Research progress on association between periodontitis and inflammatory bowel disease

Inflammatory bowel disease (IBD) is a group of chronic, non-specific inflammatory diseases of the gastrointestinal tract including primarily Crohn’s disease and ulcerative colitis, which are affected by multiple factors. Periodontitis is a type of disease characterized by plaque biofilm as the initiating factor and chronic destruction of alveolar bone via resorption. An increasing number of studies have reported a correlation between periodontitis and IBD, but the relationship between the two remains unclear. In this study, we explore the internal relationships between the two diseases from three dimensions, including epidemiological, biological, and associated treatment evidence. Based on epidemiological evidence, periodontitis was found to be associated with an increased risk of IBD, which also affects periodontal health, although the bidirectional correlation needs to be further studied by expanding the number of data sources. From the biological evidence, both clinical studies and animal experiments show that IBD and periodontitis are interconnected. Based on evidence from association therapy, drugs that are beneficial for the treatment of IBD are also effective in the prevention and treatment of periodontitis. In addition, drugs that are good for improving periodontitis can also significantly alleviate IBD. The interaction mechanism between IBD and periodontitis includes the microbial pathway and the immunization route. The microbial pathway refers to the increase in the probability of intestinal tract ectopic colonization by oral bacteria transmitted through the mouth-gut axis or blood, resulting from the increase in the proportion of opportunistic pathogens in the oral cavity of patients with periodontitis and the influence of IBD on the secretion of gastric juice and the balance of intestinal flora. These microorganisms further aggravate IBD inflammation by releasing virulence factors, destroying the intestinal mucosal barrier, and triggering inflammatory responses. In periodontitis, adaptive immunity is activated in the mouth, leading to the production of a large number of immune cells, including Th17 containing the intestinal homing marker α4β7 integrin on their surface. Increased ligand expression of α4β7 integrin in the intestinal mucosa of patients with IBD accelerates oral Th17 cell transfer to the intestine, thereby worsening intestinal inflammation. In parallel, the abnormal expression of cytokines, such as TNF-α, IL-1β, IL-10, IL-6, IL-21, soluble CD40 ligand (sCD40L), IL-23, and INF-γ, in the oral cavity of patients with IBD was observed, suggesting that IBD may affect periodontitis through immunity. These cytokines represent targets for the treatment of both diseases and provide a research direction for their prevention and treatment in the future.