The profound psychological and social significance of hair in Man is in contrast to its complete lack of vital function. For mammals, as a whole, fur provides an insulating coat for the conservation of body heat. Its properties can be adapted to seasonal changes in the environment by periodic moulting of old hairs and their replacement by new ones, and even human hair follicles remain endowed with such cyclic activity.
The Hair Follicle
Development and Structure
The structure of the hair follicle, the method by which it manufactures hair and its cyclic activity are better made understandable by brief reference to its embryonic history. Each follicle arises from an interaction between epidermis and dermis.
A thickened plaque of epidermis, lying over an aggregation of dermal cells, extends inwards to form a peg which eventually engulfs a small papilla of dermis to form the hair bulb. The epidermal cells surrounding the dermal papilla then proliferate to push outwards a column of keratinizing cells, which is the hair shaft invested in an inner root sheath. A hair canal is formed in the process.
The bulk of the hair shaft consists of elongated, keratinized cells cemented together and is known as the cortex. Some, though not all, hairs have a continuous or intermittent medulla. The cortex is surrounded by a cuticle, which arises from a single line of cells in the bulb, but becomes five to ten overlapping layers. From the outside the cuticular scales appear imbricated, like roof tiles, with the free edges directed outwards.
The inner root sheath interlocks with the overlapping cells of the cuticle of the growing hair and moves with it, but the keratinizing cells are desquamated as the hair emerges from the skin. Thus the outer surface of the inner root sheath glides against the stationary outer root sheath, which is the innermost part of the follicular wall.
As the foetus grows, the first-formed follicles move apart and a new crop of secondary rudiments develop between them. But no new follicles are formed post-natally. The total number of follicles in an adult man is about 5 million, of which about 1 million are in the head and perhaps 100,000 in the scalp. A significant loss occurs with age; young adults have an average of 615 per cm2 on the scalp, but by the age of 80 the density has fallen to 435 per cm2. Some follicles are lost in baldness; a comparison over a wide range of ages gave averages of 306 per cm2 for bald scalps as against 459 per cm2 for hairy scalps.
The first hairs to grow from hair follicles, which are fine, unmedullated and usually unpigmented, are known as lanugo and are normally shed in utero in the seventh or eighth month of gestation. Very rarely, lanugo-like hair is found in the adult, even on areas such as the nose and ears which are not normally hairy, either as an inherited trait known as hypertrichosis lanuginosa, or as the symptom of an underlying cancer.
Postnatal hair may be divided, at the extreme, into two kinds: fine, unmedullated, short vellus on the body, and longer, darker, terminal hair on the scalp. The infantile pattern is not definitive, for at puberty vellus is replaced by terminal hair in the public and axillary regions and, in the male only, on the face. This sexual hair continues to increase in area and rate of growth until the late twenties.
Virtually all hair follicles undergo cyclic activity. An active phase, anagen, in which a hair is produced, alternates with a resting period, telogen, in which the fully formed club hair remains anchored in the follicle by its expanded base and the dermal papilla lies free of the epidermal matrix, which is reduced to a small, quiescent secondary germ. Between anagen and telogen is a relatively short transition phase, known as catagen, in which the newly formed club hair moves towards the skin surface.
The follicle becomes active again at the end of telogen by a downgrowth of the secondary germ to re-invest the dermal papilla, so that the matrix becomes reconstituted and a new hair starts to form. In effect, the follicle re-enacts its embryonic development. Ultimately the old club hair is shed, or moulted.
All hairs thus reach a terminal length which is determined mainly by the duration of anagen and partly by the rate of growth. These characteristics vary with site. In the scalp, anagen may occupy three years or more; indeed the untrimmed locks of a young woman would require 6 or 7 years of continuous growth to reach her buttocks. The aging male scalp falls far short of such achievement. On the vertex of a man aged 60, the growing period ranged from 17 to 94 weeks for coarse hairs and from 7 to 22 weeks for fine hairs. On the body, the period of the cycle is much less. In a young male it ranged from 19 to 26 weeks on the leg, 6 to 12 weeks on the arm, 4 to 18 weeks on the finger, 4 to 14 weeks in the moustache, and 8 to 24 weeks in the region under the temple.
Animals show wide differences. For example, in the rat the dorsal hair is fully formed in three weeks and the shorter ventral hair in only 12 days, and in the guinea-pig anagen lasts between 20 and 40 days.
