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男性特发性骨质疏松症成骨细胞增殖减少和骨钙素表达降低。

Reduced proliferation and osteocalcin expression in osteoblasts of male idiopathic osteoporosis.

机构信息

Unitat de Recerca en Fisipatologia Ossia i Articular, Institut Municipal d'Investigació Mèdica, Hospital del Mar, Autonomous University of Barcelona, Dr. Aiguader 88, 08003 Barcelona, Spain.

出版信息

Calcif Tissue Int. 2010 Mar;86(3):220-6. doi: 10.1007/s00223-010-9336-5. Epub 2010 Jan 26.

DOI:10.1007/s00223-010-9336-5
PMID:20101397
Abstract

Osteoporosis is characterized by low bone mineral density (BMD), resulting in increasing susceptibility to bone fractures. In men, it has been related to some diseases and toxic habits, but in some instances the cause of the primary--or idiopathic--osteoporosis is not apparent. In a previous study, our group compared histomorphometric measurements in cortical and cancellous bones from male idiopathic osteoporosis (MIO) patients to those of control subjects and found reduced bone formation without major differences in bone resorption. To confirm these results, this study analyzed the etiology of this pathology, examining the osteoblast behavior in vitro. We compared two parameters of osteoblast activity in MIO patients and controls: osteoblastic proliferation and gene expression of COL1A1 and osteocalcin, in basal conditions and with vitamin D(3) added. All these experiments were performed from a first-passage osteoblastic culture, obtained from osteoblasts that had migrated from the transiliac explants to the plate. The results suggested that the MIO osteoblast has a slower proliferation rate and decreased expression of genes related to matrix formation, probably due to a lesser or slower response to some stimulus. We concluded that, contrary to female osteoporosis, in which loss of BMD is predominantly due to increased resorption, low BMD in MIO seems to be due to an osteoblastic defect.

摘要

骨质疏松症的特征是骨矿物质密度(BMD)低,导致骨折易感性增加。在男性中,它与某些疾病和有毒习惯有关,但在某些情况下,原发性(或特发性)骨质疏松症的原因并不明显。在之前的一项研究中,我们的研究小组比较了男性特发性骨质疏松症(MIO)患者和对照组的皮质和松质骨的组织形态计量学测量值,发现骨形成减少,而骨吸收没有明显差异。为了证实这些结果,本研究分析了这种病理学的病因,体外研究了成骨细胞的行为。我们比较了 MIO 患者和对照组中两个成骨细胞活性参数:成骨细胞增殖和 COL1A1 和骨钙素的基因表达,在基础条件下和添加维生素 D(3)的情况下。所有这些实验都是从第一通道成骨细胞培养物中进行的,该培养物是从髂骨外植体迁移到平板上的成骨细胞获得的。结果表明,MIO 成骨细胞的增殖率较慢,与基质形成相关的基因表达降低,可能是由于对某些刺激的反应较小或较慢。我们得出结论,与女性骨质疏松症不同,女性骨质疏松症中 BMD 的丧失主要是由于吸收增加所致,MIO 中的低 BMD 似乎是由于成骨细胞缺陷所致。

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