Dystrophic Anagen Research Articles

Hair Loss in Systemic Disease

A careful history and examination of shed hairs will reveal the etiology of most alopecias due to systemic processes. Telogen effluvium is preceded by a severe systemic stress occurring at least two months prior to the loss of normal club hairs. Most other causes of hair loss involve damage to the hair follicle, which leads to the shedding of dystrophic, brittle anagen hairs. A history of drug ingestion or nutritional compromise or concurrent symptoms suggestive of a genetic, endocrinologic, collagen vascular, or infectious etiology will lead to an accurate diagnosis.

Alopecia areata: alterations in the hair growth cycle and correlation with the follicular pathology.

A histopathological study was performed in 17 patients with alopecia areata to elucidate the changes in hair cycle dynamics. The findings confirm the view that the initial event in alopecia areata is the premature entry of anagen follicles into telogen, although some follicles survive for a time in a dystrophic anagen state. However, after re-entry into anagen takes place, growth appears to be halted in anagen III rather than anagen IV, as has previously been suggested. Follicles then return prematurely to telogen and these truncated cycles are repeated until the disease activity subsides. A new pathogenic hypothesis is presented which relates alterations in hair cycle dynamics to pathological changes within the anagen follicle and also provides an explanation for the formation of exclamation mark hairs and the non-destructive nature of the disease.

The pathogenesis of alopecia areata.

SUMMARY.— The pathogenesis of alopecia areata was studied by plucking hairs from each of a series of concentric zones, using felt patterns placed over lesions. It was possible to group lesions according to the zone with the greatest proportion of club hairs. The results are logically interpreted to mean that a wave of hair follicle damage or arrest moves centrifugally from a focal point beyond the area of alopecia. It is suggested that follicles may react in I of 3 ways. Firstly, severe damage may weaken the hair in the keratogenous zone, this being followed by breakage when the weak zone reaches the plane of the scalp; at the same time the follicle is precipitated into catagen and the hair is extruded as an exclamation mark. Secondly, the follicle may be precipitated into catagen with loss of the club in a normal manner, followed by replacement with a dystrophic anagen hair. Thirdly, the follicle may become dystrophic without a catagen phase.