Hairloss (androgenetic alopecia) treatment

Recent research indicates that the DHT that harms hair follicles comes from the the skin's sebocytes and sweat glands (sebaceous glands). (Chen et al 1996) 5 alpha-Reductase, the enzyme system that converts testosterone into DHT occurs into two enzyme forms. Type 1 represents the 'cutaneous type'; it is located primarily in the skin's sebocytes but also in epidermal and follicular keratinocytes, dermal papilla cells and sweat glands as well as in fibroblasts. Type 2 is located mainly in the seminal vesicles, prostate and in the inner root sheath of the hair follicle.

With the therapy, sometimes, it is possible to assist to the inversion of the follicle miniaturization, then the progressive enlargement and the formation of hair bigger, more pigmented, up to hair type terminal.

It is important that therapy is mixed, striking the problem from the varied anglings, in particular way if baldness is advanced.

Estrogens, the feminizing hormones, can inhibit or counteract the follicle-shrinking effect of the androgens. Women have more estrogens circulating in their blood than men. Women having a genetic predisposition for pattern hair loss are protected from losing their hair because of the high level of estrogens in their blood. When these women reach menopause however, their estrogens level may decrease and the protective effect may be overridden by the DHT message. Then hair can begin to thin rapidly. Some women are genetically pre-disposed to have pattern hair loss.

This type of hair loss or Androgenetic Alopecia or pattern baldness affects over 70% of men but also 15% of women. Women usually do not develop bald spots, but rather have overall thinning hair. Over 50% of the hair can be lost before the results are readily apparent.

Estrogens help to restore the emotional and physical condition of the patient to the pre-menopause states. It may also slow or stop hair loss triggered by menopause. Hormone replacement therapy has been a controversial treatment for menopause but newer methods are finding reductions in the risk of some cancers and in the risk of heart diseases.

The best known DHT (dihydrotestosterone) blocker is Propecia®, a drug from Merck, but Merck does not recommend Propecia for women: a one year study of hair growth in 136 post-menopausal women found no significant effect of Propecia on hair growth.

Whether thinning, receding, or completely gone, hair loss is often tied into heredity and various environmental factors. For some people, it starts later in life. For others, hair loss may begin to occur during early adulthood.

Hair follicles repeatedly go through stages in a cycle of growth and resting. It is the disruption of this cycle that results in excessive hair loss, or alopecia. The specialized cells in the follicle that become the hair shaft itself can be depleted during the resting or Latent phase in the hair cycle, resulting in less and less active follicles (and hair) over time.

ANAGEN.
The hair growing stage is called Anagen.

The bottom of the hair follicle (the bulb) is attached to the dermis and its blood supply through the dermal papilla.

The precursor cells, called keratinocytes, and assocated melanocytes multiply at the bottom of the bulb.

The growing keratinocytes become part of the hair shaft. The upward pressure of the multiplying keratinocytes pushes the shaft up out of the follicle, where is appears as a hair.

Hair grows outward from the bulb at about 1 cm per month. The Anagen phase lasts 3 years on average but can vary from a few months to as much as ten years.

The length of time the hair follicle remains in Anagen, and keeps growing, depends on the signals it receives from the surrounding scalp and its blood supply.

The cells that make up the hair follicle also communicate via the fibers in the Extracellular Matrix that provides the structure of the skin in the scalp.

The hair follicle then enters the next phase of the cycle.



CATAGEN.
When matrix cells in the hair follicle exhaust their proliferative capacity or chemical signals are received from the skin or blood, hair growth stops.
The hair follicle begins to die and enters the CATAGEN phase.
This process of programmed cell death or apoptosis, results in the lower two-thirds of the hair follicle degenerating.
The cells remaining form a pocket surrounding the old hair.
This process occurs in a matter of a few weeks.
The “bulb” of the hair follicle is drawn toward the skin surface via fibers in the Extracellular matrix, and essentially separates from the dermal papilla.
















TELOGEN.: In the Telogen phase, the remains of the hair bulb are inactive and the attached hair easily falls out.; The telogen phase can last for 2 to 3 months.; In the meantime, the dermal papilla remains attached to the remains of the bulb through the interconnecting network of the Extracellular Matrix.; The fibers in this matrix maintain both a structural linkage and a chemical communication between the two components of the hair follicle.

LATE TELOGEN.: In the final phase of Telogen, lasting a few weeks, a chemical signal causes the “bulge” and dermal papilla to re-assemble within the scalp Matrix and form a new hair follicle around the empty follicle.; Stem cells within their reservoir in the bulge begin to form new keratinocytes and the cycle starts over with a new Anagen phase.; It is during the “re-awakening” process that stem cells can die and the hair follicles lose the capacity to form a new hair shaft.; Preventing the loss of keratinocyte stem cells is extremely important to altering the course of hair loss and baldness.