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Updated: Jan 23, 2026

Application of Retinoic Acid to Obtain Osteocytes Cultures from Primary Mouse Osteoblasts
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Osteocyte Death and Bone Overgrowth in Mice Lacking Fibroblast Growth Factor Receptors 1 and 2 in Mature Osteoblasts

Jennifer McKenzie1,2, Craig Smith3, Kannan Karuppaiah3

  • 1Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO, USA.

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research
|June 18, 2019
PubMed

Insights

Fibroblast growth factor receptor (FGFR) signaling is crucial for bone development. Loss of FGFR1 in mature osteoblasts leads to high bone mass, increased porosity, and osteocyte loss, impacting bone regulation.

Area of Science:

  • Skeletal Biology
  • Bone Metabolism
  • Cell Signaling

Background:

  • Fibroblast growth factor (FGF) signaling is vital for skeletal development, influencing chondrogenesis and osteogenesis.
  • Previous studies suggested distinct roles for FGF receptor 1 (FGFR1) and FGF receptor 2 (FGFR2) in osteogenesis, but redundancy and stage-specific regulation remained unclear.

Purpose of the Study:

  • To investigate the roles of FGFR1 and FGFR2 signaling in mature osteoblasts and osteocytes.
  • To elucidate the consequences of conditional inactivation of Fgfr1 and Fgfr2 on postnatal bone growth and regulation.

Main Methods:

  • Conditional inactivation of Fgfr1 and Fgfr2 in mature osteoblasts using Osteocalcin (OC)-Cre and Dentin matrix protein 1 (Dmp1)-CreER drivers in mice.
  • Phenotypic analysis, including bone mass, periosteal apposition, endocortical bone organization, porosity, and biomechanical testing.
  • Histopathological examination and gene expression analysis to assess cellular changes and signaling pathway activation.

Main Results:

  • Young mice lacking FGFR1 and/or FGFR2 were phenotypically normal.
  • Between 6 and 12 weeks, conditional knockout mice exhibited a high bone mass phenotype with increased periosteal apposition and disorganized endocortical bone.
  • This phenotype was associated with significant osteocyte loss, increased bone porosity, impaired material properties, and activation of the Wnt/β-catenin signaling pathway.

Conclusions:

  • FGFR1 signaling in mature osteoblasts/osteocytes is essential for osteocyte survival during postnatal bone growth.
  • FGFR1 signaling plays a critical role in regulating bone mass and maintaining bone quality.
  • These findings highlight a novel function of FGFR1 in the adult bone remodeling process.
Keywords:
APOPTOSISFIBROBLAST GROWTH FACTORSMOLECULAR PATHWAYS-REMODELINGOSTEOBLASTSOSTEOCYTES

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