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An algorithm for bone mechanoresponsiveness: implementation to study the effect of patient-specific cell mechanosensitivity on trabecular bone loss

Bríanne M. Mulvihill and Patrick J. Prendergast

Computer Methods in Biomechanics and Biomedical Engineering, 2008, vol. 11, issue 5, 443-451

Abstract: The rate of bone loss is subject to considerable variation between individuals. With the ‘mechanostat’ model of Frost, genetic variations in bone mechanoresponsiveness are modelled by different mechanostat ‘setpoints’ – which may also change with age or disease. In this paper, the following setpoints are used: ϵmin (strain below which resorption is triggered); ϵmax (strain above which deposition occurs); ωcrit (microdamage-level above which damage-stimulated resorption occurs). To simulate decreased mechanosensitivity, ϵmax is increased. Analyses carried out on a simplified model of a trabecula show that ϵmax is a critical parameter: if it is higher in an individual (genetics) or increases (with age) the mass deficit each remodelling cycle increases. Furthermore, there is a value of ϵmax above which trabecular perforation occurs, leading to rapid loss of bone mass. Maintaining bone cell mechanosensitivity could therefore be a therapeutic target for the prevention of osteoporosis.

Date: 2008
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DOI: 10.1080/10255840802136150

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