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Methotrexate and low-dose prednisolone downregulate osteoclast function by decreasing receptor activator of nuclear

Inês Pedro Perpétuo1, Joana Caetano-Lopes1, Ana Maria Rodrigues1

  • 1Rheumatology Research Unit, Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.

RMD Open
|September 29, 2017
PubMed
Abstract

Insights

Methotrexate (MTX) and low-dose prednisolone (PDN) treatment in rheumatoid arthritis (RA) patients downregulates osteoclast (OC) function. This occurs by decreasing RANK surface expression on monocytes, reducing bone resorption and damage.

Area of Science:

  • Immunology
  • Rheumatology
  • Bone Biology

Background:

  • Rheumatoid arthritis (RA) is an autoimmune disease causing joint destruction.
  • Methotrexate (MTX) is a common treatment that slows bone damage, but its mechanism is unclear.
  • Osteoclasts (OCs) are key cells in bone erosion.

Purpose of the Study:

  • To investigate the effects of MTX and low-dose prednisolone (PDN) on OC precursors.
  • To analyze OC differentiation in RA patients undergoing treatment.
  • To understand the role of monocytes and RANK ligand in RA bone damage.

Main Methods:

  • Compared RA patients before and after MTX+PDN therapy to healthy donors.
  • Assessed RANK ligand surface expression on leukocytes and monocyte subpopulations.
  • Measured serum bone turnover markers, cytokines, and performed OC differentiation assays.

Main Results:

  • RA patients showed increased monocyte activation markers and RANK at baseline.
  • MTX+PDN treatment normalized these markers to control levels.
  • Reduced bone resorption by OCs was observed post-treatment, linked to decreased RANK expression.

Conclusions:

  • MTX+PDN therapy effectively downregulates OC function in RA.
  • The mechanism involves reducing RANK surface expression on monocytes.
  • This contributes to slowing bone erosion in rheumatoid arthritis.
Keywords:
BoneDMARDMonocytesOsteoclastRheumatoid arthritis

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