Recently, an oral–gut communication axis has been proposed. Herein, we review clinical studies reporting differences in oral microbial communities in inflammatory bowel diseases (IBDs), with a focus on Crohn’s Disease (CD), as well as evidence from experimental models. While available studies support evidence for the direct transmission of oral-derived bacteria to gut, further work is needed to clarify whether such transmission results in stable colonization of intestinal niches and the establishment of a persistent host–microbe state that influences host physiology. To date, evidence from clinical and murine studies suggests three routes of the oral–gut axis, which in turn directly or indirectly exacerbate intestinal inflammation and contribute to IBD pathogenesis: (i) direct invasion of pathobionts through swallowing, (ii) migration of the oral pathogen activated pro-inflammatory immune cells, (iii) systemic inflammation triggered by oral pathogens such as Porphyromonas gingivalis. Although the role of oral microbiome in systemic diseases is becoming more apparent, sophisticated clinical and experimental studies are needed to elucidate the direct and indirect oral–gut communication mechanisms, including the contribution of oral microbial metabolites. Future directions may include evaluating the diagnostic and therapeutic potential of the oral microbiome and metabolome.
Ozkul et al. (Thu,) studied this question.