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MicroRNA-29b Promotes Subchondral Bone Loss in TMJ Osteoarthritis.

J L Sun1,2, J F Yan1, S B Yu1

  • 1State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases and Shaanxi Key Laboratory of Stomatology, School of Stomatology, The Fourth Military Medical University, Xi'an, China.

Journal of Dental Research
|July 23, 2020
PubMed
Summary

MicroRNA-29b (miR-29b) levels are reduced in bone marrow mesenchymal stem cells (BMSCs) of temporomandibular joint osteoarthritis (TMJ-OA) mice, contributing to abnormal bone remodeling. Restoring miR-29b in BMSCs can rescue bone loss and cartilage degradation in TMJ-OA.

Keywords:
RNA aptamerWnt-5aagomirsantagomirsbone marrow mesenchymal stem cells (BMSCs)osteogenesis

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Area of Science:

  • Biomedical Sciences
  • Molecular Biology
  • Orthopedics

Background:

  • Abnormal subchondral bone remodeling is central to osteoarthritis (OA) pathology.
  • Bone marrow mesenchymal stem cells (BMSCs) in osteoarthritic subchondral bone promote osteoclastogenesis, but the mechanism is unclear.

Purpose of the Study:

  • To investigate the role of microRNA-29b (miR-29b) in the pro-osteoclastic effects of BMSCs in temporomandibular joint osteoarthritis (TMJ-OA).
  • To explore miR-29b as a potential therapeutic target for TMJ-OA.

Main Methods:

  • A unilateral anterior crossbite (UAC) mouse model was used to induce TMJ-OA-like changes.
  • Aptamer-based delivery systems (agomiR-29b and antagomiR-29b) were employed for BMSC-specific modulation of miR-29b levels.
  • Micro-computed tomography (micro-CT), gene expression analysis, and histological assessments were performed.

Main Results:

  • BMSCs from UAC mice showed significantly lower miR-29b levels compared to controls.
  • Overexpression of miR-29b in BMSCs rescued subchondral bone loss and reduced osteoclast activity in UAC mice.
  • miR-29b targeted Wnt5a, and its modulation in BMSCs affected both subchondral bone remodeling and OA-like cartilage degradation.

Conclusions:

  • miR-29b is a critical regulator of BMSC pro-osteoclastic activity in TMJ-OA subchondral bone.
  • BMSC-specific miR-29b restoration offers a potential therapeutic strategy for TMJ-OA by mitigating bone and cartilage damage.