The Role of Oral Pathobionts in Dysbiosis during Periodontitis Development

被引:79
作者
Jiao, Y. [1 ]
Hasegawa, M. [1 ]
Inohara, N. [1 ]
机构
[1] Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI 48109 USA
基金
美国国家卫生研究院;
关键词
NOD1; ligands; revised keystone pathogen hypothesis; microbiota; alveolar bone resorption; commensal bacteria; Pasteurellaceae; PORPHYROMONAS-GINGIVALIS; BONE LOSS; BACTEROIDES-INTERMEDIUS; STREPTOCOCCUS-GORDONII; NEUTROPHIL RECRUITMENT; TREPONEMA-DENTICOLA; SUBGINGIVAL PLAQUE; IN-VIVO; COMPLEMENT; DISEASE;
D O I
10.1177/0022034514528212
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
An emerging concept is the tight relationship between dysbiosis (microbiota imbalance) and disease. The increase in knowledge about alterations in microbial communities that reside within the host has made a strong impact not only on dental science, but also on immunology and microbiology as well as on our understanding of several diseases. Periodontitis is a well-characterized human disease associated with dysbiosis, characterized by the accumulation of multiple bacteria that play individual and critical roles in bone loss around the teeth. Dysbiosis is largely dependent on cooperative and competitive interactions among oral microbes during the formation of the pathogenic biofilm community at gingival sites. Oral pathobionts play different and synergistic roles in periodontitis development, depending on their host-damaging and immunostimulatory activities. Host immune responses to oral pathobionts act as a double-edged sword not only by protecting the host against pathobionts, but also by promoting alveolar bone loss. Recent studies have begun to elucidate the roles of individual oral bacteria, including a new type of pathobionts that possess strong immunostimulatory activity, which is critical for alveolar bone loss. Better understanding of the roles of oral pathobionts is expected to lead to a better understanding of periodontitis disease and to the development of novel preventive and therapeutic approaches for the disease.
引用
收藏
页码:539 / 546
页数:8
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