Modified titanium surfaces promote accelerated osteogenic differentiation of mesenchymal stromal cells in vitro

被引:236
|
作者
Wall, Ivan [1 ]
Donos, Nikos [2 ]
Carlqvist, Karin [1 ]
Jones, Francis [1 ]
Brett, Peter [1 ]
机构
[1] UCL Eastman Dent Inst, Div Biomat & Tissue Engn, London WC1X 8LD, England
[2] UCL Eastman Dent Inst, Dept Periodontol, London WC1X 8LD, England
关键词
Gene arrays; Osseointegration; Mesenchymal stromal cells; Adult stem cells; Titanium implant surfaces; STEM-CELLS; DENTAL IMPLANTS; HUMAN BONE; MARROW; OSTEOBLASTS; ATTACHMENT; ENERGY; HYDROPHILICITY; PROLIFERATION; INTEGRATION;
D O I
10.1016/j.bone.2009.03.662
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Titanium (Ti) is the material of choice for dental and orthopaedic implants due to its highly biocompatible nature. Modification of the implant Surface, either topographically (as roughness) or chemically, call promote accelerated osteogenesis ill vivo and greatly increase bone-implant contact and bonding strength. In this paper, we Sought to characterise the cellular and molecular responses Of human bone marrow-derived mesenchymal stromal cells (hMSCs) to two modified Ti surfaces: a rough hydrophobic surface that was sand-blasted and acid-etched (SLA) and an SLA Surface of the same toughness that was chemically modified to have high wettability/hydrophilicity (SLActive). A smooth polished (SMO) Ti Surface was used as a control. Whilst no differences in initial cell attachment to any of the surfaces were observed, we found that hMSCs cultured oil the rough surfaces underwent a decrease in cell number early ill Culture. yet simultaneously expressed higher levels of the osteogenic markers SPP1, RUNX2 and BSP. Furthermore, deposits of calcified matrix were observed at earlier time points on both SLA and SLActive surfaces Compared to SMO and this correlated with increased expression of the osteogenic promoter WNT5A in response to the rough Surfaces. Osteogenic responses to SLActive were moderately better than the hydrophobic SLA surface and gene expression studies indicate that WNT5A activation may be responsible for this increased osteogenic differentiation. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:17 / 26
页数:10
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