Figure 1.

Pathogenic effect of periodontal pathogenic bacteria on systemic diseases via the oral-gut axis. In a pathogenic environment with excessive plaque accumulation, the dynamic equilibrium between microbial invasion and host defense is disrupted, and the periodontal pathogenic bacteria and commensal bacteria together give rise to oral dysbiosis and disease states. The oral cavity is directly connected to the gastrointestinal tract, and the progression of the ecological niche from the oral cavity to the gut has been defined as the ‘oral-gut microbiome axes. These periodontal pathogenic bacteria and their virulence products then breakthrough the barrier between the oral cavity and the gut and translocate in large numbers into the gut, causing gut dysbiosis, which is characterized by (i) a reduction in overall microbial community diversity, (ii) an alteration of the Firmicutes/Bacteroidetes (F/B) ratio, and (iii) as well as a reduction in probiotics and a corresponding increase in opportunistic pathogens. In addition to microbiota dysbiosis, the transition from health to disease requires a susceptible host (including genetic/environmental factors), accompanied by a complex set of interacting mechanisms that ultimately trigger destructive immune and inflammatory responses in the host. In addition to oral diseases, systemic diseases in which the oral microbiota may be involved in regulation via the oral-gut axis include intestinal diseases (e.g. inflammatory bowel disease and colorectal cancer), rheumatoid arthritis, brain diseases (e.g. Alzheimer’s disease, Parkinson’s disease, autism spectrum disorders, and major depressive disorder), liver diseases (e.g. non-alcoholic fatty liver disease, cirrhosis, and hepatocellular carcinoma), obesity, diabetes, atherosclerosis, and skin diseases.