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β-catenin Orchestrates Gli1+ Cell Fate in Condylar Development and TMJOA.

J Wang1, X Dong1, J Lei2

  • 1Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, China.

Journal of Dental Research
|October 14, 2024
PubMed
Summary

Researchers identified Gli1+ fibrocartilage stem cells (FCSCs) crucial for condyle health. Targeting Wnt/β-catenin signaling in these cells prevents cartilage degeneration in temporomandibular joint osteoarthritis (TMJOA).

Keywords:
Gli1+ cellsfibrocartilage stem cellsosteoarthritispostnatal developmentsingle-cell transcriptome analysistemporomandibular joint

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Area of Science:

  • Stem cell biology
  • Regenerative medicine
  • Orthopedics

Background:

  • Fibrocartilage stem cells (FCSCs) are vital for condyle cartilage homeostasis and regeneration.
  • Identifying specific markers for FCSCs is crucial for understanding their fate and regulation.
  • Current knowledge on FCSCs in temporomandibular joint osteoarthritis (TMJOA) is limited.

Purpose of the Study:

  • To identify novel markers for FCSCs and elucidate their role in condyle development and TMJOA.
  • To investigate the involvement of Wnt/β-catenin signaling in Gli1+ FCSC fate.
  • To explore therapeutic potential of targeting Gli1+ FCSCs in TMJOA.

Main Methods:

  • Transcriptional landscape mapping of condylar cartilage.
  • Label-retaining cell analysis and lineage tracing to identify FCSCs.
  • Conditional knockout of β-catenin in Gli1+ cells.
  • Induction of TMJOA via discectomy and subsequent analysis.

Main Results:

  • A Gli1+ subset of FCSCs was identified and validated through lineage tracing.
  • Conditional knockout of β-catenin in Gli1+ cells inhibited their differentiation into hypertrophic chondrocytes.
  • Gli1+ cells were activated and showed accelerated hypertrophic differentiation in TMJOA, leading to stem cell depletion.
  • Deletion of β-catenin in Gli1+ cells preserved the FCSC pool and reduced TMJOA cartilage degeneration.

Conclusions:

  • A Gli1+ FCSC subpopulation plays a key role in condyle development and TMJOA.
  • Wnt/β-catenin signaling critically regulates the fate of Gli1+ FCSCs.
  • Targeting Gli1+ FCSCs and Wnt/β-catenin signaling offers a potential therapeutic strategy for TMJOA.