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Related Experiment Video

Updated: Jul 7, 2026

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
09:41

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Published on: October 17, 2017

Statins attenuate polymethylmethacrylate-mediated monocyte activation.

Alan J Laing1, John P Dillon, Kevin J Mulhall

  • 1Department of Surgical Research, Cork University Hospital, Cork, Ireland. alanjlaing1@hotmail.com

Acta Orthopaedica
|February 20, 2008
PubMed
Summary

Statins, like cerivastatin, may prevent aseptic loosening in joint arthroplasty by inhibiting monocytic activation and inflammatory cytokine production, potentially increasing implant longevity.

Related Experiment Videos

Last Updated: Jul 7, 2026

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
09:41

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Published on: October 17, 2017

Area of Science:

  • Biomaterials Science
  • Immunology
  • Pharmacology

Background:

  • Periprosthetic osteolysis is a major cause of joint arthroplasty failure, leading to aseptic loosening and complicating revision surgeries.
  • Statins (HMG-CoA reductase inhibitors) are known for their anti-inflammatory effects.
  • This study investigates statins' role in preventing the initial stage of osteolysis: monocytic activation.

Purpose of the Study:

  • To investigate the potential role of statins in inhibiting monocytic activation in response to biomaterial particles.
  • To determine if cerivastatin can modulate the inflammatory response to polymethylmethacrylate (PMMA) particles in vitro.
  • To elucidate the intracellular signaling pathways involved in this process.

Main Methods:

  • An in vitro model using human monocytes/macrophages exposed to PMMA particles was employed.
  • Cells were pretreated with cerivastatin, a potent statin.
  • Tumor necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1) production was measured.
  • The Raf-MEK-ERK intracellular signaling pathway was analyzed via western blot.

Main Results:

  • Cerivastatin pretreatment significantly reduced the production of TNF-alpha and MCP-1 by monocytes stimulated with PMMA particles.
  • This anti-inflammatory effect appears to be mediated by the intracellular Raf-MEK-ERK signaling pathway.
  • Statins may intervene in the early stages of the osteolytic cascade.

Conclusions:

  • Statins, through their anti-inflammatory properties, may suppress osteoclast activation and osteolysis by inhibiting upstream monocytic activation.
  • Statins could potentially serve a prophylactic role in preventing aseptic loosening and extending the longevity of joint implants.
  • Targeting early inflammatory responses offers a promising strategy for improving arthroplasty outcomes.