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dc.contributor.authorDriver, Madeleine
dc.contributor.otherQueen's University (Kingston, Ont.). Theses (Queen's University (Kingston, Ont.))en
dc.date.accessioned2019-01-04T18:24:11Z
dc.date.available2019-01-04T18:24:11Z
dc.identifier.urihttp://hdl.handle.net/1974/25900
dc.description.abstractOsteoporosis is a degenerative bone disease that causes an increase of fracture risk. The present method of diagnosing the disease is through a bone mineral density (BMD) scan which neglects bone quality. Due to the complexity of bone, experimental testing is difficult; hence the use of finite element models can assist in understanding deformation behaviour and failure mechanisms. The aim of this study is to construct specimen specific-finite element models to investigate stiffness sharing and axial strain distributions of cortical versus trabecular bone of rat L4 vertebral bodies with and without the inclusion of vascular apertures. In a previous experimental study, healthy (SHAM), osteoporotic (OVX) and treated osteoporotic (OVX+E) rat vertebrae underwent uniaxial compression while synchronously imaged with a micro-CT machine [1]. For the present study, these images have been processed into 3D FE models. The ratio of cortical shell stiffness to total vertebral body apparent stiffness was 70.1 ± 4.5% across all models with no significant difference across health conditions. However, since this value is significantly (P<0.01) higher than previously reported values in humans, caution should be taken when extrapolating rat vertebrae behaviour to those of humans. When viewing the axial strain, it was found that in the OVX models, the trabeculae had statistically significantly lower mean strains but a larger proportion of high strain elements creating more strain heterogeneity. Another confounding issue in these rat vertebrae is the presence of large vascular apertures in the dorsal surface of the cortical shell, that have been shown to be associated with cracks [2]. Additional models were created that removed these holes by virtually filling them in. The apparent stiffness of the cortical shell was found to increase by only 0.5%. Looking at the average axial strain distributions with the removal of the vascular apertures, the trabeculae strains showed minimal change, but the cortical shell experienced a significant (P<0.01) increased average axial strain across all health conditions. These results suggest that failure likely originates in the cortical shell and is affected by the presence of the vascular apertures, before progressing into the reduced trabecular network in the region adjacent to the vascular apertures.en_US
dc.language.isoenen_US
dc.relation.ispartofseriesCanadian thesesen
dc.rightsQueen's University's Thesis/Dissertation Non-Exclusive License for Deposit to QSpace and Library and Archives Canadaen
dc.rightsProQuest PhD and Master's Theses International Dissemination Agreementen
dc.rightsIntellectual Property Guidelines at Queen's Universityen
dc.rightsCopying and Preserving Your Thesisen
dc.rightsThis publication is made available by the authority of the copyright owner solely for the purpose of private study and research and may not be copied or reproduced except as permitted by the copyright laws without written authority from the copyright owner.en
dc.subjectFinite Element Analysisen_US
dc.subjectUniaxial Compressionen_US
dc.subjectRat Vertebraeen_US
dc.subjectCortical Shellen_US
dc.subjectTrabecular Networken_US
dc.subjectOsteoporosisen_US
dc.titleFinite Element Analysis of Cortical Shell Contributions to Apparent Stiffness and the Effect of Vascular Apertures in Rat Vertebrae Under Uniaxial Compressionen_US
dc.typeThesisen
dc.description.degreeMaster of Applied Scienceen_US
dc.contributor.supervisorPilkey, A. Keith
dc.contributor.supervisorLievers, W. Brent
dc.contributor.departmentMechanical and Materials Engineeringen_US


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