Hair, which has an essential physiological role in animals, is mainly of psychological importance in man.
A good head of hair provides some degree of warmth for the human head and also protection from ultraviolet radiation, but its significance is otherwise in the eye of the beholder.
In the form of wool, hair is of economic importance and considerable research has been carried out into the cycles of growth and the structure of wool keratin in sheep.
Too much hair, particularly on the face of women, is an embarrassment and cosmetic problem and loss of hair from the scalp is equally troublesome.
Changes in hair growth are not only of cosmetic significance but can also be associated with underlying diseases.
Diseases occurring in the skin of the scalp can damage hair follicles leading to loss of hair.
This chapter covers:
(a) the normal pattern of hair growth;
(b) causes of hair loss;
(c) skin diseases involving the scalp;
(d) causes of excess hair growth;
(e) abnormalities of the hair itself; and
(f) treatment.
The normal pattern of hair growth
Unlike other epidermal structures which grow continuously, hair has a cyclical pattern of growth.
The growing phase or anagen lasts an average of 1000 days on the scalp followed by an involutional phase known as catagen which is quite short, lasting only a few days.
The hair then enters a resting phase, telogen, lasting about 100 days.
In man, hair growth is normally asynchronous, with each individual hair following its own cycle independently of the others.
The basal layer of the hair bulb from which the hair itself is produced is known as the matrix and contains melanocytes from which melanin pigment is incorporated into the hair.
The type of melanin determines the colour and in grey or white hair, pigment production is reduced or absent.
The body surface with the exception of the palms, soles, the lips, and the genitalia, is covered with fine vellus hairs that do not have a medulla and are not pigmented.
These hairs develop into longer coarse, medullated, terminal hair on the scalp and eyebrows.
At puberty a similar change occurs in the pubic area and the axillae, also on the face and trunk, in the male.
These changes are androgen dependent, even in females, but testicular androgen is required to produce beard growth and balding in men.
Racial characteristics and the genetic make-up of the individual determine the type and colour of the hair. Straight black oriental hair is clearly different from the nordic blonde type.
Hair loss
This is known as alopecia, said to be derived from the
Latin “alopex”, a fox, presumably because of the bald patches of mange seen in wild foxes.
Adult male pattern alopecia is so common as to be considered normal.
Circulating levels of testosterone are not raised in bald men but there is evidence that availability of the hormone to the hair follicle is increased.
In postmenopausal women there may be widespread thinning of the hair but loss of hair at the temples often occurs to some degree at an earlier age.
Alopecia may be diffuse or localised.
If it is simply due to a physiological derangement of hair growth, the follicles remain intact, whereas inflammation may lead to scarring and loss of the hair follicles.
Hence, hair loss can be classified into the categories shown in the illustration on the right.
Diffuse hair loss
An interruption of the normal hair cycle leads to generalised hair loss.
This may be due to changes in circulating hormones, drugs, inflammatory skin disease, and “stress” of various types.
Telogen effluvium occurs if all the hairs enter into the resting phase together, most commonly after childbirth or severe illness.
Two or three months later the new anagen hair displaces the resting telogen hair, resulting in a disconcerting, but temporary, hair loss from the scalp.
Stress of any type, such as an acute illness or an operation, causes a similar type of hair loss. Postfebrile alopecia occurs when a fever exceeds 39°C, particularly with recurrent episodes.
It has been reported in a wide range of infectious diseases, including glandular fever, influenza, malaria, and brucellosis.
It also occurs in fever associated with inflammatory bowel disease. Dietary factors such as iron deficiency and hypoproteinaemia may play a role, but are rarely the sole cause of diffuse alopecia.
Severe malnutrition with a protein deficiency results in dystrophic changes with a reduction in the rate of hair growth.
Congenital alopecia may occur in some hereditary syndromes.
Anagen effluvium occurs when the normal development of hair and follicle is interfered with, resulting in inadequate growth.
As a result, hairs are shed earlier than usual, while still in the anagen phase.
