牙周感染是口腔多种细菌协同作用结果，牙龈卟啉单胞菌（P.gingivalis，Pg）和具核梭杆菌（F.nucleatum，Fn）是慢性牙周炎重要致病菌。Pg感染牙龈上皮细胞激活PI3K/AKT通路，促进细胞增殖。前期研究发现，Pg持续感染口腔上皮细胞，细胞恶性度增强，proMMP-2/9增高，而Pg和Fn协同感染KB细胞可引起IL-6/8升高，E-cadherin降低，细胞间连接减弱，提示感染的上皮细胞具有向间充质细胞转化的潜能。基因芯片筛查发现长链非编码RNAs－CCAT1表达上调。本研究推测Pg和Fn协同感染牙龈上皮细胞后，通过EGFR启动CCAT1，抑制miR-218-5p表达，激活AKT和NF-κB通路，促进SNAIL1表达，并直接上调ZEB2表达，促进牙龈上皮细胞间充质样转化。本研究将为牙龈上皮细胞间充质转化及远隔转移寻找有效的阻断途径，并为口腔慢性炎症向恶性肿瘤转化提供新的依据

Periodontal infection is the consequence of synergistic effect of various bacteria colonized in oral cavity. Porphyromonas gingivalis (Pg) and Fusobacterium nucleatum (Fn) are important pathogens of chronic periodontitis. Pg infection could accelerate proliferation of gingival epithelial cells by activating PI3K/AKT pathway. According to our previous studies, long-term infection of Pg could increase malignant degree of oral epithelial cells. The expression of proMMP-2/9 was increased. Meanwhile, the synergistic infection of Pg and Fn in KB cells could increase the expression of IL-6/8 and decrease the expression of E-cadherin with the weakening of cell junction, which indicated that epithelial cells gained the potency of mesenchymal transition. From the results of gene microarray, the expression of long non-coding RNA CCAT1 was increased. We speculate that the synergistic infection of Pg and Fn may promote cell mesenchymal-like transition in gingival epithelial cells firstly by binding EGFR and activating CCAT1 with the targeted inhibition of miR-218-5p expression. Accordingly, AKT and NF-κB pathway would be activated in order to increase the expression of SNAIL1 and ZEB2. We aim to look for effective blocking ways for mesenchymal transition and distal migration of gingival epithelial cells, and provide new theoretical basis on transformation from oral chronic inflammation to malignant neoplasm.