Martin T, Gooi Jonathan H, Sims Natalie A
St. Vincent's Institute of Medical Research and University of Melbourne Department of Medicine, Fitzroy, 3065, Victoria, Australia.
Crit Rev Eukaryot Gene Expr. 2009;19(1):73-88. doi: 10.1615/critreveukargeneexpr.v19.i1.40.
Bone remodeling is the process of removal and replacement of bone, taking place at many sites throughout the skeleton and regulated mainly by locally generated factors. Its purposes are to repair damaged bone, remove old bone, and facilitate skeletal responses to changes in loading requirements. Cells of the osteoblast lineage control the formation and activity of osteoclasts, which are responsible for initiation and execution of resorption at remodeling sites. The bone resorbed by osteoclasts is replaced through the differentiation and activity of osteoblasts. The consequent formation must match closely the amount of bone that is resorbed at each site. This coupling of the two processes is essential for bone balance. Both resorption products and osteoclast-derived factors contribute to the coupling of bone formation to resorption in bone remodeling. This review considers the molecular mechanisms and intercellular communication processes involved in remodeling and coupling.
骨重塑是骨骼去除和替换的过程,发生在整个骨骼的多个部位,主要受局部产生的因子调节。其目的是修复受损骨骼、去除旧骨,并促进骨骼对负荷需求变化的反应。成骨细胞谱系的细胞控制破骨细胞的形成和活性,破骨细胞负责在重塑部位启动和执行吸收过程。破骨细胞吸收的骨通过成骨细胞的分化和活性得以替换。随后的形成必须与每个部位吸收的骨量紧密匹配。这两个过程的耦合对于骨平衡至关重要。吸收产物和破骨细胞衍生因子都有助于骨重塑中骨形成与吸收的耦合。本综述探讨了参与重塑和耦合的分子机制及细胞间通讯过程。