Abstract

A particular role for Porphyromonas gingivalis (Pg) and Aggregatibacter actinomycetemcomitans (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.

Highlights

  • The prevalence of periodontitis according to this cut-off was not significantly different between rheumatoid arthritis (RA) patients and the non-RA controls (NC)

  • In the RA patients, there was no difference in the periodontal inflamed surface area (PISA) between patients treated with DMARDs and those that were not (p = 0.908)

  • We showed that in both RA patients and the NC from an Indonesian cohort, the levels of serum anti-Porphyromonas gingivalis (Pg) and anti-Aa antibodies were associated with the detection of subgingival Pg and Aa

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Summary

Introduction

Periodontitis is epidemiologically associated with rheumatoid arthritis (RA), a chronic autoimmune disease characterized by inflammation of the joints, causing pain, bone damage, and disability, the directionality of this relationship is not known [1]. The development of RA is a multistep process in which early phases are characterized by the presence of genetic and environmental risk factors and the systemic autoimmunity associated with RA, such as rheumatoid factor (RF) and anticitrullinated protein antibodies (ACPA) [2]. Periodontitis shares genetic and environmental risk factors with RA, and periodontitis by itself has been regarded as a risk factor for RA development [3,4].

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