title: An algorithm for bone mechanoresponsiveness: implementation to study the effect of patient-specific cell mechanosensitivity on trabecular bone loss.
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: epsilonmin (strain below which resorption is triggered); epsilonmax (strain above which deposition occurs); omegacrit (microdamage-level above which damage-stimulated resorption occurs). To simulate decreased mechanosensitivity, epsilonmax is increased. Analyses carried out on a simplified model of a trabecula show that epsilonmax 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 epsilonmax 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.
authors.affiliation: Trinity Centre for Bioengineering, School of Engineering, Parson's Building, Trinity College, Dublin, Ireland.
authors.forename: Bríanne M
authors.initials: BM
authors.lastname: Mulvihill
authors.forename: Patrick J
authors.initials: PJ
authors.lastname: Prendergast
mesh_terms: D000375:Aging / Q000502:physiology; D000465:Algorithms; D001696:Biomechanical Phenomena; D015519:Bone Density / Q000502:physiology; D001842:Bone and Bones / Q000503:physiopathology*; D006801:Humans; D008954:Models, Biological; D010024:Osteoporosis / Q000503:physiopathology* / Q000517:prevention & control