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Title: An algorithm for bone mechanoresponsiveness: implementation to study the effect of patient-specific cell mechanosensitivity on trabecular bone loss. Author: Mulvihill BM, Prendergast PJ. Journal: Comput Methods Biomech Biomed Engin; 2008 Oct; 11(5):443-51. PubMed ID: 18608340. 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.[Abstract] [Full Text] [Related] [New Search]