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Orthopaedic Proceedings
Vol. 102-B, Issue SUPP_1 | Pages 106 - 106
1 Feb 2020
Wise C Oladokun A Maag C
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Introduction

Femoral neck impingement occurs clinically in total hip replacements (THR) when the acetabular liner articulates against the neck of a femoral stem prosthesis. This may occur in vivo due to factors such as prostheses design, patient anatomical variation, and/or surgical malpositioning, and may be linked to joint instability, unexplained pain, and dislocation. The Standard Test Method for Impingement of Acetabular Prostheses, ASTM F2582 −14, may be used to evaluate acetabular component fatigue and deformation under repeated impingement conditions. It is worth noting that while femoral neck impingement is a clinical observation, relative motions and loading conditions used in ASTM F2582-14 do not replicate in vivo mechanisms. As written, ASTM F2582-14 covers failure mechanism assessment for acetabular liners of multiple designs, materials, and sizes. This study investigates differences observed in the implied and executed kinematics described in ASTM F2582-14 using a Prosim electromechanical hip simulator (Simulation Solutions, Stockport, Greater Manchester) and an AMTI hydraulic 12-station hip simulator (AMTI, Watertown, MA).

Method

Neck impingement testing per ASTM F2582-14 was carried out on four groups of artificially aged acetabular liners (per ASTM F2003-15) made from GUR 1020 UHMWPE which was re-melted and cross-linked at 7.5 Mrad. Group A (n=3) and B (n=3) consisted of 28mm diameter femoral heads articulating on 28mm ID × 44mm OD acetabular liners. Group C (n=3) and D (n=3) consisted of 40mm diameter femoral heads articulating on lipped 40mm ID × 56mm OD 10° face changing acetabular liners. All acetabular liners were tested in production equivalent shell-fixtures mounted at 0° initial inclination angle. Femoral stems were potted in resin to fit respective simulator test fixtures. Testing was conducted in bovine serum diluted to 18mg/mL protein content supplemented with sodium azide and EDTA. Groups A and C were tested on a Prosim; Groups B and D were tested on an AMTI. Physical examination and coordination measurement machine (CMM) analyses were conducted on all liners pre-test and at 0.2 million cycle intervals to monitor possible failure mechanisms. Testing was conducted for 1.0 million cycles or until failure.

An Abaqus/Explicit model was created to investigate relative motions and contact areas resulting from initial impingement kinematics for each test group.


Orthopaedic Proceedings
Vol. 99-B, Issue SUPP_4 | Pages 16 - 16
1 Feb 2017
Hippensteel E Wise C Ross M Langhorn J Narayan V
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INTRODUCTION

Multiple sources have consistently reported oxidation indices less than 0.1 with Marathon® inserts implanted up to 10 years. Understanding effects of oxidation level on UHMWPE wear in vivo is of great value. The objective of this study is to characterize the wear performance of Marathon® acetabular inserts at various levels of artificially induced oxidation, quantified using Bulk Oxidation Index (BOI) as determined per ASTM F2102, and to ascertain if wear rate is affected by progressive polyethylene oxidation.

METHODS

GUR 1050 UHMWPE acetabular inserts, re-melted and cross-linked at 5.0Mrad (Marathon®, DePuy Synthes Joint Reconstruction, Warsaw, IN), were artificially aged per ASTM F-2003 in a stainless steel chamber at 5 atm. oxygen pressure and 70°C. Samples were maintained at temperature for 9, 10.4 and 11 weeks. After aging was completed, Fourier Transform Infra-Red (FTIR) spectroscopy was employed on one insert from each time point to evaluate the induced oxidation as a result of artificial aging. Resulting induced BOI values measured by FTIR were 0.195, 0.528 and 1.184. UHMWPE inserts had an inner diameter of 28mm and an outer diameter of 48mm and were articulated against 28mm diameter M-Spec® metal femoral heads (DePuy Synthes Joint Reconstruction, Warsaw, IN). Testing was conducted on a 12-station AMTI ADL hip simulator (AMTI, Watertown, MA) with load soak controls per ISO 14242-1:2014(E) in bovine serum (18mg/mL total protein concentration) supplemented with 0.056% sodium azide (preservative) and 5.56mM EDTA (calcium stabilizer). The UHMWPE inserts were removed from the machine, cleaned, and gravimetric wear determined per ISO 14242-2:2000(E) every 0.5 million cycles (MCyc) for 4.0 MCyc total. A two-tailed student's t-test was used (variance determined by F-test results) to analyze differences in wear rates between the three test groups.


