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Related Concept Videos

Bone Remodeling01:40

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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Related Experiment Video

Updated: Aug 6, 2025

Author Spotlight: An Economic and Efficient Method for Quantitative Evaluation of Bone Microarchitecture in a Murine Osteoporosis Model
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Trabecular bone remodeling in the aging mouse: A micro-multiphysics agent-based in silico model using single-cell

Daniele Boaretti1, Francisco C Marques1, Charles Ledoux1

  • 1Institute for Biomechanics, ETH Zurich, Zurich, Switzerland.

Frontiers in Bioengineering and Biotechnology
|March 20, 2023
PubMed
Summary

This study developed a 3D computational model to simulate bone remodeling. The model identified sclerostin as key to bone equilibrium and RANKL/OPG as drivers of bone volume changes, offering insights into aging bone.

Keywords:
bone adaptationbone cellsmechanical signalmicro-FEnumerical simulations

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Area of Science:

  • Computational biology
  • Biophysics
  • Skeletal biology

Background:

  • Bone remodeling involves complex cellular and tissue interactions across scales.
  • In silico models are crucial for understanding signaling pathways in bone remodeling.
  • Trabecular bone microarchitecture is vital for skeletal integrity.

Purpose of the Study:

  • To develop and validate a 3D multiscale micro-multiphysics agent-based (micro-MPA) in silico model of trabecular bone remodeling.
  • To investigate the roles of osteoprotegerin (OPG), receptor activator of nuclear factor kB ligand (RANKL), and sclerostin (Scl) in regulating bone remodeling.
  • To simulate age-related bone changes using a premature aging mouse model.

Main Methods:

  • Established a 3D micro-MPA in silico model incorporating cells, receptor-ligand kinetics, mechanomics, and cytokine diffusion.
  • Utilized longitudinal in vivo data from the CV6 of PolgA(D257A/D257A) mice.
  • Simulated trabecular bone remodeling over 4 weeks, evaluating bone morphometry and responses to modulated OPG, RANKL, and Scl levels.

Main Results:

  • The model successfully simulated homeostatic (basal) trabecular bone remodeling.
  • Simulations demonstrated anabolic, anti-anabolic, catabolic, and anti-catabolic responses by altering OPG, RANKL, and Scl levels.
  • Changes in OPG and RANKL levels showed significant positive and negative correlations with bone volume fraction (BV/TV), respectively.
  • Sclerostin primarily influenced bone equilibrium, while RANKL and OPG modulated BV/TV, relevant to age-related bone conditions.

Conclusions:

  • The micro-MPA model provides valuable insights into cellular responses to the mechanical environment in bone.
  • Sclerostin is identified as a key regulator of bone remodeling equilibrium.
  • RANKL and OPG play significant roles in modulating bone volume fraction, with implications for aging bone.
  • This model can help identify critical pathways affected by degenerative conditions and aging.