Diagnostic Study Of Androgenetic Alopecia

Male Pattern Baldness
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Androgenetic Alopecia - Clinical Presentation and Diagnosis

A Standard Model for Androgenetic Alopecia

Traditionally it was believed that most models of androgenetic alopecia showed follicular miniaturization occurring in a gradually progressive fashion. But now this view has changed. Now it is believed that the transition from terminal to vellus hair occurs as an abrupt, single step process.

Researchers have found that cross-sectional area of individual hair shafts remains constant throughout fully developed anagen phase. That indicates that the hair follicle, and its dermal papilla, remains the same size. The observation indicates that follicular miniaturization does not occur within an anagen cycle but between anagen cycles.

This model also explains the lengthy delay experienced between clinical response and the commencement of therapy for medical hair restoration with minoxidil.
The pharmacological intervention may not able to affect the anagen phase. It will only have an effect at the point of miniaturization as the hair follicle move from telogen to a new anagen phase.
Histological Support for the Model
Histological studies have revealed that after follicular miniaturization, the dermal remnants of it are left behind as the stellae. These stellae, also known as fibrous tracts or streamers, extend from the subcutaneous tissue to the base of the miniaturized hair follicle. It marks the former position of the original terminal follicle.

Arao-Perkins bodies seen with elastic stains within the follicular stellae are first observed as a small cluster of elastic fibers in the neck of the dermal papilla. These are clumped in catagen and remain situated at the lowest point of origin of the follicular stellae.

With the shortening of anagen hair follicles seen in androgenetic alopecia, multiple elastic clumps can be found in a stella, like the rungs of a ladder.

A moderate perifollicular, lymphohistiocytic infiltrate, perhaps with concentric layers of perifollicular collagen deposition, is present in 40% of androgenetic alopecia cases. But it is found in only 10% of normal control subjects. Occasional eosinophils and mast cells can be seen.

The cellular inflammatory changes also occur around lower follicles in some cases. And they occasionally involve follicular stellae further supporting the above model.
Pathogenesis Vs Aging?
The Changes Affecting the Androgens have also been shown to occur in experimental conditions. It has been found that in vitro (in an artificial environment outside the living organism), dermal papilla cells from balding scalp grow less well than those obtained from the non-balding scalp. The hairs these dermal papilla cells are derived from are very fine as compared to normal hair and similar to miniaturized hair.

As the disease progresses, eventually all the hair can be involved in the process. With time the region may be entirely covered with fine vellus hairs. The pigment production is also terminated with progressive miniaturization. So the area may appear bald after the vellus hair covering is finally lost.

Women are also affected by androgenetic alopecia but the degree of hair miniaturization is not uniform. Neither is it potentially as extreme in a given area of female scalp as in some men. The degree of hair miniaturization in women is always less than in men with a mosaic of variable-diameter hairs found in the affected region on the top of the scalp.

A progressive miniaturization of hair and reduced terminal scalp hair density can also be observed in both sexes as a normal effect of aging. The decrease in density of terminal scalp hair starts becoming evident when a person is around 20 to 30 years of age and becomes more pronounced at the age of around 30 to 50 years. There is also a gradual decline in the number of hairs present per square cm and average hair diameter.

The normal age-related decrease in hair density and diameter is always greater in the central region of the scalp. This is true for both men and women. The changes in the dynamics of hair growth and hair characteristics can be termed as exaggerations of the normal aging process.

With increase in age, there is a gradual increase in the time interval between shedding of telogen hair and appearance of a replacement anagen hair. This time interval can be called the lag phase. It is the prolongation of the lag phase which also accounts, along with the decreased anagen duration, for the increased number of hairs in telogen seen in pattern hair loss.

It is universally accepted that dihydrotestosterone causes baldness, but the mechanism is not yet properly understood.

Probably there are 3 mechanisms which are at work:
  • Miniaturization of the hair follicles by a dihydrotestosterone-induced acceleration of the mitotic rate of the matrix that leaves less and less time for differentiation.
  • The increased number of hair follicles in telogen and increased duration of the lag phase. It is this mechanism of action of dihydrotestosterone which needs further research.
  • An increased telogen shedding resulting from the shortening of the hair cycles that increases the telogen number per unit of time.
One day, experts will successfully determine how androgenetic alopecia causes balding and that will help a lot in the development of an androgenetic alopecia cure.