Impact of anti-TNF and anti-IL-12/IL-23 antibody therapy on periodontal inflammation and gingival crevicular fluid IL-6 in patients with inflammatory bowel diseases.

INTRODUCTION

Periodontitis prevalence is elevated in patients with inflammatory bowel diseases (IBD). Biological therapies targeting cytokines such as tumor necrosis factor (TNF) and interleukin-12/23 (IL-12/23) are central to IBD management, yet their impact on periodontal health remains unclear.

METHODS

In a cross-sectional, hypothesis-generating design, 45 patients with IBD were examined and stratified into three groups according to their biological therapy: anti-TNF therapy (n = 15), anti-IL-12/23 therapy (n = 15), and a control group not receiving these biologics (n = 15). Periodontal status was assessed using the Periodontal Screening Index (PSI; codes 0-4) across all sextants as a standardized screening measure. Medical history, oral hygiene behavior, and prior periodontal diagnoses were documented. To assess local immune activity, interleukin-6 (IL-6) concentrations in gingival crevicular fluid (GCF) were quantified by enzyme-linked immunosorbent assay (ELISA).

RESULTS

Overall, 16 patients exhibited either known or previously undiagnosed periodontitis, with interindividual variability in severity. Patients receiving anti-IL-12/23 therapy exhibited lower mean and maximal PSI scores compared with anti-TNF-treated patients, and no sextants with advanced periodontal inflammation (PSI 3-4) were detected in this group. In contrast, active or latent periodontitis was observed in both the anti-TNF and control cohorts. Concordantly, IL-6 levels in GCF were significantly reduced in patients undergoing IL-12/23 blockade compared with controls, indicating attenuated local inflammatory signaling at the periodontal interface. These findings were observed despite no statistically significant differences in clinical or endoscopic disease activity between groups.

CONCLUSIONS

These exploratory findings suggest that systemic inhibition of the IL-12/23 axis in IBD is associated with reduced periodontal inflammatory burden and decreased local IL-6 activity, supporting a role for IL-23-dependent immune pathways in linking intestinal and oral mucosal inflammation. While causality cannot be inferred from this cross-sectional study, the data provide a mechanistic rationale for further longitudinal investigations into the impact of cytokine-targeted biologic therapy on the oral-gut immune axis.