Immunomicrobial pathogenesis of periodontitis: keystones, pathobionts, and host response

被引:739
作者
Hajishengallis, George [1 ]
机构
[1] Univ Penn, Sch Dent Med, Dept Microbiol, Philadelphia, PA 19104 USA
基金
美国国家卫生研究院;
关键词
dysbiosis; inflammation; keystone pathogen; pathobiont; periodontitis; PORPHYROMONAS-GINGIVALIS; T-CELLS; SIGNALING MECHANISMS; FILIFACTOR-ALOCIS; TH17; PATHWAY; BONE LOSS; DISEASE; INNATE; NEUTROPHILS; HEALTH;
D O I
10.1016/j.it.2013.09.001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Recent studies have uncovered novel mechanisms underlying the breakdown of periodontal host microbe homeostasis, which can precipitate dysbiosis and periodontitis in susceptible hosts. Dysbiotic microbial communities of keystone pathogens and pathobionts are thought to exhibit synergistic virulence whereby not only can they endure the host response but can also thrive by exploiting tissue-destructive inflammation, which fuels a self-feeding cycle of escalating dysbiosis and inflammatory bone loss, potentially leading to tooth loss and systemic complications. Here, I discuss new paradigms in our understanding of periodontitis, which may shed light into other polymicrobial inflammatory disorders. In addition, I highlight gaps in knowledge required for an integrated picture of the interplay between microbes and innate and adaptive immune elements that initiate and propagate chronic periodontal inflammation.
引用
收藏
页码:3 / 11
页数:9
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