what actually happens to the hair when an individual is affected by alopecia areata
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What actually happens to the hair when an individual is affected by alopecia areata?

Most of the earlier histopathological studies on the deterioration of hair follicles in alopecia areata patients were conducted on scalp tissues of already bald or severely affected individuals. These studies indicated damage to the upper part of the hair bulbs while the lower and the root sheath were found to be relatively normal. Hence alopecia areata was previously identified as a disease in which there was substantial differentiation in the immune systems targeting of the cortical keratinocytes.

In this study, the early stages of hair follicle modifications in alopecia areata were studied. A 13 year old boy who had a patch of hair loss in his occipital region, was subjected to detailed histopathological studies. The scalp tissue from his parietal region was removed and prepared for sectioning by embedding in paraffin. Longitudinal sections of the tissue were then stained with hematoxylin and eosin. Hematoxylin is a natural stain obtained from the heart wood of log wood tree Haematoxylon compachianum and is a basic stain that reacts with the cell nucleus to stain it blue or purple. Eosin is a synthetic stain obtained from the xanthene group of chemicals. It is acidic and reacts with the basic salts of the cell cytoplasm to color it orange or pink. The sections were then studied under a light microscope and two distinct changes in the hair bulb were noticed. The integrity of the epithelium in the bulb had started deteriorating and there was a change in the shape of the bulb from its normal inverted cup shape to round or club shape.

Normally, the hair follicles in the anagen growth phase are in close physical association with the surrounding dermis. A normal hair follicle has the following parts. The follicles are embedded in a matrix. Rows of cells towards the upper region constitute the upper bulb. This extends upwards to form the pre-elongation region that develops vertically into the elongation region. Here the bulb narrows to form a column of cells that are long and have very sharply defined boundaries due to fibrils piling up against them. Just above it is the cortical pre keratinization zone. Here the fibrils are very coarse and many in number. The keratogenous zone is the next region in which the fibrils are marked and the cells are crystalline. In patients with Alopecia areata, the anagen hair bulb disintegrates by way of losing cortical keratinocytes especially in the upper bulb region, displacement of medullary cells, and presence of peribulbular lymphocytic infiltrates while the matrix region remians intact.

The epithelial cells in the follicles are seen to lose their structural identity and are seen to have degenerating cell nuclei and loss of intercellular integrity. The changes in the bulbs were very similar to normal catagen follicles but the frequency with which they occurred were greater in Alopecia areata patients.

The patient was treated with intravenous pulse methyl prednisolone after which he recovered from drastic hair fall. However he later developed another patch of hair loss which was treated by injecting corticosteroid into the affected area.

One of the most characteristic features of alopecia areata is the short broken hair on the scalp which is referred to as the exclamation mark hair. This seems to be a result of the above hair follicle disruption process. The process of degeneration of the follicle and the formation of club shaped root take a few weeks from the onset of the inflammation. Further histopathological studies may help scientists evaluate the changes in hair follicles and think of various methods and medications to alleviate this supposedly autoimmune disorder.

What actually happens to the hair when an individual is affected by alopecia areata references

  • Ihm CW, Hong SS, Mun JH, Kim HU. Histopathological pictures of the initial changes of the hair bulbs in alopecia areata. Am J Dermatopathol. 2004 Jun;26(3):249-53. PMID: 15166518
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