Xue-mei Meng1, Shi-feng Yu, Ming-jie Wei. 1. Department of Periodontology, School of Stomatology, Tianjin Medical University, Tianjin 300070, China.
Abstract
OBJECTIVE: To detect the expression of RANKL and OPG protein in the giant cell lesions of jaw and to study the mechanism of this lesion. METHODS: RANKL and OPG were detected by immunohistochemistry (SP) in 24 paraffin-embedded and 2 frozen specimens of central giant cell lesion of jaw. RESULTS: RANKL signals were strongly positive in the vascular epithelial cells. They also could be found in fibrous stroma, bone matrix, and stromal spindle cells, even in some cytomembrane of multinucleated giant cells. OPG was detected in multinucleated giant cells and a fraction of round mononuclear cells. CONCLUSIONS: Active vascular epithelial cells are contributed to the formation of multinucleated giant cells through regulating RANKL, and RANKL could play its role by paracrine and autocrine, which might be inhibited by OPG.
OBJECTIVE: To detect the expression of RANKL and OPG protein in the giant cell lesions of jaw and to study the mechanism of this lesion. METHODS:RANKL and OPG were detected by immunohistochemistry (SP) in 24 paraffin-embedded and 2 frozen specimens of central giant cell lesion of jaw. RESULTS:RANKL signals were strongly positive in the vascular epithelial cells. They also could be found in fibrous stroma, bone matrix, and stromal spindle cells, even in some cytomembrane of multinucleated giant cells. OPG was detected in multinucleated giant cells and a fraction of round mononuclear cells. CONCLUSIONS: Active vascular epithelial cells are contributed to the formation of multinucleated giant cells through regulating RANKL, and RANKL could play its role by paracrine and autocrine, which might be inhibited by OPG.