BACKGROUND: Acquired bilateral naevus of Ota-like macules (ABNOM) is similar to melasma with regard to their clinical features, including female predominance, acquired onset, and predominant involvement of the malar area. The similar clinical features suggest the possibility of a shared pathogenesis. Dermal factors including vascularity and melanogenic paracrine networks such as the stem cell factor (SCF)/c-kit pathway have recently been suggested to play an important role in the pathogenesis of melasma. However, the role of dermal factors in ABNOM remains unknown. OBJECTIVES: To provide a novel view on the pathogenesis of ABNOM, we studied the expression of melanogenic paracrine cytokines such as SCF/c-kit, and assessed dermal vascularity. METHODS: Thirty-seven patients with ABNOM and 20 patients with melasma were enrolled in this study. Skin samples were obtained from lesional and perilesional normal skin. Immunohistochemistry was performed. RESULTS: Solar elastosis was slightly more intense in the lesional skin of ABNOM. In contrast to dermal pigmentation and melanocytes, the amounts of epidermal pigmentation and melanocytes were not increased in the lesional skin of patients with ABNOM. The expression of dermal SCF and c-kit was increased; however, the expression of epidermal SCF and c-kit and dermal factor VIII-related antigen was not increased in the lesional skin of ABNOM. CONCLUSIONS: These results suggest that the increased expression of the SCF/c-kit pathway between dermal fibroblasts and dermal melanocytes may play an important role in the pathogenesis of ABNOM.
BACKGROUND: Acquired bilateral naevus of Ota-like macules (ABNOM) is similar to melasma with regard to their clinical features, including female predominance, acquired onset, and predominant involvement of the malar area. The similar clinical features suggest the possibility of a shared pathogenesis. Dermal factors including vascularity and melanogenic paracrine networks such as the stem cell factor (SCF)/c-kit pathway have recently been suggested to play an important role in the pathogenesis of melasma. However, the role of dermal factors in ABNOM remains unknown. OBJECTIVES: To provide a novel view on the pathogenesis of ABNOM, we studied the expression of melanogenic paracrine cytokines such as SCF/c-kit, and assessed dermal vascularity. METHODS: Thirty-seven patients with ABNOM and 20 patients with melasma were enrolled in this study. Skin samples were obtained from lesional and perilesional normal skin. Immunohistochemistry was performed. RESULTS: Solar elastosis was slightly more intense in the lesional skin of ABNOM. In contrast to dermal pigmentation and melanocytes, the amounts of epidermal pigmentation and melanocytes were not increased in the lesional skin of patients with ABNOM. The expression of dermal SCF and c-kit was increased; however, the expression of epidermal SCF and c-kit and dermal factor VIII-related antigen was not increased in the lesional skin of ABNOM. CONCLUSIONS: These results suggest that the increased expression of the SCF/c-kit pathway between dermal fibroblasts and dermal melanocytes may play an important role in the pathogenesis of ABNOM.