Document Detail

Local effect of IL-4 delivery on polyethylene particle induced osteolysis in the murine calvarium.
MedLine Citation:
PMID:  23225668     Owner:  NLM     Status:  MEDLINE    
Wear particles generated with use of total joint replacements incite a chronic macrophage-mediated inflammatory reaction, which leads to implant failure. Macrophage activation may be polarized into two states, with an M1 proinflammatory state dominating an alternatively activated M2 anti-inflammatory state. We hypothesized that IL-4, an activator of M2 macrophages, could modulate polyethylene (PE) particle-induced osteolysis in an experimental murine model. Four animal groups included (a) calvarial saline injection with harvest at 14 days (b) single calvarial injection of PE particles subcutaneously (SC) without IL-4 (c) PE particles placed as in (b), then IL-4 given SC for 14 consecutive days and (d) PE particles as in (b) then IL-4 beginning 7 days after particle injection for 7 days. The calvarial bone volume to total tissue volume was measured using microCT and histomorphometry. Calvaria were cultured for 24 h to assess release of RANKL, OPG, TNF-α, and IL-1ra and isolation and identification of M1 and M2 specific proteins. MicroCT and histomorphometric analysis showed that bone loss was significantly decreased following IL-4 administration to PE treated calvaria for both 7 and 14 days. Western blot analysis showed an increased M1/M2 ratio in the PE treated calvaria, which decreased with addition of IL-4. Cytokine analysis showed that the RANKL/OPG ratio and TNF-α/IL-1ra ratio decreased in PE-treated calvaria following IL-4 addition for 14 days. IL-4 delivery mitigated PE particle-induced osteolysis through macrophage polarization. Modulation of macrophage polarization is a potential treatment strategy for wear particle induced periprosthetic osteolysis.
Allison J Rao; Christophe Nich; Lakshmi S Dhulipala; Emmanuel Gibon; Roberto Valladares; Stefan Zwingenberger; R Lane Smith; Stuart B Goodman
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-12-05
Journal Detail:
Title:  Journal of biomedical materials research. Part A     Volume:  101     ISSN:  1552-4965     ISO Abbreviation:  J Biomed Mater Res A     Publication Date:  2013 Jul 
Date Detail:
Created Date:  2013-05-28     Completed Date:  2013-10-29     Revised Date:  2014-07-01    
Medline Journal Info:
Nlm Unique ID:  101234237     Medline TA:  J Biomed Mater Res A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1926-34     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Wiley Periodicals, Inc.
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MeSH Terms
Acid Phosphatase / metabolism
Biological Markers
Blotting, Western
Bone Remodeling / drug effects
Cytokines / metabolism
Drug Delivery Systems
Enzyme-Linked Immunosorbent Assay
Interleukin-4 / pharmacology*
Isoenzymes / metabolism
Lectins / metabolism
Mice, Inbred C57BL
Nitric Oxide Synthase Type II / metabolism
Osteoclasts / drug effects
Osteolysis / chemically induced*,  prevention & control*
Polyethylenes / toxicity*
RANK Ligand / chemistry
Skull / drug effects*
Tomography, X-Ray Computed
Tumor Necrosis Factor-alpha / metabolism
beta-N-Acetylhexosaminidases / metabolism
Grant Support
1R01 AR063717-01/AR/NIAMS NIH HHS; 2R01 AR055650-05/AR/NIAMS NIH HHS; R01 AR055650/AR/NIAMS NIH HHS; R01 AR063717/AR/NIAMS NIH HHS
Reg. No./Substance:
0/Biological Markers; 0/Cytokines; 0/Isoenzymes; 0/Lectins; 0/Polyethylenes; 0/RANK Ligand; 0/Tumor Necrosis Factor-alpha; 207137-56-2/Interleukin-4; EC Oxide Synthase Type II; EC 3.1.3.-/tartrate-resistant acid phosphatase; EC Phosphatase; EC protein, mouse; EC

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