Purpose of Review: There is increasing evidence on the connections between chronic oral inflammation/infection and the pathophysiological conditions of the gastrointestinal tract and accessory organs of digestion. The aim of this review is to provide a critical synthesis regarding the epidemiological, clinical, and in vivo associations between periodontitis and the most relevant diseases of the digestive system. Recent Findings: An increasing body of dental and medical literature is supporting the gum-gut axis as a relevant mechanism to explain the associations between periodontitis and systemic diseases. Indeed, shared microbiological and immunological pathways have been identified between periodontitis and gut diseases, and translocation of oral bacteria to the lower parts of the digestive system has been postulated as a driver for peptic ulcers, inflammatory bowel disease, liver disease, and ultimately digestive cancers. Summary: For the upper digestive tract, epidemiologic association between periodontitis and gastroesophageal reflux disease or squamous cell carcinoma remains conflicting, despite oral keystone pathogens having been consistently found in esophageal and gastric cancer tissue biopsies. The oral cavity represents a reservoir for Helicobacter pylori, with periodontal therapy increasing the eradication and the non-recurrence rate of the infection. Regarding bowel diseases, gut dysbiosis is being progressively ascertained in close relation to periodontal infection, and periodontitis is being investigated among the risk indicators for colorectal cancer. Lastly, non-alcoholic fatty liver disease and cirrhosis were epidemiologically linked to periodontitis, while its association with pancreatic tumors represents one of the most intriguing fields of research in periomedicine.

Can Periodontitis Affect the Health and Disease of the Digestive System? A Comprehensive Review of Epidemiological Evidence and Biological Mechanisms

Baima G.
Co-first
;
Ribaldone D. G.
Co-first
;
Romano F.;Citterio F.;Armandi A.;Aimetti M.
Last
2021-01-01

Abstract

Purpose of Review: There is increasing evidence on the connections between chronic oral inflammation/infection and the pathophysiological conditions of the gastrointestinal tract and accessory organs of digestion. The aim of this review is to provide a critical synthesis regarding the epidemiological, clinical, and in vivo associations between periodontitis and the most relevant diseases of the digestive system. Recent Findings: An increasing body of dental and medical literature is supporting the gum-gut axis as a relevant mechanism to explain the associations between periodontitis and systemic diseases. Indeed, shared microbiological and immunological pathways have been identified between periodontitis and gut diseases, and translocation of oral bacteria to the lower parts of the digestive system has been postulated as a driver for peptic ulcers, inflammatory bowel disease, liver disease, and ultimately digestive cancers. Summary: For the upper digestive tract, epidemiologic association between periodontitis and gastroesophageal reflux disease or squamous cell carcinoma remains conflicting, despite oral keystone pathogens having been consistently found in esophageal and gastric cancer tissue biopsies. The oral cavity represents a reservoir for Helicobacter pylori, with periodontal therapy increasing the eradication and the non-recurrence rate of the infection. Regarding bowel diseases, gut dysbiosis is being progressively ascertained in close relation to periodontal infection, and periodontitis is being investigated among the risk indicators for colorectal cancer. Lastly, non-alcoholic fatty liver disease and cirrhosis were epidemiologically linked to periodontitis, while its association with pancreatic tumors represents one of the most intriguing fields of research in periomedicine.
2021
8
4
96
106
Dysbiosis; Gum-gut axis; Microbiome; Pancreas; Periodontal diseases
Baima G.; Ribaldone D.G.; Muwalla M.; Romano F.; Citterio F.; Armandi A.; Aimetti M.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1846101
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