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

Immunomicrobial pathogenesis of periodontitis: keystones, pathobionts, and host response.
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DOI:
10.1016/j.it.2013.09.001
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发表时间:
2014-01
影响因子:
16.8
通讯作者:
Hajishengallis G
Hajishengallis G
中科院分区:
医学1区
文献类型:
--
作者:
Hajishengallis G

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最近的研究发现了牙周宿主-微生物动态平衡破坏的新机制,这可能导致易感宿主的生物失调和牙周炎。Keystone病原体和病原体的非生物微生物群落被认为具有协同毒力,它们不仅可以承受宿主的反应,还可以通过利用组织破坏性炎症来蓬勃发展,后者助长了不断升级的失调和炎症性骨丢失的自我喂养循环,可能导致牙齿脱落和全身并发症。在这里,我们讨论了我们对牙周炎的理解的新范式,这可能有助于揭示其他多菌炎症性疾病。此外,我们还强调了微生物与启动和传播慢性牙周炎的先天和获得性免疫元件之间相互作用的综合图景所需的知识差距。
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 we discuss new paradigms in our understanding of periodontitis, which may shed light into other polymicrobial inflammatory disorders. In addition, we 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.
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