The Emu as a Model for Necrotic Femoral Head Collapse
University Of Iowa, Iowa City IA
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Abstract
DESCRIPTION (provided by applicant): Femoral head osteonecrosis remains a major unsolved problem in orthopedic surgery of the hip. Because total hip replacement often proves unsatisfactory for patients with this disorder, means are needed to forestall necrotic femoral head collapse. Much could be learned from an animal model reliably mimicking the human disorder's natural history of structural collapse. Existing quadrupedal models fail to replicate this key aspect of the pathogenesis, presumably owing to unduly benign biomechanical demand. Cryogenically-induced osteonecrosis in the emu, a large and very active biped, shows great promise for overcoming this difficulty. The central goal of the proposed work is to bring this new emu model optimally into concordance with human disorder. Aim 1 is to establish quantitative linkage between cryo-insult parameters and resulting distributions of osteocyte death. This will involve thermal finite element analysis of temperature fields produced by a specially developed cryo-insult probe, and prediction of corresponding patterns of osteocyte death. Validation will be provided by osteocyte death distributions resulting from corresponding insults delivered intraoperatively. Aim 2 is to quantify the functional similarity of femoral head mechanical load transmission in emus versus humans. In vivo joint loading of the emu hip will be determined from force plate and optoelectronic recordings. Bench tests will be performed to measure hip joint contact stress distributions, and to map cancellous bone stiffness distributions. A whole-gait-cycle structural finite element model of the emu femoral head will be developed, for comparison with corresponding data for the human. Aim 3 is to compare the pathogenesis of osteonecrosis in emus with that in a (non-collapsing) canine model. Parameters of interest include the speed and patterns of revascularization, cell types, histomorphometric alterations of the trabecular lattice, and mechanical compromise. Aim 4 is to correlate the speed and severity of collapse in the emu osteonecrosis model with quantifiable structural compromise. This will again involve the structural finite element model, coupled with CT-based assessments of bony structural degradation. At the project's conclusion, we expect to have filled a longstanding need in the field of osteonecrosis research: an animal model suitable for systematic study of human-implementable interventions to forestall femoral head collapse.
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