Induction and Inhibition of Hair Growth
For practical reasons the dermatologist is interested chiefly in whether hair growth can be regulated by therapeutic measures. The trichological literature contains many studies on ways of inducing and inhibiting hair growth; the majority are concerned with the effects of various physical and chemical factors supposed to be able to stimulate the rate of hair production.
In theory, the hair growth rate can increase: (a) if mitotic activity in the growing anagen follicle increases, (b) if new follicles or follicles producing several hair shafts are formed, (c) if follicular activity can be successfully modified so that the growth phase is prolonged and the resting phase is shortened, (d) if the telogen phase can be postponed or, better still, prevented altogether, and lastly (e) if, in the resting phase, the onset of a new anagen can be speeded up.
The only one of these five theoretical possibilities which has practical prospects today is the last one, i. e. acceleration of growth of a new generation hair in the telogen follicle.
One of the physical factors which can induce growth of a new hair in the resting follicle is mechanical epilation, which shortens telogen in a number of animals and also in man. Epilation accelerates growth only if the follicle is in telogen. Anagen hairs continue to grow from the residual matrix and in 24—48h the destructive changes in the bulb are repaired. After a brief period of restitution the hair grows again, but for a shorter time and to a lesser extent than the hairs in intact follicles in the vicinity. Epilation of anagen hair evidently does not influence the length of the resting phase after which the nexr anagen appears.
Other traumatizing measures — e. g. traumatizatior. of the skin, surgical measures (including transplantation) and cold, etc. — have similar effects to epilation. Some authors are of the opinion that normal homoeostatic inhibitors are impaired in these situations, or that stimulative metabolites are released from damaged cells.
The theory of an inductive control mechanism which is set in motion by epilation or some other trauma has recently been brought up to date. The increased mitotic activity which leads to tissue restitution is ascribed to prostaglandins released from damaged cells. Prostaglandins stimulate adenylcyclase activity, thereby raising the production of mitogeneticaily active cyclic adenosine monophosphate (AMP), the outcome of the whole process being increased proliferation of the cells in the traumatized tissue.
In evaluation of the effect of massage, the results of different authors are at variance, but most of them evaluate massage as a growth stimulant, which must be taken into account when testing various external remedies which are rubbed into the skin. To some extent massage resembles shaving, which is generally assumed to stimulate growth of the beard. Objective measurement shows that the effect of shaving is minimal, although mild erythema develops near the follicle, irrespective of whether an electric or a safety razor is used for shaving. There is even a theory that the rate of growth of the beard rises immediately after shaving, only to fall compensatorily again later on, so that the result is the same as after a haircut, i. e. nil.
As far as radiation is concerned, some animals are highly sensitive to visible radiation and it seems as though the other wavelengths of the solar spectrum might also be a physiological stimulus for a new hair growth cycle. In the case of wild animals, solar radiation is supposed to influence seasonal hair change rhythms, but the situation here is actually more complex, since it includes other factors such as temperature changes and, in particular, genetic factors and cyclic changes in endocrine functions. Photic and thermic factors influence hair growth in man on a very minor scale (chiefly after a move to a place with a different climate).
Other methods which have been tried include the percutaneous administration of a large number of chemical irritants, or of substances which it was supposed might, in various ways, induce the growth of new hair. Irritants are discussed mainly in older studies on the effects of substances like tar, phenol, chrysarobin, croton oil, anthralin, capsicum tincture and other chemicals, many of which have become stock hair preparations. According to Flesch, all irritants have one thing in common: they all induce increased vascularization, which is characteristic of the anagen phase of hair growth. The mechanism by which hyperaemia activates telogen follicles is not clear, however. Since most of the above substances were tested in animals (very often without reference to the phase of the growth cycle), it is not clear whether they can also influence hair growth in man. Clinical observations, however, showed that prolonged and sufficiently intensive stimulation of the skin can lead in some cases to coarsening of the terminal hair.
Far more convincing results have been obtained with the external use of corticosteroids, especially on increasing resorption by means of an occlusive dressing. The exact mechanism by which externally applied corticoids act on hair growth is not known, but it evidently involves a complex general effect similar to the one in systemic therapy, an anti inflammatory effect and an effect on keratinization and pigmentation, especially in pathological conditions. Other, systematically administered remedies can also induce more intensive growth, from lanuginous to terminal hair. Undesirable, but only temporary iatrogenic hypertrichosis of the trunk, the limbs and sometimes the face as well has been described, for instance, after streptomycin, penicillamine, psoralens and di phenylhydantoin. The hirsutism which occurs relatively frequently in prediposed women after androgen and progesterone therapy has a poorer prognosis.
A diversity of substances which are supposed to be able to influence hair growth are used in the production of shampoos and other cosmetic hair preparations; they include, for example, cholesterol, egg yolk emulsions, vitamin F, oestrogens and tissue and plant extracts. Their action is mostly restricted to keratin, however, i.e. mainly to the cuticle and the adjacent part of the hair cortex, where they can limit the negative effect of external factors.
With greater exposure, or in a higher concentration, most physical factors and some chemicals which induce growth can produce the reverse phenomenon, i. e. inhibition or complete arrest of hair growth. For instance, regular strong pressure from a clasp, a cap or an unsuitable hair style can lead to irreversible alopecia in the relevant localization. The same applies to mechanical, thermic and chemical trauma, which can destroy the follicles completely.
Unlike inductive factors, inhibitory factors affect the anagen follicle, reduce or completely suppress the mitotic activity of the matrix and impair keratinization. The concentration or exposure time needed for an inductive effect to change to an inhibitory effect is unknown. The one exception is X-ray irradiation, which can be dosed exactly, so that its effect can be progressively intensified from reversible to irreversible damage to the bulb.
Growth can also be inhibited after chemicals, as a side effect of general poisoning (e. g. in individual intolerance or after overdosing with salts of heavy metals, quinine, atebrin, etc.) or after the direct toxic effect on the follicle of specific depilatories with different mechanisms of action (cytostatics and anticoagulants inhibiting mitosis, a tripanarol block of plasma cholesterol synthesis in the liver, thallium interference with cell differentiation and a thallium block of cystine binding to the keratin molecule). Chloroprene derivatives, large doses of vitamin A and the non saturated fatty acids of human sebum have a depilatory effect, evidently by inhibiting the free SH groups of protein. Inhibitory factors attack only the active anagen follicle and transform the growing anagen hair to a dysplastic hair.