**8. Histopathology**

Histopathology depends on the stage of the disease [30]. In the acute stage, there is a dense inflammatory infiltrate surrounding the terminal anagen hair bulb situated in the deep subcutaneous tissue. Inflammatory infiltrate consists primarily of T lymphocytes and Langerhans cells, with occasional eosinophils, mast cells, and plasma cells [31, 32]. An early and typical feature is the presence of eosinophils in stellae and within hair bulbs [29]. Anagen hairs cycle through catagen then into telogen. A dense lymphocytic inflammation can cause breaking of the hair shaft with a trichorrhexis nodosa-like fracture. This is the exclamation point hair, which is in telogen phase and therefore shed [31, 32]. The horizontal section demonstrates a significant decrease in the anagen:telogen ratio. There is also a decrease in the number of terminal hairs with a slight increase in the number of vellus hairs [31].

In the subacute stage, the number of catagen hairs is markedly increased [30]. The number of telogen hairs also increases after a few weeks. The amount of terminal hairs decreases and the vellus hair increases [31, 32].

In the chronic stage, either no or a mild chronic peribulbar lymphocytic inflammation around the miniaturized hairs situated in the papillary dermis is observed [30, 31]. The terminal:vellus hair ratio decreases to 1.3:1 rather than 7:1, which is found in the normal population. Fibrosis is an uncommon finding. However, in approximately 10% of the patients with a long history of alopecia areata, fibrosis of the upper follicle can be detected [31].

Of note, diagnosis of alopecia areata does not depend on the presence of an inflammatory infiltrate. Histopathological examination reveals increased numbers of telogen hairs in the acute and chronic stages, increased miniaturized hairs in chronic stage, and markedly increased catagen hairs in the subacute stage, helping in the diagnosis of alopecia areata [30].