In many animals waves of follicular activity, followed by moulting, pass over the body in symmetrical patterns. In the rat, for example, replacement of hairs starts in the venter and bands of activity and shedding move over the flanks to the dorsum, subsequently spreading to the head and the tail regions. In contrast, in the human scalp each follicle appears to be independent of its neighbours. At any one time an average of 13 per cent (4-24 per cent) of the follicles are in telogen and about 1 per cent in catagen. Thus in a scalp containing around 100,000 follicles with an average cycle of 1000 days, about 100 club hairs should be shed each day. This is approximately the number covered in practice.
The guinea-pig has been said to resemble man in that moulting is continuous and at random. However, in the newborn animal all follicles are simultaneously active and it seems that for at least 50 days, and probably for much longer, follicles show a measure of synchrony with others producing the same type of fibre, if out of phase with those producing different fibre types. It would thus appear to be erroneous to regard the guinea-pig follicle as an experimental model from which information relevant to the human condition can be drawn. However, at an early stage human follicles may also show some synchrony, for there is evidence of the passage of a wave of growth from front to back in the scalp of newborn infants.
Rate of Growth of Hair
The rate of growth of human hair has been determined by direct measurement of marked hairs in situ, by shaving or clipping at selected intervals and by pulse labelling S cystine and autoradiography. The average growth per 24 hours has been stated to range from about 0-21 mm on the female thigh to 0-38 mm on the male chin. Another study, in which graduated capillary tubes were fitted around growing hairs, gave 0-44 mm for the male vertex, 0-39 mm for the temple, 0-27 mm for the beard and 0-44 mm for the chest. The average for the vertex in women was 0-45 mm per 24 hours. Though scalp hair appears to grow faster in women than in men, before puberty the rate is greater in boys than in girls. In both sexes the growth rate is highest between the ages of 50 and 69 years. Some workers believe that the growth rate remains constant in any follicle, others that it usually decreases or increases.
While daily variations in temperature have no effect on hair growth, it seems likely that there are longer-term seasonal changes; for example, the beard grows faster in summer than in winter. It is generally agreed that shaving does not alter the rate of growth, though prolonged irritation may affect the follicle.
Rates may differ considerably between species. Hair growth can be more than 1-0 mm per 24 hours in the rat and up to 0-6 mm in the guinea-pig, in which it has been clearly shown that the rate depends on the time for which activity of the follicle has been in progress.
There is ample experimental and clinical evidence that hormones influence hair growth. The analysis of their actions is, however, extremely complicated. In considering the extent to which animal models may illuminate the human condition, it is important to distinguish the control of the follicular cycle, concerned with the adaptive function of the moulting, from the control of sexual hair, concerned with adult social interactions. Moreover, hormones may act at more than one point; an action which modifies the structure of the hair, the rate of growth or the duration of the growing phase must be distinguished from one which simply reduces or prolongs the resting period. The failure to make such distinctions has led to many useless experiments and even more fallacious conclusions.
The control of the follicular cycle appears to be exercised at several different levels. First, experiments on rats have demonstrated that each follicle has an intrinsic rhythm which continues when its site is changed or, at least for a period, when it is transplanted to another animal in a different phase of the moult. When hairs are plucked from resting follicles, activity is initiated and at least for a time the follicles remain out of phase with their neighbours. Whether the intrinsic control of the follicle involves the build-up and dispersal of inhibitors of the release of wound hormones when the follicle is epilated, or both, continues to be debated.
The intrinsic cycle is, in turn, influenced by systemic factors, so that, for example, follicles on homografts gradually come into phase with their hosts. Several hormones have been shown to affect the moult cycles in animals. Thus, the passage of the moult in the female rat is accelerated by removal of the ovaries or the adrenals, or by administration of thyroid hormone and, conversely, is delayed by administration of oestrogens or adrenocortical steroids, or by inhibition of the thyroid. In a number of mammals moulting is influenced by seasonal changes, in particular of the photoperiod. It seems likely that these act through the hypothalamus, the anterior pituitary and the endocrine system.
Hormones also influence the rate of hair growth and the duration of anagen in the rat. Oestrogen decreases both; thyroxine increases growth but reduces the growing period. This finding suggests that the two hormonal systems act at different points.
Such experimental studies on animals have only a limited relevance in relation to human hair growth, but there are several points of interest. First, it appears that post-partum alopecia (see below) is caused by a disturbance of the hair follicle cycle brought about by circulating hormones, probably by the high level of oestrogens, in late pregnancy. Secondly, thyroid disturbances are frequently associated with diffuse alopecia. Thirdly, even the human scalp may not be free from environmental influences, for hair fall shows significant seasonal fluctuations.
