Role of Periodontitis in Inflammatory Bowel Disease 2256065

Abstract Introduction Periodontitis is a prevalent oral infection linked to the initiation/exacerbation of inflammatory bowel disease (IBD), yet its causal and mechanistic basis remains unclear. We sought to elucidate how periodontitis contributes to IBD pathogenesis through integrated clinical and animal studies. Methods We conducted a case-control clinical study assessing the periodontal status of 180 IBD patients and 180 healthy controls. Each subject underwent a comprehensive oral examination and provided saliva and fecal samples. To mimic human conditions, we induced periodontitis in mice using ligature-induced periodontitis (LIP) and oral gavage models, utilizing mice with genetic gut barrier defects or gut barrier weakened by piroxicam medication. Results IBD patients exhibited prevalence of periodontitis compared to healthy controls. Severe periodontitis, bleeding scores were positive risk indicators for IBD. 16S rRNA sequencing identified the presence of oral taxa in the feces of IBD patients with periodontitis compared to healthy controls. Corroborating these human findings, LIP in mice facilitated the colonization of native oral bacteria in the intestine, leading to colitis. Similarly, oral gavage of human periodontal pathogens induced colitis in mice with gut barrier deficiencies, compared to untreated mice or those inoculated with oral commensals. Periodontal pathogens promoted infiltration of IgG+ B cells into the colonic lamina propria and increased IgG activation, triggered elevated IL1b and IL-17 production, leading to induction of colitis. Remarkably, the resolution of LIP in mice diminished the intestinal load of oral bacteria and reversed colitis in mice. Conclusion The oral cavity may serve as a reservoir for bacteria that can induce colitis via B-cell-mediated responses, especially in the presence of compromised intestinal barriers. Dental care can reduce the risk of IBD by limiting the influx of colitogenic oral pathogens and should be considered as an integral part of IBD evaluation and care. Funding Source n/a Topic Categories Mucosal and Regional Immunology (MUC)

Authors

Institutions

Publication Details

Journal
The Journal of Immunology
Published
2026-07-28
DOI
https://doi.org/10.1093/jimmun/vkag141.304
Primary Topic
Oral microbiology and periodontitis research
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Role of Periodontitis in Inflammatory Bowel Disease 2256065

Himanshi Tanwar, Mario Aimetti, Massimo Costalonga, Davide Giuseppe Ribaldone et al.
The Journal of Immunology
Oral microbiology and periodontitis research
article

Role of Periodontitis in Inflammatory Bowel Disease 2256065

Himanshi Tanwar, Mario Aimetti, Massimo Costalonga, Davide Giuseppe Ribaldone, Giacomo Baima, Jean Pierre Raufman, Cynthia Sears, Vivek Thimbigere-Math, Saurabh Mehandru, Devon Allison, Jeba Gnanasekaran, Xuesong He
article en

Abstract

Abstract Introduction Periodontitis is a prevalent oral infection linked to the initiation/exacerbation of inflammatory bowel disease (IBD), yet its causal and mechanistic basis remains unclear. We sought to elucidate how periodontitis contributes to IBD pathogenesis through integrated clinical and animal studies. Methods We conducted a case-control clinical study assessing the periodontal status of 180 IBD patients and 180 healthy controls. Each subject underwent a comprehensive oral examination and provided saliva and fecal samples. To mimic human conditions, we induced periodontitis in mice using ligature-induced periodontitis (LIP) and oral gavage models, utilizing mice with genetic gut barrier defects or gut barrier weakened by piroxicam medication. Results IBD patients exhibited prevalence of periodontitis compared to healthy controls. Severe periodontitis, bleeding scores were positive risk indicators for IBD. 16S rRNA sequencing identified the presence of oral taxa in the feces of IBD patients with periodontitis compared to healthy controls. Corroborating these human findings, LIP in mice facilitated the colonization of native oral bacteria in the intestine, leading to colitis. Similarly, oral gavage of human periodontal pathogens induced colitis in mice with gut barrier deficiencies, compared to untreated mice or those inoculated with oral commensals. Periodontal pathogens promoted infiltration of IgG+ B cells into the colonic lamina propria and increased IgG activation, triggered elevated IL1b and IL-17 production, leading to induction of colitis. Remarkably, the resolution of LIP in mice diminished the intestinal load of oral bacteria and reversed colitis in mice. Conclusion The oral cavity may serve as a reservoir for bacteria that can induce colitis via B-cell-mediated responses, especially in the presence of compromised intestinal barriers. Dental care can reduce the risk of IBD by limiting the influx of colitogenic oral pathogens and should be considered as an integral part of IBD evaluation and care. Funding Source n/a Topic Categories Mucosal and Regional Immunology (MUC)

The Journal of ImmunologyVol. 215(Supplement_1)
Johns Hopkins University (US), Johns Hopkins Medicine (US), University of Minnesota System (US), University of Turin (IT), University of Maryland, College Park (US), Icahn School of Medicine at Mount Sinai (US)
Good health and well-being
Openalex Percentile: Top 8%
Oral microbiology and periodontitis research
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.