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Macrophage-Pulp Fibroblast Interactions Modulate Initial Dental Pulp Regeneration In Vitro.

Chloé Le Fournis1, Thomas Giraud1,2, Sandra Roumani1

  • 1Aix Marseille Univ, CNRS, Inst Movement Sci, Marseille, France.

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|January 20, 2026
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Summary
This summary is machine-generated.

Pulp fibroblasts influence macrophage types (M1/M2), which then control pulp stem cell (DPSC) behavior and blood vessel growth, impacting pulp regeneration. This study reveals key cell interactions in early pulp healing.

Keywords:
angiogenesismacrophage differentiationpulp fibroblastpulp regeneration

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Area of Science:

  • Dental Pulp Biology
  • Tissue Engineering
  • Immunology

Background:

  • Injured fibroblasts are crucial for pulp inflammation and regeneration.
  • Fibroblasts direct macrophage differentiation into pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes.
  • Understanding these interactions is key to modulating pulp healing.

Purpose of the Study:

  • To investigate the effects of fibroblast-conditioned macrophages on dental pulp stem cell (DPSC) proliferation and migration.
  • To assess the impact of these macrophages on neo-angiogenesis in pulp regeneration.
  • To elucidate the role of fibroblast-macrophage crosstalk in initial pulp repair mechanisms.

Main Methods:

  • Isolation and characterization of human dental pulp stem cells (DPSCs) and pulp fibroblasts.
  • Stimulation of fibroblasts mimicking carious lesions (injury and Lipoteichoic Acid - LTA).
  • Incubation of macrophages (M0) with stimulated fibroblast supernatants to induce M1/M2 differentiation; assessment of DPSC viability, migration, VEGF secretion, and endothelial cell neo-angiogenesis.

Main Results:

  • Fibroblast supernatants induced macrophage differentiation, influencing DPSC and endothelial cell viability.
  • M2-like macrophage secretomes promoted DPSC proliferation and endothelial cell organization (neo-angiogenesis).
  • M1-like macrophage secretomes (from LTA-stimulated fibroblasts) enhanced DPSC migration and VEGF secretion.

Conclusions:

  • Pulp fibroblasts dictate macrophage polarization (M1/M2) based on stimulation.
  • Macrophage phenotypes subsequently modulate DPSC proliferation/migration and neo-angiogenesis.
  • Cell-cell interactions are critical for initiating pulp tissue regeneration.