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Mathematical modeling of elasticity changes in the cortical bone of HIP/RPL29‐ deficient mice
Author(s) -
Sloofman Laura Gail,
Pelesko John A.,
Schleiniger Gilberto F.,
KirnSafran Catherine B.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.668.1
Subject(s) - elasticity (physics) , cortical bone , phenotype , mutant , genetically modified mouse , biology , endocrinology , anatomy , transgene , genetics , materials science , gene , composite material
Mathematical modeling, or using equations to describe a system, is a powerful technique in transgenic research. Our laboratory created the first viable mutant mouse model lacking an individual ribosomal protein (HIP/RPL29). A short stature phenotype associated with increased bone fragility is observed in HIP/RPL29 null mice. We recently noted that a decrease in collagen cross‐linking during the growth of HIP/RPL29 null bone precedes an overall enhancement in the mineral‐to‐matrix ratio in adult bone. We hypothesize that we can build on existing mathematical models to describe the changes in bone structure and composition resulting from HIP/RPL29 deficiency. Hierarchical multi‐scale models of wild type and HIP/RPL29 null cortical bone will be used to simulate adult control and mutant bone. We aim to relate the changes in null bone samples to elasticity measurements collected via three‐point bending tests. Since the equations describing mutant and control bone are interrelated, we can extrapolate relationships among the mentioned properties. We will also use this model to predict the elasticity in control and mutant bones at three months of age. All calculations will be compared with accepted experimental values. This model will be altered as the three‐month mutant bone phenotype is refined. Funding was provided by the Howard Hughes Medical Institute to LGS and NIH P20‐ RR016458 to CBKS.