Pathophysiology
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Pathophysiology of Hair

Physiology of hairs

Normal Hair density is around 300 follicles/sq cm

Follicles follow a hair growth cycle.

It has three phases and almost all the hairs which you see is in anagen phase and the growth is approx. ½ inch per month.the anagen phase last for 2-5 years.At any given time approx. 90% of hairs are in anagen phase.

The catagen phase is the transitional period of 2 to 4 weeks, when the productivity of the follicle is shutting down.

When the dermal papilla reaches the region of the bulge, follicles enter the telogen or resting phase. Telogen lasts approximately 100 days (3 to 4 months). At the end of the telogen phase, the hair shaft sheds, but it can persist into the early next anagen phase, in which case you can see two hair shafts emerging from one canal.

Causes of hair loss

  1. Physical stress – Surgery, illness, anemia, rapid weight change
  2. Emotional stress – Mental illness.
  3. Thyroid abnormalities
  4. Medications – High doses of vitamin A (sometimes present in diet supplements), blood pressure medications, gout medications
  5. Hormonal changes – Pregnancy, birth control pills, menopause
  6. Androgenetic Alopecia – Male/Female Pattern Baldness

Hair transplant for male pattern baldness

It is >90% cause of loss of Hairs in men The androgenic alopecia involves both genetic  and hormonal factor. The genetic factor determines the density and location of androgen sensitive hair on scalp and hormonal factor plays dominant role at puberty. These two factor together result in shortening of anagen phase and miniaturization of hair follicles.

Classification of hair loss

Most the surgeon worldwide follow the Norwood’s classification

The classifiaction is from Type 1 to type 7 with variant

The cause of male pattern or androgenic alopecia

It is sure that androgen metabolism in our body involves two steroidal enzymes 5 alpha reductase and androgen recepor protein (ARP). These iso enzymes are present in hair follicles. 5α-reductase isoenzymes, type I and II, are both part of the normal androgen metabolism and their function is to reduce testosterone to dihydrotestosterone (DHT). The 5α type I isoenzyme is located mainly in sebaceous glands, epidermal and follicular keratinocytes, dermal papilla cells, and sweat glands. The 5 α reductase type II isoenzyme is located mainly in the root sheaths of the scalp hair follicle.

The isoenzymes is found to be found in increase concentration in frontal hairs then occipital areas.

ARPs are the other class of metabolites present in androgen sensitive areas. These ARPs are also found in the outer root sheath and dermal papilla fibroblasts of scalp hair follicles. Since the levels of these ARPs are found to be 30% greater in the balding frontal hair follicles than in non-balding occipital follicles of both men and women, these are thought to play some role in the disease, but the mechanism of their action is not very clear yet.

Technically, the follicle is still alive and connected to a good blood supply (that’s why it can nurture a transplanted follicle that is immune to the effects of DHT), but it will grow smaller and smaller. Some follicles will die, but most will simply shrink in size and produce weaker hairs. The progressively shorter anagen growing cycle means more hairs are shed and remaining hairs become so thin that they cannot survive daily wear and tear, experts say. Hairs in balding areas gradually change from long, coarse, thick, colored hairs into fine, unpigmented, fuzzy hairs.

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