Crosstalk between the oral microbiota, mucosal immunity, and the epithelial barrier regulates oral mucosal disease pathogenesis

• Published in: Mucosal immunology Vol. 14; no. 6; pp. 1247 - 1258
• Main Authors: Lin, Dongjia, Yang, Lisa, Wen, Liling, Lu, Huanzi, Chen, Qianming, Wang, Zhi
• Format: Journal Article
• Language: English
• Published: New York Nature Publishing Group US 01.11.2021; Elsevier Limited
• Subjects: Allergology; Animals; Antibodies; Biodiversity; Biomedical and Life Sciences; Biomedicine; Candidiasis; Cell Communication; Disease; Disease Susceptibility; Dysbacteriosis; Dysbiosis; Etiology; Gastroenterology; Homeostasis; Host Microbial Interactions - immunology; Host-Pathogen Interactions - immunology; Humans; Immune response; Immune System - immunology; Immune System - metabolism; Immunity (Disease); Immunity, Mucosal; Immunology; Leukokeratosis; Lichen planus; Literature reviews; Microbial Interactions; Microbiota; Microorganisms; Mouth Mucosa - immunology; Mouth Mucosa - metabolism; Mouth Mucosa - microbiology; Mucosal immunity; Oral carcinoma; Oral cavity; Oral squamous cell carcinoma; Review Article; Saliva; Signal Transduction
• ISSN: 1933-0219; 1935-3456
• DOI: 10.1038/s41385-021-00413-7

Oral mucosal disease (OMD), which is also called soft tissue oral disease, is described as a series of disorders or conditions affecting the mucosa and soft tissue in the oral cavity. Its etiology is unclear, but emerging evidence has implicated the influence of the composition of the oral mucosa and saliva-resident microbiota. In turn, this dysbiosis effects the immune response balance and epithelial barrier function, followed by the occurrence and progression of OMD. In addition, oral microbial dysbiosis is diverse in different types of diseases and different disease progressions, suggesting that key causal pathogens may exist in various oral pathologies. This narrative literature review primarily discusses the most recent findings focusing on how microbial dysbiosis communicates with mucosal adaptive immune cells and the epithelial barrier in the context of five representative OMDs, including oral candidiasis (OC), oral lichen planus (OLP), recurrent aphthous ulcer (RAU), oral leukoplakia (OLK), and oral squamous cell carcinoma (OSCC), to provide new insight into the pathogenetic mechanisms of OMDs.