The biology of hypertrichosis and how it occurs

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Hypertrichosis Biology

Hypertrichosis is an excessive hair disorder characterized by abnormal hair length and density for a particular racial, age or sex group. It could be generalized, that is, spread throughout the body, with few exceptions, or localised, that is, restricted to small areas of the body. It affects practically all people of all races, ages and sex. The abnormal appearance of the affected people can cause social ostracism causing considerable mental stress in them.

While this disorder is mainly a cosmetic problem, it may also be a sign of underlying systemic problems. Hypertrichosis can therefore aid in the diagnosis of such systemic diseases.

Hypertrichosis is manifested in many forms. In this article we will use the existing knowledge base to explore the biological causes of this disorder.

To understand the biology of hypertrichosis, it is first necessary to know the kind of hairs involved and the terms used to name them. There are essentially three kinds of hair involved viz. lanugo, vellus and terminal.

Lanugo refers to long, fine, unmedullated and unpigmented hairs, which in normal cases appear on the entire fetus during the 3rd to 7th month of pregnancy and are shed in utero in the 7th or 8th month. After birth, the entire body of the newborn, with the exception of the scalp and eyebrows, is covered with short and very fine un-pigmented vellus hairs. Vellus hairs are variably medullated and are produced by hair follicles that penetrate only into the papillary dermis. Hair shafts of the vellus hairs are no wider than the inner root sheath of the follicles that produce them. Terminal hairs are coarser and medullated and the follicles producing them penetrate to the reticular dermis. Terminal hair shafts are wider than the inner root sheath of the follicles that produce them being twice that of the vellus hairs. In their anagen phase (the growth phase) the terminal hairs can be more than 2 centimeters long, whereas vellus hair usually grows significantly less than 2 centimeters in length.

The biology of hypertrichosis involves two major mechanisms

One method of hypertrichosis development involves the conversion of vellus hairs into terminal hairs. The sudden increase in androgen during adolescence causes the follicles in the axillae, groin and in males, the beard and chest, to grow bigger and penetrate more deeply into the dermis and transform into terminal hairs. This mechanism sometimes also involves the transformation of vellus hairs into terminal hairs even on sites where there are normally no terminal hairs. But the mechanism of vellus to terminal changeover is as yet poorly understood. Even though the mechanism is androgen driven, it is not known why it should result in an increase in hair growth in places like the axillae and groin and cause a reduction of growth on the scalp.

The second major mechanism in hypertrichosis biology involves changes in hair cycling. Hair follicle cycle has three stages. These are the anagen stage, which is the growth phase, the catagen stage, where the follicle growth stops and the cycling portion of the follicle undergoes apoptosis and the telogen stage where the shedding of hair takes place.

It is well established that longer hair is the result of longer time spent by the follicle in the anagen phase. It is also well known that higher hair density can be caused by a reduction in hair shedding as a result of a reduction in the percentage of hair follicles in the telogen phase. It is seen that some places on the body, such as the scalp, which has longer hairs and greater hair density, have more hair follicles in the anagen stage. Like the vellus to terminal transformation, the medical world has just started understanding the control and alteration of the hair cycle. Hair follicles growing in every site of the body have their own distinctive growth pattern, which can be changed by systemic influences such as androgens, thyroid and growth hormones. Hypertrichosis can be the result of hair follicles spending more than their normal time duration in the anagen phase

A third but less well established mechanism of hypertrichosis is one involving an increase in hair follicle density. The density of hair follicles differs from place to place on the body. According to this mechanism, hypertrichosis is exhibited in those areas of the body that have a higher density of hair follicles than is normal for those sites. Such a cause of hypertrichosis can only occur during fetal development as no new hair follicles are formed in the skin after birth. As such, someone born with hypertrichosis as a result of greater than normal density of hair follicles is born with such a condition and the problem persists throughout life.

Despite there being a limited number of mechanisms for hypertrichosis, the causes that trigger the mechanism are still by and large unknown.


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