Kenkre J S, Bassett Jhd
1 Section of Investigative Medicine, Imperial College London, London, UK.
2 Molecular Endocrinology Laboratory, Department of Medicine, Imperial College London, London, UK.
Ann Clin Biochem. 2018 May;55(3):308-327. doi: 10.1177/0004563218759371. Epub 2018 Mar 4.
The bone remodelling cycle replaces old and damaged bone and is a highly regulated, lifelong process essential for preserving bone integrity and maintaining mineral homeostasis. During the bone remodelling cycle, osteoclastic resorption is tightly coupled to osteoblastic bone formation. The remodelling cycle occurs within the basic multicellular unit and comprises five co-ordinated steps; activation, resorption, reversal, formation and termination. These steps occur simultaneously but asynchronously at multiple different locations within the skeleton. Study of rare human bone disease and animal models have helped to elucidate the cellular and molecular mechanisms that regulate the bone remodelling cycle. The key signalling pathways controlling osteoclastic bone resorption and osteoblastic bone formation are receptor activator of nuclear factor-κB (RANK)/RANK ligand/osteoprotegerin and canonical Wnt signalling. Cytokines, growth factors and prostaglandins act as paracrine regulators of the cycle, whereas endocrine regulators include parathyroid hormone, vitamin D, calcitonin, growth hormone, glucocorticoids, sex hormones, and thyroid hormone. Disruption of the bone remodelling cycle and any resulting imbalance between bone resorption and formation leads to metabolic bone disease, most commonly osteoporosis. The advances in understanding the cellular and molecular mechanisms underlying bone remodelling have also provided targets for pharmacological interventions which include antiresorptive and anabolic therapies. This review will describe the remodelling process and its regulation, discuss osteoporosis and summarize the commonest pharmacological interventions used in its management.
骨重塑周期可替换陈旧和受损的骨骼,是一个高度受调控的终身过程,对于维持骨骼完整性和矿物质稳态至关重要。在骨重塑周期中,破骨细胞吸收与成骨细胞骨形成紧密耦合。重塑周期发生在基本多细胞单元内,包括五个协调步骤:激活、吸收、逆转、形成和终止。这些步骤在骨骼内的多个不同位置同时但异步发生。对罕见人类骨病和动物模型的研究有助于阐明调节骨重塑周期的细胞和分子机制。控制破骨细胞骨吸收和成骨细胞骨形成的关键信号通路是核因子κB受体激活剂(RANK)/RANK配体/骨保护素和经典Wnt信号通路。细胞因子、生长因子和前列腺素作为该周期的旁分泌调节因子,而内分泌调节因子包括甲状旁腺激素、维生素D、降钙素、生长激素、糖皮质激素、性激素和甲状腺激素。骨重塑周期的破坏以及由此导致的骨吸收与形成之间的任何失衡都会导致代谢性骨病,最常见的是骨质疏松症。对骨重塑潜在细胞和分子机制理解的进展也为药物干预提供了靶点,包括抗吸收和促合成疗法。本综述将描述重塑过程及其调控,讨论骨质疏松症,并总结其治疗中最常用的药物干预措施。