The Influence of Intracortical Microarchitecture on the Mechanical Fatigue of Bone

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dc.contributor.advisorEdwards, William Brent
dc.contributor.authorLoundagin, Lindsay Lessel
dc.contributor.committeememberBoyd, Steven Kyle
dc.contributor.committeememberSchmidt, Roel Kuijer Tannin
dc.contributor.committeememberDuncan, Neil A.
dc.contributor.committeememberCooper, David Michael Lane
dc.contributor.committeememberTaylor, David
dc.contributor.committeememberManske, Sarah Lynn
dc.date2020-11
dc.date.accessioned2020-07-10T20:41:20Z
dc.date.available2020-07-10T20:41:20Z
dc.date.issued2020-07-07
dc.description.abstractMechanical fatigue is the predominant etiology of stress fracture, a known contributor to atypical femoral fracture, and may also play a critical role in fragility fracture. While these fatigue-related fractures are well-documented in humans, they are poorly understood. Extensive research has attempted to characterize the fatigue behavior of cortical bone; however, owing to the inherent variability in bone tissue, samples that appear identical in macrostructure can exhibit a large degree of scatter in fatigue life. The overarching hypothesis of this thesis is that the variance in fatigue-life data can be attributed to intracortical microarchitecture, including the size, spacing, and density of vascular canals and osteocyte lacunae. A series of studies were conducted that utilized ex vivo mechanical testing, high-resolution imaging, and finite element modeling to establish the relationship between intracortical microarchitecture and the fatigue life of bone in compression. Both porosity and canal diameter demonstrated a strong negative relationship with fatigue life, whereas lacunar density was positively correlated. The reduced fatigue life associated with higher porosity was a result of larger, rather than more abundant canals, indicating that canals act as stress concentrators that may impair the fatigue resistance of bone beyond increasing overall porosity. The stress concentrations caused by vascular canals were quantified as stressed volume (i.e., the volume of material above yield) which was positively correlated to porosity and canal diameter. Furthermore, stressed volume proved to be a strong predictor of fatigue-life variance across multiple loading magnitudes. The findings from this thesis suggest that a majority of the fatigue-life variance of cortical bone in compression is driven by intracortical microarchitecture, and fatigue failure may be predicted by quantifying the stress concentrations associated with vascular canals.en_US
dc.identifier.citationLoundagin, L. L. (2020). The Influence of Intracortical Microarchitecture on the Mechanical Fatigue of Bone (Doctoral thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca.en_US
dc.identifier.doihttp://dx.doi.org/10.11575/PRISM/38005
dc.identifier.urihttp://hdl.handle.net/1880/112283
dc.language.isoengen_US
dc.publisher.facultyKinesiologyen_US
dc.publisher.institutionUniversity of Calgaryen
dc.rightsUniversity of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission.en_US
dc.subjectCortical boneen_US
dc.subjectVascular canalsen_US
dc.subjectStress concentrationsen_US
dc.subjectFinite element analysisen_US
dc.subjectOsteocyte Lacunaeen_US
dc.subjectStress Fractureen_US
dc.subjectFatigue fractureen_US
dc.subject.classificationEngineeringen_US
dc.subject.classificationEngineering--Biomedicalen_US
dc.subject.classificationEngineering--Mechanicalen_US
dc.titleThe Influence of Intracortical Microarchitecture on the Mechanical Fatigue of Boneen_US
dc.typedoctoral thesisen_US
thesis.degree.disciplineKinesiologyen_US
thesis.degree.grantorUniversity of Calgaryen_US
thesis.degree.nameDoctor of Philosophy (PhD)en_US
ucalgary.item.requestcopytrueen_US
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