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骨质疏松症的细胞与分子机制

Cellular and molecular mechanisms of osteoporosis.

作者信息

Manolagas S C

机构信息

Division of Endocrinology and Metabolism, University of Arkansas for Medical Sciences, Little Rock 72205-7199, USA.

出版信息

Aging (Milano). 1998 Jun;10(3):182-90. doi: 10.1007/BF03339652.

DOI:10.1007/BF03339652
PMID:9801728
Abstract

Osteoblasts and osteoclasts are derived from progenitors originating in the bone marrow, and the process of bone remodeling is controlled by growth factors and cytokines which regulate the birth and death of these cells. An overproduction of osteoclasts relative to the need for remodeling, and an undersupply of osteoblasts relative to the need for cavity repair, represent the fundamental pathophysiologic changes in postmenopausal and age-related osteopenia, respectively. As in these two forms of the disease, the osteoporosis induced by glucocorticoid excess is also caused by changes in the birth and death of bone cells, and in particular a decrease in osteoblastogenesis in the bone marrow, and an increased rate of osteoblast and osteocyte apoptosis.

摘要

成骨细胞和破骨细胞起源于骨髓中的祖细胞,骨重塑过程由生长因子和细胞因子控制,这些因子调节这些细胞的生成与凋亡。相对于重塑需求而言破骨细胞产生过多,以及相对于腔隙修复需求而言成骨细胞供应不足,分别代表绝经后骨质疏松症和年龄相关性骨质减少的基本病理生理变化。与这两种疾病形式一样,糖皮质激素过多所致的骨质疏松症也是由骨细胞生成与凋亡的变化引起的,尤其是骨髓中成骨细胞生成减少,以及成骨细胞和骨细胞凋亡率增加。

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