The growth of the sexual hair is brought about by androgens, that is, by male hormones. The first sexual hair to appear is that in the public region. In boys it reaches the classical ‘female’ pattern at an average age of 15-2 years, in girls about 1½ years earlier. In about 80 per cent of men and 10 per cent of women the public hair spreads further over the abdomen in a sagittal, acuminate or disperse pattern; this growth may not be complete until the mid-twenties. Axillary hair appears about two years after the start of pubic hair growth and continues to increase until the late twenties. The rate of growth of the beard levels out after the age of 35, but the area continues to increase until the later decades of life.
Castration virtually prevents the development of the beard if it is carried out before the age of 16 years. Performed after the age of 21, it only reduces the extent, and the weight of hair growth per day. There is little doubt that the rising levels of androgen at puberty account for the successive development of pubic and axillary hair in both sexes, and for the growth of the male beard. Equally, androgens are necessary for the development of female hirsutism, that is body and facial hair in part or whole of the male pattern. Either abnormally high levels of androgen or an increased response of the pilo-sebaceous apparatus, or both, may be involved. Anti-androgens, namely substances which block the attachment of male hormones to the receptors within the target cells, effectively reduce such hair growth.
Paradoxically, androgens are also a prerequisite for the development of male pattern alopecia or alopecia androgenetica in subjects who are genetically disposed. Eunuchs retain their scalp hair, even when they have a family history of baldness, unless they are treated with testosterone. However, castration of balding men, though it arrests the process, does not appear to restore luxurious hair growth to areas that are already bald. The condition will be further considered below.
The nutritional requirements of skin and the general consequences of dietary deficiency have been reviewed. Attention was drawn to the necessity of certain vitamins, particularly some of the B complex, for normal hair growth and keratinization of the epidermis. On the other hand, evidence was presented that vitamin A inhibits the differentiation of the stratified squamous epithelium. Thus hyperkeratotic popular dermatitis is a symptom of vitamin A deficiency, and excess of the vitamin, for example when used in the treatment of psoriasis, appears to cause loss of hair.
Protein deficiency is the cause of the condition kwashiorkor and has serious consequences for hair growth. The hair becomes sparse, thin and brittle and loses its pigment. The linear growth may be decreased by as much as one-half: children with kwashiorkor produced only 59 μm3 hair tissue per follicle per day compared to a normal figure of 514 μm3, and the hair was weaker even when corrected for the difference in diameter.
The changes in the hair reflect considerable alterations in the follicles themselves. Thus in a sample of Andean children with kwashiorkor the proportion of follicles in anagen was only 26±6 per cent compared with 66±6 per cent in healthy children of the same age, and even the anagen follicles were severely atrophied, with depletion of pigment and loss of internal and external root sheaths. Even more severe changes were found in children suffering from marasmus; less than 1 per cent of the follicles were in anagen. Marasmus appears to be a condition of chronic protein–calorie undernutrition in which the hair follicles have ceased activity in order to conserve nitrogen, whereas kwashiorkor is an acute condition following more or less normal growth.
The hair bulb is rapidly affected by experimental protein malnutrition. In male volunteers, the mean root diameters became significantly reduced by the eleventh day of protein deprivation, pigmentation was visibly reduced by the fourteenth day, and there was progressive atrophy and loss of root sheaths. The changes were reversible within days when protein was given. Thus while claims that administration of amino acids will, in certain conditions, improve hair growth should be treated with great caution, the possibility should not be rejected out of hand.
Chemistry of Hair
The greater part of hair and wool is made up of an insoluble protein material called keratin, which is formed as the ultimate product of the keratinization process which takes place in the follicle. There are also present the vestigial cell membranes, nucle, etc., but these form a very small fraction of the substance of hair. Small quantities of water-soluble substances are also present, such as pentoses, phenols, uric acid, glycogen, glutamic acid, valine and leucine.
Keratin, like other proteins, is composed of amino acids, substances of the general formula which give rise to the majority of the most characteristic properties of the proteins.
About 25 different amino acids are known to occur in proteins, and of these 18 are found in measurable amounts in keratin.
Formation of Hydrogen Bonds between Parallel Polypeptide Chains. The hydrogen bonds are formed by the interaction of the NH group with a suitably placed CO group.
Formation of Salt Linkages between Acidic and Basic Side-chains. As some of the side-chains of the polypeptide contain acidic groups and others contain basic groups, there is the possibility of salt formation between them if the groups are favourably placed; thus:
(aspartic acid residue)
Formation of Disulphide Linkages. The extreme strength and insolubility of hair keratin is attributed to its large cystine content. This amino acid contains two amino and two carboxyl groups; it can thus enter into two polypeptide chains which are then linked together by a disulphide bond:
A few disulphide bonds are also believed to be along the main chains. Other linkages such as ether cross-links between serine, threonine and tyrosine have been suggested, but there is little evidence for such linkages and the known chemical behaviour of hair can be explained in terms of hydrogen bonds, salt linkages and disulphide bonds.
