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Updated: Aug 3, 2025

Analysis of Craniomaxillofacial Malformations in Mice Using Three-dimensional Microcomputed Tomography
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Osteoblastic RAR Inhibition Causes VAD-Like Craniofacial Skeletal Deformity.

Q Dai1,2,3,4,5,6, S Sun2,3,4,5,7, A Jin2,3,4,5,7

  • 1The 2nd Dental Center, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Journal of Dental Research
|April 10, 2023
PubMed
Summary
This summary is machine-generated.

Maternal vitamin A deficiency (VAD) causes craniofacial deformities. Inhibiting retinoic acid receptor (RAR) in osteoblasts in mice mimicked VAD skeletal defects, revealing RAR

Keywords:
craniofacial abnormalitiesosteoblastsretinoic acid receptor (RAR)vitamin A deficiency (VAD)

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Area of Science:

  • Developmental Biology
  • Genetics
  • Orthopedics

Background:

  • Retinoid signaling disorders, particularly vitamin A deficiency (VAD), are linked to craniofacial deformities in infants.
  • Previous studies elucidated eye and palate defects in VAD mice but faced challenges in understanding craniofacial skeletal deformities, their cellular origins, and mechanisms.
  • Retinoic acid receptor (RAR) is crucial for retinoid signaling, yet individual gene knockouts do not fully replicate pathway inhibition.

Purpose of the Study:

  • To investigate the role of osteoblastic retinoic acid receptor (RAR) activity in craniofacial skeletal development.
  • To elucidate the mechanisms by which RAR dysfunction in osteoblasts leads to craniofacial deformities mimicking VAD.
  • To establish a mouse model that conditionally inhibits RAR transcription activity in osteoblasts.

Main Methods:

  • Conditional expression of a dominant-negative RARα mutation (dnRARα) in osteoblasts of mice to specifically inhibit RAR transcription activity.
  • Micro-computed tomography (micro-CT) for 3D reconstruction and analysis of craniofacial bone morphology, size, and ossification.
  • Histological analysis and transcriptome sequencing of calvaria to assess bone formation, resorption, and gene expression changes.
  • Cell-autonomous and crosstalk mechanisms involving osteoblast and osteoclast differentiation were investigated.

Main Results:

  • Osteoblastic dnRARα expression successfully mimicked VAD-associated craniofacial skeletal deformities, including cranial bone hypomineralization, mandibular deformity, and clavicular hypoplasia.
  • Micro-CT confirmed significant abnormalities in the shape, size, and ossification of craniofacial bones.
  • Histology and transcriptome data revealed impaired osteoblast differentiation (cell-autonomous) and osteoclast differentiation (via impaired Rankl transcription and osteoblast-osteoclast crosstalk).

Conclusions:

  • Osteoblastic RAR activity is essential for normal craniofacial skeletal development.
  • Inhibition of osteoblastic RAR leads to skeletal deformities that closely resemble clinical VAD craniofacial defects.
  • This study provides novel insights into the pathogenesis of VAD-induced craniofacial skeletal malformations by highlighting the critical role of RAR signaling in osteoblasts.