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Related Concept Videos

Bone Remodeling01:40

Bone Remodeling

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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Related Experiment Video

Updated: May 11, 2026

Improved Methodology for Studying Postnatal Osteogenesis via Intramembranous Ossification in a Murine Bone Marrow Injury Model
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Bone refilling in cortical basic multicellular units: insights into tetracycline double labelling from a

Pascal R Buenzli1, Peter Pivonka, David W Smith

  • 1School of Mathematical Sciences, Monash University, Melbourne, VIC, 3800, Australia, pascal.buenzli@uwa.edu.au.

Biomechanics and Modeling in Mechanobiology
|May 2, 2013
PubMed
Summary

Bone multicellular units (BMUs) coordinate bone remodeling. A mathematical model reveals osteoblast activity and number influence bone formation rates, explaining observed relationships in cortical bone and suggesting synchronous osteoblast behavior during remodeling.

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Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair
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Last Updated: May 11, 2026

Improved Methodology for Studying Postnatal Osteogenesis via Intramembranous Ossification in a Murine Bone Marrow Injury Model
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Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair
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Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair

Published on: May 23, 2014

Area of Science:

  • Biomaterials Science
  • Cell Biology
  • Computational Biology

Background:

  • Bone remodeling is a continuous process mediated by bone multicellular units (BMUs), involving coupled activity of osteoclasts and osteoblasts.
  • Osteoblast refilling rate is dependent on cell number and secretory activity, with a known linear relationship between matrix apposition rate and BMU cavity radius in cortical bone.
  • The underlying mechanisms governing this linear relationship from complex cellular regulations remain unclear.

Purpose of the Study:

  • To extend a mathematical model of cellular development within a single cortical BMU.
  • To investigate how osteoblast number and secretory activity vary along the BMU's closing cone.
  • To explore the influence of BMU cavity shrinkage on osteoblast development and activity.

Main Methods:

  • Developed a mathematical model incorporating biochemical coupling between osteoclasts and osteoblasts of varying maturity.
  • Included osteoblast differentiation into osteocytes and bone lining cells within the model.
  • Compared model-predicted matrix apposition rates with experimental data from tetracycline double labeling.

Main Results:

  • The model accurately predicts the linear relationship between matrix apposition rate and BMU cavity radius for most of the bone refilling phase.
  • Deviations from linearity were observed at the beginning and end of the refilling phase, supporting synchronous osteoblast behavior.
  • Model suggests variability in experimental data may stem from BMUs being at different life stages (initiation, progression, termination).

Conclusions:

  • The mathematical model provides insights into the regulation of osteoblast activity and number during bone remodeling.
  • Findings support the hypothesis of synchronous osteoblast function and offer explanations for observed phenomenological relationships.
  • Slower quasi-steady state attainment by osteoblasts compared to osteoclasts may locally influence Haversian canal diameter.