A coupled mechano-biochemical model for bone adaptation
Language English Country Germany Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Models, Biological * MeSH
- Biomechanical Phenomena physiology MeSH
- Adaptation, Physiological physiology MeSH
- Humans MeSH
- RANK Ligand physiology MeSH
- Osteoporosis physiopathology MeSH
- Osteoprotegerin physiology MeSH
- Computer Simulation MeSH
- Receptor Activator of Nuclear Factor-kappa B physiology MeSH
- Bone Remodeling physiology MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- RANK Ligand MeSH
- Osteoprotegerin MeSH
- Receptor Activator of Nuclear Factor-kappa B MeSH
- TNFRSF11A protein, human MeSH Browser
- TNFSF11 protein, human MeSH Browser
Bone remodelling is a fundamental biological process that controls bone microrepair, adaptation to environmental loads and calcium regulation among other important processes. It is not surprising that bone remodelling has been subject of intensive both experimental and theoretical research. In particular, many mathematical models have been developed in the last decades focusing in particular aspects of this complicated phenomenon where mechanics, biochemistry and cell processes strongly interact. In this paper, we present a new model that combines most of these essential aspects in bone remodelling with especial focus on the effect of the mechanical environment into the biochemical control of bone adaptation mainly associated to the well known RANKL-RANK-OPG pathway. The predicted results show a good correspondence with experimental and clinical findings. For example, our results indicate that trabecular bone is more severely affected both in disuse and disease than cortical bone what has been observed in osteoporotic bones. In future, the methodology proposed would help to new therapeutic strategies following the evolution of bone tissue distribution in osteoporotic patients.
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