Endocrine causes of diffuse alopecia include both hypoand hyperthyroidism, hypopituitarism, and diabetes mellitus.
In hypothyroidism the hair is thinned and brittle, whereas in hypopituitarism the hair is finer and soft but does not grow adequately.
Systemic drugs cytotoxic agents, anticoagulants, immunosuppressants, and some antithyroid drugs may cause diffuse hair loss, usually an “anagen effluvium” as mentioned above.
Inflammatory skin disease, when widespread, can be associated with hair loss, for example in erythroderma due to psoriasis or severe eczema.
Deficiency states are a rare cause of alopecia. Patients who suffer from hair loss are often convinced that there is some deficiency in their diet and may sometimes produce the results of an “analysis” of their hairs which show deficiencies in specific trace elements.
In fact it is very difficult to cause actual hair loss even in gross malnutrition and in those dying from starvation in refugee camps, the hair growth in the scalp is usually present.
In chronic malnutrition or kwashiorkor, the hair assumes a curious red/brown colour which may be due to iron deficiency.
Treatment
Wherever possible, the cause should be treated.
This may be a matter of replacement therapy in hormonal deficiency. In alopecia due to stress, once this cause is removed hair growth may revert to normal.
Treatment of inflammatory skin disease will result in some improvement of the hair loss.
Androgenic alopecia in men is best accepted, with assurance that it indicates normal virility. Minoxidil causes hair growth and is commercially available as a lotion.
This has to be applied continuously every day as the scalp reverts to a level of loss which would have occurred without treatment as soon as it is stopped.
It is effective in about half the patients with male pattern alopecia.
Localised alopecia
Alopecia areata is a common form of hair loss.
It is seen in 2% of patients attending the average dermatology clinic in the United Kingdom.
There may be small patches of hair loss or the whole scalp may be affected. Resolution occurs in a few months or the condition may persist for years.
There may be slight inflammation of the skin in the affected areas in keeping with the possibility of an underlying immune reaction against the hair follicles.
There is also an association with autoimmue disease and atopy.
In the affected areas the follicles are visible and empty.
The hairs about to be lost have an “exclamation mark” appearance and in some areas that are resolving, fine vellus hairs are seen.
Patches commonly occur on the scalp, face, or eyebrows.
In alopecia totalis, the whole head is involved, and in alopecia universalis hair is lost from the whole of the body.
In many patients, particularly if it is a first episode, regrowth occurs within a few months with fine pale hairs appearing first, being replaced by normal adult hair.
In older patients, non-pigmented hair may persist in previous patches of alopecia.
Factors associated with a poor prognosis are:
(1) Repeated episodes of alopecia
(2) Very extensive or complete hair loss (alopecia totalis)
(3) Early onset before puberty
(4) In association with atopy
Differential diagnosis includes trauma from the habit of plucking hair (trichotillomania) in mentally disturbed patients and traction alopecia from tight hair rollers or hair styles that involve tension on the hair.
In fungal infections (tinea capitis) there is scaling and broken hairs.
Fungal spores or hyphae are visible in hair specimens on microscopy.
Inflammation is present with loss of hair follicles in lupus erythematosus and lichen planus.
Treatment
An initial limited area of alopecia areata in adult life can be expected to regrow and treatment is generally not needed.
Treatments that are carried out include:
(1) Injection of triamcinolone diluted with local anaesthetic which usually stimulates localised regrowth of hair.
Unfortunately it often falls out again and there is a risk of causing atrophy.
Topical steroid lotion can be used but results are variable.
(2) Ultraviolet light or psoralen with ultraviolet
A can give good, if transient, results in a few patients but it has little effect in the majority.
It may act by suppressing an immune reaction around the hair root.
(3) Induced contact dermatitis and irritants are occasionally effective.
Cantharadin and dithranol have been used for many years as irritants. Primula leaves or chemicals (for example, diphencyprone) can be applied to produce an acute contact dermatitis.
