Treatment resistance of rheumatoid arthritis relates to infection of periodontal pathogenic bacteria: a case–control cross-sectional study

Abstract

Recent studies have shown that periodontitis is associated with rheumatoid arthritis (RA) and periodontal bacteria, such as Aggregatibacter actinomycetemcomitans (Aa) and Porphyromonas gingivalis (Pg) are involved in the pathogenesis of RA via citrullinated proteins. Smoking has also been shown to be involved in the pathogenesis of RA; however, the extent of this involvement is still poorly understood. In addition, RA and polymyalgia rheumatica (PMR) are sometimes difficult to differentiate; however, the relationship between PMR and the factors from smoking and periodontal bacteria is unclear. The aim of this study was to clarify the relationship between periodontal pathogenic bacterial infections and smoking in patients with RA or PMR. This case–control study included 142 patients with untreated RA or PMR. This study evaluated the serum antibody titers against periodontal pathogenic bacterial antigens and an anti-citrullinated peptide antibody (ACPA). In patients with RA, the relationship between antibody titers and disease activity of RA and response after 3 months of treatment was also investigated. Additionally, the effects of smoking were evaluated. Although there was no significant difference in serum antibody titer against periodontal pathogenic bacteria between the ACPA-positive RA group and the ACPA-negative PMR group, we found an association between the elevated antibody titer against Pg and the degree of ACPA value, especially between negative group and high-value positive group (≥ 100 U/mL). The antibody titers against Aa and Pg did not differ depending on disease activity score 28 (DAS28) at baseline; however, patients with high antibody titers had poor RA therapeutic response as judged by DAS28 after 3 months. We could not find any association between smoking and any of these parameters. Periodontal pathogenic bacteria, especially Pg, are associated with elevated ACPA levels. Our findings suggest that Pg and Aa infections interfere with the therapeutic response of RA.

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

“…The results indicated a significantly higher ESR and a trend toward a higher DAS28-ESR in 16 RA patients positive for anti- P. gingivalis IgG than in 22 RA patients without anti- P. gingivalis IgG [78] . Similar results were obtained in recent studies [141] , [142] , and both concluded that baseline serum anti- P. gingivalis IgG, but not anti- A. actinomycetemcomitans IgG, was predictive of the response to treatment with bDMARDs and csDMARDs. However, these are serum IgG responses to sonicated preparations of P. gingivalis , and their target antigens are unclear.…”

“…Since 2013, eight original intervention studies have been conducted to assess the effect of periodontitis and periodontopathic bacterial infection on the response to pharmacological treatment with DMARDs in RA patients [78] , [137] , [138] , [139] , [140] , [141] , [142] , [143] . A summary of the study method and outcome in each study is presented in Table 2 .…”

The Effects of Periodontal Treatment on Rheumatoid Arthritis and of Anti-Rheumatic Drugs on Periodontitis: A Systematic Review

“…It has been demonstrated that all periodontal indexes are worse in RA patients, with an adjusted odds ratio of 2.66 [87]. There is also a linear correlation between clinical and laboratoristic parameters of RA and periodontitis, such as the high Disease Activity Score Calculator for Rheumatoid Arthritis (DAS28), RF, ACPAs, CRP, ESR, and disease duration [88][89][90][91].…”

Comorbidity of rheumatoid arthritis and periodontal diseases

“…Авторы предполагают, что антитела IgA против RgpB в слюне могут быть связаны с активностью заболевания РА. В японском перекрестном исследовании «случай -контроль» [95] отмечено, что пародонтальные патогенные бактерии, особенно P. gingivalis, связаны с повышенным уровнем ACPA. Пациенты с РА, которые имели высокие титры антител, имели плохой ответ на терапию.…”