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Intramembranous ossification and endochondral ossification are impaired differently between glucocorticoid-induced osteoporosis and estrogen deficiency-induced osteoporosis

机译:糖皮质激素诱导的骨质疏松症和雌激素缺乏症引起的骨质疏松症的膜内骨化和软骨内骨化受到不同的损害

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摘要

A fracture is the most dangerous complication of osteoporosis in patients because the associated disability and mortality rates are high. Osteoporosis impairs fracture healing and prognosis, but how intramembranous ossification (IO) or endochondral ossification (EO) during fracture healing are affected and whether these two kinds of ossification are different between glucocorticoid-induced osteoporosis (GIOP) and estrogen deficiency-induced osteoporosis (EDOP) are poorly understood. In this study, we established two bone repair models that exhibited repair via IO or EO and compared the pathological progress of each under GIOP and EDOP. In the cortical drill-hole model, which is repaired through IO, osteogenic differentiation was more seriously impaired in EDOP at the early stage than in GIOP. In the periosteum scratch model, in which EO is replicated, chondrocyte hypertrophy progression was delayed in both GIOP and EDOP. The in vitro results were consistent with the in vivo results. Our study is the first to establish bone repair models in which IO and EO occur separately, and the results strongly describe the differences in bone repair between GIOP and EDOP.
机译:骨折是患者骨质疏松症最危险的并发症,因为相关的残疾和死亡率很高。骨质疏松症损害骨折的愈合和预后,但是在骨折愈合过程中膜内骨化(IO)或软骨内骨化(EO)受到怎样的影响,糖皮质激素诱导的骨质疏松症(GIOP)和雌激素缺乏症引起的骨质疏松症(EDOP)这两种骨化是否有所不同)了解甚少。在这项研究中,我们建立了两种通过IO或EO表现出修复作用的骨修复模型,并比较了GIOP和EDOP下每种骨的病理进展。在通过IO修复的皮质钻孔模型中,与GIOP相比,EDOP早期对成骨分化的损害更为严重。在复制EO的骨膜刮擦模型中,GIOP和EDOP均延缓了软骨细胞肥大进程。体外结果与体内结果一致。我们的研究是第一个建立IO和EO分别发生的骨修复模型的,结果强烈描述了GIOP和EDOP之间的骨修复差异。

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