A potential pathogenic association between periodontal disease and Crohn’s disease

Abstract

Oral conditions are relatively common in patients with inflammatory bowel disease (IBD). However, the contribution of oral maladies to gut inflammation remains unexplored. Here, we investigated the effect of periodontitis on disease phenotypes of patients with IBD. In all, 60 patients with IBD (42 with ulcerative colitis [UC] and 18 with Crohn’s disease [CD]) and 45 healthy controls (HCs) without IBD were recruited for this clinical investigation. The effects of incipient periodontitis on the oral and gut microbiome as well as IBD characteristics were examined. In addition, patients were prospectively monitored for up to 12 months after enrollment. We found that, in both patients with UC and those with CD, the gut microbiome was significantly more similar to the oral microbiome than in HCs, suggesting that ectopic gut colonization by oral bacteria is increased in patients with IBD. Incipient periodontitis did not further enhance gut colonization by oral bacteria. The presence of incipient periodontitis did not significantly affect the clinical outcomes of patients with UC and CD. However, the short CD activity index increased in patients with CD with incipient periodontitis but declined or was unchanged during the study period in patients without periodontitis. Thus, early periodontitis may associate with worse clinically symptoms in some patients with CD.

Periodontitis may induce gut microbiota dysbiosis via salivary microbiota

“… 5 , 17 – 20 Source Tracker analysis revealed that more oral-derived bacteria existed in the altered faecal samples of the SP group (Fig. 3f ), and Iima et al also revealed the similarity of the oral and gut microbiota, 21 supporting our hypothesis that the salivary microbiota of patients with periodontitis may induce gut microbiota dysbiosis by entering the gastrointestinal tract.…”

Pyroptosis-Mediated Periodontal Disease

“…Inflammasome mutations can lead to inappropriate caspase-1 activation, which is associated with autoinflammatory syndromes [ 80 ]. Moreover, caspase-1 is involved in the pathogenesis of several diseases, including periodontal disease [ 4 ], Alzheimer’s disease [ 81 , 82 ], cardiovascular disease [ 83 ], rheumatoid arthritis [ 84 ], endometriosis [ 70 ], and Crohn’s disease [ 85 ], all of which are characterised by cell death and inflammation. Caspase-1 deficiency or inhibition protects against cell death, inflammation, and tissue dysfunction, associated with these diseases.…”

“…This can be noticed from the articles retrieved from the search strategy applied herein. It is also clear that other areas of medical knowledge besides dentistry focus on understanding pyroptosis-mediated inflammation processes [ 12 , 75 , 85 , 86 , 87 , 88 , 89 , 90 ]. Regarding periodontitis and periodontal therapies, the included articles present similarities regarding methods, type of cells involved, concentration, and kind of pyroptosis stimulation, as the outcomes point to the same direction considering the cellular events.…”

“…When focusing on rheumatoid arthritis, the disseminated P. gingivalis and A. actinomycetemcomitans may enhance pyroptosis of synovial cells [ 84 ]. Early periodontitis may also worsen clinical symptoms in patients with Crohn’s disease [ 85 ] as Porphyromonas strains were identified in the colonic mucosa of patients with ulcerative colitis and Crohn’s disease [ 119 ]. Taken together, there is reason to assume that periopathogens do not exclusively provoke pyroptosis in periodontal tissues.…”

Site-specific adaptation mechanisms of an oral pathobiont in the oral and gut mucosae

“…It has been reported that IBD patients display an increased prevalence of periodontitis [10, 11]. Also, early periodontitis may worsen clinical outcomes in some IBD patients [12]. Furthermore, the oral administration of P. gingivalis and F. nucleatum exacerbates the severity of dextran sulfate sodium (DSS)–induced colitis in mice by disrupting the intestinal barrier [13–15].…”