Modelling the anabolic response of bone using a cell population model

DOI10.1016/J.JTBI.2012.04.019zbMATH Open1337.92037arXiv1112.5685OpenAlexW2148851290WikidataQ47775040 ScholiaQ47775040MaRDI QIDQ292702FDOQ292702

D. W. Smith, Bruce S. Gardiner, Peter Pivonka, Pascal R. Buenzli

Publication date: 9 June 2016

Published in: Journal of Theoretical Biology (Search for Journal in Brave)

Abstract: To maintain bone mass during bone remodelling, coupling is required between bone resorption and bone formation. This coordination is achieved by a network of autocrine and paracrine signalling molecules between cells of the osteoclast lineage and cells of the osteoblastic lineage. Mathematical modelling of signalling between cells of both lineages can assist in the interpretation of experimental data, clarify signalling interactions and help develop a deeper understanding of complex bone diseases. In this paper, we further develop a mathematical model of bone cell interactions by Pivonka et al. (2008) to include the proliferation of precursor osteoblasts into the model. This inclusion is important to be able to account for Wnt signalling, believed to play an important role in anabolic responses of bone. We show that an increased rate of differentiation to precursor cells or an increased rate of proliferation of precursor osteoblasts themselves both result in increased bone mass. However, modelling these different processes separately enables the new model to represent recent experimental discoveries such as the role of Wnt signalling in bone biology and the recruitment of osteoblast progenitor cells by transforming growth factor �eta. Finally, we illustrate the power of the new model's capabilities by applying the model to prostate cancer metastasis to bone. In the bone microenvironment, prostate cancer cells are believed to release some of the same signalling molecules used to coordinate bone remodelling (i.e. Wnt and PTHrP), enabling the cancer cells to disrupt normal signalling and coordination between bone cells. This disruption can lead to either bone gain or bone loss. We demonstrate that the new computational model developed here is capable of capturing some key observations made on the evolution of the bone mass due to metastasis of prostate cancer to the bone microenvironment

Full work available at URL: https://arxiv.org/abs/1112.5685

zbMATH Keywords

mathematical modelproliferationosteoblast formationprostate cancer metastasiswnt signalling

Mathematics Subject Classification ID

Physiology (general) (92C30) Cell biology (92C37)

Cites Work

• Theoretical investigation of the role of the RANK-RANKL-OPG system in bone remodeling
• Modeling the interactions between osteoblast and osteoclast activities in bone remodeling

Cited In (12)

• Computational model of the dual action of PTH -- application to a rat model of osteoporosis
• A new non targeted bone remodeling model combined with an interpolation meshless method
• Osteocytes as a record of bone formation dynamics: a mathematical model of osteocyte generation in bone matrix
• A mathematical model for fibrous dysplasia: the role of the flow of mutant cells
• Fractionated follow-up chemotherapy delays the onset of resistance in bone metastatic prostate cancer
• Coupling systems biology with multiscale mechanics, for computer simulations of bone remodeling
• A model for bone mechanics and remodeling including cell populations dynamics
• A mathematical model for bone cell population dynamics of fracture healing considering the effect of energy dissipation
• Bone remodeling as a spatial evolutionary game
• Mathematical model of bone remodeling captures the antiresorptive and anabolic actions of various therapies
• The Cellular Dynamics of Bone Remodeling: A Mathematical Model
• An integrative model of prostate cancer interaction with the bone microenvironment

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