Best Practice & Research Clinical Endocrinology & Metabolism
3Bone remodelling: its local regulation and the emergence of bone fragility
Section snippets
Bone modelling and remodelling
The material composition and structure of bone determine the loads it can tolerate.1 While this is self-evident, the converse – that the loads on bone determine its structure – is less evident. Adaptation of the material composition and structure of bone to prevailing loads is carried out by the cellular machinery of bone modelling and remodelling.2 Bone modelling and remodelling optimize bone strength and minimize mass, serving the needs of strength for loading and lightness for mobility. Bone
Cellular and molecular events in bone remodelling
While resorption of a volume of bone by osteoclasts precedes formation of a comparable volume of bone by osteoblasts5, these sequential functions are probably regulated by cellular and molecular events that are contemporaneous and multidirectional. Bone remodelling is tightly regulated by central, systemic and local factors that provide signals to and between the members of this multicellular unit. The osteoblasts and osteoclasts are the executive cells of the BMU, but this multicellular unit
Aging and changes in the remodelling machinery leading to bone loss and structural decay
There are at least four age-related changes in the cellular machinery of bone modelling and remodelling that compromise the material and structural properties of bone.116 Remodelling rate is rapid during growth, because each remodelling event deposits only a small amount of bone.9 As growth nears its ‘programmed’ completion, rapid remodelling is no longer needed, and the remodelling rate slows. With the completion of longitudinal growth, the only requirement for bone formation is the repair of
Summary and conclusion
Adaptive and reparative bone remodelling may be initiated from signals by the osteocyte to the bone lining cell. In adaptive modelling, bone formation occurs without resorption altering the size and shape of bone, while bone resorption during growth without bone formation is also bone modelling and excavates the marrow cavity. Bone remodelling, the resorption of bone followed by focal bone formation by the BMU, is carried out by actively resorbing osteoclasts, generated through the action of
Acknowledgements
Work from the authors' laboratories is supported by NHMRC Program (TJM) and Project (ES) grants.
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2022, Clinical BiochemistryCitation Excerpt :Cancellous bone provides strength to the skeleton due to its architecture without adding too much weight and is also metabolically more active due to the larger surface area. The adult bone is continuously being remodelled in order to repair microdamage, preserve bone strength and mechanical competence as well as maintain calcium homeostasis [3]. Remodelling is a surface phenomenon and occurs focally in bone remodelling units (BRU) with parathyroid hormone (PTH), as well as cell signalling molecules such as osteoprotegerin and Receptor Activator of Nuclear κ B ligand (RANK-L) being major regulators of this process.
Co-encapsulation of combinatorial flavonoids in biodegradable polymeric nanoparticles for improved anti-osteoporotic activity in ovariectomized rats
2021, Environmental Technology and InnovationCitation Excerpt :Remodelling and maintenance of bone requires a coordinated balance between osteoclast which causes resorption of bone and osteoblasts that causes formation of bone (Martin and Seeman, 2008; Ming et al., 2013).
Post-natal bone physiology
2020, Seminars in Fetal and Neonatal MedicineCitation Excerpt :Siddiqui and Partridge [46] reviewed the role of cytokines in osteoclast development and reported that interleukins-1 (IL-1), IL-6 and tumor necrosis factor (TNF) stimulate osteoclast development, while IL-4, IL-18, and interferon- γ inhibit osteoclast development. Post-natal bone remodeling is a dynamic process of balancing osteoclast-mediated bone resorption and osteoblast-mediated bone formation, with the skeletal responses to changes in loading and physiologic needs is met to ensure mineral homeostasis [47]. Remodeling is initiated by stimulation of osteoclast formation, followed by osteoclast-mediated bone resorption which takes few weeks, a reversal period, lag time between the end of resorption and the beginning of formation it takes four or five weeks, and then a long period of bone matrix formation and mineralization mediated by osteoblasts which takes 3–4 months for one packet (Fig. 1).