Little syndrome: cicatricial alopecia of the scalp, non-cicatricial alopecia of the axillae and
pubis,and a lichenoid follicular eruption.
•Tufted folliculitis:Fibrosis of the follicles can cause tortional changes so that more than one hair can grow
from the follicle.
•Morphoea(en coup de sabre).
•Lupus erythematosus.
6-Clinical syndromes e.g.
•Pseudopelade:There are multiple asymptomatic, irregularly shaped cicatricial patches. Affected areas are
ivory-white or slightly pink and atrophic. Some cases are due to lichen planus or DLE
•Folliculitis decalvans:chronic folliculitis leads to patchy scarring lesions. Frequently, tufts of hair persist, so
that several hairs emerge from one follicle.
Treatment
•None is known. Surgical treatment may be considered
III-ABNORMALITIES OF HAIR SHAFT
Monilithrix
•It is an autosomal dominant condition
•The hair at birth is most commonly normal, and is progressively replaced by
short, fragile, beaded hairs
with follicular keratosis during the first months of life
•It affects the nape and occiput but may involve the entire scalp.
•
Pili torti
•Hairs are flattened and at irregular intervals completely rotated through 180° around their long axis.
•It may be a manifestation of some syndromes e.g. Menkes' syndrome: a hereditary defect of intestinal
copper transport with light-colored, twisted hair.
•The hair is usually normal at birth, but is gradually replaced by abnormal hair, as early as the third month,
or not until the second or third year of life.
•Hair is short(< 5 cm), coarse, brittle and dry over the whole scalp or there may be circumscribed baldness,
irregularly patchy or occipital.
Trichorrhexis nodosa
•It is a response of the hair shaft to injury e.g. hairdressing procedures, sea bathing and sunlight.
•The cuticular cells become disrupted, allowing the cortical cells to splay out to form nodes.
Clinically
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•Often it is discovered incidentally and only a few whitish nodules are seen near the ends of scattered hairs.
•If many hairs are affected the patient may complain that the hair is dry, dull or brittle.
•It is reversible with the avoidance of physical and chemical trauma. Complete resolution may take 2-4
years, depending on the growth of new anagen hairs.
IV-HAIR PIGMENTATION DISORDERS
•Whatever the hair color seen by the eye, isolated melanin is brown in color and gives a dark brown solution
in aqueous alkaline hydrogen peroxide.
•The whole range of human hair color is due to two types of melanin: eumelanins, which are mainly found in
black and brown hair, and pheomelanins, which are yellow or red and are found in auburn(red) and blonde
hair.
•Dark hair shows a great number of melanin granules(melanosomes).
•Lighter-colored hair shows less melanin deposition, and blonde hair follicles show melanosomes with a
moth-eaten appearance.
Greying of hair (canities)
•It is due to a gradual but progressive reduction in melanocyte function and their final death in hair follicle.
•In Caucasoid races, white hair first appears at the age of ± 35 years, and by the age of 50 years 50% of the
population have at least 50% grey hairs.
•The onset in black people is ± 43 years.
•The beard and moustache areas commonly become grey before scalp or body hair. On the scalp the temples
usually show greying first.
•'overnight' greying of the hair occurs in diffuse AA due to selective shedding of pigmented hairs, the nonpigmented hairs being retained.
Premature greying of hair
•It is the onset of greying before 20 years of age in white people and 30 years of age in black people.
•It is associated with some autoimmune diseases e.g. pernicious anemia and hyperthyroidism due to genetic
linkage.
•Other conditions with premature greying of hair are progeria
Poliosis
•It is the presence of a localized patch of white hair due to the absence of melanin in a group of neighboring
follicles.
Causes
•Vitiligo
•Tuberous sclerosis
•Piebaldism: a white forelock with a white patch in the central portion of the forehead.
V-SCALP DISORDERS
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Pruritic scalp
•It may occur as an isolated symptom in the absence of any objective changes. The patient is often middleaged, the pruritus is spasmodic and may be intense, and exacerbations are frequently related to periods of
stress or fatigue.
•In children and in women of any age, pediculosis should be excluded no matter what the social status of the
patient.
•Pruritus is also the predominant manifestation of acne necrotica, in which scattered vesicles followed by
small crusts are a source of severe discomfort.
•Lichen simplex is a frequent cause of pruritus of the nape and occipital region.
•Seborrheic and atopic dermatitis and other inflammatory disorders e.g. psoriasis may be pruritic, but
pruritus is seldom a presenting symptom.
Pityriasis capitis (Dandruff)
Etiology
•It is relatively rare and mild in children.
•At age 20 years, some 50% of white people are affected in some degree.
•It becomes less frequent after 50 years.
•The age incidence suggests that an androgenic influence is important, and the level of sebaceous activity
may be a factor.
•The role of malassezia furfur is still disputed.
