抑制核因子-κB受体活化因子及其配体通路治疗牙周炎的研究进展  

Research advances on inhibition receptor activator of nuclear factor-κB and its ligand in periodontal treatment

作　　者：陈斌[1] 孙卫斌[1] 

机构地区：[1]南京大学医学院附属口腔医院牙周科,南京210008

出　　处：《国际口腔医学杂志》2012年第1期101-104,共4页International Journal of Stomatology

基　　金：南京市卫生局青年科技人才启动基金资助项目(QYK-10166);南京市留学回国人员科技活动基金资助项目(人社厅发[2008]86)

摘　　要：核因子-κB受体活化因子(RANK)及其配体(RANKL)在牙周炎患者的牙槽骨吸收中具有重要的作用,抑制RANKL/RANK通路,可有效抑制破骨细胞的分化和激活,从而抑制牙槽骨的吸收。骨保护蛋白(OPG)可和RANKL结合,干扰RANKL和RANK的结合,从而防止骨组织的过度破坏。本文就RANKL/RANK/OPG轴、RANKL/RANK/OPG与牙周炎、抑制RANKL/RANK通路治疗牙周炎的可行性等研究进展作一综述。Receptor activator of nuclear factor-κB （RANK） /receptor activator of nuclear factor-κB ligand（RANKL） play a critical role in alveolar bone resorption though affecting osteoclasts formation and activation, therefore,we can inhibit periodontal bone resorption though RANKL/RANK inhibition. Osteoprotegerin （OPG） protects bone from excessive resorption by binding to RANKL and preventing it from binding to RANK. In this paper, we will review the relationship between RANKURANK/OPG signaling pathway and periodontal disease, and we will mainly focus on the possibility of periodontal treatment with RANKL/RANK inhibition.

关 键 词：核因子-κB受体活化因子/核因子-κB受体活化因子配体通路 牙周治疗 牙槽骨吸收 

分 类 号：R781.42[医药卫生—口腔医学]