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Orthopaedic Proceedings
Vol. 92-B, Issue SUPP_III | Pages 450 - 450
1 Jul 2010
Maurer-Ertl W Kürzl G Fröhlich E Leithner A Ghaffari-Tabrizi N Bodo K Liegl B Windhager R
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Although fibrous dysplasia is a benign bone disease, in few cases patient are suffering from severe pain of the skeletal system. The aim of this study was to evaluate the current state regarding pain of patients with fibrous dysplasia treated at our hospital.

We searched our digital database since 1990 for patients with fibrous dysplasia. Subsequent we verified the histological diagnosis by reviewing the final pathologic report. Additional we called the identified patients by phone to make an enquiry about their pain course and associated treatment. For rating pain intensity we used a numeric rating scale with a range within zero to ten.

We identified 43 patients (21 male, 22 female) with an average age at initial diagnosis of 40 years (range 10 to 72years). The mean follow up was 6 years (range 1 to 23 years). Among these 43 patients we were able to contact 33 by phone. Initial diagnosis was made due to pain in 23 cases, nearly coequal by coincidental examination in 20 cases, for fracture in two cases and for local swelling and bone deformity each time in two cases. Thirty-six patients revealed monostotic and seven patients polyostotic involvement. The following locations were found: three times craniofacial, four times within the spine, eight times at the upper extremity, ten times in the pelvis and 31 times at the lower limb. Two patients were suffering additionally from Mazabraud Syndrome. Actual values at the numeric rating scale regarding pain ranged from 0 to 9 with a mean value of 1. Specific in the polyostotic group we found an average value of 3 and three of seven patients stated a value greater than 5 for persistent pain. Five patients with polyostotic involvement were treated with bisphosphonat for pain control with good response.

It is remarkable that patients with polyostotic involvement have marked higher values for pain intensity at the numeric rating scale. So therefore we should have a closer look for potential reasons explaining that fact. In accordance with previous published studies we found that pain decreased by intermittent intravenous application of bisphosphonates.


Orthopaedic Proceedings
Vol. 91-B, Issue SUPP_II | Pages 293 - 293
1 May 2009
Ogunwale B Brewer J Schmidt-Ott A Tabrizi N Meek R
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Unlike metal-on-Polyethylene, metal-on-metal (MoM) implants seem to affect the adaptive immune response as evident from the associated perivascular infiltrate containing lymphocytes and plasma cells. This is more pronounced in implant failure secondary to aseptic loosening, and may represent the failure mode. A reduction in CD8+ T lymphocyte counts has also been described with Hip Resurfacing. MoM articulations produce a much smaller order of size of wear particles (nanoparticles) than metal-on- Polyethylene, which may be responsible for the observed adaptive immune system effects. We therefore analyzed the effects of CoCr nanoparticles (CoCrNP) on Dendritic Cells, T cells & B cells.

We produced CoCrNP using repetitive short spark discharges between electrodes of prosthetic CoCr alloy. Electron micrography and Brunauer-Emmet-Teller method both confirmed nanoparticle size. The following experiments were then undertaken.

Dendritic Cells were cultured from mouse bone marrow and incubated with CoCrNP of varying concentrations for 24hrs, or lipopolysaccharide as a positive control. Activation status was then characterized by CD40 expression on fluorescence activated cell sorting (FACS) analysis.

T Cell Viability; Cells from mouse lymph nodes were incubated with CoCrNP in varying concentrations. At 48hrs, Propidium Iodide (PI) was added and proportion of CD4+ lymphocytes that were PI+ve determined by FACS analysis.

T Cell proliferation; Cells from mouse lymph nodes were cultured in medium without phenol red and incubated with μCD3 (anti CD3), μCD3 + CoCrNP, μCD3 + μCD28 or μCD3 + μCD28 + CoCrNP. At 48hrs, Almar Blue was added & difference in light absorbance at 570nm & 600nm was then used to determine T cell proliferation at 72hrs.

Cells from lymph nodes of an MD4 (Hen Egg Lysozyme (HEL) specific B cell receptor transgenic) mouse were incubated with CoCrNP, HEL (positive control) or CoCrNP + HEL. B cell activation at 48hrs was characterised by CD40 and CD86 expression on FACS analysis.

We found CoCrNP did not significantly increase CD40 expression on DCs, neither did it alter CD40 or CD86 expression on B cells. Using a sublethal concentration of CoCrNP as determined from the viability tests, CoCrNP inhibited CD3 & CD3/CD28 dependent T-cell proliferation. This would indicate CoCrNP reduces T cell proliferation and/or survival, which may explain the observed reduction in CD8+ count with hip resurfacing. Understanding the development of the Peri-vascular infiltrate associated with MoM implants will however, probably require more complex (most likely in vivo) models.