Macrophages-Key cells in the response to wear debris from joint replacements.
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Adverse Biological Effect of TiO₂ and Hydroxyapatite Nanoparticles Used in Bone Repair and ReplacementThe pathobiology and pathology of aseptic implant failureInteraction of Materials and Biology in Total Joint Replacement - Successes, Challenges and Future Directions.Interleukin-1 receptor-associated kinase-4 (IRAK4) promotes inflammatory osteolysis by activating osteoclasts and inhibiting formation of foreign body giant cells.Can wear explain the histological variation around metal-on-metal total hips?Modulation of mouse macrophage polarization in vitro using IL-4 delivery by osmotic pumps.Contributions of human tissue analysis to understanding the mechanisms of loosening and osteolysis in total hip replacement.Do genetic susceptibility, Toll-like receptors, and pathogen-associated molecular patterns modulate the effects of wear?Establishment of Green Fluorescent Protein and Firefly Luciferase Expressing Mouse Primary Macrophages for In Vivo Bioluminescence Imaging.The BCL2 -938C>A Promoter Polymorphism Is Associated with Risk for and Time to Aseptic Loosening of Total Hip Arthroplasty.Immune modulation as a therapeutic strategy in bone regeneration.Lentivirus-mediated short hairpin RNA interference targeting TNF-alpha in macrophages inhibits particle-induced inflammation and osteolysis in vitro and in vivoInflammation, fracture and bone repair.Autophagy mediated CoCrMo particle-induced peri-implant osteolysis by promoting osteoblast apoptosis.Increased migration of uncemented acetabular cups in female total hip arthroplasty patients with low systemic bone mineral density. A 2-year RSA and 8-year radiographic follow-up study of 34 patientsVitamin D attenuates inflammation, fatty infiltration, and cartilage loss in the knee of hyperlipidemic microswine.Osteolysis around total knee arthroplasty: a review of pathogenetic mechanisms.Chronic inflammation in biomaterial-induced periprosthetic osteolysis: NF-κB as a therapeutic target.Novel biological strategies for treatment of wear particle-induced periprosthetic osteolysis of orthopaedic implants for joint replacement.Toll-like receptors-2 and 4 are overexpressed in an experimental model of particle-induced osteolysis.Contribution of human osteoblasts and macrophages to bone matrix degradation and proinflammatory cytokine release after exposure to abrasive endoprosthetic wear particles.The effects of immunomodulation by macrophage subsets on osteogenesis in vitro.Recombinant CC16 protein inhibits the production of pro-inflammatory cytokines via NF-κB and p38 MAPK pathways in LPS-activated RAW264.7 macrophages.Osseointegration of Zirconia in the Presence of Multinucleated Giant Cells.Mesenchymal stem cells in the aseptic loosening of total joint replacements.Gene Expression in Osteolysis: Review on the Identification of Altered Molecular Pathways in Preclinical and Clinical Studies.Comprehensive study on the roles of released ions from biodegradable Mg-5 wt% Ca-1 wt% Zn alloy in bone regeneration.Bioeffects of micron-size magnesium particles on inflammatory cells and bone turnover in vivo and in vitro.The effect of local IL-4 delivery or CCL2 blockade on implant fixation and bone structural properties in a mouse model of wear particle induced osteolysis.Probiotics protect mice from CoCrMo particles-induced osteolysis.Immune response and innervation signatures in aseptic hip implant looseningNetrin-1 is highly expressed and required in inflammatory infiltrates in wear particle-induced osteolysis.Role of macrophages in the biological reaction to wear debris from joint replacements.Macrophage polarization and activation in response to implant debris: influence by "particle disease" and "ion disease"Innate immune reactions in septic and aseptic osteolysis around hip implants.Correlations between macrophage polarizing cytokines, inflammatory mediators, osteoclast activity, and toll-like receptors in tissues around aseptically loosened hip implants.* Murine Model of Progressive Orthopedic Wear Particle-Induced Chronic Inflammation and Osteolysis.Biological effects of metal degradation in hip arthroplasties.Mutant CCL2 protein coating mitigates wear particle-induced bone loss in a murine continuous polyethylene infusion model.Particle disease really does exist.
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P2860
Macrophages-Key cells in the response to wear debris from joint replacements.
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
@pt
bilimsel makale
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scientific article published on 09 April 2013
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Macrophages-Key cells in the response to wear debris from joint replacements.
@en
Macrophages-Key cells in the response to wear debris from joint replacements.
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type
label
Macrophages-Key cells in the response to wear debris from joint replacements.
@en
Macrophages-Key cells in the response to wear debris from joint replacements.
@nl
prefLabel
Macrophages-Key cells in the response to wear debris from joint replacements.
@en
Macrophages-Key cells in the response to wear debris from joint replacements.
@nl
P2093
P2860
P50
P356
P1476
Macrophages-Key cells in the response to wear debris from joint replacements
@en
P2093
Allison J Rao
Christophe Nich
Jukka Pajarinen
Michiaki Takagi
Stuart B Goodman
Yasunobu Tamaki
Yuya Takakubo
P2860
P304
P356
10.1002/JBM.A.34599
P577
2013-04-09T00:00:00Z