Hair is thus an intensely cross-linked structure and can be considered as a series of submicroscopic fibrils with both parallel and linked polypeptide chains: X-ray studies show that a considerable proportion of hair has a crystalline structure (effectively a regular structure, though not necessarily crystalline in the sense associated with inorganic materials) known as the α-keratin structure. This has been described in X-ray diffraction terms by MacArthur and Giroud and Leblond.
Mineral Constituents of Hair
The mineral content of hair, in particular the trace metal content, has been a subject of interest for many years, especially since analytical techniques have been developed that permit the analysis to be carried out on the small samples of hair generally available. Apart from scientific curiosity there is always the possibility that metals present in trace amounts might influence the action of hair treatments such as bleaching or dyeing.
Bagchi and Ganguly have determined the mineral constituents of human hair and point out that the amounts of carbon, hydrogen, nitrogen, sulphur and phosphorus are approximately of the same magnitude irrespective of age, race and sex. They also quote figures for the trace metal contents of the same samples of hair, but the data obtained are insufficient to allow generalizations to be made.
Discoloration of hair during permanent waving is frequently attributed to the presence of metals, particularly iron or lead, in the hair. In cases known to one of the authors, it appeared that the hair was contaminated by iron from the use of old and worn hair grips or clips. The origin of the lead, which often amounted to 1000 ppm or more, was less easy to explain. The complaints, which concerned a slightly pinkish brown colour, generally came from subjects with perfectly white or naturally blonde hair, and it was not reasonable to suppose that they had used lead-containing hair colorants.
Tompsett has shown that when the calcium metabolism of the body is disturbed, lead which is normally accumulated in the bones becomes mobile and can disperse into the blood stream, and hence into all the soft tissues and organs of the body. Unfortunately hair was not included in this investigation, but by analogy with arsenic, which has long been known to deposit in hair and nails, it seems highly probable that this could be the origin of lead in the hair. Further evidence for this theory comes from the work of Strain et al, who showed that the zinc content of hair reflected the zinc content of body tissues. Similar results have been found with other metals and there seems little doubt that metals in the blood stream find their way into the hair.
Chemical Properties of Hair
While there is no space here to classify exhaustively all the chemical properties of hair, certain reactions are reviewed which have a direct bearing on the structural details already dealt with.
At the outset, it must be realized that about 50 per cent of the weight of hair keratin is made up of the side-chains of the amino acids, so these have a correspondingly great effect on the properties of the whole material. Because of the variety of these side-chains, the reactions are not clearcut, but the influence of certain groups may be detected in their contribution to the total chemical reactivity. For instance, if the disulphide bonds are broken the hair is weakened, but not destroyed as long as the salt links are intact. Similarly, the action of strong acids in breaking the salt links (by suppressing the ionization of the carboxylic acid groups) will not disrupt the hair unless the disulphide bonds are simultaneously broken. If the hydrogen bonds remain intact it is very difficult to carry out any other reactions with the hair, because it does not swell to admit any other reagents; it is certainly difficult to cause hair to react in non-polar solvents. Alexander suggests, in fact, that most of the mechanical strength of dry hair resides in the hydrogen bonds.
Under normal conditions, however, the hydrogen bonds always contain some water absorbed from the air, usually around 9 per cent—more or less, according to the humidity of the atmosphere, etc. In liquid water, hair can take up bound water to about 30 per cent of its own weight.
Physical methods of evaluating hair damage such as extensometer tests and stress relaxation measurements are well known. Later work has been aimed at obtaining suitable chemical methods for estimating hair damage and a number of different principles, including the swelling effect of lithium bromide, the effect of enzymes and the copper uptake of hair, have been evolved.
Melanin and Melanocytes
Hair colour is caused by pigment granules in the cells of the hair shaft. The effect is produced by the large amount of pigment in the cortex, but granules also occur in the medulla. The pigment is manufactured within melanocytes situated around the apex of the dermal papilla and transferred to the newly formed hair cells from the tips of their finger-like dendrites.
The granules themselves are the end product of melanosomes. These originate as colourless pre-melanosomes in the region of the Golgi and become progressively darker as pigment is synthesized on them and they move peripherally. The granules themselves are ovoid or rod-shaped and vary in length from 0-4 μm. The darker the hair, the larger the average size of the granules, and Negroids generally have larger and fewer granules than Caucasoids. Melanogenesis has been reviewed by Collins and by Fitzpatrick.
