Recent studies have shown that oral microbiota play an important role in the esophageal cancer (EC) initiation and progression, suggesting that oral microbiota is a new risk factor for EC. The composition of the microbes inhabiting the oral cavity could be perturbed with continuous factors such as smoking, alcohol consumption, and inflammation. The microbial alteration involves the decrease of beneficial species and the increase of pathogenic species. Experimental evidences suggest a significant role of oral commensal organisms in protecting hosts against EC. By contrast, oral pathogens, especially Porphyromonas gingivalis and Fusobacterium nucleatum, give rise to the risk for developing EC through their pro-inflammatory and pro-tumorigenic activities. The presences of oral dysbiosis, microbial biofilm, and periodontitis in EC patients are found to be associated with invasive cancer phenotypes and poor prognosis. The mechanism of oral bacteria in EC progression is complex, which involves a combination of cytokines, chemokines, oncogenic signaling pathways, cell surface receptors, the degradation of extracellular matrix, and cell apoptosis. From a clinical perspective, good oral hygiene, professional oral care, and rational use of antibiotics bring positive impacts on oral microbial balance, thus helping individuals reduce the risk of EC, inhibiting postoperative complications among EC patients, and improving the efficiency of chemoradiotherapy. However, current oral hygiene practices mainly focus on the oral bacteria-based predictive and preventive purposes. It is still far from implementing microbiota-dependent regulation as a therapy for EC. Further explorations are needed to render oral microbiota a potential target for treating EC.
Keywords: Carcinogenesis; Chronic inflammation; Dysbiosis; Esophageal cancer; Oral hygiene; Oral microbiota,.
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.