Bacterial invasion and persistence: critical events in the pathogenesis of periodontitis?

被引:121
作者
Ji, S. [1 ]
Choi, Y. S. [2 ,3 ]
Choi, Y. [2 ,3 ]
机构
[1] Korea Univ, Anam Hosp, Dept Periodontol, Seoul, South Korea
[2] Seoul Natl Univ, Sch Dent, Dept Immunol & Mol Microbiol, Seoul 110749, South Korea
[3] Seoul Natl Univ, Sch Dent, Dent Res Inst, Seoul 110749, South Korea
基金
新加坡国家研究基金会;
关键词
microbiology; periodontal immunology; periodontal pathogens; periodontal risk factor; GINGIVAL EPITHELIAL-CELLS; REGULATORY T-CELLS; EARLY-ONSET PERIODONTITIS; CHEDIAK-HIGASHI-SYNDROME; TIGHT-JUNCTION PROTEINS; PAPILLON-LEFEVRE-SYNDROME; PORPHYROMONAS-GINGIVALIS; FUSOBACTERIUM-NUCLEATUM; TREPONEMA-DENTICOLA; IN-VITRO;
D O I
10.1111/jre.12248
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Periodontitis is chronic inflammation of the periodontium caused by the host's inflammatory response to plaque biofilm, which destroys tooth-supporting soft and hard tissues. Periodontitis is a complex disease that involves interactions among three main features - microbial challenge, the host immune response, and environmental and genetic risk factors - in its pathogenesis. Although periodontitis has been regarded as the result of hyperimmune or hyperinflammatory responses to plaque bacteria, recent studies indicate that periodontal pathogens are rather poor activators and/or suppressors of the host immune response. This raises the question of how periodontal pathogens cause inflammation. To resolve this issue, in the present review we propose that bacterial invasion into gingival tissue is a key event in the initiation of periodontitis and that the persistence of these bacteria within host tissue results in chronic inflammation. In support of this hypothesis, we present the ways in which microbial, environmental and genetic risk factors contribute to bacterial invasion. It is hoped that the current model will instigate active discussion and new research to complete the puzzle of this complex disease process.
引用
收藏
页码:570 / 585
页数:16
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