The shades of human hair result mainly from two kinds of pigment, eumelanin, which is brown or black, and phaeomelanin, which is yellow or reddish. Eumelanin is formed from the amino acid tyrosine by oxidation with the enzyme tyrosinase. Tyrosine is also the precursor of phaeomelanin, but it seems that the presence of an o-aminophenol derived from tryptophane is also necessary.
Other pigments, which appear to be iron complexes, have been extracted from human red hair, red rabbits and red mongrel dogs, and given the name of trichosiderins. At least three distinct compounds have been isolated. The importance of these pigments is questionable. Boldt has shown that their colour is not due to the iron content, since it has been possible to isolate iron-free alcohols, named pyrrotrichols, which have the same colours as the iron complexes. Moreover, the red colour of human hair is not substantially altered by extraction of the trichosiderins. Thus, although it is admitted that red hair does contain greater amounts of iron than any other shade, its colour is now believed to be due to phaeomelanin.
Biochemistry of Melanogenesis
The first stage in the formation of either eumelanin or phaeomelanin is the oxidation of tyrosine to 3,4-dihydroxyphenylalanine (dopa) by the enzyme tyrosinase. The second stage, also catalysed by tyrosinase, is the dehydrogenation of dopa to form dopa quinone (Figure 23.6).
Eumelanins involve the formation of indole-5,6-quinone. It now seems likely that eumelanin is not, as once believed, a simple polymer of indole-5,6-quinone units linked through a single bond, but a poikilopolymer of several types of monomer joined by multiple types of bonds, with the incorporation of an assortment of oxidized intermediates. According to Dalgliesh there are four sites at which the molecules could join together. The eumelanin becomes linked to protein.
A large number of materials can inhibit tyrosinase activity, and therefore pigmentation. Such materials include competitors for tyrosine (3-fluorotyrosine, N-acetyltyrosine, N-formyltyrosine, phenylalanine, 3-aminotyrosine), agents with a complexing activity with the copper prosthetic group of the enzyme (phenylthiourea, diethyldithiocarbamate, BAL, cysteine, glutathione, hydrogen sulphide, cyanides, etc.), compounds which alter the redox potential of the system (hydroquinone, indophenol, etc.), substances which combine with one or other of the intermediates in the melanin synthesis (aniline, p-aminobenzoic acid, p-phenylenediamine, etc.) and one or two materials (ethers of hydroquinone, pentachloronaphthalenes) where the mode of action is unknown. Useful reviews of such inhibitors are given by Lorincz and Fitzpatrick.
For obvious reasons, few of these materials have been tested in vivo. However, α-naphthylthiourea and phenylurea cause graying of hair in rats as long as they remain in the diet, and thiouracil has suppressed pigmentation in man.
Greying of Hair
Greying of hair involves a loss of pigment from the hair shafts and a progressive loss of tyrosinase activity from he hair bulbs. It must be considered as a normal part of aging; in Caucasoids white hairs first appear at the temples at the average age of 34, and by age 50 half the population has at least 50 per cent grey hairs.
Rapid graying of hair (as judged by its overall appearance) after severe emotional stresses has often been recorded, though the belief that the hair of Marie Antoinette and Sir Thomas More turned white overnight may stretch credulity. It is not conceivable that pigment could be destroyed in hair which has already grown. However, there are two possible explanations. One is that telogen effluvium (see below, Hair, Disorders) causes sudden shedding of dark hairs from a mixed population, leaving a predominance of white or grey hairs in situ; the other is that a traumatic event precipitates loss of hairs by an episode of alopecia areata — the first hairs to regrow are invariably white. However, such a process would take weeks or months rather than hours. Green and Patterson recorded such a case of an engine driver who fell fro ma stationary engine. His hair came out on the day of the accident, at first in a round patch, which was diagnosed as alopecia. Eventually it spread, until after four months he was completely bald. Two months later a few white downy hairs appeared.
Greying of hair can be experimentally produced in animals by copper or by pantothenic acid deficiency; greying due to copper can be reversed by panthothenic acid. Though it has been claimed that huge doses of p-aminobenzoic acid will occasionally restore pigment to grey hair in man there is no known medical treatment by which greying can be consistently reversed. Hair follictes can, however, sometimes produce pigmented or grey hair intermittently; one such condition is a rare anomaly known as ringed hair or pili annulati.
