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牙周炎和牙周病原菌作为类风湿性关节炎的风险因素:过去十年综述

Periodontitis and periodontopathic bacteria as risk factors for rheumatoid arthritis: A review of the last 10 years.

作者信息

Kobayashi Tetsuo, Bartold Peter Mark

机构信息

General Dentistry and Clinical Education Unit, Faculty of Dentistry & Medical and Dental Hospital, Niigata University, 2-5274 Gakkocho-dori, Chuo-ku, Niigata 951-8514, Japan.

Division of Periodontology, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, 2-5274 Gakkocho-dori, Chuo-ku, Niigata 951-8514, Japan.

出版信息

Jpn Dent Sci Rev. 2023 Dec;59:263-272. doi: 10.1016/j.jdsr.2023.08.002. Epub 2023 Aug 26.

DOI:10.1016/j.jdsr.2023.08.002
PMID:37674898
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10477376/
Abstract

Rheumatoid arthritis (RA) is characterized by chronic inflammatory destruction of joint tissue and is caused by an abnormal autoimmune response triggered by interactions between genetics, environmental factors, and epigenetic and posttranslational modifications. RA has been suggested to be interrelated with periodontitis, a serious form or stage of chronic inflammatory periodontal disease associated with periodontopathic bacterial infections, genetic predisposition, environmental factors, and epigenetic influences. Over the last decade, a number of animal and clinical studies have been conducted to assess whether or not periodontitis and associated periodontopathic bacteria constitute risk factors for RA. The present review introduces recent accumulating evidence to support the associations of periodontitis and periodontopathic bacteria with the risk of RA or the outcome of RA pharmacological treatment with disease-modifying antirheumatic drugs. In addition, the results from intervention studies have suggested an improvement in RA clinical parameters after nonsurgical periodontal treatment. Furthermore, the potential causal mechanisms underlying the link between periodontitis and periodontopathic bacteria and RA are summarized.

摘要

类风湿性关节炎(RA)的特征是关节组织的慢性炎症性破坏,它是由遗传、环境因素以及表观遗传和翻译后修饰之间的相互作用引发的异常自身免疫反应所导致。有研究表明,RA与牙周炎相关,牙周炎是慢性炎症性牙周疾病的一种严重形式或阶段,与牙周病原菌感染、遗传易感性、环境因素以及表观遗传影响有关。在过去十年中,已经开展了多项动物和临床研究,以评估牙周炎及相关牙周病原菌是否构成RA的风险因素。本综述介绍了最近积累的证据,以支持牙周炎和牙周病原菌与RA风险或RA使用改善病情抗风湿药物治疗结果之间的关联。此外,干预研究的结果表明,非手术牙周治疗后RA的临床参数有所改善。此外,还总结了牙周炎和牙周病原菌与RA之间联系的潜在因果机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e335/10477376/f258c7b31d1c/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e335/10477376/f258c7b31d1c/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e335/10477376/f258c7b31d1c/gr1.jpg

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Int Dent J. 2025 Sep 2;75(6):103856. doi: 10.1016/j.identj.2025.103856.
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Probiotic-derived extracellular vesicles: the next breakthrough in postbiotics for rheumatoid arthritis.益生菌衍生的细胞外囊泡:类风湿性关节炎后生元的下一个突破。
Front Immunol. 2025 Aug 7;16:1620185. doi: 10.3389/fimmu.2025.1620185. eCollection 2025.
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Bibliometric and visualized analysis of the relationship between rheumatoid arthritis and periodontitis-related bacteria using CiteSpace software.

本文引用的文献

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J Clin Periodontol. 2023 Mar;50(3):295-306. doi: 10.1111/jcpe.13756. Epub 2022 Dec 16.
2
Host and bacterial factors linking periodontitis and rheumatoid arthritis.牙周炎和类风湿性关节炎相关的宿主和细菌因素。
Front Immunol. 2022 Aug 25;13:980805. doi: 10.3389/fimmu.2022.980805. eCollection 2022.
3
Does periodontal treatment improve rheumatoid arthritis disease activity? A systematic review.
使用CiteSpace软件对类风湿性关节炎与牙周炎相关细菌之间关系的文献计量学及可视化分析。
Front Microbiol. 2025 Jul 16;16:1589331. doi: 10.3389/fmicb.2025.1589331. eCollection 2025.
4
Blockade of IL-1 family cytokines in the treatment of rheumatoid arthritis.白细胞介素-1家族细胞因子阻断剂在类风湿关节炎治疗中的应用
Front Pharmacol. 2025 May 30;16:1577628. doi: 10.3389/fphar.2025.1577628. eCollection 2025.
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Periodontal Pathogens Correlate with Rheumatoid Arthritis Disease Parameters: A Systematic Review Based on Clinical Studies.牙周病原体与类风湿性关节炎疾病参数的相关性:基于临床研究的系统评价
Dent J (Basel). 2025 May 15;13(5):214. doi: 10.3390/dj13050214.
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The potential crosstalk genes and molecular mechanisms between systemic lupus erythematosus and periodontitis.系统性红斑狼疮与牙周炎之间潜在的串扰基因及分子机制。
Front Genet. 2025 Apr 16;16:1527713. doi: 10.3389/fgene.2025.1527713. eCollection 2025.
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