Alam A S, Huang C L, Blake D R, Zaidi M
Department of Cellular and Molecular Sciences, St. George's Hospital Medical School, London, U.K.
Biosci Rep. 1992 Oct;12(5):369-80. doi: 10.1007/BF01121500.
Several important conclusions have recently emerged from in vitro studies on the resorptive cell of bone, the osteoclast. First, it has been established that osteoclast function is modulated locally, by changes in the local concentration of Ca2+ caused by hydroxyapatite dissolution. It is thought that activation by Ca2+ of a surface membrane Ca2+ receptor mediates these effects, hence providing a feedback control. Second, a number of molecules produced locally by the endothelial cell, with which the osteoclast is in intimate contact, have been found to affect bone resorption profoundly. For instance, the autocoid nitric oxide strongly inhibits bone resorption. Finally, reactive oxygen species have been found to aid bone resorption and enhance osteoclastic activity directly. Here, we will attempt to integrate these control mechanisms into a unified hypothesis for the local control of bone resorption.
最近，对骨吸收细胞破骨细胞的体外研究得出了几个重要结论。首先，已经确定破骨细胞功能受到局部调节，这种调节是由羟基磷灰石溶解导致的局部Ca2+浓度变化引起的。据认为，Ca2+对表面膜Ca2+受体的激活介导了这些效应，从而提供了一种反馈控制。其次，已发现与破骨细胞密切接触的内皮细胞局部产生的一些分子会深刻影响骨吸收。例如，自分泌物质一氧化氮强烈抑制骨吸收。最后，已发现活性氧有助于骨吸收并直接增强破骨细胞活性。在此，我们将尝试把这些控制机制整合为一个关于骨吸收局部控制的统一假说。