The cosmetician may need to be able to recognize several abnormalities of the hair shaft of genetic origin, each of which may be associated with sparse, brittle and often short hair. From these disorders must be differentiated various types of hair loss in which the shafts remain structurally normal.
Hair loss may be either rapid or gradual. Sudden shedding of hair is often, though not invariably, transient, whereas gradual loss, observed only by its long-term effect, is usually hopelessly chronic.
Rapid loss can be further subdivided into two types, according to whether the fallen hair is a club, or a growing hair shed from an active follicle.
Loss of club hairs is known as telogen effluvium and seems to have several possible causes. One, namely childbirth, is well established and the ensuing condition is known as postpartum alopecia. Loss of growing hairs is known as anagen effluvium. It occurs after cytotoxic drugs, and it seems likely that the shedding of hairs in patchy baldness, or alopecia areata, is a similar process.
Slowly developing hair loss, causing baldness in a symmetrical pattern, is well known in males, where it is named male-pattern alopecia or ulopecia androgenetica. Diffuse alopecias have been attributed to several causes. It seems likely that much, probably most, diffuse alopecia in women is an inherited androgen-potentiated condition which is the female equivalent of male-pattern baldness.
Defects of the Hair Shaft
Monilethrix: a condition in which the hair shaft is beaded with elliptical nodes about 0.7-1.00 mm apart alternating with constricted internodes which lack any medulla. The hair is brittle and breaks off a centimeter or two above mergence.
Pili torti. The hair shaft is twisted on its axis at intervals, and usually breaks off short.
Trichorrhexis nodosa: a response to physical or chemical injury in which an apparently normal hair becomes swollen and split to form a node at which the hair subsequently fractures. In trichorrhexis invaginata the fractured hair.
Excessive shedding of normal club hairs after febrile illness (post-febrile alopecia) is well authenticated, and other causes, for example antithyroid drugs, anticoagulants and psychogenic stress have been suggested. Kligman has recounted the case of a prisoner who suffered a daily shed of 600-1500 hairs over a period of three months after conviction for murder, but subsequently recovered after a pardon had been granted.
The shedding of hair within two or three months of parturition appears to be a telogen effluvium similar to post-febrile alopecia. The cause seems to be a prolongation of anagen by the hormonal conditions of late pregnancy. Lynfield first described, and others have confirmed, that prior to childbirth as many as 95 per cent of the scalp follicles may be in anagen, but that the proportion falls to less than 70 per cent within 2-4 months after parturition, suggesting that the follicles have been precipitated into catagen.
In contrast to telogen effluvium, loss of anagen hairs is a rapid event. Cytotoxic drugs such as cyclophosphamide, adriamycin and vincristine can produce it in a few days.
Alopecia areata, or patchy baldness, is usually easy to recognize. The lesions are sited asymmetrically, and each starts at a focal point and spreads outwards. The process may take two or more weeks or may, to quote Behrman, be so rapid that a completely denuded plaque may appear overnight with the lost hairs found in a heap on the pillow in the morning.
The margins of the lesions are characterized by the occurrence of short protruding club hairs with a prayed point, often named ‘exclamation marks.’ As the lesions progress, many follicles in a state of arrested anagen can be found. By plucking hairs successively from a series of concentric rings around the focus of the lesions, it has been shown that an area from which only club hairs can be removed develops at the centre and moves centripetally.
The simplest hypothesis to explain these observations is that initially hairs are shed from all active follicles, leaving only the clubs unaffected. The shearing of hair from follicles moving into catagen produces the protruding stumps of the exclamation marks. However, it is quite possible that follicles are also precipitated into catagen. It should be added that the process does not always produce patchy lesions, but may sometimes occur diffusely, so-called diffuse alopecia areata.
The cause of alopecia areata is a subject of debate. It seems likely that there are several types, probably four, of the disease, differing from each other in the age of onset, clinical features and prognosis. Authors are divided about the role of heredity, some favouring a family history in 10-20 per cent of cases, others finding it in none. Some believe psychological factors are important, others that they play do role. It seems however, difficult to deny that the condition is in some instances precipitated by mental shock.
Various treatments such as ultraviolet light or miscellaneous irritants have been used for alopecia areata, but there is no objective evidence that they are of any value. One half of all patients recover within a year of the initial attack, though the incidence of relapse is high. Conticosteroids, given systemically, have been shown to induce regrowth in many cases, though the growth is not always maintained after discontinuation of the treatment. More justifiable is the use of intralesional injections.
No particular expertise is needed to recognize pattern alopecia in the male, for the recession of the hair line, loss of hair from the crown, and the bald pate are only too familiar. In the affected areas the hairs become steadily shorter and liner and, ultimately, cosmetically useless. About a third of the follicles may disappear. A reduction in the length of the growing period is reflected in the increased ratio of telogen to anagen in samples of plucked hair.
