Targeted disruption of the dentin sialophosphoprotein (DSPP) gene in the mice (Dspp-/-) results in dentin mineralization defects with enlarged predentin phenotype similar to human dentinogenesis imperfecta type III. Using DSPP/biglycan (Dspp-/-Bgn-/0) and DSPP/decorin (Dspp-/-Dcn-/-) double knockout mice, here we determined that the enlarged predentin layer in Dspp-/- teeth is rescued in the absence of decorin, but not in the absence of biglycan. However, Fourier transform infrared (FTIR) spectroscopy analysis reveals similar hypomineralization of dentin in both Dspp-/-Bgn-/0 and Dspp-/-Dcn-/- teeth. Atomic force microscopy (AFM) analysis of collagen fibrils in dentin shows subtle differences in the collagen fibril morphology in these genotypes. The reduction of enlarged predentin in Dspp-/-Dcn-/- mice suggests that the elevated level of decorin in Dspp-/- predentin interferes with the mineralization process at the dentin mineralization front. On the other hand, the lack of DSPP and biglycan leads to the increased number of calcospherites in Dspp-/-Bgn-/0 predentin, suggesting that a failure in coalescence of calcospherites was augmented in Dspp-/-Bgn-/0 teeth as compared to Dspp-/- teeth. These findings indicate that normal expression of small leucine rich proteoglycans, such as biglycan and decorin, plays an important role in the highly orchestrated process of dentin mineralization.
- Dentin mineralization
- Dentin sialophosphoprotein (DSPP)
- Dentinogenesis imperfecta (DGI)
- Knockout mouse
ASJC Scopus subject areas
- Molecular Biology