Bacteriome and mycobiome dysbiosis in oral mucosal dysplasia and oral cancer

Abstract

It has long been considered that the oral microbiome is tightly connected to oral health and that dysbiotic changes can be detrimental to the occurrence and progression of dysplastic oral mucosal lesions or oral cancer. Improved understanding of the concepts of microbial dysbiosis together with advances in high-throughput molecular sequencing of these pathologies have charted in greater microbiological detail the nature of their clinical state. This review discusses the bacteriome and mycobiome associated with oral mucosal lesions, oral candidiasis, and oral squamous cell carcinoma, aiming to delineate the information available to date in pursuit of advancing diagnostic and prognostic utilities for oral medicine.

Keywords: bacteriome; dysbiosis; microbiome; mycobiome; oral cancer; oral candidiasis; oral dysplasia; oral medicine; oral mucosa; oral pathology.

FIGURE 1

Potential contribution of bacteria and fungi on the development of OSCC. Bacteria may enter the bloodstream (A) or translocate from the periodontal pocket or microinjury (B) to the tumoral site. Proposed contributing mechanisms of bacteria and fungi to the development of OSCC include the production of carcinogenic metabolites (1), induction of proinflammatory microenvironment (2), and alteration of the balance between host cell proliferation and apoptosis (3). Figure was generated and adapted from “Tumor Microenvironment 2,” by BioRender.com (2023), retrieved from https://app.biorender.com/biorender‐templates.

FIGURE 2

Significantly altered taxa repeatedly reported in OPMD‐associated studies on oral bacteriota. List of phyla (A), genera (B), and species (C) significantly increased or decreased in the indicated number of studies (only taxa reported in two or more studies are shown). *All three OPMDs have same direction with OSCC; ^†Different between OL and Smoking; ^#Different between OLP and Smoking; +, increased in OSCC; −, decreased in OSCC.