Institute of Musculoskeletal Medicine, University Hospital Muenster, Germany.
Institute of Inflammation and Ageing, University of Birmingham, United Kingdom.
Swiss Med Wkly. 2020 Feb 7;150:w20187. doi: 10.4414/smw.2020.20187. eCollection 2020 Jan 27.
Although the impact of osteoblast-osteoclast crosstalk in bone remodelling has been intensively studied, the importance of osteocytes, descendants of osteoblasts, in this process has for a long time been neglected. During their embedding phase, osteocytes undergo considerable phenotypic transformation, from a cuboidal, highly metabolically active osteoblast secreting extracellular matrix to a small, stellate, quiescent osteocyte with numerous long dendrites. Osteocytes are encysted in cavities (lacunae) and their dendritic extensions are located in tunnels (canaliculi) forming a remarkable, highly branched, lacunar-canalicular signalling network that spans the entire bone matrix. Osteocytes and their dendrites can communicate directly with each other and through the release of effector proteins such as sclerostin and nuclear factor κB ligand (RANKL), influence osteoblast and osteoclast formation. This allows osteocytes embedded within the bone matrix to communicate and coordinate activity of cells on the bone surface to adapt to mechanical needs and hormonal changes. Besides their importance in sustaining physiological bone homeostasis, accumulating evidence suggests that dysregulated osteocyte function and alterations in the osteocyte lacunar-canalicular network structure are characteristics of skeletal diseases. This review highlights some aspects of osteocyte communication with osteoclasts and mesenchymal stromal cells, the importance of blood vessel-osteocyte interaction and describes central functions of these cells in rheumatoid arthritis, osteoarthritis, osteomyelitis and osteoporosis. Within the last decade new technologies and tools have facilitated the study of osteocyte biology and the search for therapeutic targets to address bone fragility in the near future.
虽然破骨细胞与成骨细胞的相互作用在骨重建中受到了深入研究，但成骨细胞的后代——骨细胞在这一过程中的重要性长期以来一直被忽视。在其嵌入阶段，骨细胞经历了相当大的表型转变，从分泌细胞外基质的立方体形、高代谢活性的成骨细胞转变为具有许多长树突的小、星状、静止的骨细胞。骨细胞被包裹在腔（陷窝）中，其树突延伸位于隧道（小管）中，形成一个显著的、高度分支的陷窝小管信号网络，跨越整个骨基质。骨细胞及其树突可以直接相互交流，并通过释放效应蛋白（如硬化蛋白和核因子 κB 配体（RANKL））来影响成骨细胞和破骨细胞的形成。这使得嵌入骨基质中的骨细胞能够与骨表面的细胞进行通讯和协调活动，以适应机械需求和激素变化。除了在维持生理骨稳态方面的重要性外，越来越多的证据表明，骨细胞功能失调和骨细胞陷窝小管网络结构的改变是骨骼疾病的特征。这篇综述强调了骨细胞与破骨细胞和间充质基质细胞的通讯的一些方面，描述了血管与骨细胞相互作用的重要性，并描述了这些细胞在类风湿关节炎、骨关节炎、骨髓炎和骨质疏松症中的核心功能。在过去的十年中，新技术和工具促进了骨细胞生物学的研究，并为寻找治疗靶点以解决骨脆弱性提供了帮助。
