Bisphosphonates inhibit surface-mediated osteogenesis.

Bisphosphonates inhibit surface-mediated osteogenesis.
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DOI:
10.1002/jbm.a.36944
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发表时间:
2020-08-01
期刊:
Journal of biomedical materials research. Part A
影响因子:
--
通讯作者:
Schwartz Z
Schwartz Z
中科院分区:
其他
文献类型:
--
作者:
Lotz EM;Lohmann CH;Boyan BD;Schwartz Z

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Bisphosphonates target osteoclasts, slowing bone resorption thus providing rationale to support osseointegration. However, bisphosphonates may negatively affect osteoblasts, impairing peri-implant bone formation. The goal of this study was to assess the effects bisphosphonates have on surface mediated osteogenesis of osteoblasts. MG63 cells were cultured on 15mm grade 2 titanium disks: smooth PT, hydrophobic-microrough SLA, or hydrophilic-microrough mSLA (Institut Straumann AG, Basel, Switzerland). Tissue culture polystyrene (TCPS) was used as a control. At confluence, cells were treated with 0M, 10−8M, 10−7M, and 10−6M of alendronate, zoledronate, or ibandronate for 24h. Sprague Dawley rats were also treated with 1μg/kg/day ibandronate or phosphate buffered saline control for 5wk. Calvarial osteoblasts (rOBs) were isolated, characterized, and cultured on surfaces. Osteogenic markers in the media were quantified using ELISAs. Bisphosphonate treatment reduced osteocalcin, osteoprotegerin, osteopontin, BMP2, PGE2, TGFβ1, IL10, and VEGF in MG63 cells. The effect was more robust on rough surfaces, and higher concentrations of bisphosphonates stunted production to TCPS/PT levels. Ibandronate conditioned rOBs produced less osteogenic markers similar to direct bisphosphonate treatment. These results suggest bisphosphonate exposure jeopardizes the pro-osteogenic response osteoblasts have to microstructured surfaces. Their effects persist in vivo and negatively condition osteoblast response in vitro. Clinically, bisphosphonates could compromise osseointegration.
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