Defense mechanisms of periapical inflammation by endothelial cells in persistent apical periodontitis

为探讨慢性根尖周炎的发病机制，采用免疫组织化学和分子生物学技术，对慢性根尖周炎患者牙周组织中一氧化氮（NO）、糖基化终末产物受体（RECEPTOR for Advanced Glycation End Products，RECEPTOR）和中期因子（Midkine）进行了检测。内皮细胞共表达NO和中期因子。表达AGE的内皮细胞也表达AGEs。此外，共表达的中期因子和趋化因子的内皮细胞进行了测定。提示内皮细胞在根尖周炎症的扩展和防御中起重要作用。

To determine the mechanisms of persistent apical periodontitis, nitric oxide (NO), receptor for advanced glycation end products (RAGE) and midkine were analyzed using immunohistochemical and molecular biological techniques. NO and midkine were co-expressed by endothelial cells. RAGE was also expressed by AGE- expressing endothelial cells. In addition, co-expression of midkine and chemokines by endothelial cells were determined. The data suggested that endothelial cells could play a central role in extension and defense of periapical inflammation.