Effects of transforming growth factor-beta 1 (TGF-β1) on in vitro mineralization of human osteoblasts on implant materials

被引:79
|
作者
Zhang, H
Ahmad, M
Gronowicz, G
机构
[1] Univ Connecticut, Ctr Hlth, Dept Orthopaed Surg, Farmington, CT 06030 USA
[2] Univ Connecticut, Ctr Hlth, Dept Prosthodon & Operat Dent, Farmington, CT 06030 USA
[3] Univ Minnesota, Dept Oral & Maxillofacial Radiol, Minneapolis, MN 55455 USA
关键词
implant; growth factor; osteoblast; mineralization;
D O I
10.1016/S0142-9612(02)00616-6
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
An in vitro cell-implant mineralization model system was used to study the effect of transforming growth factor-beta 1 (TGF-beta1) on mineralization in human osteoblast cultures. SaOs-2 and primary human osteoblast (HOB) cells were cultured on Tivanium (Ti-6Al-4V) disks. Administration of different concentrations of TGF-beta1 (0.02, 0.01, 0.2, 1.0, 2.0 ng/ml) to these cultures demonstrated a biphasic dose response with 0.2 ng/ml TGF-beta1 maximally increasing the calcium Content compared to control Culture. Results with SaOs-2 and HOB cultures were similar. An optimal dose of TGF-beta1 (0.2 ng/ml) was provided to the cultures either in one single dose or multiple doses. Continuous administration of 0.2 ng/ml TGF-beta1 caused 77% (SaOs-2) and 60% (HOB) increases in calcification compared to the control and 0.2ng/ml single dose groups. Single administration of the accumulative dose at 1.6ng/ml had no significant effect on the calcium content in either cell culture compared to control. Two weeks continuous administration of 0.2 ng/ml TGF-beta1 in both cell cultures resulted in significant increases in the expression of bone specific extracellular matrix proteins which included alkaline phosphatase, Type I collagen, and osteocalcin as measured by Northern blot analysis and RT-PCR. At 4 weeks, the mRNA level of Type I collagen was still significantly higher in the TGF-beta1 treatment group compared to control. In conclusion, TGF-beta1 enhances mineralization of HOB on implant materials. Published by Elsevier Science Ltd.
引用
收藏
页码:2013 / 2020
页数:8
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