Scalp hair contributes significantly to a person’s appearance and self-esteem. In this chapter, alopecias and hair shaft disorders will be discussed.
Alopecia, or hair loss, may be non-scarring or scarring in nature. Non-scarring alopecia occurs when there is hair loss without destruction to the permanent portion of the hair follicle, while scarring alopecia occurs when hair follicles are irreversibly damaged. When faced with a diagnostic dilemma in cases of scalp alopecia, scalp biopsies may be performed. Histopathologically, non-scarring alopecias show preservation of follicular unit architecture, hair follicle numbers, and presence of sebaceous glands. Scarring alopecias show disruption of follicular unit architecture, decrease in hair follicle numbers with replacement by fibrous tissue, and diminished or absent sebaceous glands.
Non-scarring alopecia occurs when there is hair loss without destruction to the permanent portion of the hair follicle, namely the bulge area. Clinically, follicular ostia are patent and visible. There is a potential for hair follicle recovery and regrowth in most non-scarring alopecias. However, in certain advanced, end-stage forms of non-scarring alopecia such as androgenetic alopecia, traction alopecia, and alopecia areata, regrowth potential may be limited.
Alopecia areata is a T-cell-mediated autoimmune hair loss condition that occurs in about 2% of the population (Figures 19–1, 19–2, 19–3, 19–4). The main pathogenetic mechanism of alopecia areata is believed to be the collapse of the immune privilege status of the hair follicle, leading to the presentation of autoantigens by major histocompatibility antigen (MHC) class I molecules in the hair bulb and resultant attack by CD8+ cytotoxic T cells.
This patient presents with two months of hair loss and examination shows a well-demarcated circular area of non-scarring alopecia on the vertex. Alopecia areata commonly presents as round or oval patches of non-scarring hair loss. Short “exclamation mark” hairs are often seen, particularly at the margins of the alopecia.
This child presents at six years of age with diffuse alopecia areata, which later progressed to loss of all scalp and body hair. Her condition remains refractory despite various treatments including a two-month course of oral prednisolone, topical diphencyprone immunotherapy, topical psoralen with ultraviolet A therapy, and excimer laser.
The characteristic dermoscopic features of alopecia areata include yellow dots, black dots, broken hairs, short vellus hairs, and tapering hairs.
Acute alopecia areata—histology
The photo shows a transverse section of the scalp skin at the level of the subcutis. There are prominent peribulbar infiltrates of lymphocytes in a “swarm of bees” ...