The oral‑gut axis in periodontitis: Current evidence and emerging therapeutic targets (Review) 

The oral‑gut axis has emerged as an important biological pathway linking periodontitis with gut microbiota dysbiosis and systemic immune‑metabolic disturbances. In periodontitis, the expansion of oral pathobionts, such as Porphyromonas gingivalis and Fusobacterium nucleatum may promote enteric colonisation, impair gut barrier integrity, alter microbial metabolite profiles and sustain low‑grade systemic inflammation. The present narrative review synthesises evidence from the PubMed, Scopus and Web of Science databases up to January, 2026 on oral‑gut microbial crosstalk in periodontitis, with an emphasis on microbial translocation, barrier dysfunction, immune signalling, metabolite‑mediated pathways and emerging therapeutic strategies. Unlike recent reviews, it also integrates Mendelian randomisation evidence, the oral‑gut‑bone axis, implant‑related implications and a global‑health perspective. Current evidence supports bidirectional interactions between oral and gut dysbiosis in periodontitis. Experimental and clinical studies indicate that oral pathobionts can reach the intestine, disrupt tight‑junction integrity, reduce short‑chain fatty acid production and promote Th17/Treg imbalance, thereby amplifying mucosal and systemic inflammation. These alterations are linked to osteoclastogenesis, alveolar and peri‑implant bone loss, and broader associations with gastrointestinal, cardiometabolic, autoimmune and neuroinflammatory disorders. Adjunctive therapeutic approaches under investigation include probiotics, prebiotics, synbiotics, dietary modulation, faecal microbiota transplantation, and combined host‑ and microbiota‑directed interventions. Conclusions: The oral‑gut axis provides a biologically plausible framework connecting periodontitis with systemic disease through microbial, immune and metabolic pathways. However, a large amount of the currently available evidence remains observational or derived from animal models, and heterogeneity in study design limits formal comparison across studies. Large longitudinal human studies, standardised multi‑omics approaches, and rigorously designed randomised trials are required to establish causality and to guide precision, microbiome‑informed periodontal care.