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首页> 外文期刊>European Cells & Materials >The effect of bisphosphonate treatment on the biochemical and cellular events during bone remodelling in response to microinjury stimulation
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The effect of bisphosphonate treatment on the biochemical and cellular events during bone remodelling in response to microinjury stimulation

机译：双膦酸盐治疗对微损伤刺激引起的骨重塑过程中生化和细胞事件的影响

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Osteoporosis is one of the most prevalent bone diseases worldwide and is characterised by high levels of bone turnover, a marked loss in bone mass and accumulation of microdamage, which leads to an increased fracture incidence that places a huge burden on global health care systems. Bisphosphonates have been used to treat osteoporosis and have shown great success in conserving bone mass and reducing fracture incidence. In spite of the existing knowledge of the in vivo responses of bone to bisphosphonates, the cellular responses to these drugs have yet to be fully elucidated. In vitro model systems that allow the decoupling of complex highly integrated events, such as bone remodelling, provide a tool whereby these biological processes may be studied in a more simplified context. This study firstly utilised an in vitro model system of bone remodelling and comprising all three major cell types of the bone (osteocytes, osteoclasts and osteoblasts), which was representative of the bone’s capacity to sense microdamage and subsequently initiate a basic multicellular unit response. Secondly, this system was used to study the effect of two commonly utilised aminobisphosphonate treatments for osteoporosis, alendronate and zoledronate. We demonstrated that microinjury to osteocyte networks being treated with bisphosphonates modulates receptor activator of nuclear factor kappa-B ligand and osteoprotegerin activity, and subsequently osteoclastogenesis. Furthermore, bisphosphonates increased the osteogenic potential following microinjury. Thus, we have shown for the first time that bisphosphonates act at all three stages of bone remodelling, from microinjury to osteoclastogenesis and ultimately osteogenesis.
机译：骨质疏松症是世界上最流行的骨病之一，其特征是高水平的骨转换，骨量明显减少和微损伤的积累，这导致骨折发生率增加，给全球卫生保健系统带来沉重负担。双膦酸盐已用于治疗骨质疏松症，并且在保存骨量和减少骨折发生率方面显示出巨大的成功。尽管已有关于骨骼对双膦酸盐的体内反应的现有知识，但尚未完全阐明对这些药物的细胞反应。允许去耦复杂的高度整合事件（例如骨骼重塑）的体外模型系统提供了一种工具，可以在更简化的背景下研究这些生物学过程。这项研究首先利用了骨骼重塑的体外模型系统，该系统包含骨骼的所有三种主要细胞类型（成骨细胞，破骨细胞和成骨细胞），这代表了骨骼感知微损伤并随后引发基本的多细胞单位反应的能力。其次，该系统用于研究两种常用的氨基双膦酸盐治疗骨质疏松的效果，阿仑膦酸盐和唑来膦酸盐。我们证明了用双膦酸盐治疗的对骨细胞网络的微损伤可调节核因子κB配体的受体激活剂和骨保护素的活性，进而破坏破骨细胞。此外，双膦酸盐增加了微损伤后的成骨潜能。因此，我们首次证明了双膦酸酯在骨骼重塑的所有三个阶段都起作用，从微损伤到破骨细胞形成，最终到成骨。

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