Orthopaedic Proceedings
Vol. 94-B, Issue SUPP_XXVII | Pages 46 - 46
1 Jun 2012
Wise C Sharma S Gao X Londono D Mauldin KN Brandon J King V Zhang D Gordon D Herring J
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Introduction

Adolescent idiopathic scoliosis (AIS) is the most common paediatric spinal deformity, affecting about 3% of school-aged children worldwide. This disorder occurs in otherwise healthy children who bear no obvious deficiencies in the components of the spinal column itself. The cause of AIS is poorly understood, as is implied by the name. Lesions of the bony composition of the vertebrae, the vertebral endplates, the paraspinous muscles, or the neurological system each have been proposed to explain disease pathogenesis. Progress has been hampered by the absence of an obvious AIS animal model. Consequently we have used genetic studies in human populations to identify factors underlying AIS susceptibility.

The complex inheritance and population frequency of AIS suggest that many genetic factors are involved in this disease. To search comprehensively for such factors we previously undertook the first genome-wide association study (GWAS) of AIS susceptibility in a cohort of 419 families in Texas, USA. We found that chromosome 3 SNPs in the proximity of the CHL1 gene yielded strongest results, which we replicated in additional cohorts (rs10510181 OR 1·49, 95% CI 1·29–173, p=2·58×10–8). CHL1 is of interest because it encodes an axon guidance protein and is functionally related to the ROBO3 gene that causes hereditary gaze palsy with progressive scoliosis (HGPPS), a rare disease marked by severe scoliosis. Here we expanded the study to 702 Texas families.

Methods

We tested more than 327 000 single-nucleotide polymorphisms (SNPs) across all human autosomes for association with disease.


Orthopaedic Proceedings
Vol. 90-B, Issue SUPP_III | Pages 446 - 446
1 Aug 2008
Gao X Herring J Cain N Gillum J Browne R Helms C Swaney S Zhang D Shoemaker S Lovett M Bowcock A Wise C
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Background and methods: Adolescent idiopathic scoliosis (AIS) is the most common spinal deformity in children, with a prevalence of 1–2%. The disease generally displays complex inheritance. Various family studies have produced many first reports of AIS susceptibility regions, but confirmation of these is lacking. In the present study we investigated extension of our own data, and reproducibility of other published results, by testing linkage in a new collection of fifty-four AIS families. Altogether fifteen candidate regions were evaluated in a two-stage design.

Results: Strongest results were obtained for linkage to microsatellite loci within a candidate region of proximal 8q previously identified by chromosomal breakpoint mapping. Although positive lod scores were obtained for other regions, none exhibited significance less than or equal to P = .05. Lod scores remained stable after analysis of an independent panel of SNP loci in the 8q candidate region and were strengthened with inclusion of additional affected family members (multipoint NPL = 3.02, P = 0.001). Two SNPs near the peak of linkage produced evidence of association to AIS susceptibility. Both SNPs are found within plausible candidate genes for AIS susceptibility.

Conclusion: These results support linkage of the 8q11-8q13 region to AIS susceptibility. Bashiardes et al. previously described a chromosomal break in the 8q11 region that disrupted the gamma-1- syntrophin (SNTG1) gene and segregated with AIS in an extended kindred. In that study, possible rare splice site mutations were identified an additional affected family and one sporadic case. The peak of linkage and association detected in this study appears to be distinct from the SNTG1 gene. This suggests the possibility that more than one gene in the region may contribute to disease. A more detailed analysis of the region encompassing this linkage peak, and the SNTG1 gene, is warranted in larger family collections.