Search

Your search keyword '"Wooley, Paul"' showing total 36 results
Start Over Author "Wooley, Paul" Publisher wiley
36 results on '"Wooley, Paul"'

34. Polymethylmethacrylate and titanium alloy particles activate peripheral monocytes during periprosthetic inflammation and osteolysis.

Author

Yang SY, Zhang K, Bai L, Song Z, Yu H, McQueen DA, and Wooley PH

Subjects
Alloys, Animals, Arthroplasty, Replacement adverse effects, Bone Transplantation, Humans, Leukocytes, Mononuclear drug effects, Mice, Mice, SCID, Transplantation, Heterologous, X-Ray Microtomography, Inflammation physiopathology, Leukocytes, Mononuclear transplantation, Osteolysis physiopathology, Polymethyl Methacrylate pharmacology, Titanium pharmacology
Abstract

We investigated the interactions of particulate PMMA or titanium alloy, patient blood monocytes, and periprosthetic tissues using a SCID-hu model of aseptic loosening. Periprosthetic tissues and bone chips obtained at revision surgery for loosening were transplanted into muscles of SCID mice. Peripheral blood monocytes (PBMCs) isolated from the same donors were fluorescently labeled and co-cultured with PMMA or Ti-6Al-4V particles before intraperitoneal injection. Control mice with periprosthetic tissue or non-inflammatory ligament xenografts received naive PBMCs transfusion. Mice were euthanized 2 weeks after PBMC transfusion. The human tissues were well accepted in SCID mice. Transfused fluorescent-labeled PBMCs were markedly accumulated in transplanted periprosthetic tissues. Multinucleated osteoclast-like cells were commonly seen within retrieved xenograft tissue, and focal bone erosions were ubiquitous. Total cell densities and CD68+ cells within the xenograft were significantly increased in mice transfused with PMMA and Ti-provoked PBMCs compared to the naïve PBMC animals (p < 0.05). Immunohistochemical staining identified much stronger positive IL-1 and TNF stains in xenografts from either PMMA or Ti-stimulated monocytes transfusion groups (p < 0.05). TRAP+ cells were found around bone chips in both activated-PBMCs groups, although markedly more aggregated TRAP+ cells in the PMMA-challenged group than in the titanium group (p < 0.05). MicroCT assessment confirmed the significant decrease of bone mineral density in chips interacted with activated-monocytes/osteoclasts. In conclusion, PMMA or titanium particles readily activate peripheral monocytes and promote the cell trafficking to the debris-containing prosthetic tissues. Particles-provoked PBMCs participated in and promoted the local inflammatory process, osteoclastogenesis, and bone resorption., (Copyright © 2010 Orthopaedic Research Society.)

Published
2011
Full Text
View/download PDF

35. Erythromycin inhibits wear debris-induced osteoclastogenesis by modulation of murine macrophage NF-kappaB activity.

Author

Ren W, Li XH, Chen BD, and Wooley PH

Subjects
Animals, Bone Resorption metabolism, Bone Resorption physiopathology, Carrier Proteins metabolism, Cell Line, Gene Expression drug effects, Interleukin-1 genetics, Macrophages cytology, Macrophages metabolism, Membrane Glycoproteins metabolism, Mice, Prosthesis Failure, RANK Ligand, Receptor Activator of Nuclear Factor-kappa B, Skull cytology, Tumor Necrosis Factor-alpha genetics, Anti-Bacterial Agents pharmacology, Erythromycin pharmacology, Macrophages drug effects, NF-kappa B metabolism, Osteoclasts cytology
Abstract

Activation of nuclear factor kappa B (NF-kappaB) signaling in response to cell stimulation by wear debris may be critical in the pathogenesis of aseptic loosening. Erythromycin (EM), a macrolide antibiotic, has been shown to effectively suppress some types of inflammatory reactions. In this study, we examined the effect of EM on wear debris-induced osteoclastic bone resorption in vitro. EM inhibited Ca+ release from neonatal calvaria co-cultured with conditioned medium from mouse RAW264.7 macrophages activated by wear debris. Inhibition of Ca+ release was associated with a decreased number of tartrate-resistant acid phosphatase (TRAP)-positive cells in cultured bones. To investigate the mechanism whereby EM inhibits bone-resorption, RAW cells were incubated with wear debris in the presence EM. Real time RT-CR analysis revealed that EM (5 microg/ml) significantly inhibited mRNA expression of NF-kappaB, cathepsin K (CPK), IL-1beta and TNFalpha, but not RANK in RAW cells stimulated with wear debris. Furthermore, electrophoretic mobility-shift assay showed that EM (0.2 microg-5 microg/ml) could reduce DNA-binding activity of NF-kappaB in RAW cells stimulated with wear debris. The inhibition of inflammatory osteoclastogenesis by EM treatment was further confirmed by an osteoclast (OC) formation assay using primary cultures of mouse bone marrow progenitor cells stimulated with macrophage colony-stimulating factor and RANK ligand (RANKL). EM treatment (5 microg/ml) resulted in more than 70% reduction in multinucleated OC formation and 50% reduction of TRAP+ cells by bone marrow progenitor cells. Our findings support that EM suppresses wear debris-induced osteoclastic bone resorption by, at least, down-regulation of NF-kappaB signaling pathway. It appears that EM represents a potential therapeutic candidate for the treatment and prevention of aseptic loosening.

Published
2004
Full Text
View/download PDF

36. Evaluation of the biocompatibility of a chitosan scaffold in mice.

Author

VandeVord PJ, Matthew HW, DeSilva SP, Mayton L, Wu B, and Wooley PH

Subjects
Animals, Biocompatible Materials standards, Bone Substitutes pharmacology, Cell Division, Chitin therapeutic use, Chitosan, Collagen metabolism, Female, Immunity, Cellular, Mice, Mice, Inbred BALB C, Models, Animal, Neovascularization, Physiologic, Neutrophils, Prosthesis Implantation, Tissue Engineering methods, Biocompatible Materials pharmacology, Bone Substitutes chemistry, Chitin analogs & derivatives, Chitin pharmacology
Abstract

Chitosan scaffolds appear to be suitable for a variety of tissue engineering applications. This study addressed the biocompatibility of chitosan in a mouse implantation model. Porous chitosan scaffolds were implanted in mice, and animals were sacrificed after 1, 2, 4, 8, or 12 weeks. Macroscopic inspection of the implantation site revealed no pathological inflammatory responses. Histological assessment indicated marked neutrophil accumulation within the implant, which resolved with increasing implantation time. Gram staining and limulus assays revealed no evidence of infection or endotoxin. Collagen was observed within the chitosan pore spaces, indicating that connective tissue matrix was deposited within the implant. Angiogenic activity associated with the external implant surface was also observed. Cellular immune responses were determined by lymphocyte proliferation assays, and antibody responses were measured using ELISA techniques. These assays indicated a very low incidence of chitosan-specific reactions. Although there was a large migration of neutrophils into the implantation area, there were minimal signs of any inflammatory reaction to the material itself. This preliminary study demonstrates that chitosan has a high degree of biocompatibility in this animal model. Overall, the findings suggest that chitosan may be suitable for the development of implantable materials., (Copyright 2001 John Wiley & Sons, Inc.)

Published
2002
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results