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Depletion and Reconstitution of Macrophages in Mice
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Macrophage Polarization during MRONJ Development in Mice.

A Soundia1, N Elzakra2, D Hadaya2

  • 1Private practice, Kennewick, WA, USA.

Journal of Dental Research
|August 6, 2024
PubMed
Summary

Medication-related osteonecrosis of the jaws (MRONJ) involves M1 macrophage polarization. Rosiglitazone reversed this M1 predilection and reduced MRONJ burden in mice, suggesting M2 promotion as a therapeutic strategy.

Keywords:
bone biologyimmunityinflammationosteonecrosisperiodontal disease(s)/periodontitisperiodontal tissues/periodontium

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Area of Science:

  • Oral and Maxillofacial Surgery
  • Immunology
  • Bone Biology

Background:

  • Macrophages regulate bone remodeling, with M1 polarization implicated in medication-related osteonecrosis of the jaws (MRONJ).
  • Zoledronate (ZA) is a common medication associated with MRONJ.
  • Early macrophage phenotypes in MRONJ development are not fully understood.

Purpose of the Study:

  • To characterize macrophage polarization during early MRONJ development in a mouse model.
  • To investigate the therapeutic potential of rosiglitazone in mitigating MRONJ burden.

Main Methods:

  • Zoledronate (ZA) administration and experimental periodontal disease (EPD) induction in mice.
  • Micro-computed tomography, histology, and immunohistochemistry for analysis.
  • Assessment of MRONJ burden with and without rosiglitazone treatment.

Main Results:

  • M1 macrophage polarization, positive for MMP-13, was observed in early stages of MRONJ development in ZA-treated mice.
  • Rosiglitazone treatment reversed M1/M2 macrophage polarization.
  • Rosiglitazone significantly decreased osteonecrosis and bone exposure in ZA-treated mice with EPD.

Conclusions:

  • M1 macrophage polarization and MMP-13 overexpression play a critical role in early MRONJ pathogenesis.
  • Promoting an M2 macrophage phenotype via interventions like rosiglitazone may offer a preventative strategy for MRONJ.