1,25二羟维生素D3缺乏对小鼠继发性牙本质生成、矿化和龋损的影响

目的探讨1,25二羟维生素D3[1,25（OH）2D3]对小鼠继发性牙本质生成和矿化的作用。方法利用苏木精-伊红（HE）染色、免疫组织化学染色和碱性磷酸酶（ALP）组织化学染色方法,比较分析6周龄野生型和1α 羟化酶基因敲除小鼠[1α（OH）ase-/-小鼠]下颌骨矿化的差异。结果与野生型小鼠相比,1α（OH）ase-/-小鼠下颌第一磨牙龋损明显增加,面继发性牙本质面积明显减少,Ⅰ型胶原及OCN在继发性牙本质的阳性比例明显减少,Biglycan在继发性牙本质的阳性比例明显增加,ALP明显减少。结论1,25（OH）2D3缺乏会导致小鼠继发性牙本质生成、矿化减少和龋损增加。

The effect of 1,25 (OH)2D3 deficiency in the secondary dentin formation and mineralization and caries of the mice

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.