Candida albicans is a predominant fungal commensal of the oral cavity that normally maintains a balanced relationship with the host without causing tissue damage. However, alterations in local and systemic host conditions can disrupt this equilibrium, enabling C. albicans to transition from a commensal organism to an opportunistic pathogen and cause oral candidiasis. This review aims to provide a comprehensive overview of the major virulence mechanisms that facilitate this commensal-to-pathogen transition, with particular emphasis on adhesion, morphological switching, biofilm formation, epithelial invasion, and host tissue damage. Initial adherence to oral epithelial surfaces is mediated by fungal adhesins, particularly the agglutinin-like sequence proteins and hyphal wall protein 1. Subsequent yeast-to-hyphal transition enhances adhesion, biofilm development, and tissue invasion through highly regulated polarized hyphal growth. Biofilm formation further promotes fungal persistence and resistance to antifungal agents and host immune responses. Epithelial invasion occurs through induced endocytosis and active penetration and is facilitated by fungal invasins and secreted hydrolytic enzymes, particularly secreted aspartyl proteinases. Understanding the coordinated interplay of these virulence mechanisms provides insight into the pathogenesis of oral candidiasis.