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Macrophages modulate mesenchymal stem cell function via tumor necrosis factor alpha in tooth extraction model.

Aung Ye Mun1, Kentaro Akiyama1, Ziyi Wang2

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Depleting macrophages impairs bone regeneration by reducing mesenchymal stem cells (MSCs) and inflammatory cells. TNF-α activation of MSCs is crucial for tooth extraction socket healing.

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Area of Science:

  • Regenerative Medicine
  • Immunology
  • Oral Biology

Background:

  • Mesenchymal stem cells (MSCs) and macrophages are key players in bone regeneration.
  • The precise mechanisms of MSC-macrophage interaction, particularly with M1 macrophages, are not fully understood.

Purpose of the Study:

  • To investigate the role of macrophages in bone regeneration after tooth extraction.
  • To elucidate the interaction between MSCs and M1 macrophages during the healing process.
  • To identify molecular mechanisms, including TNF-α signaling, involved in MSC-macrophage crosstalk.

Main Methods:

  • A macrophage-depleted mouse model using clodronate liposomes was established.
  • Histochemical analysis quantified M1, M2, MSC, and TNF-α+ cells in tooth extraction sockets.
  • In vitro bulk RNA-sequencing (RNA-Seq) analyzed TNF-α-stimulated MSCs.

Main Results:

  • Macrophage depletion significantly reduced bone regeneration and the number of M1, MSC, and TNF-α+ cells.
  • A temporal reduction and subsequent recovery of these cells were observed after depletion.
  • RNA-Seq identified 15 candidate genes in MSCs potentially regulating immunomodulatory capacity.

Conclusions:

  • Macrophages, especially M1, are essential for effective bone regeneration after tooth extraction.
  • TNF-α signaling plays a critical role in activating MSCs during socket healing.
  • Specific genes like Clec4e, Gbp6, and Cxcl10 are implicated in inflammation and bone formation, influencing MSC osteogenic differentiation.