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可疑口腔病原体在关节炎发展中无明显作用。

No Obvious Role for Suspicious Oral Pathogens in Arthritis Development.

机构信息

Department of Oral and Maxillofacial Surgery, Dr. Sardjito General Hospital, Yogyakarta 55281, Indonesia.

University Medical Center Groningen, Department of Oral and Maxillofacial Surgery, University of Groningen, P.O. Box 30.001, 9700 RB Groningen, The Netherlands.

出版信息

Int J Environ Res Public Health. 2021 Sep 10;18(18):9560. doi: 10.3390/ijerph18189560.

DOI:10.3390/ijerph18189560
PMID:34574484
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8471642/
Abstract

A particular role for (Pg) and (Aa) has been suggested in periodontitis and rheumatoid arthritis (RA), as these bacteria could initiate the formation of rheumatoid factor (RF) and anticitrullinated protein autoantibodies (ACPA). We assessed whether serum antibodies against Pg and Aa in RA patients and non-RA controls reflect the subgingival presence of Pg and Aa, and evaluated the relationship of these antibodies to the severity of periodontal inflammation and RA-specific serum autoantibodies. In 70 Indonesian RA patients and 70 non-RA controls, the subgingival presence of Pg and Aa was assessed by bacterial 16S rRNA gene sequencing, and serum IgG levels specific for Pg and Aa were determined. In parallel, serum levels of ACPA (ACPA:IgG,IgA) and RF (RF:IgM,IgA) were measured. The extent of periodontal inflammation was assessed by the periodontal inflamed surface area. In both RA patients and the controls, the presence of subgingival Pg and Aa was comparable, anti-Pg and anti-Aa antibody levels were associated with the subgingival presence of Pg and Aa, and anti-Pg did not correlate with ACPA or RF levels. The subgingival Pg and Aa were not related to RA. No noteworthy correlation was detected between the antibodies against Pg and Aa, and RA-specific autoantibodies.

摘要

(Pg)和(Aa)在牙周炎和类风湿关节炎(RA)中具有特定作用,因为这些细菌可能引发类风湿因子(RF)和抗瓜氨酸蛋白自身抗体(ACPA)的形成。我们评估了 RA 患者和非 RA 对照组血清中针对 Pg 和 Aa 的抗体是否反映了 Pg 和 Aa 的龈下存在,并评估了这些抗体与牙周炎炎症严重程度和 RA 特异性血清自身抗体的关系。在 70 名印度尼西亚 RA 患者和 70 名非 RA 对照组中,通过细菌 16S rRNA 基因测序评估 Pg 和 Aa 的龈下存在,并测定针对 Pg 和 Aa 的血清 IgG 水平。同时,测量 ACPA(ACPA:IgG,IgA)和 RF(RF:IgM,IgA)的血清水平。牙周炎炎症程度通过牙周炎炎症表面面积评估。在 RA 患者和对照组中,龈下 Pg 和 Aa 的存在相似,抗 Pg 和抗 Aa 抗体水平与 Pg 和 Aa 的龈下存在相关,抗 Pg 与 ACPA 或 RF 水平无关。龈下 Pg 和 Aa 与 RA 无关。未检测到针对 Pg 和 Aa 的抗体与 RA 特异性自身抗体之间存在显著相关性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c086/8471642/a1345ae694cc/ijerph-18-09560-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c086/8471642/d27daa80f6c5/ijerph-18-09560-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c086/8471642/a1345ae694cc/ijerph-18-09560-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c086/8471642/d27daa80f6c5/ijerph-18-09560-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c086/8471642/a1345ae694cc/ijerph-18-09560-g002.jpg

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本文引用的文献

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Effect of Anti-Rheumatic Treatment on the Periodontal Condition of Rheumatoid Arthritis Patients.抗风湿治疗对类风湿关节炎患者牙周状况的影响。
Int J Environ Res Public Health. 2021 Mar 4;18(5):2529. doi: 10.3390/ijerph18052529.
2
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Rheumatology (Oxford). 2021 Feb 1;60(2):658-666. doi: 10.1093/rheumatology/keaa219.
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Increased IgA anti-citrullinated protein antibodies in the periodontal inflammatory exudate of healthy individuals compared to rheumatoid arthritis patients.
Front Cell Infect Microbiol. 2022 Jul 18;12:956417. doi: 10.3389/fcimb.2022.956417. eCollection 2022.
4
Influence of Oral Microbiota on the Presence of IgA Anti-Citrullinated Protein Antibodies in Gingival Crevicular Fluid.口腔微生物群对龈沟液中抗瓜氨酸化蛋白抗体IgA存在情况的影响。
Front Oral Health. 2022 Jun 16;3:904711. doi: 10.3389/froh.2022.904711. eCollection 2022.
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Periodontitis in First Degree-Relatives of Individuals With Rheumatoid Arthritis: A Short Narrative Review.类风湿关节炎患者一级亲属中的牙周炎:一篇简短的叙述性综述。
Front Oral Health. 2022 May 6;3:895753. doi: 10.3389/froh.2022.895753. eCollection 2022.
与类风湿关节炎患者相比,健康个体牙周炎症渗出物中 IgA 抗瓜氨酸化蛋白抗体增加。
J Clin Periodontol. 2020 May;47(5):552-560. doi: 10.1111/jcpe.13277. Epub 2020 Mar 17.
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Gingimaps: Protein Localization in the Oral Pathogen .牙龈卟啉单胞菌:口腔病原体中的蛋白质定位。
Microbiol Mol Biol Rev. 2020 Jan 2;84(1). doi: 10.1128/MMBR.00032-19. Print 2020 Feb 19.
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