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    Statins attenuate polymethylmethacrylate-mediated monocyte activation.

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    Authors
    Laing, Alan J
    Dillon, John P
    Mulhall, Kevin J
    Wang, J H
    McGuinness, Anthony J
    Redmond, Paul H
    Affiliation
    Department of Surgical Research, Cork University Hospital, Cork, Ireland., alanjlaing1@hotmail.com
    Issue Date
    2012-02-03T15:13:40Z
    MeSH
    Anti-Inflammatory Agents/*pharmacology
    Arthroplasty, Replacement/adverse effects
    Cytokines/biosynthesis
    Humans
    Hydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology
    Inflammation/immunology
    Models, Biological
    Monocytes/*drug effects/immunology
    Osteolysis/etiology/immunology
    Polymethyl Methacrylate/*pharmacology
    *Prosthesis Failure
    Pyridines/*pharmacology
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    Citation
    Acta Orthop. 2008 Feb;79(1):134-40.
    Journal
    Acta orthopaedica
    URI
    http://hdl.handle.net/10147/209153
    DOI
    10.1080/17453670710014888
    PubMed ID
    18283585
    Abstract
    BACKGROUND: Periprosthetic osteolysis precipitates aseptic loosening of components, increases the risk of periprosthetic fracture and, through massive bone loss, complicates revision surgery and ultimately is the primary cause for failure of joint arthroplasty. The anti-inflammatory properties of HMG-CoA reductase inhibitors belonging to the statin family are well recognized. We investigated a possible role for status in initiating the first stage of the osteolytic cycle, namely monocytic activation. METHODS: We used an in vitro model of the human monocyte/macrophage inflammatory response to poly-methylmethacrylate (PMMA) particles after pretreat-ing cells with cerivastatin, a potent member of the statin family. Cell activation based upon production of TNF-alpha and MCP-1 cytokines was analyzed and the intracellular Raf-MEK-ERK signal transduction pathway was evaluated using western blot analysis, to identify its role in cell activation and in any cerivastatin effects observed. RESULTS: We found that pretreatment with cerivastatin significantly abrogates the production of inflammatory cytokines TNF-alpha and MCP-1 by human monocytes in response to polymethylmethacrylate particle activation. This inflammatory activation and attenuation appear to be mediated through the intracellular Raf-MEK-ERK pathway. INTERPRETATION: We propose that by intervening at the upstream activation stage, subsequent osteoclast activation and osteolysis can be suppressed. We believe that the anti-inflammatory properties of statins may potentially play a prophylactic role in the setting of aseptic loosening, and in so doing increase implant longevity.
    Language
    eng
    ISSN
    1745-3682 (Electronic)
    1745-3674 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1080/17453670710014888
    Scopus Count
    Collections
    Cork University Hospital

    entitlement

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