Yoshikawa H, Takaoka K
Department of Orthopaedic Surgery, Osaka University Medical School.
Nihon Rinsho. 1994 Sep;52(9):2262-7.
Both cortical and trabecular bones continuously renew themselves to maintain their mechanical strength and bone volume. The sequence of cellular events at the site of bone remodeling is as follows: (1) Activation; osteoclast precursors are activated and differentiated. (2) Resorption; osteoclasts resorb a certain volume of bone by removing mineral and matrix. (3) Formation; osteoblasts differentiate and form new bone. The cellular coupling in space and time between osteoclastic resorption and osteoblastic formation is regulated not only by systemic hormones such as estrogen, PTH, calcitonin, or vitamin D, but also by local factors such as TGF-beta, BMP, IGF-I, IGF-II, prostaglandins, IL-1, IL-4, IL-6, or TNF-alpha. We explain here the mechanism of bone remodeling and review the various regulators for bone remodeling.
皮质骨和小梁骨都会持续自我更新,以维持其机械强度和骨量。骨重塑部位的细胞事件顺序如下:(1) 激活;破骨细胞前体被激活并分化。(2) 吸收;破骨细胞通过去除矿物质和基质来吸收一定体积的骨。(3) 形成;成骨细胞分化并形成新骨。破骨细胞吸收和成骨细胞形成在空间和时间上的细胞偶联不仅受雌激素、甲状旁腺激素、降钙素或维生素D等全身激素调节,还受转化生长因子-β、骨形态发生蛋白、胰岛素样生长因子-I、胰岛素样生长因子-II、前列腺素、白细胞介素-1、白细胞介素-4、白细胞介素-6或肿瘤坏死因子-α等局部因子调节。我们在此解释骨重塑的机制,并综述骨重塑的各种调节因子。