The mechanism by which acute inflammation stimulates hair growth is not understood.
Scarring alopecia
The absence of hair follicles is an important physical sign as it indicates:
(1) The presence of an inflammatory process that requires further investigation.
(2) That there is unlikely to be any substantial recovery of hair growth.
The presence of inflammation does not necessarily produce marked erythema—in lichen planus and lupus erythematosus, the inflammatory changes are often chronic.
Systemic lupus erythematosus produces areas of inflammation that extend, leaving residual scarring.
In discoid lupus erythematosus there is more scaling with keratotic plugs in the follicle.
Localised scleroderma (morphoea) also causes alopecia, often with a linear atrophic lesion the en coup de sabre pattern.
More acute inflammatory changes are seen as a result of pyogenic infection or kerion in which there is a marked inflammatory reaction to fungal infection from cattle.
In “folliculitis decalvans” there is florid folliculitis with deep seated pustules and scarring.
Treatment is with prolonged antibiotics.
Tinea capitis can be associated with alopecia.
Trauma can also cause scarring with alopecia.
Skin disease involving the scalp
The scalp can be involved in any skin disease, but most commonly in psoriasis and seborrhoeic eczema.
A mild degree of scaling from accumulation in skin scales is so common as to be normal (dandruff).
Increased accumulation of scales is seen in seborrhoeic dermatitis in which pityrosporum organisms may play a part.
Sometimes masses of thick adherent scales develop in pityriasis amiantacea, usually due to psoriasis.
Eczema and contact dermatitis can also involve the scalp.
Treatment
Scaling and inflammatory changes can be improved with the use of sulphur and salicylic ointment.
It is effective but messy and best applied at night.
Tar preparations, oil of cade, and coconut oil in various formulations are all effective.
Topical steroids can also be used to suppress inflammation.
Hair shaft abnormalities
Congenital abnormalities of the hair shaft itself lead to weak, thin and broken hairs.
In some cases there is a characteristic appearance, for example “spun glass” appearance of pili torti with a twisted hair.
In monilethrix there are regular nodes in the hair shaft.
There are other abnormalities of the hair shaft which are not associated with increased fragility, such as the Willi hair syndrome, progressive kinking of the hair and uncombable hair, in which the hair grows in disorderly profusion, completely resistant to combing and brushing.
In pili annulati there may be a spangled appearance due to bright bands in the hair shaft.
Excessive hair
Two types of overgrowth of hair occur:
Hirsuties
This is the growth of coarse terminal hair in a male distribution occurring in a woman.
This is not always easy to assess since what is unacceptable and emotionally disturbing to one woman may be quite acceptable to another.
The amount of hair growth may appear to be within normal limits in a patient complaining of excessive hair but it should never be dismissed as of no consequence if it is important to the woman concerned.
Nevertheless, it is important to limit the number of investigations once it is clear that there is no underlying abnormality.
Strong reassurance may then be the most helpful management.
It is of course most apparent on the face but is often present on the thighs, abdomen and back as well.
Hirsuties occurs most commonly after the menopause and may be present to some degree in normal women as a result of familial or racial traits.
It may arise without any underlying hormonal disorder or as a result of virilising hormones.
These causes are listed in the box on the right.
In addition to androgens, a number of drugs can cause hirsuties.
It is important to remember that hirsuties may be part of a virilising syndrome or polycystic ovaries.
It is useful to measure the serum testosterone and oestrogen level, as well as urinary 17 oxosteroid concentrations.
Hypertrichosis
This is an excessive growth of hair which may be generalised or localised.
It may be due to metabolic disturbance or drugs, or simply a feature of a localised lesion such as a mole.
Treatment
It is clearly important to treat any underlying cause and this will usually improve the condition. Otherwise treatment is symptomatic and includes:
• Removal of hair by shaving or hair removing creams.
• Electrolysis and diathermy, which gives permanent destruction of the hair follicle.
• Antiandrogen drugs such as cyproterone can be used under specialist supervision.
