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 …