Document Detail


Contributions of angiogenesis to inflammation, joint damage, and pain in a rat model of osteoarthritis.
MedLine Citation:
PMID:  21538326     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To determine the contributions of angiogenesis to inflammation, joint damage, and pain behavior in a rat meniscal transection model of osteoarthritis (OA).
METHODS: OA was induced in male Lewis rats (n=8 per group) by meniscal transection. Animals were orally dosed with dexamethasone (0.1 mg/kg/day), indomethacin (2 mg/kg/day), or the specific angiogenesis inhibitor PPI-2458 (5 mg/kg every other day). Controls consisted of naive and vehicle-treated rats. Synovial inflammation was measured as the macrophage fractional area (expressed as the percentage), thickness of the synovial lining, and joint swelling. Synovial angiogenesis was measured using the endothelial cell proliferation index and vascular density. Channels positive for vessels at the osteochondral junction were assessed (osteochondral angiogenesis). Medial tibial plateaus were assessed for chondropathy, osteophytosis, and channels crossing the osteochondral junction. Pain behavior was measured as weight-bearing asymmetry.
RESULTS: Dexamethasone and indomethacin each reduced pain behavior, synovial inflammation, and synovial angiogenesis 35 days after meniscal transection. Dexamethasone reduced, but indomethacin had no significant effect on, the total joint damage score. PPI-2458 treatment reduced synovial and osteochondral angiogenesis, synovial inflammation, joint damage, and pain behavior.
CONCLUSION: Our findings indicate that synovial inflammation and joint damage are closely associated with pain behavior in the meniscal transection model of OA. Inhibition of angiogenesis may reduce pain behavior both by reducing synovitis and by preventing structural change. Targeting angiogenesis could therefore prove useful in reducing pain and structural damage in OA.
Authors:
Sadaf Ashraf; Paul I Mapp; David A Walsh
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Arthritis and rheumatism     Volume:  63     ISSN:  1529-0131     ISO Abbreviation:  Arthritis Rheum.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-09-07     Completed Date:  2011-11-08     Revised Date:  2011-12-01    
Medline Journal Info:
Nlm Unique ID:  0370605     Medline TA:  Arthritis Rheum     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2700-10     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2011 by the American College of Rheumatology.
Affiliation:
Arthritis Research UK Pain Centre, Department of Academic Rheumatology, University of Nottingham, City Hospital, Nottingham, UK. sadaf.ashraf@nottingham.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Animals
Anti-Inflammatory Agents, Non-Steroidal / pharmacology,  therapeutic use
Behavior, Animal / drug effects
Cartilage, Articular / drug effects,  pathology,  physiopathology
Dexamethasone / pharmacology,  therapeutic use
Glucocorticoids / pharmacology,  therapeutic use
Indomethacin / pharmacology,  therapeutic use
Inflammation / complications,  pathology,  physiopathology
Joints / drug effects,  pathology*,  physiopathology
Male
Neovascularization, Pathologic / complications,  pathology*,  physiopathology
Osteoarthritis / complications,  pathology*,  physiopathology
Pain / complications,  drug therapy,  pathology*,  physiopathology
Pain Measurement
Rats
Rats, Inbred Lew
Weight-Bearing / physiology
Grant Support
ID/Acronym/Agency:
18769//Arthritis Research UK
Chemical
Reg. No./Substance:
0/Anti-Inflammatory Agents, Non-Steroidal; 0/Glucocorticoids; 50-02-2/Dexamethasone; 53-86-1/Indomethacin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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