破骨细胞分化因子和骨保护因子在颌骨中心性巨细胞病变组织中的表达

目的 检测破骨细胞核因子κB受体活化因子配体(RANKL，又称破骨细胞分化因子)和骨保护因子(OPG)蛋白在颌骨中心性巨细胞病变中的表达，探讨此类病变发生骨破坏的作用机制。方法采用免疫组织化学的方法检测26例颌骨中心性巨细胞病变中RANKL和OPG蛋白的表达。结果 RANKL在颌骨中心性巨细胞病变中的血管、基质中有强烈表达，某些病变中的部分短梭形单核基质细胞和多核巨细胞的胞膜也为RANKL阳性；病变中大部分的多核巨细胞和少部分圆形单核基质细胞的胞质OPG表达为阳性。结论 激活的血管内皮细胞通过调节RANKL的表达来促进颌骨中心性巨细胞病变中的多核破骨样巨细胞的形成；RANKL可以通过旁分泌和自分泌的方式发挥作用。同时在颌骨中心性巨细胞病变中存在由OPG介导的抑制多核破骨样巨细胞生成和骨吸收的负反馈机制。

Expression of receptor activator of NF-kappa B ligand and osteoprotegerin protein in the giant cell lesions of jaw

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.