title: Using smooth particle hydrodynamics to investigate femoral cortical bone remodelling at the Haversian level.
abstract: In the neck of the femur, about 70% of the strength is contributed by the cortical bone, which is the most highly stressed part of the structure and is the site where failure is almost certainly initiated. A better understanding of cortical bone remodelling mechanisms can help discern changes at this anatomical site, which are essential if an understanding of the mechanisms by which hips weaken and become vulnerable to fracture is to be gained. The aims of this study were to (i) examine a hypothesis that low strain fields arise because of subject-specific Haversian canal distributions causing bone resorption and reduced bone integrity and (ii) introduce the use of a meshless particle-based computational modelling approach SPH to capture bone remodelling features at the level of the Haversian canals. We show that bone remodelling initiated by strain at the Haversian level is highly influenced by the subject-specific pore distribution, bone density, loading and osteocyte density. SPH is shown to be effective at capturing the intricate bone pore shapes that evolved over time.
authors.affiliation: Auckland Bioengineering Institute, The University of Auckland, Auckland, New Zealand. j.fernandez@auckland.ac.nz
authors.forename: J W
authors.initials: JW
authors.lastname: Fernandez
authors.forename: R
authors.initials: R
authors.lastname: Das
authors.forename: P W
authors.initials: PW
authors.lastname: Cleary
authors.forename: P J
authors.initials: PJ
authors.lastname: Hunter
authors.forename: C D L
authors.initials: CD
authors.lastname: Thomas
authors.forename: J G
authors.initials: JG
authors.lastname: Clement
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001862:Bone Resorption; D005260:Female; D005272:Femur Neck / Q000473:pathology / Q000503:physiopathology; D006620:Hip Fractures / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D057446:Hydrodynamics; D008297:Male; D008954:Models, Biological; D013312:Stress, Physiological