Role of Periodontitis in Inflammatory Bowel Disease 2256065

H Himanshi Tanwar (University of Maryland) J Jeba Gnanasekaran (University of Maryland) D Devon Allison (University of Maryland) G Giacomo Baima (University of Turin) M Mario Aimetti (University of Turin) D Davide Giuseppe Ribaldone (University of Turin) M Massimo Costalonga (University of Minnesota) S Saurabh Mehandru (Icahn School of Medicine at Mount Sinai, New York) J Jean Pierre Raufman (University of Maryland) C Cynthia Sears (Johns Hopkins University School of Medicine) X Xuesong He V Vivek Thimbigere-Math (University of Maryland)

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)

Article Details

Volume / Issue Vol. 215, Issue Supplement_1
Published August 01, 2026
ISSN 0022-1767
Publisher American Association of Immunologists

Authors (12)

H

Himanshi Tanwar

University of Maryland

J

Jeba Gnanasekaran

University of Maryland

D

Devon Allison

University of Maryland

G

Giacomo Baima

University of Turin

M

Mario Aimetti

University of Turin

D

Davide Giuseppe Ribaldone

University of Turin

M

Massimo Costalonga

University of Minnesota

S

Saurabh Mehandru

Icahn School of Medicine at Mount Sinai, New York

J

Jean Pierre Raufman

University of Maryland

C

Cynthia Sears

Johns Hopkins University School of Medicine

X

Xuesong He

V

Vivek Thimbigere-Math

University of Maryland