Periodontitis and inflammatory bowel disease (IBD) are both chronic inflammatory diseases that are characterized by abnormal host immune responses and microbiota dysbiosis. Emerging evidence implies potential associations between periodontitis and IBD. Porphyromonas gingivalis (P. gingivalis), a primary cause of periodontitis, is thought to play a role in the development of IBD through the oral–gut disease axis. However, the precise mechanisms of its involvement remain enigmatic. In this narrative review, we begin with a discussion of the bidirectional relationship between periodontitis and IBD and the involvement of P. gingivalis in each of the two diseases. Further, we summarize the possible routes by which P. gingivalis links periodontitis and IBD through the oral–gut axis, as well as the underlying mechanisms of its involvement in the pathogenesis of IBD. Collectively, P. gingivalis participates in the progression of IBD through gut dysbiosis, impairment of the intestinal barrier, release of inflammatory mediators, and disturbance of the immune response. The above findings may provide new insights for exploring novel biomarkers and potential therapeutic approaches for IBD.

Periodontitis and diabetes are both chronic diseases with a complex bidi- rectional relationship. Diabetes increases the risk of periodontitis by two to three times when compared to people who do not have diabetes. In this study, we used microarray analysis to identify differentially expressed lncRNAs and mRNAs in response to advanced glycosylation end prod- ucts (AGEs) and conventional osteogenic induction, and we identified LINC00673 as the target. LINC00673, a recently discovered lncRNA, has been studied in various cancers. However, the function and regulatory mechanism of LINC00673 in PDLSCs exposed to the AGEs microenvi- ronment have never been fully explored. Following that, we predicted an interaction between LINC00673 and miR188-3p and confirmed the direct binding sites of miR-188-3p on LINC00673. MiR-188-3p overexpres- sion resulted in increased osteogenic differentiation, whereas LINC00673 overexpression reversed its suppression, indicating that LINC00673 acts as a competing endogenous RNA for miR-188-3p. By suppressing one another, LINC00673 and miR-188-3p form a network that controls LEP, its target gene. By inhibiting the canonical Wnt pathway, LEP decreased bone formation in PDLSCs. In conclusion, our findings provide new evi- dence that this lncRNA-miRNA (microRNA) regulatory network plays an important role in the osteogenic differentiation of PDLSCs and has the potential to be a therapeutic target for diabetes-related periodontitis.