抄録
Developing skull sutures are the place in which osteogenic cell proliferation-differentiation balance is maintained. Mutations in fibroblast growth factor receptors (FGFRs) and TWIST cause congenital anomaly called craniosynostosis defined as early closure of one or more cranial sutures. Previous studies have suggested: 1) TWIST is expressed in the sutural mesenchyme maintaining undifferentiated condition; 2) FGFR2 expression is associated with proliferation of osteogenic progenitor cells; 3) FGFR1 expression regulates osteoblast differentiation. In order to evaluate this hypothesis we carried out immunohistochemical detection of cell cycle regulators in mouse developing suture. Cell cycle regulators which promote cell proliferation are mainly present where Fgfr2 is expressed, they are also detected in some of the sutural cells. Other cell cycle regulators that inhibit cell cycle progression localize in cells adjacent to the osteoid in which Fgfr1 is expresssed. These results support the hypothesis and suggest that mutations in the genes induce the imbalanced osteogenic differentiation resulting in early suture fusion.
