Androgenetic Alopecia Affects The Hair Growth Cycle Of The Person Suffering From It

Male Pattern Baldness
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How Does Androgenetic Alopecia Affect hair Growth Cycle?

Androgenetic Alopecia is the most common cause of balding in aging men. This disease is caused by hormonal and genetic factors.

How does it start?

The condition results from increased binding of androgens (especially dihydrotestosterone) to the androgen receptors in the dermal papilla of sensitive hair follicles. The sensitive follicles react to the change in the level of androgens by an increased rate of hair shedding.

The origin of male pattern baldness is characterized by the following three factors:
  • The alteration of hair cycle dynamics
  • Follicular miniaturization
  • Inflammation
The biochemical stimulation for these changes is provided by androgens. The latter induces a transformation in the growth factor beta (TGF-B) to cause cyclical miniaturization of the entire hair follicle.

The resulting hair produced from the follicle is shorter and finer and it provides less complete scalp coverage. Due to the progressive shrinking of the dermal papilla, less and less nutrition is available to these shortened hair follicles. The latter ultimately fall leading to an occurrence of bald spots on the scalp.
Topical Oxygen Free Radical Scavengers
Hair growth is a cyclical process with three alternating phases:
  • Anagen growth phase,
  • Catagen involutional phase
  • Telogen resting phase.
Anagen lasts for 3-5 years, catagen for 2 weeks and telogen for 3 months. The usual ratio of anagen hair to telogen hair is 12:1. Normal hair shedding occurs within the telogen or the resting phase. The telogen phase can be subdivided into exogen (which is the proper resting phase) and the latent phase (the transitional phase between telogen and anagen).
The Pathological Condition Causing Androgenetic Alopecia
Androgenetic alopecia results due to a pathological condition where androgen concentration is quite high. The action of these hormones on dermal papilla cells alters the growth factors produced in the hair follicle. The alteration of growth factors causes a decrease in the length of anagen with each cycle whereas the length of telogen remains constant or is prolonged. This results in a reduction of the anagen to telogen ratio and the ratio of new hair to resting hair over the scalp.

With progression of the disease, more and more hairs are in the resting phase. Due to this prolonged resting phase, balding patients often experience periods of excessive hair shedding, most noticeable while combing or washing.
Reduction in the Duration of Anagen
The growth rate of hair remains relatively constant. The duration of anagen growth phase determines maximal hair length. Thus, with each successively foreshortened hair cycle, the length of each hair shaft is reduced. Ultimately, the anagen duration becomes so short that the growing hair fails to achieve sufficient length to reach the surface of the skin. And that leaves an empty follicular pore. The gradual reduction in the number of hair follicles contributes finally to the balding process.
Changes in Hair Follicles
The step-wise miniaturization (shortening) of hair follicle and alteration of hair-cycle dynamics in the pre-programmed follicles results in considerable changes going on the scalp. The shortening of anagen duration causes the maximum length of the new anagen hair to start becoming shorter than that its predecessor.

Eventually, the anagen phase becomes so short that no new hair reaches the surface. Nothing is left behind as its remnant except the pore, leading to a reduction in the number of hairs present on the scalp.

The follicular miniaturization - caused by hair-cycle changes - affects the hair follicle to a great extent. It affects the follicle's growth, structure and function. Thus, it affects the papilla, the matrix and ultimately the hair shaft. In association with the changes in hair cycle dynamics, there is progressive, stepwise miniaturization (of the entire follicular apparatus).

Hair follicle apparatus consists of mesenchymal and ectodermal components. The ectodermal part consists of an invagination of epidermis into the dermis and subcutaneous fat. The hair bulb contains the hair matrix producing the hair shaft.

The mesenchymal component is the dermal papilla, a small collection of specialized fibroblasts that is almost totally surrounded by the hair bulb. Being central in the maintenance and control of hair growth, the dermal papilla is likely to be the target of androgen-mediated events leading to miniaturization and hair cycle changes. The constant geometric relation between the dermal papilla size and the size of the hair matrix suggests that the size of the dermal papilla determines the size of the hair bulb and ultimately the hair shaft produced.
Characteristics of Hair Shaft
A miniaturized or shortened hair follicle has about greater than tenfold reduction in its overall cell numbers. The reason for the change is not very clear. But it is certain that it has something to do with dermal adhesion, leading to dermal papilla fibroblasts dropping off into the dermis, or migration of dermal papilla cells into the dermal sheath associated with the outer root sheath of the hair follicle. These changes result in the alteration of hair follicular function. Smaller follicles result in finer hairs.

The caliber of hair shafts reduces from 0.08 mm to less than 0.06 mm. This is also followed by a reduction in pigment production. On the scalp which is gradually balding, three types of hairs are seen, the terminal hair, the thin and short vellus hair and transitional indeterminate hairs which are the bridge between full-sized terminal hairs and miniaturized hairs.
Histopathological Changes
The blood flow in the scalp in early male pattern baldness has been found to be quite diminished as compared to the controls.

The miniaturization of hairs seen clinically in affected scalp areas of male pattern hair loss is reflected in the typical histologic findings. Besides, there are the changes observed in decrease in diameter, decreased number of terminal hairs and increased telogen count and associated increase in the number of vellus hairs.

The earliest (but relatively nonspecific) histologic sign of androgenetic alopecia may be a spotty perivascular degeneration of the lower third of the connective tissue sheath of affected anagen follicles. This is recognized by a characteristic basophilic smudging in the otherwise pink and fibrillary collagen fibers in the connective tissue sheath.

Later, the connective tissue stele, seen in all telogen follicles, may become broader and more cellular in male pattern hair loss than the collapsed sheath seen with normal follicles.

Moderate inflammation is also more common in balding scalp. This inflammation or fibrosis may have prognostic value for re-growth in pattern hair loss. It is indicated by the fact that a good response to minoxidil therapy is observed only in those patients who have little or no inflammation.

What is the other change? It is the decrease in the thickness of the epidermis, dermis, and subcutaneous tissue in advanced male pattern hair loss compared with normal controls. The decreased skin thickness is supposedly related to the loss of substance of the normal hair follicles.