Candida albicans in the Oral Cavity: A Critical Review of Taxonomy, Virulence Factors, Host Interactions, Diagnosis, and Modern Therapeutic Strategies
Keywords:
Candida albicans, oral candidiasis, oral mycobiome, biofilm, candidalysin, IL-17, MALDI-TOF MS, antifungal resistance, photodynamic therapy, precision dentistryAbstract
Candida albicans is a prevalent member of the oral mycobiome and the principal cause of oral candidiasis, yet its detection does not by itself establish disease. This review critically integrates fungal taxonomy, oral ecology, virulence, mucosal immunology, diagnostic reasoning, antifungal therapy, and emerging interventions. A targeted structured update of PubMed-indexed and publisher-indexed literature was combined with a supplied bibliographic corpus; mechanistic studies, clinical cohorts, diagnostic evaluations, guidelines, and recent translational evidence were prioritized. The evidence supports a threshold model in which candidiasis emerges from convergence of fungal fitness, ecological disruption, and impaired host containment. Adhesins and morphogenetic circuits enable stable colonization and hyphal invasion; biofilm extracellular matrix and metabolic plasticity promote persistence; and the Ece1-derived toxin candidalysin links hyphal growth to epithelial injury and danger signaling. Protection is site-specific and depends on salivary function, epithelial pattern-recognition, neutrophils, and IL-17-dominant immunity, while bacterial–fungal interactions can either restrain or amplify pathogenicity. Diagnosis remains primarily clinicopathological: microscopy and culture are confirmatory, species identification is useful when treatment failure or epidemiological risk makes it consequential, and molecular or mass-spectrometric methods improve identification but cannot independently distinguish colonization from infection. Established treatment pairs correction of predisposing factors and oral reservoirs with topical or systemic antifungals selected according to severity, host status, prior azole exposure, species, and—when indicated—susceptibility testing. Biofilm tolerance, efflux, target alteration, and sterol-pathway remodeling complicate recurrent disease. Photodynamic therapy, probiotics, anti-biofilm materials, nanoparticles, vaccines, and host-directed or anti-candidalysin strategies are promising but unevenly mature. Future studies require standardized case definitions, lesion-targeted sampling, clinically anchored fungal-load thresholds, longitudinal multi-omics, and trials that measure recurrence and patient-reported outcomes rather than culture clearance alone.
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