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Joint contact stresses calculated for acetabular dysplasia patients using discrete element analysis are significantly influenced by the applied gait pattern.

ABSTRACT: Gait modifications in acetabular dysplasia patients may influence cartilage contact stress patterns within the hip joint, with serious implications for clinical outcomes and the risk of developing osteoarthritis. The objective of this study was to understand how the gait pattern used to load computational models of dysplastic hips influences computed joint mechanics. Three-dimensional pre- and post-operative hip models of thirty patients previously treated for hip dysplasia with periacetabular osteotomy (PAO) were developed for performing discrete element analysis (DEA). Using DEA, contact stress patterns were calculated for each pre- and post-operative hip model when loaded with an instrumented total hip, a dysplastic, a matched control, and a normal gait pattern. DEA models loaded with the dysplastic and matched control gait patterns had significantly higher (p?=?0.012 and p?

SUBMITTER: Thomas-Aitken HD

PROVIDER: S-EPMC6237088 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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Joint contact stresses calculated for acetabular dysplasia patients using discrete element analysis are significantly influenced by the applied gait pattern.

Thomas-Aitken Holly D HD Willey Michael C MC Goetz Jessica E JE

Journal of biomechanics 20180731

Gait modifications in acetabular dysplasia patients may influence cartilage contact stress patterns within the hip joint, with serious implications for clinical outcomes and the risk of developing osteoarthritis. The objective of this study was to understand how the gait pattern used to load computational models of dysplastic hips influences computed joint mechanics. Three-dimensional pre- and post-operative hip models of thirty patients previously treated for hip dysplasia with periacetabular o ...[more]

PMID: 30104055

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Project description:BackgroundDevelopmental dysplasia of the hip (DDH) is a debilitating condition whose distinguishing signs include incomplete formation of the acetabulum leading to dislocation of the femur, accelerated wear of the articular cartilage and joint laxity resulting in osteoarthritis. It is a complex disorder having environmental and genetic causes. Existing techniques fail to detect milder forms of DDH in newborns leading to hip osteoarthritis in young adults. A sensitive, specific and cost effective test would allow identification of newborns that could be non-invasively corrected by the use of a Pavlik harness. Previously, we identified a 2.5 MB candidate region on human chromosome 3 by using linkage analysis of a 4 generation, 72 member family. Whole exome sequencing of the DNA of 4 severely affected members revealed a single nucleotide polymorphism variant, rs3732378 co-inherited by all 11 affected family members. This variant causes a threonine to methionine amino acid change in the coding sequence of the CX3CR1 chemokine receptor and is predicted to be harmful to the function of the protein To gain further insight into the function of this mutation we examined the effect of CX3CR1 ablation on the architecture of the mouse acetabulum and on the murine gait.MethodsThe hips of 5 and 8 weeks old wild type and CX3CR1 KO mice were analyzed using micro-CT to measure acetabular diameter and ten additional dimensional parameters. Eight week old mice were gait tested using an inclined treadmill with and without load and then underwent micro-CT analysis.Results(1) KO mice showed larger a 5-17% larger diameter left acetabula than WT mice at both ages. (2) At 8 weeks the normalized area of space (i.e. size discrepancy) between the femur head and acetabulum is significantly larger [38% (p = 0.001)-21% (p = 0.037)] in the KO mice. (3) At 8 weeks gait analysis of these same mice shows several metrics that are consistent with impairment in the KO but not the WT mice. These deficits are often seen in mice and humans who develop hip OA.ConclusionThe effect of CX3CR1 deletion on murine acetabular development provides suggestive evidence of a susceptibility inducing role of the CX3CR1 gene on DDH.

Project description:We have previously investigated an association between the genome copy number variation (CNV) and acetabular dysplasia (AD). Hip osteoarthritis is associated with a genetic polymorphism in the aspartic acid repeat in the N-terminal region of the asporin (ASPN) gene; therefore, the present study aimed to investigate whether the CNV of ASPN is involved in the pathogenesis of AD.Acetabular coverage of all subjects was evaluated using radiological findings (Sharp angle, centre-edge (CE) angle, acetabular roof obliquity (ARO) angle, and minimum joint space width). Genomic DNA was extracted from peripheral blood leukocytes. Agilent's region-targeted high-density oligonucleotide tiling microarray was used to analyse 64 female AD patients and 32 female control subjects. All statistical analyses were performed using EZR software (Fisher's exact probability test, Pearson's correlation test, and Student's t-test).CNV analysis of the ASPN gene revealed a copy number loss in significantly more AD patients (9/64) than control subjects (0/32; p = 0.0212). This loss occurred within a 60 kb region on 9q22.31, which harbours the gene for ASPN. The mean radiological parameters of these AD patients were significantly worse than those of the other subjects (Sharp angle, p = 0.0056; CE angle, p = 0.0076; ARO angle, p = 0.0065), and all nine patients required operative therapy such as total hip arthroplasty or pelvic osteotomy. Moreover, six of these nine patients had a history of operative or conservative therapy for developmental dysplasia of the hip.Copy number loss within the region harbouring the ASPN gene on 9q22.31 is associated with severe AD. A copy number loss in the ASPN gene region may play a role in the aetiology of severe AD.Cite this article: T. Sekimoto, M. Ishii, M. Emi, S. Kurogi, T. Funamoto, Y. Yonezawa, T. Tajima, T. Sakamoto, H. Hamada, E. Chosa. Copy number loss in the region of the ASPN gene in patients with acetabular dysplasia: ASPN CNV in acetabular dysplasia. Bone Joint Res 2017;6:439-445. DOI: 10.1302/2046-3758.67.BJR-2016-0094.R1.

Dataset Information

Joint contact stresses calculated for acetabular dysplasia patients using discrete element analysis are significantly influenced by the applied gait pattern.

Publications

Joint contact stresses calculated for acetabular dysplasia patients using discrete element analysis are significantly influenced by the applied gait pattern.

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