Abstract:

Objective To determine the role of 1,25（OH）2D3 on the secondary dentin formation and mineralization of the mice. Methods The differences of the mandible mineralization between the wild-type and 1-α-hydroxylase gene knockout mice at 6 weeks old were assessed by hematoxylin-eosin（HE） staining, immunohistochemistry, alkaline phosphatase（ALP） histochemistry staining. Results The ratio of caries were increased significantly, while the secondary dentin was reduced significantly, the deposition of type Ⅰ collagen and osteocalcin on the secondary dentin of occlusion surface was decreased significantly, but the deposition of the Biglycan on the dentin was increased significantly, the active of ALP on the odontoblasts were reduced significantly in 1-α-hydroxylase gene knockout mice compared to that in the wild-type littermates. Conclusion 1,25（OH）2D3 deficiency lead to a defect in the secondary dentin formation and mineralization and caries of the mice.

Key words: 1,25（OH）2D3, secondary dentin, mineralization, caries