Our Hair

Every hair grows from a hair follicle. These mini-organs are embedded in large numbers in the skin of almost the entire body surface. Apart from the mucous membranes, only the palms of the hands and feet, the lips and the surfaces of the eyelids are left out. What is special about the follicular organs is their cyclical dynamics: Normally, they go through life-long phases of build-up, breakdown and rest, which bring with them the characteristic growth, stagnation and loss of head and body hair.

human hair and hair follicles

The three types of human hair

Depending on their location on the body, but also on other circumstances, hair follicles can produce different hair. The mature, so-called terminal hair forms the predominant head and body hair in adulthood (with obvious differences in length and thickness, e.g. between head and pubic hair). “Immature” hair variants are the fluffy, colourless lanugo hair of the embryo and the short, thin vellus hair, the prepubertal body hair, which is also retained in larger parts in many adult women and some men.

Terminal hair

  • forms further parts of the body hair (chest hair, etc.) in adults: head hair, eyebrows and eyelashes, pubic hair, underarm hair and hormone status-dependent
  • completely pigmented (if not greyed…)
  • diameter between about 0.02 and 0.12 millimetres (= very thin and very thick hair)
  • can become very long, depending on the length of the growth phase (the world record set in the Guinness Book of Records is 5.76 metres, measured in 2004 for the Chinese woman Xi Qiuping)
  • three-layer structure (cuticle, bark, medulla) with thick, stable bark
  • Follicle is connected to a sebaceous gland

Vellus hair

  • prepubertal body hair, remains partially intact even after puberty (especially in women)
  • weakly pigmented
  • very thin: not thicker than 0.3 millimetres
  • Length maximum 2 millimetres
  • two-layer structure without mark
  • Follicle is not connected to a sebaceous gland

The transition between vellus and terminal hair is indeed fluid: in the course of several follicle cycles, the hair growing out of the follicle can become increasingly thicker, longer and more pigmented. This happens when a baby’s first visible hair grows, when body hair transforms from vellus to terminal type during puberty – or when the follicles are treated with medication. Hair in this intermediate state is also called intermediate hair by some experts [1].

Lanugo Hair

  • embryonic body hair, usually falls out before birth or soon after
  • normally pigment-free
  • very thin: not thicker than 0.3 millimetres
  • slightly longer than vellus hair, but normally not longer than 10 millimetres
  • two-layer structure without mark
  • Follicle is connected to a sebaceous gland

Even from “adult” follicles lanugo or vellus hair can grow again. Often this happens under rather unfavourable conditions, such as very poor nutritional status, diseases and/or when taking certain medications. But also quite normal aging processes, changes in the hormone balance without a particular disease value or genetically determined sensitivities can cause the follicles to produce vellus hair again instead of terminal hair and cause receding hairline corners or the typical hair loss pattern of male alopecia.

The hair follicles

Hair follicles of different body regions and stages of development differ in size and shape, but essentially all hair follicles are of the same structure. During the cyclically successive growth, decomposition and resting phases, a follicle undergoes constant changes in which its size and even its internal structure changes significantly: all follicles have this in common, too.

Hair follicles are elongated invaginations of the epidermis into the dermis. The inside of the follicle is lined by several superimposed cell layers, the connective tissue and epithelial root sheaths. The outer cells of the hair shaft and root sheath inside the follicle overlap like scales. As this scaly structure of the hair and root sheath is oriented in opposite directions, the scales interlock and ensure that the hair shaft is held relatively firmly in the follicle.

By the way: Whether the hair grows straight, wavy or curly out of the follicle is determined by the shape of the follicle cross-section. A follicle with a round cross-section produces a round and therefore smooth hair, an oval follicle produces an oval (i.e. preferably bendable in one direction) and therefore wavy or curly hair.

At the edge of the follicle a small “bulge” is noticeable. It contains the most precious good of every hair follicle: a small heap of stem cells from which the follicle is cyclically renewed. If these stem cells are damaged – by radiation, highly cytotoxic drugs or aggressive inflammatory processes – no more hair can grow from the follicle.

At its lower end, the follicle thickens to form the so-called hair bulb (hair bulb). The hair papilla protrudes into the bulb from below. In addition to a blood vessel loop that supplies the cells of the bulb with oxygen and nutrients, this papilla contains various specialised cells that are involved in controlling the follicle cycle. In the bulb – in the anagen phase (growth phase) of the hair follicle – the magic of hair growth happens. Then the hair bulb is filled with so-called matrix cells and melanocytes (pigment cells).

The matrix cells, from which the hair cells originate, are among the most dynamic cells in the body: in the anagen phase, they divide on average daily and thus ensure the growth of the hair shaft. The offspring of the matrix cells push their way up the follicle. On the way, they are still stained with brownish, reddish or black melanin by the melanocytes.

