Periodontitis increases the risk of gastrointestinal dysfunction: an update on the plausible pathogenic molecular mechanisms

Periodontitis is an inflammatory disease affecting the soft tissues surrounding the teeth. It is linked to various communicable and non-communicable diseases, including diabetes, cardiovascular disease, rheumatoid arthritis, and cancer. The link between periodontal disease and systemic diseases is attributed to inflammation, microbial products, and microbes spreading to distant organ systems. Oral bacteria can reach the gut via swallowed saliva, inducing gut dysbiosis and gastrointestinal dysfunction. Some periodontal pathogens, such as Porphyromonas gingivalis, Klebsiella, Helicobacter, pylori, Streptococcus, Veillonella, Parvimonas micra, Fusobacterium nucleatum, Peptostreptococcus, Haemophilus, and Aggregatibacter actinomycetemcomitans can survive in the acidic gut environment and result in dysbiosis.

Gut dysbiosis increases gut inflammation and induces dysplastic changes that lead to gut dysfunction. Various studies have linked oral bacteria and the oral-gut axis to gastrointestinal (GI) tract disorders such as inflammatory bowel disease, liver disease, hepatocellular carcinoma, pancreatic ductal adenocarcinoma, ulcerative colitis, and Crohn's disease. While the correlation between periodontitis and GI disorders is well established, the molecular mechanisms by which oral microflora induce these changes have not been extensively discussed. This review comprehensively discusses the molecular and immunological mechanisms by which periodontal pathogens can induce gut dysbiosis and induce organ dysfunction leading to various GIT disorders.