Abstract Craniosynostosis is a congenital condition characterized by the premature fusion of the craniofacial sutures. The Crouzon mouse (Fgfr2cC342Y/+) is a well-established model of this condition which shows premature fusion of the coronal suture. Our group has recently shown that postnatal, cyclic loading can potentially rescue the coronal suture and normalize skull morphology in Crouzon mice. This study aimed to investigate the underlying biological mechanism of the treatment. Wild-type (WT) and Crouzon (MUT) mice underwent in vivo loading sessions. Loading did not significantly affect skull shape. The patency across the coronal suture did not change between treated and untreated MUT animals. Orientation and coherence of the coronal suture collagen fibres were statistically different when comparing WT untreated with MUT untreated and WT treated with MUT treated. Treatment increases the number of proliferative cells in both the WT and MUT sutures compared to their untreated counterparts. The mechanobiological mechanisms driving the differences need further investigation into molecular mechanotransduction pathways. Understanding the biological principles affected during bone loading, a more refined cyclical bone loading protocol can be developed and refined for potential clinical use.
Steacy et al. (Wed,) studied this question.