The periodontal inflamed surface area is associated with the clinical response to biological disease-modifying antirheumatic drugs in rheumatoid arthritis: a retrospective study

Abstract

Objectives: We evaluated whether the periodontal inflamed surface area (PISA), a measure of the inflammatory burden posed by periodontitis, is associated with the clinical response to biological disease-modifying antirheumatic drugs (bDMARDs) in patients with rheumatoid arthritis (RA).

Methods: We conducted a retrospective study that collected rheumatologic and periodontal data from 54 patients with RA who had received corticosteroid, conventional synthetic DMARDs, or non-steroidal anti-inflammatory drugs before (baseline) and after 6 months of bDMARD therapy. After the patients were divided into two groups based on high or low PISA according to the median measurements at baseline, the rheumatologic condition was compared between the groups.

Results: The patients with a low PISA showed significantly lower values for the Clinical Disease Activity Index (CDAI) (p = .008), swollen joint count (p = .02), and patient’s and evaluator’s global assessment (p = .01 and p = .03) and significantly greater decreases in changes in the CDAI from baseline to 6 months than the patients with a high PISA (p = .01), although these values were comparable at baseline. Both univariate and multivariate analyses revealed a significantly positive correlation between the baseline PISA and changes in the CDAI (p = .04 and p < .001).

Conclusion: The PISA is associated with the clinical response to bDMARDs in patients with RA.

Keywords:

• Biological disease-modifying antirheumatic drug
• clinical response
• periodontal inflamed surface area
• rheumatoid arthritis

Acknowledgements

The authors would like to acknowledge all of the staff of the Niigata Rheumatic Center for their assistance in the present study.

Conflict of interest

None.

Additional information

Funding

The present study was partially supported by KAKENHI Grant-in Aid for Scientific Research [17K11983 to Tetsuo Kobayashi] from the Japan Society for the Promotion of Science.