Bone Cell Biology and Disease Unit, St. Vincent's Institute of Medical Research, Melbourne, Victoria 3065, Australia; email:
Department of Medicine, The University of Melbourne, St. Vincent's Hospital, Melbourne, Victoria 3065, Australia.
Annu Rev Physiol. 2020 Feb 10;82:507-529. doi: 10.1146/annurev-physiol-021119-034425. Epub 2019 Sep 25.
Bone remodeling is essential for the repair and replacement of damaged and old bone. The major principle underlying this process is that osteoclast-mediated resorption of a quantum of bone is followed by osteoblast precursor recruitment; these cells differentiate to matrix-producing osteoblasts, which form new bone to replace what was resorbed. Evidence from osteopetrotic syndromes indicate that osteoclasts not only resorb bone, but also provide signals to promote bone formation. Osteoclasts act upon osteoblast lineage cells throughout their differentiation by facilitating growth factor release from resorbed matrix, producing secreted proteins and microvesicles, and expressing membrane-bound factors. These multiple mechanisms mediate the coupling of bone formation to resorption in remodeling. Additional interactions of osteoclasts with osteoblast lineage cells, including interactions with canopy and reversal cells, are required to achieve coordination between bone formation and resorption during bone remodeling.
骨重建对于受损和老化骨骼的修复和替换至关重要。该过程的主要原则是，破骨细胞介导的骨吸收伴随着成骨细胞前体细胞的募集；这些细胞分化为产生基质的成骨细胞，形成新的骨骼来替代被吸收的部分。来自骨质增生综合征的证据表明，破骨细胞不仅吸收骨，还提供信号来促进骨形成。破骨细胞通过促进从吸收基质中释放生长因子、产生分泌蛋白和微泡以及表达膜结合因子，在成骨细胞系细胞的整个分化过程中发挥作用。这些多种机制介导了骨形成与吸收在重塑中的偶联。破骨细胞与成骨细胞系细胞的额外相互作用，包括与覆盖细胞和逆转细胞的相互作用，对于在骨重建期间实现骨形成和吸收之间的协调是必需的。
