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Why does the hair follicle cycle at all?


Why does the hair follicle cycle at all?

Source - In search of the “hair cycle clock”: a guided tour
Volume 72 Issue 9-10 Page 489-511, December 2004

A standard answer to this question is that synchronized hair follicle cycling and rhythmic shedding of hair shafts provide an excellent tool for adapting a mammal’s fur/hair coat to seasonal changes in habitat conditions as well as in procreational activities and needs (allowing for seasonal molting and changes in coat density and color during the mating season) (Stenn and Paus, 2001). However, besides primates, many other mammalian species (e.g., pigs) show a mosaic hair cycle, where every hair follicle more or less follows its own cycling rhythm—completely incongruent with seasonal changes. And even in species with fairly well-synchronized cycling activity (such as mice, rats, and rabbits), the latter becomes increasingly heterogeneous as the animals age, and is not at all stringently coupled to seasonal changes, e.g., in the length of the light period or temperature. While the seasonal and perennial endocrine changes that mammalian systems are subject to certainly can all modulate hair follicle cycling profoundly in one way or another (Ebling, 1988), they fail to explain the initiaton and termination of the individual waves of hair follicle cycling that travel through the skin of these animals. Therefore, additional arguments must be invoked when trying to explain the selection advantage during evolution that mammalian species may have obtained from developing cyclic transformations of their hair follicles.

During evolution, hair follicle cycling may have originated from the need to regenerate a (originally continuously produced) hair shaft, when it had been lost, and may have evolved only fairly recently, as a result of wear-and-tear environmental pressures (Jahoda in Stenn et al., 1999). Hair follicle cycling also allows to limit the maximal length of a hair shaft in a given location (e.g., overly long eyelashes, eyebrows, ear, nose and facial hair would severely compromise an animal’s capacity to see, smell and hear, while overly long truncal hair would seriously impede an animal’s movement). Its cycling capacity thus serves as an essential basis for generating distinct, appropriate hair shaft lengths in different regions of the integument—simply by modulating the duration of the hair shaft-producing anagen phase, which does indeed differ greatly between defined skin sites (cf. Chase, 1954; Dawber, 1997; Paus and Peker, 2003). The regular shedding of hair shafts, furthermore, rhythmically cleanses the skin surface from debris and even parasites that have accumulated in the follicular canal, and serves as an instrument of excretion for potentially deleterious chemicals (e.g., heavy metals, organic compounds) that are removed from the system by depositing them in “dead” trichocytes (Stenn and Paus, 2001). From an evolutionary point of view, hair follicle cycling may, thus, have awarded distinct survival and propagation advantages for mammalian species that developed this capacity.

Furthermore, its cycling activity makes the hair follicle a marvel of regeneration: in contrast to the non-cycling nail apparatus, even massive damage to the hair follicle does not abrogate its astounding capacity for regeneration—as long as its epithelial stem cell populations and contact between them and the dermal papilla have not been lost or damaged beyond repair. When hair follicles are severely damaged by chemotherapy, they can even accelerate the speed of cycling: by rapid deletion of the damaged anagen hair bulb and massive, premature onset of catagen, followed by a dramatically shortened telogen phase, a new anagen hair bulb is constructed at maximal speed (“dystrophic catagen” pathway; Paus et al., 1994a; Müller-Röver et al., in press). Given how vital an appropriate hair/fur coat is for the survival of most mammalian species in their adopted habitats, cycling may, therefore, also keep this miniorgan continuously in an optimal regeneration mode.

In addition, the hair follicle is an incredibly productive “biofactory” for numerous growth-modulatory agents, which are synthesized and/or metabolized here, including cytokines, neurotrophins, and hormones characteristically found in the hypothalamus, pituitary, or adrenal gland (Hoffmann, 2001a; Foitzik et al., 2003; Paus and Peker, 2003; Botchkarev et al., 2004). While these predominantly seem to be utilized by the hair follicle to modulate its own growth and pigmentation activity, its vasculature, and innervation (Paus et al., 1997b; Botchkarev et al., 2001; Peters et al., 2002; Tobin et al., 2003; Botchkareva et al., 2004), the hair follicle rhythmically may also secrete these agents into the surrounding skin or even into the circulation. (Unfortunately, this intriguing endocrine aspect of hair biology has remained almost completely unexplored.)

Given that, typically, all these agents are expressed in a strikingly hair cycle-dependent manner (usually with an expression maximum during anagen or catagen (e.g., Paus et al., 1997a; Welker et al., 1997; Foitzik et al., 2003; Botchkarev et al., 2004), hair follicle cycling may also be a means of regulating the para- or even endocrine secretory activity of this potent “biofactory”. The dramatic effects of synchronized hair follicle cycling on the architecture and functional properties of the surrounding skin can best be observed in mice. Subsequent to the onset of a wave of anagen development, epidermis, dermis, and subcutis become substantially thicker, and even show substantial angiogenesis only to get get thinner again during catagen/telogen (Chase et al., 1953; Hansen et al., 1984; Paus et al., 1990; Mecklenburg et al., 2000). Taken together, this invites the hypothesis that, via its cycling activity, the pilosebaceous unit serves as the “chief secretory agent” in skin biology.

Finally, hair follicle cycling may represent a highly efficient safe-guarding system against malignant degeneration: its most rapidly dividing and metabolically most active cell populations in the hair matrix, which must also be subjected to the greatest oxidative damage from reactive oxygen species (generated during this massive proliferative activity as well as during follicular melanogenesis), are rhythmically deleted during catagen—probably long before they can undergo malignant degeneration. In fact, while numerous tumors do arise from skin appendages, the vast majority of those develop from the “non-cycling”, distal hair follicle compartments, including from its epithelial stem cell region (e.g., basal cell carcinomas from the bulge), while malignant melanoma arising from the—regularly deleted!—hair follicle pigmentary unit is an extreme rarity.


What purpose does baldness serve ? I can totally understand why our hairs cycle & why our skin sheds but why the f**k do we bald? Why do people bald with various degrees? Why not lose it all?
It is such a stupid thing! Whoever created us must really enjoy torturing people.The fact that no one can even find a cure shows that some people are born to suffer.
I am sorry for the rant,I promise this is my last post here.This place is driving me nuts.I need to preoccupy my time with something else.
Goodbye everyone & good luck.