Abstract

The objective of this study was to explore the molecular mechanisms of adhesion of endothelial cells (ECs) to implant grades of titanium alloy (Ti) and stainless steel (SS), compared to tissue culture polystyrene (PS). The idea is that promotion of EC adhesion to implant surfaces during the initial stages of healing may be critical in the formation of a capillary bed intimately associated with the implant surface. Ultimately this could be expected in turn to promote bone formation close to the surface and a more stable implant/bone interface. Surfaces were coated with either peak 1 fibrinogen gammaAgammaA, fibrinogen Fr I-9, fibrinogen fragment D1, fibronectin, vitronectin, or fetal calf serum and then post-coated with bovine serum albumin (BSA) to block non-specific cell adhesion. Surfaces with BSA alone and no other protein coating were also evaluated. Fibronectin coating maximized cell adhesion on all three surfaces, and adhesion was highest on PS. BSA blocked cell adhesion to PS (and most adhesion to SS) much better than to Ti. These results provide evidence that BSA adsorption on the metal surface is unable to effectively block the adhesion of the cells to the Ti. These data may provide a basis for understanding in vivo observations that soft tissue becomes attached to a Ti surface more rapidly and with more bone formation than to SS. Evidence is also presented that alphavbeta3 plays an important role in adhesion of ECs to the Ti surface. These experiments also provide preliminary data which may reflect some of the features of initial EC adhesion to metal implants.

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