Depending on whether the freshly baked hair cells are located rather in the middle or rather at the edge of the future hair, they develop somewhat differently. Thus, on the way up, the medulla, cortex and cuticle of the hair gradually develop: Slightly looser arranged hair cells in the middle, firmly cemented cells in the thick cortex and dead, scale-like cells at the edge. As long as they live, all hair cells do one thing in particular: as so-called keratinocytes (horny cells) they synthesize the protein keratin, the chains of which purr together by themselves to form elastic, spiral-wound threads, and the cells soon fill up completely.

As long as new hair cells are formed at the bottom of the hair bulb, the hair grows and pushes itself further and further out of the follicle. At the base it is closely connected to the so-called papilla – a small invagination of surrounding skin tissue that contains blood vessels and supplies the hair cells with oxygen and nutrients.

The follicle cycle

Sooner or later, however (in the case of scalp hair, usually after months or years) the growth phase comes to an end; hair and hair follicles enter the next phase of their cycle. The growth phase is followed by the regression or catagen phase: the matrix cells no longer divide, the hair detaches from the papilla and is only held in the follicle by the scaly cuticle. At the same time the follicle shrinks. The catagen phase lasts two to three weeks, after which the shortened, shrunken follicle enters its well-deserved resting phase, the telogen phase. Essentially nothing happens during a few weeks to months – except that the aged hair may spontaneously fall out or be torn out by the hairbrush at some point during this period. At a certain point in time, the follicle is then reactivated, lengthens, new matrix cells develop from stem cells – a new anagen phase and a new hair begins [2].

For a long time it was assumed that the old hair, if it is still in the follicle, is simply pushed out by the hair that is now developing. In more recent textbooks, there is often a somewhat revised view, motivated by recent research, that the old hair is actively pushed out in a process controlled by the follicle. In this model of events, the follicle remains empty for a while before the new hair begins to grow. For these two phases the new terms exogenous and kenogenic phase were coined [3].

The length of the anagen and telogen phases is on the one hand genetically programmed, but is also influenced by various external factors – especially by the body’s own chemicals (hormones, among others) and foreign chemicals (drugs) to which the follicle is exposed.

Anagen phase

  • active growth of a new hair
  • any old hair that may still be present is pressed out by the new hair
  • Hair is closely connected to the papilla at the base of the follicle and is nourished by blood vessels
  • Duration: several months (e.g. around ten weeks for eyebrows, around twenty weeks for eyelashes) to many years (scalp hair) – the duration of the anagen phase determines the maximum achievable hair length

Catagen Phase

  • Regression of the follicle (shrinkage to about half the length of the anagen phase, regression of the papilla, no more cell division activity)
  • Hair detaches from the papilla, but remains anchored in the follicle
  • Duration: about two weeks

Telogen Phase

  • resting phase of the follicle, hardly any metabolic activity of the cells
  • Hair is still in the follicle, but can fall out/be ripped out more easily than in the other phases
  • Duration: several months (head hair: about three months, eyebrows about seven months)

Exogenous and Kenogene phase (more recent hypotheses)

  • Exogenous phase: active, controlled repulsion of the old hair at the end of the telogen phase
  • Kenogen phase: temporarily “empty” follicle after telogen phase

What controls the development and cycle of hair follicles?

In the course of individual development, the follicles of the scalp (and of course many other parts of the body that are less important for the problem of hair loss) develop from lanugo to vellus to terminal hair-producing organ. At the same time, each follicle alternates cyclically between growth and resting phases.

In men, undesirable changes in the hair cycle (e.g. increasing shortening of the anagen phase) can already occur in early adulthood, which can lead to regression of the follicle from mature back to vellus hair follicle.

How are these changes controlled? The hair papilla has a decisive influence on the behaviour of a follicle. The cells of the papilla secrete a variety of growth factors that control the growth of the follicle and the formation of the bulb by stimulating the stem cells belonging to each follicle to divide at certain times and produce new matrix cells and melanocytes. The secretory activity of the papilla determines the size of the bulb (and thus the thickness of the growing hair), the speed of hair growth and the duration of the anagen phase.

The papilla has its own “timing” mechanism that determines the lengths of the anagen and catagen phases. Researchers have some hypotheses about the nature of this mechanism, but it is far from clear. What is certain is that both the timing and the structure-giving properties of the papilla are largely hereditary. However, they are also influenced by external circumstances. For example, papillae develop different characteristics in different parts of the human body (for example, with regard to their androgen sensitivity), which may remain even after the follicle has been moved to another part of the body.

The most important factor influencing hair growth in humans are the androgens, a group of sex hormones, with testosterone and its close relative dihydrotestosterone (DHT) as the most important representatives. Other modulators of hair growth include stress hormones (cortisol and adenocorticotropin).

