Abstract

The effects of dietary sucrose feeding, intragastric sucrose feeding and dietary calcium-deficiency on primary dentinogenesis of the pulp-dentin organ and caries progression were examined in an experimental rat model. The possible role of calcium balance and reduced mineralization of dentin organic matrix as a cause of reduced dentin formation in young, fast growing, rats were also studied. During 3-6 weeks of feeding, immediately after weaning at 3 weeks the urinary calcium, phosphorus, potassium and sodium levels and excretion rates were determined. The areas of dentin formed, the width of the predentin layer, serum mineral and insulin levels, and the areas of dentinal caries lesions were quantified at the end of the experiment. Also the occurrence and progression level of caries lesions were measured. In rat pups, dietary sucrose reduced dentin formation both during the lactation and experimental periods, increased urinary Ca²⁺ excretions, reduced urinary P, K and Na excretions, and enhanced dental caries occurrence and progression, but it did not affect the width of the predentin layer or the serum mineral and insulin levels. Intragastric sucrose reduced dentin formation and increased Ca²⁺ excretion, but did not affect the width of the predentin layer, serum mineral and insulin levels in the blood or induce dental caries. Dietary calcium-deficiency reduced dentin formation, increased the width of the predentin layer, caused hypocalcemia, and reduced urinary Ca²⁺ excretion. These results show that sucrose and calcium-deficiency reduce the rate of primary dentinogenesis through different mechanisms. Calcium imbalance or reduced mineralization of the dentin organic matrix does not explain the reduced dentinogenesis in sucrose fed rats. In conclusion, the present findings indicate that a sucrose load reduces dentinogenesis by impairing the synthesis rate of the dentin organic matrix, but also points out the importance of the local sucrose challenge in initiating dental caries.