BACKGROUND/ OBJECTIVES: Alopecia areata (AA) is a non-scarring inflammatory hair loss disease. We investigated the early pathological changes of AA to identify possible factors participating in its pathogenesis. METHODS: Clinical, laboratory and pathological features of 87 AA patients were investigated. RESULTS: Anti-nuclear antibody was found in 11 of 85 patients tested (13%), with a higher percentage in women (21%) than men (5%) (P = 0.026). In early AA lesions, inflammatory infiltration in the upper dermis and epithelial cell damage of the hair follicle infundibulum, just above the sebaceous gland, was observed. Liquefaction and disarrangement of peripheral infundibular epithelial cells coexisted with T-lymphocytic invasion and regression of the lower follicle. The latter findings positively correlated with the presence of eosinophils and perivascular mononuclear cell infiltration in the upper dermis. Eosinophilic infiltration was found in 35 patients (40%) and was positively correlated to elevated serum IgE levels (r = 0.21, P = 0.044), a more severe perivascular lymphocytic inflammation in the upper dermis (r = 0.24, P = 0.026), as well as a prominent swarm of bees-like peri-follicular infiltration (r = 0.41, P < 0.001). Mast cells were abundant in the upper dermis, especially around blood vessels, and positively correlated with eosinophil presence (r = 0.30, P = 0.027). CONCLUSION: Damage to the hair follicle infundibulum in the upper dermis might be an important component of early changes in AA lesions, possibly caused by lymphocyte cell infiltration in the same area. AA may involve damage of the upper hair follicle as well as the bulb, possibly involving hypersensitivity and autoimmunity.
BACKGROUND/ OBJECTIVES: Alopecia areata (AA) is a non-scarring inflammatory hair loss disease. We investigated the early pathological changes of AA to identify possible factors participating in its pathogenesis. METHODS: Clinical, laboratory and pathological features of 87 AA patients were investigated. RESULTS: Anti-nuclear antibody was found in 11 of 85 patients tested (13%), with a higher percentage in women (21%) than men (5%) (P = 0.026). In early AA lesions, inflammatory infiltration in the upper dermis and epithelial cell damage of the hair follicle infundibulum, just above the sebaceous gland, was observed. Liquefaction and disarrangement of peripheral infundibular epithelial cells coexisted with T-lymphocytic invasion and regression of the lower follicle. The latter findings positively correlated with the presence of eosinophils and perivascular mononuclear cell infiltration in the upper dermis. Eosinophilic infiltration was found in 35 patients (40%) and was positively correlated to elevated serum IgE levels (r = 0.21, P = 0.044), a more severe perivascular lymphocytic inflammation in the upper dermis (r = 0.24, P = 0.026), as well as a prominent swarm of bees-like peri-follicular infiltration (r = 0.41, P < 0.001). Mast cells were abundant in the upper dermis, especially around blood vessels, and positively correlated with eosinophil presence (r = 0.30, P = 0.027). CONCLUSION:Damage to the hair follicle infundibulum in the upper dermis might be an important component of early changes in AA lesions, possibly caused by lymphocyte cell infiltration in the same area. AA may involve damage of the upper hair follicle as well as the bulb, possibly involving hypersensitivity and autoimmunity.