Biological and physicochemical implications of the aging process on titanium and zirconia implant material surfaces

Abstract

Statement of problemChanges in physicochemical properties because of implant material aging and natural deterioration in the oral environment can facilitate microbial colonization and disturb the soft-tissue seal between the implant surfaces. PurposeThe purpose of this in vitro study was to investigate the effect of aging time on the physicochemical profile of titanium (Ti) and zirconia (ZrO2) implant materials. Further microbiology and cell analyses were used to provide insights into the physicochemical implications of biological behavior. Material and methodsDisk-shaped specimens of Ti and ZrO2 were submitted to roughness, morphology, and surface free energy (SFE) analyses before nonaging (NA) and after the aging process (A). To simulate natural aging, disks were subjected to low-temperature degradation (LTD) by using an autoclave at 134 ºC and 0.2 MPa pressure for 20 hours. The biological activities of the Ti and ZrO2 surfaces were determined by analyzing Candida albicans (C. albicans) biofilms and human gingival fibroblast (HGF) cell proliferation. For the microbiology assays, a variance analysis method (ANOVA) was used with the Tukey post hoc test. For the evaluation of cellular proliferation, the Kruskal-Wallis test followed by Dunn multiple comparisons were used. ResultsTi nonaging (TNA) and ZrO2 nonaging (ZNA) disks displayed hydrophilic and lipophilic properties, and this effect was sustained after the aging process. Low-temperature degradation resulted in a modest change in intermolecular interaction, with 1.06-fold for TA and 1.10-fold for ZA. No difference in biofilm formation was observed between NA and A disks of the same material. After 48 hours, the viability of the attached HGF cells was very similar to that in the NA and A groups, regardless of the tested material. ConclusionThe changes in the physicochemical properties of Ti and ZrO2 induced by the aging process do not interfere with C. albicans biofilm formation and HGF cell attachment, even after long-term exposure.