Candida albicans is a dimorphic fungus that normally colonizes the oral cavity as a commensal yeast form. Under conditions of immune suppression or microbial dysbiosis, Candida undergoes a morphogenetic switch from yeast to hyphal form, which is critical for tissue invasion. The hyphal form produces invasive filaments that penetrate the epithelial barrier, triggering mucosal inflammation and the characteristic white pseudomembranous plaques. Mucosal immune defense against Candida depends heavily on the T-helper 17 (Th17) cell axis. Th17 cells produce interleukin-17 (IL-17) and IL-22, which recruit neutrophils to the oral mucosa and stimulate epithelial cells to produce antimicrobial peptides such as β-defensins and histatins. When Th17 immunity is compromised - as in HIV/AIDS, chemotherapy-induced lymphopenia, or chronic corticosteroid use - the IL-17 signaling pathway is disrupted, allowing Candida to proliferate unchecked and transition to its invasive hyphal form. Biofilm formation is another key virulence mechanism. Candida adheres to mucosal surfaces and denture materials, forming structured biofilms that are resistant to host immune clearance and antifungal penetration. Biofilm-associated Candida can be up to 1000 times more resistant to fluconazole than planktonic cells. This...