Effect of compressive force on human osteoblast-like cells and bone remodelling: An in vitro study

被引:56
作者
Tripuwabhrut, Polbhat [1 ]
Mustafa, Manal [1 ]
Gjerde, Cecilie G. [2 ]
Brudvik, Pongsri [2 ]
Mustafa, Kamal [1 ]
机构
[1] Univ Bergen, Fac Med & Dent, Dept Clin Dent, Ctr Clin Dent Res, N-5020 Bergen, Norway
[2] Univ Bergen, Fac Med & Dent, Dept Clin Dent, N-5020 Bergen, Norway
关键词
Osteoblasts; Mechanical stress; Bone remodelling; In vitro; Alveolar bone; PROSTAGLANDIN E-2 PRODUCTION; ORTHODONTIC TOOTH MOVEMENT; KAPPA-B LIGAND; ALKALINE-PHOSPHATASE; OSTEOCLAST DIFFERENTIATION; RECEPTOR ACTIVATOR; MECHANICAL-STRESS; EXPRESSION; OSTEOPROTEGERIN; MINERALIZATION;
D O I
10.1016/j.archoralbio.2013.01.004
中图分类号
R78 [口腔科学];
学科分类号
100302 [口腔临床医学];
摘要
Objective: The aim of this study was to determine the effect of continuous compressive force (CF) on expression by human alveolar bone-derived osteoblasts (HOBs) of some specific molecules involved in bone remodelling. Design: HOBs were cultured with or without CF (control, 2.0, 4.0 g cm(-2)) for 1, 3 and 7 days. Expression of alkaline phosphatase (ALP), type I collagen (Coil), osteopontin (OPN), osteocalcin (OCN), transcription factor Runx2, receptor activator of nuclear factor kappa B ligand (RANKL), osteoprotegerin (OPG) and prostaglandin E2 (PGE(2)) was analysed by real-time-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA) and/or immunostaining. Results: The results revealed that CF upregulated ALP and Coil expression at both messenger RNA (mRNA) and protein levels but did not affect expression of OPN and OCN mRNA. Runx2 mRNA was inhibited by CF, which also altered the expression of molecules involved in osteoclastogenesis, by enhancing RANKL expression and suppressing OPG expression. At 4.0 g cm(-2) of CF, the expression of RANKL and PGE(2) was significantly upregulated. Conclusion: The results suggest that initial application of CF on HOBs can simultaneously affect expression of markers related to both osteogenesis and osteoclastogenesis. (C) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码:826 / 836
页数:11
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