Pattern alopecia is inherited, apparently as an autosomal dominant trait, but it is only manifested in the presence of male hormone. Eunuchs retain their scalp hair, even when they have a family history of baldness, unless they are treated with testosterone. Though a correlation with hairiness of the chest has been suggested, baldness does not seem to be associated with other induces of masculinity, such as sebum secretion, muscle size and body hair in general. While the finding that bald scalp has a greater capacity than non-bald scalp to convert testosterone to 5α-dihydrotestosterone in vitro suggests that the key to understanding baldness lies in the field of steroid metabolism, no plausible hypothesis of how androgens promote baldness of the scalp but hair growth on the body has yet been proposed.
Loss of hair is by no means uncommon in women. Occasionally such loss involves obvious recession of the hair line as in males, but usually it is diffuse.
A number of causes have been proposed. It has long been recognized that thin hair may be associated with hypothyroidism (myxoedema) as well as with hyperthyroidism.
There is some evidence pointing to other factors, such as, for example, iron deficiency and ingestion of amphetamines for weight reduction. However, in many cases (over half of the total in one series studied) no possible cause could be found. It seems likely that these were androgenetic alopecias which had become manifested even within the normal range of female androgen levels.
Hirsutism may be defined as growth in the female of coarse terminal hair in part or whole of the adult male sexual pattern. At one end of the scale the condition may be obviously associated with other signs of virilism, excessive androgen production and an endocrine pathology. But most cases show no signs of masculinization except hirsutism, and have only slightly or moderately raised androgen levels; some lie well within the range for normal, non-hirsute subjects. The condition appears to result either from abnormal levels of free androgens or from an abnormal response of the hair follicle, or both. Anti-androgens, such as the steroid cyproterone acetate given orally, have proved effective in management of the condition.
Definition and Etiology
Dandruff is a condition of the scalp characterized by the massive desquamation of small flakes of stratum corneum. It has already been mentioned as a sealing disorder in Chapter I, where its occurrence and debatable etiology were briefly reviewed.
Discussion about the cause of dandruff revolves around the relative roles of physiological, traumatic and infective factors. Many authors have attempted to correlate dandruff with body disorders or environmental factors. Thus Lubowe has discussed the possible roles of hormones, metabolic faults, diet and nervous tension as well as inflammatory reactions to topical mediaments and cosmetics. Sefton noted that prisoners of war in Japanese camps in Singapore in 1942-45 had little dandruff and attributed this to shortage of fats in the diet, and it has been claimed that vitamin therapy is effective for some types of dandruff.
The yeast-like organisms, Pityrosporum ovale and Pityrosporum orbiculare are common members of the scalp flora. Pityrosporum can be easily detected with stains such as methylene blue and Nile blue. It does not appear to exist in nature away from human beings and has proved difficult to culture, though this problem has been solved. Its ultrastructure has been described by Swift.
Pityrosporum ovale was first described in 1874 by Malassez who believed it to be the sole cause of dandruff. This opinion was later supported by reddish. The role of Pityrosporum in dandruff has been much debated. What is the evidence? Koch laid down the original postulates for proving an organism is the specific cause of a disease as follows:
the organism must be present in every case of the disease;
it should be collected and cultivated in pure culture;
inoculation from such culture and reproduce the disease in susceptible animals;
the organism must be re-obtained from such animals and again grown in pure culture.
There is little doubt that Pityrosporum is generally present in cases of dandruff; so are many other micro-organisms, including a number of bacterial and moulds. The first postulate might thus appear to be satisfied, were it not for the fact that Pityrosporum is also present on scalps which do not have dandruff. The question therefore arises whether there is any relationship between dandruff and the level of infection. Some authors have failed to find any such correlation, others have produced evidence that Pityrosporum is in fact more abundant in affected than in non-affected persons.
The question of whether inoculation of cultured Pityrosporum ovale could produce dandruff was investigated by Moore and his associates. Their results are quoted in Table 23.3. The evidence is not overwhelming, but it supports the view that Pityrosporum is a causative agent.
Some further support comes from studies on the effect of antimicrobial preparations. When an aqueous solution of neomycin and nystatin was massaged into the scalp, both the scurf and the microbial flora were reduced. Moreover, it appeared that a reduction in the yeast flora was more effective in controlling dandruff than a reduction in the number of bacteria.
