During skull development, the calvarial bones are formed by intramembranous ossification.As calvarial bones advance to envelop the brain, fibrous sutures form between the calvarial plates.Brain expansion is coupled with calvarial growth through a series of tissue interactions within the cranial suture complex.Craniosynostosis, the premature fusion of the skull bones at the sutures, represents a disruption in the coordinated growth and development of the expanding brain and calvarial vault, and is the second most common birth defect that affects the craniofacial complex.Mutations in fibroblast growth factor receptors (FGFRs) are thought to cause craniosynostosis in Crouzon syndrome andApertsyndrome.However mutations in MSX2, a bone morphogenetic protein (BMP) effector transcription factor, are thought to account for Boston-type craniosynostosis.Recent studies have demonstrated that FGFs/FGFRs interact with BMPs in calvadal bone osteogenesis.Here we show that BMP2 expression is induced by FGF2 and that co-treatment of FGF2 and BMP2 induced later-stageosteoblastic differentiation of cranial suture cells.However, inhibition of BMP2 signaling by Noggin weakens the effect of FGF2 or FGF2 plus BMP2 on induction of later-stageosteoblastic differentiation of cranial suture cells.Therefore, we suggest that BMP2 signaling is required for FGF2-lependent induction of later-stage of cranial suture cell osteoblastic differentiation.