Role of Candida albicans in chronic inflammation and the development of oral squamous cell carcinoma

Abstract

Oral cancer pathogenesis is significantly influenced by Candida species, especially C. albicans, through chronic inflammation and cellular dysregulation. Epidemiological studies highlight a strong correlation between persistent Candida infections and oral carcinogenesis. Experimental evidence has identified key biomolecular mechanisms, including biofilm formation, epithelial invasion, and immune evasion. Chronic inflammation induced by Candida fosters a pro-tumorigenic environment characterized by oxidative stress, cytokine imbalance, and genomic instability. Animal models of Candida-induced oral lesions offer insights into premalignant conditions, and case series studies further support the association between fungal infections and oral cancer. This review critically examines the role of Candida, particularly C. albicans, in oral squamous cell carcinoma (OSCC) pathogenesis by analyzing epidemiological, experimental, and mechanistic data. We emphasize the importance of early detection and therapeutic strategies, including antifungal prophylaxis, to manage Candida colonization in cancer patients. A comprehensive literature search of studies published between 2015 and 2025 was conducted using Pub Med, Scopus, and Web of Science. Key findings were synthesized to understand the relationship between Candida infections and OSCC. The persistent Candida infections create a pro-tumorigenic microenvironment that accelerates dysplastic changes and malignant progression, particularly in high-risk individuals. While the direct causative relationship is complex, the combined effects of Candida, tobacco, alcohol use, and immunosuppression are significant in oral carcinogenesis. Early detection, antifungal treatments, and personalized therapies are essential to improving patient outcomes. A multidisciplinary approach involving oncologists, microbiologists, and immunologists is crucial for developing integrated strategies to manage both Candida infections and cancer. Future research should focus on dual-action therapies targeting both Candida-induced inflammation and tumor progression.