The circumstantial and experimental evidence thus implicate Pityrosporum as an agent in dandruff, but does not establish beyond doubt that it is the only cause. Indeed it may well be that the term dandruff covers more than one condition and that dry dandruff needs to be differentiated from greasy dandruff. A further complication is the distinction between dandruff and seborrheic dermatitis. Spoor believed that it was unrealistic to try to separate the conditions, whereas Kligman and his co-workers strongly reject the view that they are in any way related.
The wide range of treatments that have been used for dandruff reflects the debate about its nature and etiology.
Inasmuch as dry dandruff might be related to external provoking agents such as unsuitable shampoos, alcoholic lotions or waving lotions used too close to the scalp, these should clearly be avoided.
Greasy dandruff has been assaulted by an armoury of materials. Before reviewing them, the difficulties of making an objective assessment of their efficacy should be mentioned. Properly controlled tests are essential, since regular washing, massage and anointment of the scalp will often alleviate dandruff, whatever the materials used.
Hair follicles are tubular inpushings of the epidermis. The hair is produced by keratinization of cells formed by division in the matrix at the base of the follicle. This epidermal matrix surrounds a small dermal papilla which becomes invaginated into its base.
There are about 120,000 follicles on the human scalp. Each one undergoes a cycle of activity in which an active phase (anagen), which lasts for 1 to 3 years or even longer, is followed by a short transition phase (catagen) and a resting phase (telogen). This process involves a cessation of mitosis in the matrix and the keratinization of the expanded base of the hair to form a ‘club’, which is retained until the follicle again becomes active, when it is shed. Thus about 100 hairs are normally lost from the scalp each day.
Such cyclic activity of hair follicle may be considered as a remnant of the moult in other mammals. In contrast to the human scalp, where the activity of each follicle appears to be independent of its neighbours, some animals, such as rats and mice, exhibit wavelike patterns of new hair growth and moulting, which start in the mid-venter and spread over the flanks to the back. These have proved interesting models for experimentation on the factors controlling hair growth, but it should not be supposed that this has any direct relevance to human baldness. It appears that their follicles have an intrinsic rhythm, of which the mechanism remains undiscovered, but that this can be greatly modified by circulating hormones and thus, in turn, by environmental factors acting through the hypothalamus and the pituitary. Thus moulting, like reproductive activity, is seasonally controlled. Perhaps even the human scalp retains a reflection of the seasonal moult, with increased shed of club hairs in the autumn.
In the axillary and pubic regions of both sexes, and on the face of the male, coarse terminal hair — as distinct from fine vellus — develops at puberty, and continues to increase in amount for several years. The growth of this hair is initiated by and dependent upon androgens (male steroid hormones) which are secreted by the testicles of the male and by the adrenal glands and the ovaries in the female. Male-type body hair is also androgen-dependent, though its amount and distribution vary greatly between individuals. Unacceptable amounts of facial and body hair in women, known as hirsutism, may result from abnormal high androgen production, but individual variations in the sensitivity of the target hair follicles is also important. Compounds which block the action of androgen, known as anti-androgens, offer possibilities for the alleviation of female hirsutism.
Male pattern alopecia, a condition in which vigorously growing terminal hair is gradually replaced by miserably small and cosmetically useless fibres over areas of the scalp, appears to be hereditary, but requires the presence of male hormone. Hence eunuchs, even if genetically disposed, do not go bald, unless treated with tes osterone, and women rarely develop conspicuous bald patches, though they frequently suffer diffuse hair loss which may be the female equivalent. Why male hormones should promote hair growth on the face and body and ruin on the vertex of the scalp, so far eludes any consistent explanation.
Dandruff. Sometimes known as pityriasis capitis, this condition is characterized by the massive desquamation of small flakes of stratum corneum from the otherwise normal scalp. The scales may be dry or trapped in a film of sebum. Dandruff is uncommon in infancy and early childhood, but by puberty about half of all males and females become affected and in many it persists throughout life. It must therefore be considered as a physiological state rather than a disease and, as such, falls very much in the cosmetic rather than the clinical field.
The causation of dandruff is still debatable. Perhaps constitution or as in acne, stimulation by androgens or other physiological factors plays a part. Micro-organisms may well be involved, both Pityrosporum ovale and Pityrosporum orbiculare are more abundant in affected than in non-affected persons. Other suggestions are that the condition is caused by an allergen in sweat, or is a physiological error in the normal process of desquamation.
Dandruff has been treated with ointments containing 2 per cent salicyclic acid. Shampoos containing selenium disulphide or zinc pyrithione are currently favoured, and appear to work by reducing epidermal turnover. Other preparations are based on supposed ability to reduce the yeast flora.