Remodeling of the sagittal suture development in sclerostin knockout male mice associated with cranial flat bone...

The purpose of this study was to examine the effect of lack of sclerostin gene (Sost) on the growth and development of cranial bone associated with sagittal suture.

10, 15, 30, and 60-day-old wild-type mice and Sost knockout (Sost^Δ26/Δ26) mice were served in this study. The calvariae including sagittal sutures were removed and observed microscopically. The activity of osteoclast was examined by tartrate-resistant acid phosphatase (TRAP) staining and the expression of sclerostin and β-catenin were evaluated by immunohistochemical methods.

It was shown that Sost^Δ26/Δ26 mice resulted in increased bone formation, leading to thickening of the calvaria. Suture stenosis and partial bone obliteration accompanied by higher expressive levels of β-catenin have also been observed in Sost^Δ26/Δ26 mice, while sagittal suture remains its patency in the late developmental stage.

These results suggest that Sost^Δ26/Δ26 mice shows accumulation of β-catenin, inducing a metabolic effect on bone remodeling during the early postnatal period, which may be related to the abnormality of cranial suture in Sost^Δ26/Δ26 mice.