Titanium surfaces influence behaviour and gene expression of soft tissue-cells

Objectives:

The aim of this study was to investigate the influence of surface wettability and surface topography of Ti implant surfaces on the behaviour and activation/differentiation of epithelial cells and primary human gingival fibroblasts (HGF).

Methods:

Hydrophobic acid-etched (A) and coarse-grit-blasted, acid-etched (SLA) surfaces and hydrophilic acid-etched (modA) and modSLA surfaces were produced. The behaviour of an oral squamous cell carcinoma cell line (HSC-2) and HGF grown on all surfaces was compared through determination of cell attachment and proliferation, time-lapse microscopy of fluorescence labeled cells and determination of gene expression by real time polymerase chain reaction.

Results:

All investigated Ti surfaces showed less initial cell attachment and cell proliferation than the controls. During the first 24h proliferation of HSC-2 was highest on plastic controls (p<0.01; ANOVA, Tukeyxs HSD test), followed by modSLA, SLA, modA and A surfaces.

After one day of incubation cell spreading and cell movements observed by time-lapse microscopy were most pronounced for A and modA surfaces compared to SLA and modSLA surfaces.

Cell proliferation of HGF was higher on smoother surfaces (A and modA) and lower on rougher surfaces (SLA and modSLA) at all tested time points, being lowest on modSLA.

The relative gene expressions of cytokeratin14, integrin alpha6, integrin beta4, vinculin, transforming growth factor (TFG)-beta, TGF-beta1 and TGF-beta3 were decreased in HSC-2 on all four types of Ti surfaces compared to control surfaces (p<0.01; ANOVA, Tukeyxs HSD-test). There was no significant difference of gene expression on the four different implant surfaces with the exception of, TGF-beta, which was higher on modSLA surface than on SLA surface (p<0.05; ANOVA, Tukeyxs HSD-test).

Conclusion:

We have demonstrated that all tested titanium surfaces downregulate cell attachment, cell proliferation, expression of adhesion promoters and cytokines involved in wound healing in HSC-2 cells and cell proliferation in HGF.

Supported by ITI-Grant-423/2005