JAK/STAT是近年来发现的由细胞因子刺激产生的信号转导通路，参与细胞的增值，分化和免疫调节等多种生物学功能。有研究发现SCOS3蛋白是此信号通路重要的负向调控因子，基于我们课题组前期实验以及已有的研究发现基础上，本课题提出这样假设，一是在根尖周炎模型中，JAK2/STAT3炎性通路和SCOS3蛋白在根尖周病不同时期有表达，同时观察病变区局部注射JAK2/STAT3抑制剂AG490后炎症和骨破坏变化情况，二是研究人牙周膜成纤维细胞在前炎症因子MIF刺激下通过一系列膜信号转导最终可以激活JAK2/STAT3信号通路，并建立破骨前体细胞与牙周膜细胞细胞共培养模型，以探讨SCOS3蛋白作为负向调控因子参与根尖周骨破坏的机制。本研究可以初步阐明JAK2/STAT3信号通路介导的炎症性骨破坏机制并为根尖周病以及其他口腔炎性疾病的预防及治疗提供理论基础。

Janus kinase (JAK)–signal transducer and activator of transcription (STAT) pathway was produced by cytokines and identified as an important member in cell proliferation, differentiation and immune regulation. Emerging evidences suggest SCOS3 protein is a negative regulatory factor of JAK2/STAT3, based on our previous studies and existing research finding, we put forward such assumption, first, JAK2/STAT3 inflammatory pathway and SCOS3 protein may express in different periods during periapical lesions, while observing the change of bone destruction after local injection of JAK2/STAT3 inhibitor AG490; second, under the stimulation of MIF, huamn periodontal ligament fibroblasts can activate JAK2/STAT3 signal pathway, and establishment of pre-osteoclast and periodontal ligament cell co-culture model to investigate the mechanism of SCOS3 protein as a negative regulatory factors involved in periapical bone destruction. This study can preliminary lead to a new mechanistic insight into the JAK2/STAT3 mediated inflammatory bone destruction and might provide the theoretical basis on prevention and treatment to periapical diseases and other oral inflammatory diseases.