Cranial bone microarchitecture in a mouse model for syndromic craniosynostosis.

ABSTRACT: Crouzon syndrome is a congenital craniofacial disorder caused by mutations in the Fibroblast Growth Factor Receptor 2 (FGFR2). It is characterized by the premature fusion of cranial sutures, leading to a brachycephalic head shape, and midfacial hypoplasia. The aim of this study was to investigate the effect of the FGFR2 mutation on the microarchitecture of cranial bones at different stages of postnatal skull development, using the FGFR2^C342Y mouse model. Apart from craniosynostosis, this model shows cranial bone abnormalities. High-resolution synchrotron microtomography images of the frontal and parietal bone were acquired for both FGFR2^C342Y/+ (Crouzon, heterozygous mutant) and FGFR2^+/+ (control, wild-type) mice at five ages (postnatal days 1, 3, 7, 14 and

SUBMITTER: Ajami S 

PROVIDER: S-EPMC11547221 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature