破骨细胞过度活跃是引发炎症性牙槽骨吸收的病理基础。IL-17A和Notch信号在破骨细胞分化及骨吸收中发挥重要作用。 但IL-17A与Notch/RBP-J信号通路间的相互关系尚不清楚。本课题组前期研究表明：IL-17A具有诱导NF-κB转录活性及促Notch2/RBP-J信号转导的生物学功能；软件分析Notch2和RBP-J启动子均存在NF-κB的结合位点。由此推测IL-17A/NF-κB对Notch2/RBP-J信号通路的调控作用可能影响破骨细胞分化和骨吸收过程。因此，本课题拟进一步探讨IL-17A诱导破骨细胞分化及炎症性牙槽骨吸收过程中，参与调控Notch2/RBP-J信号通路的NF-κB家族特定成员，明确受NF-κB信号调控的Notch2和RBP-J启动子区域具体位点。深入探讨IL-17A/NF-κB调控Notch2/RBP-J信号的分子机制，可为抑制炎症性牙槽骨吸收提供新思路。

One of the risk factors for bone loss in periodontal disease is the increase of bone-resorbing osteoclasts. Both IL-17A and Notch signaling play important roles in osteoclastogenesis and bone resorption. However, the underlying mechanism between the interaction of IL-17A and Notch/RBP-J signaling pathway is not well-defined. Our pilot study demonstrated that IL-17A augmented NF-κB transcriptional activity and Notch2 expression level. Meanwhile, IL-17A down-regulated RBP-J expression level at early stage while up-regulated RBP-J expression level at later stage. Potential NF-κB binding sites are predicted on the Notch2 and RBP-J promoter regions. These results suggested the potential effect of IL-17A/NF-κB on Notch2/RBP-J. The aim of these studies is to investigate which member of NF-κB family regulates Notch2/RBP-J in IL-17A-induced osteoclastogenesis and bone resorption．Furthermore, the NF-κB binding sites in Notch2 and RBP-J promoter regions will be explored. The results obtained from these studies will provide useful information for inhibition of inflammatory bone destruction related to periodontal disease.