Influence of prosthetic surface roughness on biofilm density and prosthesis longevity.

چکیده اصلی

Dental prosthesis failure is often associated with biofilm-mediated infections, yet the combined roles of surface roughness and material chemistry remain underexplored. This observational, retrospective study investigated associations between these factors and biofilm density, pathogen selection, and prosthesis longevity. Surface roughness (Ra) and microbial colonization were analyzed for 85 explanted prostheses (fixed, removable, implant-supported, and orthodontic) and compared to control samples (polished enamel, sealants). Biofilm formation was quantified via optical density (OD) and colony-forming units (CFU/cm2), while pathogen profiles were identified using selective culture and biochemical assays. A strong positive correlation (R2 = 0.84, interpreted as a very strong correlation according to Evans' (1996) classification) was observed between surface roughness and biofilm accumulation. Smooth surfaces like zirconia (Ra ∼320 nm) exhibited low biofilm (OD 0.45), whereas rougher surfaces, particularly removable PMMA dentures (Ra ∼1100 nm), showed dense biofilms (OD up to 1.85) dominated by Candida spp. and Pseudomonas aeruginosa. Material chemistry was associated with distinct pathogen profiles: PMMA favored fungal and Gram-negative adhesion, while titanium promoted staphylococcal colonization. In this cohort, biofilm-associated infections were associated with reduced functional longevity; for example, implant crowns designed for 15+ years were removed after a mean of 5.4 years due to peri-implantitis. The study concludes that prosthetic failure is associated with the synergistic effect of surface topography, which correlates with biofilm quantity, and material composition, which is associated with distinct microbial ecology. These findings underscore the need for prostheses engineered with optimized surface smoothness and antimicrobial material chemistry. However, the observational, retrospective design limits causal inference; the culture-based methodology likely underestimates the full microbial diversity, particularly of anaerobic species; and the heterogeneity of device types limits direct comparability between groups.

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