Nuffield Orthopaedic Centre

About: Nuffield Orthopaedic Centre is a healthcare organization based out in Oxford, United Kingdom. It is known for research contribution in the topics: Population & Arthroplasty. The organization has 2082 authors who have published 2920 publications receiving 145718 citations.

Facet joint injections as a means of reducing the need for vertebroplasty in insufficiency fractures of the spine

Abstract: Objectives Recent publications compared treatment of vertebral fractures reporting improvement in the majority but with no significant difference between the local anaesthetic and vertebroplasty groups. Potential explanations include placebo response or therapeutic response to the “control procedure”. We investigated whether preliminary facet joint injection can identify those patients whose pain arises from paravertebral structures rather than the vertebral insufficiency fracture itself.

Hypoxia-inducible factor 1-alpha does not regulate osteoclastogenesis but enhances bone resorption activity via prolyl-4-hydroxylase 2.

Abstract: Osteogenic-angiogenic coupling is promoted by the hypoxia-inducible factor 1-alpha (HIF-1α) transcription factor, provoking interest in HIF activation as a therapeutic strategy to improve osteoblast mineralization and treat pathological osteolysis. However, HIF also enhances the bone-resorbing activity of mature osteoclasts. It is therefore essential to determine the full effect(s) of HIF on both the formation and the bone-resorbing function of osteoclasts in order to understand how they might respond to such a strategy. Expression of HIF-1α mRNA and protein increased during osteoclast differentiation from CD14+ monocytic precursors, additionally inducing expression of the HIF-regulated glycolytic enzymes. However, HIF-1α siRNA only moderately affected osteoclast differentiation, accelerating fusion of precursor cells. HIF induction by inhibition of the regulatory prolyl-4-hydroxylase (PHD) enzymes reduced osteoclastogenesis, but was confirmed to enhance bone resorption by mature osteoclasts. Phd2+/- murine osteoclasts also exhibited enhanced bone resorption, associated with increased expression of resorption-associated Acp5, in comparison with wild-type cells from littermate controls. Phd3-/- bone marrow precursors displayed accelerated early fusion, mirroring results with HIF-1α siRNA. In vivo, Phd2+/- and Phd3-/- mice exhibited reduced trabecular bone mass, associated with reduced mineralization by Phd2+/- osteoblasts. These data indicate that HIF predominantly functions as a regulator of osteoclast-mediated bone resorption, with little effect on osteoclast differentiation. Inhibition of HIF might therefore represent an alternative strategy to treat diseases characterized by pathological levels of osteolysis. © 2017 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

Thermal effects of cement mantle thickness for hip resurfacing.

Abstract: Hybrid hip resurfacing arthroplasty with uncemented acetabular and cemented femoral fixation is increasingly becoming popular as an alternative to total hip arthroplasty. There is concern about femoral neck fractures, and long-term survival has not yet been demonstrated. Thermal necrosis may be an important factor for neck fracture and will affect the viability of the femoral bone. This cadaveric study investigated the thermal effect of thick (1.5 mm, n = 3) and thin (0.5 mm, n = 3) cement mantles; 5 thermocouples were used to record temperature at the femoral bone/cement interface during hip resurfacing arthroplasty. The highest recorded temperatures were significantly higher when a thick cement mantle is used (45.4 degrees C), compared to a thin cement mantle (32.7 degrees C). To reduce the potential for thermal necrosis, the thin cement mantle technique is recommended.

The X-chromosome and susceptibility to ankylosing spondylitis.

Abstract: Objective. Ankylosing spondylitis (AS) affects 0.25-1.0% of the population, and its etiology is incompletely understood. Susceptibility to this highly familial disease (lambda(s) = 58) is primarily genetically determined. There is a significant sex bias in AS, and there are differences in recurrence risk to the offspring of affected mothers and fathers, suggesting that there may be an X-linked recessive effect. We undertook an X-chromosome linkage study to determine any contribution of the X-chromosome to AS susceptibility.Methods. A linkage study of the X-chromosome using 234 affected sibling pairs was performed to investigate this hypothesis.Results. No linkage of the X-chromosome with susceptibility to AS was found. Model-free multipoint linkage analysis strongly excluded any significant genetic contribution (lambda greater than or equal to 1.5) to AS susceptibility encoded on the X-chromosome (logarithm of odds [LOD] < -2.0). Smaller genetic effects (lambda greater than or equal to 1.3) were also found to be unlikely (LOD < -1.0).Conclusion. The sex bias in AS is not explained by X-chromosome-encoded genetic effects. The disease model best explaining the sex bias in occurrence and transmission of AS is a polygenic model with a higher susceptibility threshold in females.