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Emerging evidence points to the involvement of periodontal disease (PD) in the pathogenesis of rheumatoid arthritis (RA), especially in anti-citrullinated protein antibodies (ACPA)-positive RA. The bacteria Porphyromonas gingivalis, involved in oral mucosal inflammation and PD, can citrullinate proteins via prokaryotic peptidylarginine deiminase.1 Systemic translocation of oral bacteria has been found in RA-patients with PD. These bacterial translocations have been implicated in the generation of anti-modified protein antibodies (AMPAs) as ACPA can also recognise modified bacterial proteins.2 Nevertheless, the ‘cause-consequence’ relation between PD and RA remains debatable as PD may be a risk factor (PD→RA; scenario 1; figure 1A) but also a consequence of RA (RA→PD; scenario 2).3 Additionally, the relation PD→RA may be confounded by related factors (eg, body mass index (BMI), smoking or other factors related to socioeconomic status (SES); scenario 3). Increased prevalence of periodontitis and P. gingivalis were reported in ACPA-positive/autoantibody-positive at-risk individuals in case–control/cross-sectional studies.4 5 Longitudinal studies on PD in at-risk individuals could elucidate temporal relationships and provide further insight into the relation of PD in RA-development. Therefore, we longitudinally analysed the relation between tooth loss as proxy for (preceding) PD and progression to clinically apparent inflammatory arthritis (IA) and RA in patients with clinically suspect arthralgia (CSA). We also studied whether this relation is independent of SES and SES-related factors.
Conceptual framework of hypotheses on periodontal disease and RA (A) and the development of inflammatory arthritis in …
Footnotes
Handling editor Josef S Smolen
Contributors SJHK and AvdH-vM designed the study. SJHK and EvM accessed and verified the data. SJHK analysed the data and acted as guarantor. All authors interpreted the data and wrote the report. AvdH-vM was the principal investigator. All authors approved the final version of the manuscript and were responsible for the decision to submit the manuscript for publication.
Funding This work was supported by the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program (Starting grant, agreement No. 714312) and by the Dutch Arthritis Society.
Competing interests None declared.
Patient and public involvement Patient partners were involved in the design of the CSA-cohort, and in the design and execution of the TREAT EARLIER-trial
Provenance and peer review Not commissioned; externally peer reviewed.
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