Matsumoto S, Yamaguchi M, Arai M, Togari A, Matsui H, Tajima S, Kohsaka M, Kawai M
Department of Pharmacology, School of Dentistry, Aichi-Gakuin University, Nagoya, Japan.
Aichi Gakuin Daigaku Shigakkai Shi. 1990 Sep;28(3):785-96.
The rat incisor is continuously growing throughout the animal's life recording the state of mineralization within its dentin at all times. Therefore, it was assumed that the incisor dentin was suitable material for studying the effects of various drugs on such mineralization. The present study set out to examine the effects of vitamin D3 metabolites on the remineralization of dentin and the serum calcium level in parathyroidectomized (PTX) rats. Male Wistar rats weighing about 200-250 g were parathyroidectomized. Each rat was given daily 12 g of a synthetic diet containing 0.1% Ca and 0.4% P (normal P) or 0.06% P (P deficient) without vitamin D. Exp. I: Three groups of rats given a normal P diet were orally administered vehicle, 25 (OH) D3 (50 IU/rat) or 1,25 (OH)2D3 (5 IU/rat) for 5 days from the 28th day after PTX, respectively. Exp. II: Two groups of rats given a normal P diet or a P deficient diet were further divided into 4 sub-groups and intramuscularly administered 0, 5,000, 10,000 or 20,000 IU of vitamin D3 on the 9th day after PTX, respectively. The active vitamin D3, 1,25 (OH)2D3 restored the mineralization of the dentin which had been suppressed following PTX, and elevated the serum calcium level to about 9 mg/dl. However, the 25 (OH) D3 neither restored the mineralization of the dentin nor elevated the serum calcium level in the PTX rats. At doses below 1,000 IU, vitamin D3 could not restore the mineralization of the dentin. However, at massive doses above 5,000 IU, the mineralization was restored in proportion to the dose. The serum calcium levels also increased in proportion to the dose. It is assumed that the increase of the serum calcium level was mainly due to the enhancement of calcium absorption from the intestine by vitamin D3. Both remineralization of the incisor dentin and increase of the serum calcium level were more marked in groups of rats given a P deficient diet than in those given a normal P diet. In all cases in the present experiments, the degree of mineralization of the dentin seemed to correspond with the degree of elevation of the serum calcium levels. These results suggest that the remineralization of the dentin in the PTX rats was attributable to the effect of the vitamin D3 metabolites on serum calcium regulation. Relative biological activities of 1,25 (OH)2D3, 25 (OH) D3 and vitamin D3 on the remineralization of dentin were estimated to be 1, less than 0.02 and less than 0.001, respectively.
大鼠的门齿在动物的一生中持续生长,随时记录牙本质内的矿化状态。因此,人们认为门齿牙本质是研究各种药物对这种矿化作用的合适材料。本研究旨在研究维生素D3代谢产物对甲状旁腺切除(PTX)大鼠牙本质再矿化及血清钙水平的影响。选用体重约200 - 250 g的雄性Wistar大鼠进行甲状旁腺切除术。每只大鼠每天给予12 g不含维生素D的合成饲料,其中一组含0.1%钙和0.4%磷(正常磷),另一组含0.06%磷(低磷)。实验I:PTX术后第28天起,三组给予正常磷饲料的大鼠分别口服赋形剂、25(OH)D3(50 IU/只)或1,25(OH)2D3(5 IU/只),持续5天。实验II:两组分别给予正常磷饲料或低磷饲料的大鼠进一步分为4个亚组,PTX术后第9天分别肌肉注射0、5000、10000或20000 IU维生素D3。活性维生素D3,即1,25(OH)2D3可恢复PTX后被抑制的牙本质矿化,并使血清钙水平升高至约9 mg/dl。然而,25(OH)D3既不能恢复PTX大鼠的牙本质矿化,也不能提高其血清钙水平。低于1000 IU的剂量下,维生素D3不能恢复牙本质矿化。然而,高于5000 IU的大剂量时,矿化程度与剂量成比例恢复。血清钙水平也与剂量成比例增加。推测血清钙水平的升高主要是由于维生素D3增强了肠道对钙的吸收。给予低磷饲料的大鼠组门齿牙本质的再矿化和血清钙水平的升高比给予正常磷饲料的大鼠组更明显。在本实验的所有情况下,牙本质的矿化程度似乎与血清钙水平的升高程度相对应。这些结果表明,PTX大鼠牙本质的再矿化归因于维生素D3代谢产物对血清钙调节的作用。1,25(OH)2D3、25(OH)D3和维生素D3对牙本质再矿化的相对生物活性估计分别为1、小于0.02和小于0.001。