4.6 Review

Oral microbiota and Helicobacter pylori in gastric carcinogenesis: what do we know and where next?

Journal

BMC MICROBIOLOGY
Volume 21, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s12866-021-02130-4

Keywords

Oral microbiota; H; pylori; CagA; Interaction; Gastric cancer

Categories

Funding

  1. National Institute for Medical Research Development (NIMAD), Tehran, Iran [958117]

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The oral microbiota may play a role in the development and progression of gastric cancer, but the causal relationship between oral microbiota and gastric cancer remains controversial. Exploring the interaction and relationship between the oral microbiota and Helicobacter pylori in gastric cancer, as well as the impact of oral microbiota on the mechanisms of carcinogenesis, could offer new insights for the diagnosis and prevention of gastric cancer.
Gastric cancer (GC) is one of the most common malignancies causing death worldwide, and Helicobacter pylori is a powerful inducer of precancerous lesions and GC. The oral microbiota is a complex ecosystem and is responsible for maintaining homeostasis, modulating the immune system, and resisting pathogens. It has been proposed that the gastric microbiota of oral origin is involved in the development and progression of GC. Nevertheless, the causal relationship between oral microbiota and GC and the role of H. pylori in this relationship is still controversial. This study was set to review the investigations done on oral microbiota and analyze various lines of evidence regarding the role of oral microbiota in GC, to date. Also, we discussed the interaction and relationship between H. pylori and oral microbiota in GC and the current understanding with regard to the underlying mechanisms of oral microbiota in carcinogenesis. More importantly, detecting the patterns of interaction between the oral cavity microbiota and H. pylori may render new clues for the diagnosis or screening of cancer. Integration of oral microbiota and H. pylori might manifest a potential method for the assessment of GC risk. Hence it needs to be specified the patterns of bacterial transmission from the oral cavity to the stomach and their interaction. Further evidence on the mechanisms underlying the oral microbiota communities and how they trigger GC may contribute to the identification of new prevention methods for GC. We may then modulate the oral microbiota by intervening with oral-gastric bacterial transmission or controlling certain bacteria in the oral cavity.

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