SummaryThe histopathology of the skin in hypotrichosis has been studied for a Jersey calf and comparisons made with normal skin. Other abnormalities of the hair follicle have been described in a Hereford mutant.There is considerable variation in hypotrichosis of the calf, as in mice, all forms involving retardation or arrest of the prenatal and early postnatal skin development.A feature of the skin in hypotrichosis is a high concentration of abnormally complex arteriovenous anastomoses. It is postulated that this abnormality of cutaneous vascular supply is a predisposing factor in the development of the syndrome. The poor development of the hair follicles and associated sweat glands appears to result from insufficiency of the capillary bed. An analogous situation in humans is cutaneous necrosis of the leg as a result of dilatation of the arteriovenous anastomoses.While arteriovenous anastomoses do not appear compensatory to lack of sweat glands, they do provide an alternative thermoregulatory mechanism which might be effective at moderate environmental temperature.

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