Abstract / Summary
Colonisation of maxillofacial prostheses by Candida albicans is conventionally attributed to surface roughness, porosity, and wettability properties that explain where cells accumulate rather than why particular surfaces promote biofilm formation. This review reinterprets the in vitro literature on C. albicans adhesion to maxillofacial silicone elastomers through the underlying molecular events. Nine eligible studies identified through searches of PubMed, Scopus, and ScienceDirect conducted on 31 March 2026 were appraised with the QUIN tool and mapped onto a six-stage molecular cascade: surface conditioning, reversible attachment, adhesin engagement, morphogenesis, matrix assembly, and antifungal tolerance. Three conclusions emerged. First, C. albicans senses topography through mechanically gated calcium channels and converts mechanical contact into hyphal commitment; roughness is therefore a morphogenetic cue that surface finishing can withhold. Second, the tested agents—silver nanoparticles, chitosan, thymol, and carvacrol, and a Lactobacillus brevis-derived biosurfactant—engage distinct molecular targets and are not mechanistically interchangeable. Third, most included studies evaluated silicone without salivary conditioning, whereas the clinical interface is an acquired salivary pellicle that supplies both adhesion receptors and antimicrobial peptides. All studies fell within the medium risk-of-bias band (50.0–62.5%). Pellicle-conditioned models and molecular readouts are required. The mechanistic interpretations discussed in this review are derived from the broader C. albicans literature and have not been directly demonstrated on maxillofacial silicone elastomers.