Postdoctoral Fellow University of Maryland Baltimore, Maryland, United States
Disclosure(s):
Himanshi Tanwar: No financial relationships to disclose
Introduction/Rationale: 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.