•M furfur may cause irritation that leads to increased cell turnover. The result is a large number of dead skin
cells. As the cells fall off, they tend to clump together with sebum causing dandruff to appear.
Clinically
•Small, white or grey scales accumulate on the surface of the scalp.
•After removal with an effective shampoo, the scales form again within 4-7 days.
Treatment
1-Cyto statics:They reduce epidermal turnover in the scalp:
-Selenium sulphide(Selsun Blue shampoo)
-Tar-based shampoos (Polytar liquid)
2- Anti malassezia furfur preparations:
-Zinc pyrithione(Head & Shoulders shampoo)
-ketoconazole (Nizoral shampoo)
Pityriasis amiantacea
Etiology
•It is often present without any obvious underlying cause, but may be associated with psoriasis, lichen
simplex or seborrhoeic dermatitis.
Clinically
•There are thick, yellow-white scales densely coating the scalp and adhering to the scalp hairs as they exit
the scalp. They are arranged in an overlapping manner like tiles on a roof, hence the name.
•Usually it affects only part of the scalp but may occasionally involve the whole scalp.
Treatment
•The abundant scale is removed by the use of oil of a topical tar/salicylic acid ointment.
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•Either preparation should be washed out of the scalp after 4-5h with a suitable shampoo, for example tar or
an imidazole shampoo.
•Recurrence may occur.
Cutis verticis gyrata
•There is overgrowth of the scalp in relation to the underlying skull, so the skin of the scalp has a gyrate or
cerebriform appearance.
Classification
•Primary essential: There is no other abnormality.
•Primary nonessential: Associated with mental deficiency, cerebral palsy, epilepsy, schizophrenia,
microcephaly, deafness, ophthalmologic abnormalities.
•Secondary: Cases associated with undelying systemic diseases(e.g. acromegaly), inflammatory dermatoses,
nevi, and trauma.
Clinically
•It usually affects the vertex and occipital region, but can involve the entire scalp.
•Folds are soft and spongy and cannot be corrected by pressure or traction.
•Hair over the folds may be sparse but normal in furrows.
Treatment
•Hygiene for folds and furrows is very important.
•Plastic surgery may be helpful.
HAIR COSMETICS
Shampoos
(from the Hindi word champo which means massage)
Composition
1-Principal surfactants (agents that lower the surface tension of a liquid, allowing easier spreading) for
detergency and foaming power.
2-Secondary surfactants to improve and 'condition' hair.
3-Additives which both complete the formulation and add 'special' effects. Whatever the claims of some
manufacturers, most special additives end up down the sink.
Mechanism of action
•The chemical mechanism by which shampoos clean hair is similar to that of traditional soap. While both
soaps and shampoos contain surfactants, shampoos use a different class of surfactants balanced to avoid
removing too much oil from the hair.
•The lipids do not come off easily when the hair is rinsed with plain water because hair has a hydrophobic
surface that repels water. Surfactants reduce the interfacial surface tension and allow for the removal of the
sebum from the hair shaft.
Types of shampoos
•Antidandruff, 'medicated' and scalp treatment shampoos contain antiseptics and active agents such as tar.
•Cleansing types sold for treating greasy hair.
•Cosmetic types having good conditioning action and popular among women with dry or 'normal' hair.
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Conditioners
•Dry hair lacks luster and is difficult to style. This is due to natural weathering and is worsened by chemical
& physical processes applied to hair.
•They provide lubrication and gloss and render the hair easier to comb and style.
•Conditioners are left on for up to 30 min, often with damp heat and then rinsed off.
• Conditioners contain:
•Meoisturizers to hold moisture in the hair.
•Other ingredients e.g.
-Reconstructors( hydrolyzed protein to penetrate the hair and strengthen its structure.
-Glossers(light-reflecting chemicals).
-Oils(to soften hair).
-Natural triglycerides, e.g. almond, avocado, corn and olive, beeswax, jojoba oil, mink oil,
Lanolin.
-Phospholipids, e.g. egg yolk and soya bean
- Vitamins A, B and E
-Proteins e.g. collagen, keratin (horn and hoof), gelatin.
Cosmetic hair coloring
•The penetration of dyes into hair depends on their molecular size and the aqueous swelling of the hair at the
time of application of the dye; basicity of the dye is also important. The most successful dyes contain
relatively small molecules.
•Hair-coloring materials can be divided into three groups:
1-Vegetable dyes(Henna)
•Henna gives reddish auburn shades, so it should not be used on gray hair, as it turns it orange.
•The dye is produced from dried leaves of some plants e.g. Lawsonia alba.
•Traditionally, it is applied as a thick paste which is left in situ for 5-60min. The effects last for up to 10
weeks.
•This process is non-toxic but messy. Also, concentration of Henna is difficult to control, and hence results
can be unpredictable.
2-Metallic dyes
•Traditionally, hair dyes for men have been of this type, as the color changes occur less rapidly.
