牙周致病菌引发的免疫炎症反应是牙周炎的致病机制之一，模式识别受体（PRR）是机体识别病原体相关分子模式从而启动固有免疫应答的重要途径。我们前期探索用牙龈卟啉单胞菌（Pg）刺激牙周组织细胞，发现除Toll样受体外还有多种PRR高表达，粘附分子、RANKL等破坏因子也高表达，推测PRR在牙周炎致病机制中会发挥重要作用。本课题拟通过实时荧光定量PCR芯片技术观察PRR在牙周炎组织及Pg感染的细胞中的表达全貌；利用实时定量PCR、蛋白免疫印迹等技术验证筛出的PRR在牙周炎组织和感染细胞中的表达；并利用特异的PRR激动剂和基因沉默技术从正反两方面探讨相关PRR在Pg促牙周组织细胞表达粘附分子等炎症因子和基质金属蛋白酶、RANKL等组织破坏介质中的作用及可能的信号通路，全面、深入地阐述PRR在牙周炎症反应和软硬组织破坏中的作用及机制，丰富牙周炎致病机制的理论体系，为建立新的治疗策略提供线索和理论基础。

Immunal response initiated by periodontal pathogens is one of the pathogenesis of periodontitis. Pattern recognition receptors (PRRs) can recognize pathogen associated molecular patterns (PAMPs), which are important for triggering innate immune response in many inflammatory dieases. However, the role of PRRs except Toll-like receptors in periodontitis is not clear. In our previous study, it was found that besides Toll-like receptors, the level of other PRRs (such as NOD-like receptors) as well as adhesion molecules and RANKL were increased in periodontal fibroblasts when stimulated by Porphyromonas gingivalis. Therfore we hypothesize that PRR may play an important role in pathogenesis of periodontitis. In this study, the whole PRR gene expression profile in gingival tissue from periodontitis patients and in periodontal fibroblasts treated by P.gingivalis will be analyzed by PT2 real-time PCR arrays. The PRRs which may take part in periodontitis pathogenesis will be selected and to be testified further by real-time PCR and Western-blot techniques. Then the roles of these PRRs and signal pathway mechanisms in expression of inflammatory cytokines (such as adhesion molecules), tissue-break-down media (such as matrix metalloproteinases and RANKL) will be studied by applying special receptor agonists and knocking down these PRRs gene. The results of this study will supply more evidences for our understanding the role of PRR in periodontitis, and enrich the theory of periodontal pathogenesis. Besides, it could provide clues and set up theoretical basis for a new treatment strategy of periodontal diseases.