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Related Experiment Video

Updated: Nov 10, 2025

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro
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Apremilast inhibits inflammatory osteoclastogenesis.

Yannick Degboé1,2, Flavia Sunzini1, Shatakshi Sood1

  • 1Institute of Infection, Inflammation and Immunity, University of Glasgow, Glasgow, UK.

Rheumatology (Oxford, England)
|March 31, 2021
PubMed
Summary

Apremilast (APR) directly inhibits osteoclast formation in psoriatic arthritis (PsA) by reducing inflammatory cytokines and osteoclastogenesis, suggesting a bone-protective effect in PsA patients.

Keywords:
apremilastbonecytokinesinflammationosteoclastsphosphodiesterase 4

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Area of Science:

  • Immunology
  • Rheumatology
  • Bone Biology

Background:

  • Psoriatic arthritis (PsA) involves bone erosion and loss driven by osteoclasts (OCs) and inflammatory cytokines.
  • Apremilast (APR), a phosphodiesterase 4 inhibitor, is effective in PsA by reducing cytokine production, but its direct impact on human osteoclast formation is unknown.

Purpose of the Study:

  • To investigate the direct effects of Apremilast (APR) on osteoclast formation and function in psoriatic arthritis (PsA).
  • To determine if APR modulates osteoclastogenic cytokine production and differentiation in human cells.

Main Methods:

  • Assessed osteoclastogenic cytokine production by human peripheral blood mononuclear cells (PBMCs) with and without APR.
  • Evaluated APR's effect on osteoclast differentiation in PBMC co-cultures and stimulated monocytes.
  • Measured bone resorption and compared ex vivo osteoclast differentiation in PsA, pre-PsA, psoriasis patients, and healthy controls.

Main Results:

  • APR significantly reduced key osteoclastogenic cytokines in activated PBMCs.
  • APR dose-dependently inhibited PBMC-driven osteoclast differentiation in PsA and pre-PsA patients.
  • APR suppressed TNF and IL-17A-induced osteoclastogenesis and bone resorption in PsA patient monocytes.

Conclusions:

  • Targeting phosphodiesterase 4 with APR inhibits both cytokine production and direct osteoclastogenesis.
  • APR demonstrates potential for a direct bone-protective effect in psoriatic arthritis (PsA).