Abstract：
Periodontitis is an immuno-inflammatory disease of the soft tissues surrounding the teeth. Periodontitis is linked to many communicable and non-communicable diseases such as diabetes, cardiovascular disease, rheumatoid arthritis, and cancers. The oral-systemic link between periodontal disease and systemic diseases is attributed to the spread of inflammation, microbial products and microbes to distant organ systems. Oral bacteria reach the gut via swallowed saliva, whereby they induce gut dysbiosis and gastrointestinal dysfunctions. Some periodontal pathogens like Porphyromonas. gingivalis, Klebsiella, Helicobacter. Pylori, Streptococcus, Veillonella, Parvimonas micra, Fusobacterium nucleatum, Peptostreptococcus, Haemophilus, Aggregatibacter actinomycetomcommitans and Streptococcus mutans can withstand the unfavorable acidic, survive in the gut and result in gut dysbiosis. Gut dysbiosis increases gut inflammation, and induce dysplastic changes that lead to gut dysfunction. Various studies have linked oral bacteria, and oral-gut axis to various GIT disorders like inflammatory bowel disease, liver diseases, hepatocellular and pancreatic ductal carcinoma, ulcerative colitis, and Crohn\'s disease. Although the correlation between periodontitis and GIT disorders is well established, the intricate molecular mechanisms by which oral microflora induce these changes have not been discussed extensively. This review comprehensively discusses the intricate and unique molecular and immunological mechanisms by which periodontal pathogens can induce gut dysbiosis and dysfunction.
摘要：
牙周炎是牙齿周围软组织的免疫炎性疾病。牙周炎与许多传染性和非传染性疾病有关，如糖尿病，心血管疾病,类风湿性关节炎,和癌症。牙周病和全身性疾病之间的口腔-全身联系归因于炎症的传播，微生物产品和微生物到远处的器官系统。口腔细菌通过吞咽的唾液到达肠道，从而诱发肠道菌群失调和胃肠功能失调。一些牙周病原体，如卟啉单胞菌。牙龈,克雷伯菌属,螺杆菌。Pylori,链球菌,Veillonella,Parvimonasmicra,具核梭杆菌,肽链球菌,嗜血杆菌,放线菌和变形链球菌可以承受不利的酸性，在肠道中存活并导致肠道生态失调。肠道菌群失调会增加肠道炎症，并诱导导致肠道功能障碍的发育不良变化。各种研究已经将口腔细菌联系起来，和各种GIT疾病如炎症性肠病的口肠轴，肝脏疾病,肝细胞和胰腺导管癌，溃疡性结肠炎,和克罗恩病。虽然牙周炎和GIT疾病之间的相关性已被确定，口腔微生物引起这些变化的复杂分子机制尚未得到广泛讨论。这篇综述全面讨论了牙周病原体可引起肠道菌群失调和功能障碍的复杂而独特的分子和免疫机制。
