Effect of ProRoot MTA® and Biodentine® on osteoclastic differentiation and activity of mouse bone marrow macrophages

Miri Kim1, Soojung Kim1, Hyunjung Ko1

  • 1Asan Medical Center, University of Ulsan, Department of Conservative Dentistry, Seoul, Korea.

Abstract

Insights

ProRoot MTA (PMTA) and Biodentine (BIOD) inhibit osteoclast differentiation and activity, similar to alendronate (ALD). These dental materials impact key signaling pathways involved in bone resorption.

Area of Science:

  • Biomaterials Science
  • Cell Biology
  • Dental Materials

Background:

  • Osteoclasts are crucial for bone resorption and are implicated in various bone pathologies.
  • Understanding the effects of dental materials on osteoclastogenesis is vital for clinical applications.
  • Alendronate (ALD) is a known inhibitor of osteoclast activity.

Purpose of the Study:

  • To evaluate the osteoclast differentiation inhibitory effects of ProRoot MTA (PMTA) and Biodentine (BIOD).
  • To compare the effects of PMTA and BIOD with alendronate (ALD) on osteoclasts.
  • To investigate the molecular mechanisms underlying the inhibitory actions of PMTA and BIOD.

Main Methods:

  • Murine bone marrow macrophages (BMMs) were differentiated into osteoclasts.
  • Cells were treated with PMTA, BIOD, or ALD.
  • Osteoclast differentiation, activity (resorption pits, TRAP staining), gene expression (RT-qPCR), and signaling pathways (Western blot) were assessed.

Main Results:

  • PMTA, BIOD, and ALD significantly reduced the number of TRAP-positive osteoclasts.
  • BIOD showed a lesser inhibitory effect on osteoclast-related gene expression (cathepsin K, TRAP, c-Fos) compared to PMTA and ALD.
  • PMTA and BIOD suppressed RANKL-mediated phosphorylation of ERK1/2 and IκBα signaling pathways.

Conclusions:

  • ProRoot MTA and Biodentine exhibit inhibitory effects on osteoclast differentiation and activity.
  • These effects are comparable to alendronate and are mediated through the inhibition of IκB phosphorylation and ERK signaling.
  • PMTA and BIOD represent potential therapeutic agents for conditions involving excessive osteoclast activity.

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