Autoinducer-2 produced by oral microbial flora and alveolar bone loss in periodontitis

被引:0
|
作者
Li, Cheng [1 ,2 ,3 ]
Zhou, Hancheng [1 ,2 ,3 ]
Gou, Huiqing [1 ,2 ,3 ]
Fan, Zixin [1 ,2 ,3 ]
Zhang, Yifei [1 ,2 ,3 ]
Tang, Pengzhou [1 ,2 ,3 ]
Huang, Jiaxin [1 ,2 ,3 ]
Xu, Yan [1 ,2 ,3 ]
Li, Lu [1 ,2 ,3 ]
机构
[1] Nanjing Med Univ, Affiliated Stomatol Hosp, Dept Periodont, Nanjing 210029, Peoples R China
[2] Nanjing Med Univ, Jiangsu Key Lab Oral Dis, Nanjing, Peoples R China
[3] Jiangsu Prov Engn Res Ctr Stomatol Translat Med, Nanjing, Peoples R China
基金
中国国家自然科学基金;
关键词
autoinducer-2; Fusobacterium nucleatum; macrophages; periodontal pathogens; periodontitis; quorum sensing; QUORUM-SENSING INHIBITORS; BIOFILM FORMATION; CONSENSUS REPORT; GENE-EXPRESSION; LUXS; GROWTH; CLASSIFICATION; WORKSHOP; PROPOSAL; SIGNAL;
D O I
10.1111/jre.13247
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Objective: The aim of this study was to investigate the association between autoinducer-2 (AI-2) of oral microbial flora and the alveolar bone destruction in periodontitis to determine if AI-2 may have the potential that monitor periodontitis and predict bone loss. Background: Plaque biofilm was the initiating factor of periodontitis and the essential factor of periodontal tissue destruction. The formation of biofilms depended on the complex regulation of the quorum sensing (QS) system, in which bacteria could sense changes in surrounding bacterial density by secreting the autoinducer (AI) to regulate the corresponding physiological function. Most oral bacteria also communicated with each other to form biofilms administrating the QS system, which implied that the QS system of periodontal pathogens was related to periodontitis, but the specific relationship was unknown. Method: We collected the gingival crevicular fluid (GCF) samples and measured the concentration of AI-2 in samples using the Vibrio harveyi BB180 bioluminescent-reporter system. To explore the interaction between AI-2 and bone metabolism, we utilized AI-2 purified from Fusobacterium nucleatum to investigate the impact of F. nucleatum AI-2 on osteoclast differentiation. Moreover, we constructed murine periodontitis models and multi-species biofilm models to study the association between AI-2 and periodontal disease progression. Results: The AI-2 concentration in GCF samples increased along with periodontal disease progression (p < .0001). F. nucleatum AI-2 promoted osteoclast differentiation in a dose-dependent manner. In the periodontitis mice model, the CEJ-ABC distance in the F. nucleatum AI-2 treatment group was higher than that in the simple ligation group (p < .01), and the maxilla of the mice in the group exhibited significantly lower BMD and BV/TV values (p < .05). Conclusions: We demonstrated that the AI-2 concentration varied with the alveolar bone destruction in periodontitis, and it may have the potential for screening periodontitis. F. nucleatum AI-2 promoted osteoclast differentiation in a dose-dependent manner and aggravated bone loss.
引用
收藏
页码:576 / 588
页数:13
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