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Ulcerative colitis-driven gut dysbiosis exacerbates periodontal bone loss through the gut-oral axis /Th17/Treg imbalance

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Editor's note
Patients with ulcerative colitis face accelerated bone loss in their gums—a finding that reframes periodontitis as a systemic consequence of gut barrier failure rather than a local dental problem. This work moves beyond correlation to establish causation through elegant microbiota transfer experiments, positioning dysbiosis-driven barrier dysfunction as the linchpin connecting intestinal and oral disease. Gastroenterologists and periodontists should recognize these conditions as linked mucosal disorders amenable to microbiota-targeted intervention.

Source: europepmc · Origin: CN · Huang Y, Hu Y, Zhao Y, Li Y, Liu Y, Wang M, Wang Q, Hu H. · NPJ biofilms and microbiomes · 2026-05-23

URL: https://pubmed.ncbi.nlm.nih.gov/42173912/

AI rationale (4/5, tier: unclassified): Directly addresses gut dysbiosis, barrier leakage, and Th17/Treg imbalance in UC; strong mechanistic focus on intestinal mucosa dysfunction.

Ulcerative colitis (UC) and periodontitis, both microbial dysbiosis-driven chronic inflammatory disorders, coexist and mutually exacerbate, but the causal mechanisms remain unclear. Using ligature-induced periodontitis plus DSS-colitis mice, we found UC doubles alveolar bone loss, heightens systemic inflammation, oxidative stress, and osteoclastogenesis. 16S rRNA and LC-MS metabolomics showed UC enriches oral pathogens, depletes gut Firmicutes, expands Bacteroides, and correlates with suppressed amino-acid/bile-acid biosynthesis. Fecal microbiota transplantation (FMT) from DSS donors into antibiotic-pretreated periodontitis-prone mice replicated aggravated bone loss, systemic inflammation, gut-barrier leakage, and Th17/Treg imbalance, while healthy-donor FMT protected. GC-MS revealed 35-60% reductions in acetate, propionate, and butyrate; keystone taxa Parabacteroides and Muribaculum inversely correlated with SCFAs and host inflammatory genes. Collectively, UC-driven gut dysbiosis is a transmissible causal factor that simultaneously remodels oral and intestinal biofilms, erodes epithelial barriers, and amplifies osteoclastic bone resorption. SCFAs-producing microbes or supplementation may be potential therapeutics for UC-associated periodontitis patients.

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Published 2026-05-28 · Last kit-update 2026-05-28