Current research on surface modifications has yielded advanced implant biomaterials. Various implant surface modifications have been shown to be promising in improving bone target cell response, but more comprehensive studies whether certain implant surface modifications can directly target cell behavioural features such as morphogenesis and proliferation are needed. Here, we studied the response of primary alveolar bone cells on various implant surface modifications in terms of osteoblast morphology and proliferation in vitro. Analyses of surface modifications led to surface-related test parameters including the topographical parameters micro-roughness, texture aspect and surface enlargement as well as the physicochemical parameter surface wettability. We compared osteoblast morphology and proliferation towards the above-mentioned parameters and found that texture aspect and surface enlargement but not surface roughness or wettability exhibited significant impact on osteoblast morphology and proliferation. Detailed analysis revealed osteoblast proliferation as a function of cell morphology, substantiated by an osteoblast size- and morphology-dependent increase in mitotic activity. These findings show that implant surface topography controls cell behavioural morphology and subsequently cell proliferation, thereby opening the road for cell instructive biomaterials.

Though recent studies report decisive positive effects on cells, elicited by ultraviolet (UV)-induced bioactivation of biomaterial implant surfaces, they frequently employ cells other than of human origin or cells not representing oral implant targets. Therefore, the present study aims at exploring distinct cell functions of primary human alveolar bone osteoblasts (PHABO) in response to bioactivated microstructured titanium and zirconia implant surfaces with matched controls. UV-treatment significantly reduced surface carbon, while concomitantly increasing wettability. In case of titanium or zirconia biomaterial source of equal roughness, bioactivation did not significantly improve cell functions, including initial cell attachment, morphogenesis, proliferation, and gene expression of osteogenic biomarkers osteocalcin, alkaline phosphatase and collagen type I. However, cell functions discriminated surface roughness by either comparing titanium and zirconia or interindividual zirconia surfaces. While rough surfaces primarily favored primary adhesion, proliferation appeared improved on smooth surfaces, and gene expression seemed to be stronger modulated on the smoothest biomaterial. Our results show for the first time that bioactivation appears to be not the main causative for the observed modulation of the distinct cell functions analyzed in PHABO, but add to the body of evidence that they were more governed by surface architecture rather than by bioactivation.