Cure8 research brief
The review suggests shared immune and microbial mechanisms connecting gum disease and IBD, which may explain observed epidemiologic links and point to potential targets for future research or combined oral–gut interventions. However, clinical relevance remains unproven.
Clinicians; researchers focused on mucosal immunology, microbiome, or IBD; adult patients with IBD concerned about oral health
The authors followed PRISMA guidelines and included 39 studies, mainly preclinical mechanistic work using dextran sulfate sodium (DSS) colitis models that resemble ulcerative colitis.
In the forward direction (periodontitis → IBD) mechanisms with supporting evidence include microbial translocation, metabolic changes, immune cell gut-homing, and intestinal barrier disruption. Two shared immunological hubs—Th17/Treg imbalance and dysregulated macrophage polarization—are highlighted, connected by IL-1β and IL-17A signaling.
Evidence for the reverse direction (IBD → periodontitis) comes only from preclinical studies and is presented as a hypothesis. Some preclinical interventions targeting these hubs improved both colitis and periodontitis, but clinical benefit in patients has not been established.
Most evidence is preclinical and centered on DSS colitis (UC-like) models; extrapolation to Crohn's disease is limited. Clinical trials demonstrating benefit from targeting the proposed hubs are not reported.
Review the original publication for the complete reporting, methods, and context.
Conflict statement: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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