Ultrastructural abnormalities in the dermal papillae of both lesional and clinically normal follicles from alopecia areata scalps

Abstract

Alopecia areata is a form of balding whose aetiology is uncertain. Although the dermal papilla in the hair bulb regulates the follicle and may play a part in the pathogenesis of alopecia areata, its ultrastructure has not been well described. As clinically normal, i.e. non-balding, follicles from alopecia areata scalps show abnormalities at the light microscope level, it would be expected that they should exhibit the earliest pathological changes involved in the dysfunction of the follicle. This study was designed to investigate the ultrastructure of normal human scalp follicular dermal papillae and to see if changes occurred in the ultrastructure of dermal papillae from either lesional or non-balding regions of alopecia areata. Normal dermal papillae contained well formed fibroblast-like cells with large, oval nuclei and well-developed endoplasmic reticulum; the cells were separated from each other by extracellular matrix containing small pieces of collagen and basal lamina-like material. Dermal papillae from both clinically normal and lesional alopecia areata follicles were less well organized and the dermal papilla cells exhibited signs of cell injury and contained abnormal amounts of pigment; an increased concentration of fibrous material in the extracellular matrix and thickening of the dermal papilla-epithelial junction were also seen. Follicles from lesional areas showed more pronounced changes than clinically normal ones. Ultrastructural abnormalities in the dermal papillae of clinically normal scalp follicles support the study of these follicles as a prime research target. The changes detected suggest that dermal papilla cells in alopecia areata would be less able to synthesize regulatory factors and that these may have more difficulty crossing into the epithelial compartment. They are consistent with an early pathological role for the dermal papilla in alopecia areata, but do not distinguish whether this is a primary aetiological role or a secondary response to an insult elsewhere in the follicle.