Related Experiment Video
Updated: Aug 11, 2026

Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification
Published on: December 3, 2016
FGF signaling in the developing endochondral skeleton
1Department of Molecular Biology and Pharmacology, Washington University Medical School, Campus Box 8103, 660 S. Euclid Ave., St. Louis, MO 63110, USA. dornitz@wustl.edu
Abstract:
Mutations in fibroblast growth factor receptors (Fgfrs) are the etiology of many craniosynostosis and chondrodysplasia syndromes in humans. The phenotypes associated with these human syndromes and the phenotypes resulting from targeted mutagenesis in the mouse have defined essential roles for FGF signaling in both endochondral and intramembranous bone development. In this review, I will focus on the role of FGF signaling in chondrocytes and osteoblasts and how FGFs regulate the growth and development of endochondral bone.
Insights
Fibroblast growth factor receptors (Fgfrs) mutations cause craniosynostosis and chondrodysplasia. FGF signaling is crucial for bone development, particularly in chondrocytes and osteoblasts during endochondral bone growth.
Area of Science:
- Skeletal Biology
- Developmental Biology
- Genetics
Background:
- Mutations in fibroblast growth factor receptors (Fgfrs) are linked to human craniosynostosis and chondrodysplasia syndromes.
- FGF signaling plays essential roles in both endochondral and intramembranous bone development, as evidenced by human syndromes and mouse models.
Purpose of the Study:
- This review focuses on the specific roles of FGF signaling within chondrocytes and osteoblasts.
- It aims to elucidate how FGFs regulate the intricate processes of endochondral bone growth and development.
Main Methods:
- Review of existing literature on Fgfr mutations and FGF signaling pathways.
- Analysis of phenotypic data from human craniosynostosis and chondrodysplasia syndromes.
- Examination of findings from targeted mutagenesis studies in mouse models.
Main Results:
- Fgfr mutations are established causes of significant skeletal developmental disorders.
- FGF signaling is a key regulator of chondrocyte differentiation and proliferation.
- FGFs influence osteoblast activity and the overall process of endochondral ossification.
Conclusions:
- FGF signaling is indispensable for normal skeletal development, particularly endochondral bone formation.
- Understanding FGF pathways in chondrocytes and osteoblasts offers insights into treating skeletal dysplasias.
- Further research into FGF signaling mechanisms can identify therapeutic targets for bone disorders.
Related Concept Videos
Growth of Cartilage and Bone Tissue
Bone Formation by Intramembranous Ossification
The process begins when mesenchymal cells in the embryonic skeleton gather together and differentiate into osteogenic cells, which then develop into...
Bone Remodeling and Repair
Changes in the Appendicular Skeleton with Age
Initially, the limb buds consist of a core of mesenchyme covered by a layer of ectoderm. The ectoderm at the end of the limb bud thickens to form a narrow crest called the apical ectodermal ridge. This ridge stimulates the underlying...
Development of the Limb Synovial Joints
The mesenchymal stem cells differentiate into chondrocytes that form the hyaline cartilage, and later the cartilaginous model of the bone. This model further transforms into a bone. This process is known as endochondral ossification.
During development, the limbs...
Bone Formation by Endochondral Ossification