Although testosterone is known as the male sex hormone par excellence, testosterone (and generally androgen) levels also increase in girls and women during puberty. Androgens are not only produced in the testicles, but also in smaller amounts in the ovaries and in the adrenal cortex. Testosterone causes underarm hair and pubic hair to grow. Dihydrotestosterone, which is produced from testosterone by a small chemical transformation catalysed by the enzyme 5α reductase, stimulates, among other things, the growth of the rest of the body hair and the beard hair. Dihydrotestosterone is also the “main culprit” in male hair loss.

How do androgens affect hair follicles?

The currently generally accepted hypothesis is that androgens from the blood bind to specialized receptors of cells of the hair papilla located at the base of the follicle and stimulate them to produce growth or inhibition factors, which in turn influence the division and metabolic activity of the cells of the follicle.

IGF-1 (insulin-like growth factor) is seen as the key growth factor; TGF-β (transforming growth factor) is seen as the key inhibitory factor. The intermediate receptor provides an explanation why the effect of androgens on hair follicles can be so different at different sites in the body: It ranges from growth-stimulating (pubic hair, beard hair, axillary hair) to practically non-existent (eyelashes) and growth-inhibiting (parts of the scalp in hereditary men). These effects can easily occur simultaneously. The hypothesis is that the papillae of the hair follicles, under the influence of their specific environment, express a different androgen receptor population or, in response to androgen binding to their receptors, emit different messenger substances.

Testosterone and dihydrotestosterone

It is now known that testosterone is converted into dihydrotestosterone in the cells of many target tissues by the enzyme 5α reductase. Dihydrotestosterone (DHT) binds much more strongly to many androgen receptors than testosterone and can therefore be characterised as biologically more effective. In this sense, testosterone is the transport form of the hormone or the prohormone and DHT its active form.

5α-Reductase is part of the equipment of most cell types that respond to testosterone and is also found in the hair follicles. The efficacy of 5α reductase inhibitors such as finasteride for androgenic alopecia allows us to conclude that DHT is indeed the form of testosterone crucial for hair loss.

The influence of prostaglandins on hair growth: research continues

Recent research on hair loss deals with the influence of a group of so-called tissue hormones, the prostaglandins. Unlike the classical hormones circulating in the blood, which are the body’s “long-distance mail”, so to speak, prostaglandins are something like “office memos”: messenger substances that transmit information locally, i.e. to groups of neighbouring cells. Accordingly, prostaglandins are not synthesized centrally in specialized glands, but directly in the tissue where they exert their influence. Many cells of the hair follicle are also equipped with the “machinery” for prostaglandin synthesis [4].

In the meantime it has been proven that prostaglandins have a very decisive influence on the growth and dynamics of hair follicles. However, much about the exact mechanism of this effect is still unclear. One thing is clear: Hair sprouts when exposed to prostaglandins of a certain type (prostaglandin F2α). [5] And stops growing when exposed to prostaglandins of another type (prostaglandin D2), which have also been shown to be significantly increased in bald scalp areas compared to hairy ones. [6] The hair follicles of hair follicles are also affected by prostaglandins of a different type (prostaglandin D2).

In the context of the hitherto puzzled picture of the control of hair follicle growth, it is conceivable that prostaglandins are connected as a regulatory link between androgens and local growth and inhibitors (IGF-1 and TGF-β). It is conceivable that the synthesis of prostaglandins in hair follicles or neighbouring cells is stimulated by dihydrotestosterone and that prostaglandins in turn stimulate the synthesis of local messengers. But none of this has really been proven yet.

And even under this expanded hypothesis, it remains painfully unexplained and unaddressed why in some people the hair follicles of the scalp shrink under the influence of testosterone. We now know or suspect that this happens via dihydrotestosterone and prostaglandin D2 – but these details do not get us as much further in our understanding of the causes of the problem as it might at first appear. However, the discovery of the influence of prostaglandins has opened up a new possibility of pharmacologically influencing follicular growth.

Follicular units

In modern hair transplantation medicine, there is much talk of the so-called Follicular Units (FU): The two currently most important transplantation procedures FUT (Follicular Unit Transplantation) and FUE (Follicular Unit Extraction) even have the term directly in their names.

In order to understand what a follicular unit is, it is important to know that the typical illustration, which shows a single hair follicle from which in turn a single hair sprouts, is a bit misleading in one respect. In fact, most follicles of the scalp do not actually stand isolated in the skin, but form groups of two to four terminal hair follicles and one to two vellus hair follicles, which are not only close together, but whose hair channels can even merge with each other in the upper layers of the skin, so that typically two, three or even four hairs grow from a single follicular channel on the surface of the scalp.[7] The follicles of this closely connected group, as well as the associated sebaceous glands and hair follicle muscle, form a follicular unit.