•Inorganic salts are used and coat the surface as either oxides from reduction of the metal salts by keratin, or
sulphides from the action of the sulphur in keratin on the metal.
•They all give a rather dull (metallic) appearance and may cause brittle or damaged hair if used too often.
•Lead acetate, with precipitated sulphur or sodium thiosulphate, gives brown to black shades.
•Silver nitrate used with pyrogallol produces a greenish-black color.
•Colors from blonde to black are possible by mixing silver nitrate variously with copper, cobalt or nickel;
brownish-black skin staining is the great disadvantage.
3-Synthetic organic dyes
•They are the most important type because of the comprehensive range of 'natural' colors they give.
•Synthetic organic dyes are of three types:
1-Temporary dyes:
-They wash out with one wash with a shampoo and last no longer than 1 week, so they are suitable for
artists.
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-They are available in aerosol sprays.
- Disadvantage of such dyes is their tendency to flake off onto clothing.
2-Semipermanent dyes:
- They are used frequently to brighten a natural color or modify white or grey hair but they cannot color
hair lighter than its natural shade.
- Many are now used in color shampoos.
-They are relatively easy to wash out with shampoos containing ammonia; other shampoos must be used
six to 10 times to remove them.
3-Permanent dyes:
- The process starts by stripping the hair of all the melanin by using a bleacher (20% H2O2solution)
followed by a dye and an alkaline soap or synthetic cleansing agent.
- The greatest problem is their potential to cause allergic dermatitis in up to 10% of users. All dyes in this
group have instructions to carry out patch testing , e.g. behind the ear, 24-48h before use.
- H2O2 is chiefly responsible for the structural damage to hair which may occur
- With regular professional re-tinting, using the same product, the hair can be kept the same color for as
long as required
- They must not be applied more frequently than every 2-3 weeks because hair damage will occur
Bleaches
•Bleaching is an oxidative alkaline treatment which oxidizes and bleaches melanin.
•The hair lightens to reddish or yellow tones depending on the underlying hair
color, and ultimately to
platinum.
•Bleaching is very damaging to the hair, rendering it dry, porous and more prone to tangle. Overuse may
cause disruption and fracture of the hair.
•Home bleaching is usually performed with 6% H2O2 with ammonia to speed the reaction, which otherwise
takes 12h. Salons use more powerful bleaching materials which are much faster.
•They are often applied to individual strands of hair, others being left untreated to give highlights.
•Bleaching is terminated by shampooing or an acid rinse.
•Platinum blonde color is obtained when the bleached hair is treated with a blue or lilac colorant.
Perming hair (permanent wave)
•It is a process that creates a curl in the hair shaft by altering its internal chemical structure. This curl
cannot
be destroyed except by further chemical treatment.
•Keratin is composed of cystine chains found mainly in the matrix.
•Cystine chains are linked together by disulphide bonds. These bonds keep the hair in shape.
•In order to change hair shape, the disulphide bonds have to be broken down and re-formed into a different
pattern.
•The hair is first washed and then wound on to some kind of former, such as a curler.
•The perm lotion is applied to the hair. It is an alkaline (pH 9) solution containing reducing agents to reduce
the disulphide bonds. The reducing agent most often used is thioglycolic acid plus ammonia.
•Reducing agents act on keratin, breaking the disulphide linkages. The result is that the keratin softens and
swells, and so hair can stretch to take up the shape of the formers.
•'Tepid' waving involves using a weaker thioglycolate solution plus warm air.
•Neutralising lotion is then applied. This contains oxidising agents. One that is often used is hydrogen
peroxide.
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•Oxidising agents work in the opposite way to reducing agents. They make the cysteine units link together
into pairs again, hardening the hair and giving it its new, permanent shape.
Hair straightening
•The chemistry of the straightening process is identical with that of perming.
•The oval shape and natural crimp of Afro-Caribbean hair makes it difficult to straighten without damage.
The chemical treatment can weaken the hair structure, and breakage after relaxation treatment is not
uncommon.
•Contributing factors include incorrect concentrations of relaxing solution, mistakes in timing the
application, and incomplete rinsing.
•Often the hair breakage is seen at the back of the neck. In addition, straightening leaves the hair fibers in a
high degree of torsional stress (twisting), and a slightly wavy look. This makes them liable to rapid
weathering, with the cuticle wearing down and a characteristic lengthwise splitting.
Hair setting
•It means temporarily altering hair shape.
•Some of the weak disulphide bonds are broken by water and then re-form in the newly positioned hair as the
hair dries.
•A curl can be produced by setting hair on a roller and allowing wet hair to dry while twisted round the
roller. After the rollers have been removed the hair holds its shape until it gets wet again. A hair dryer has to
be used to speed the process up.
•Softer, looser styles can be created by brushing and blow drying only, without using rollers.
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