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Hair
follicle cycle
Each individual hair is formed inside a hair bulb
deep in a hair follicle. The follicle is a tiny but powerful factory,
which throughout the human life span hardly ever stops working.
This hair shaft factory is unique in that it is the only organ
in the mammalian body which, for its entire lifetime, undergoes
cyclic transformations. The hair follicle cycles between stages
of rapid growth (anagen) to apoptosis-driven regression (catagen)
and back to anagen, via an interspersed period of relative quiescence
(telogen).
Hair is continually shed and renewed by the operation of these
alternating cycles of growth, rest, fallout and renewed growth.
Growth is not synchronized so each hair passes through the three
phases independently. The relative duration of these phases varies
with the individual's age, nutritional status, hormonal factors,
and other physiologic and pathologic factors. The duration of
anagen determines the final length of the hair and thus varies
according to body site; however catagen and telogen duration vary
to a lesser extent depending on site.
Unlike other mammals, hair growth and loss in humans is random
and not seasonal or cyclic. At any given time, a random number
of hairs will be in various stages of growth and shedding. In
older people the hair cycle becomes shorter, the follicles gradually
give up producing long, strong hair, and the hairs become thinner
and shorter. The result may be a general thinning of the hair,
or even a degree of baldness.
Although we speak of stages in the development of a hair follicle,
it should be made clear that these are actually dynamic, flowing
processes and the setting up of stages is purely for our understanding
of the human hair follicle cycle. In many reported hair biology
studies not enough emphasis has been placed on the fact that the
follicle is a dynamic structure. Most studies conducted so far
have been limited to follicles of one particular phase of the
cycle or one phase of development. However, determining the molecular
signals that orchestrate the follicle’s transit between
these three stages is one of the key challenges of hair research.
The catagen phase in the hair follicle cycling process is described
as a highly controlled process of coordinated cell differentiation
and apoptosis. Once the involution (process of progressive decline
or degeneration) of catagen is complete and a club hair is formed,
the hair follicle prepares the hair for expulsion from the scalp.
An increase in the percentage of scalp follicles in the telogen
stage leads to excessive shedding. Although telogen is the quiescent
or resting period, a telogen follicle may still have a hair fiber
in it. Telogen can be considered as an “anagen break”.
Although the key players in the underlying molecular controls
have not
been discovered as yet, drugs that reduce the percentage of follicles
in this stage would be useful in many forms of treating hair loss.
Telogen
in the hair follicle cycle
Telogen is considered as the resting stage or the period of
quiescence in the hair follicle cycling process. When hair follicles
enter
telogen and stop making hair, they dump their last cells on to
the end of the fiber. This lump of cells acts as an anchor to
hold the hair fiber in the tube of the hair follicle. The hair
is now called a "club" hair as the lump of cells on
the end gives it a club appearance. This non living hair is attached
to the skin with a "club-like" root, but will eventually
be pushed out or pulled out during combing or washing and replaced
by a new growing hair. The telogen stage typically
lasts for
two
to three months before the scalp follicles enter the anagen stage
and the cycle is repeated.
The percentage of follicles in the telogen stage varies according
to the region of the body. For example, 5 to 15 per cent of scalp
follicles are in the telogen stage at any one time, as compared
with 40 to 50 percent of follicles on the trunk. On an average,
people lose from 50 up to 150 scalp hairs a day. It is not as
yet clear whether shedding is an active, regulated process or
a passive
event that occurs at the onset of the anagen stage, as the new
hair grows in. Telogen is a heterogeneous state, since about one
percent of telogen follicles shed their hair fiber each day.
Mechanism
of telogen
By the end of catagen, the follicle extends no deeper than the
upper dermis. In telogen, the dermal papilla can become isolated
in the dermis as the remaining hair follicle regresses and sits
high up in the dermis. The telogen follicle sits in the dermis
as a small finger of “quiescent” epithelial cells
above a tight cluster of papilla fibroblasts. Matrix cells are
the living, actively proliferating group of cells which differentiate
and become keratinized to form the hair cortex, but in telogen
follicles the volume of the dermal papilla extracellular matrix
is much reduced Fibroblasts (spindle-shaped cells with cytoplasmic
processes present in connective tissue, capable of forming collagen
fibers) in this phase also have scant cytoplasm.
The epithelial cells of the lower telogen follicle do not show
significant DNA or RNA synthesis, nor is there any synthesis of
proteins characteristic of the anagen follicle, such as trichohyalin
and the hair cortical keratins. However, Keratin 14 (K14) synthesis
continues in the epithelial sac to which the telogen hair fiber
anchors. Embedded in the epithelial sac is the club hair (or telogen)
shaft. This shaft has a brush-like base attached to the two-layered
epidermal outer root sheath sac. The region of the epidermal sac
at the very base of the club hair is composed of tightly packed,
small cells known as the hair germ. Where it interfaces the papilla,
the hair germ is flattened. When the telogen follicle transits
to the next anagen phase, the cells of the germ swells and grows
down to enclose the papilla. The new hair emerges from the same
opening at the surface of the skin as the old one, and the hair
cycle begins again.
Telogen is by far the most difficult phase to identify morphologically
since the earliest phase of anagen and the latest phase of catagen
may appear structurally like telogen. However, the fact that these
phases are functionally distinguishable implies a molecular difference.
Although the molecular nature of the underlying oscillator system
remains to be clarified, animal research studies indicate that
the deletion of selected adhesion molecules (desmoglein-3) or
proteases (cathepsin L) in transgenic mice induces abnormalities
in telogen club hair formation and shaft anchorage. The evidence
gathered demonstrates that desmoglein 3 is critical for anchoring
the telogen hair to the outer root sheath of the follicle, and
that cathepsin L is an important regulator of keratinocyte and
melanocytes differentiation during hair follicle morphogenesis
and cycling.
Telogen
in the hair follicle cycle references
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