Experimental study on the pulp obriteraltion as a complication of luxation injuries of teeth.

本研究旨在建立门牙和磨牙釉质发育不全的实验动物模型。对牙釉质发育不全的动物模型进行了组织学和生化检查。体重150 ~ 160 g的雄性Wister大鼠，每天1次注射HEBP，连续一周。解剖上颌切牙及周围组织，进行组织学检查，并进行淀粉原蛋白mRNA原位杂交。沿牙本质-牙釉质交界处形成若干牙釉质小岛，小岛之间可见无牙釉质区。在无牙釉质区成釉细胞和牙釉质胰岛成釉细胞中均检测到成釉原蛋白基因的表达。用抗牛淀粉原抗体检测成釉细胞中淀粉原蛋白的免疫组化检查，发现在无釉质区成釉细胞中存在对抗体有阳性反应的颗粒。这些结果表明，注射HEBP既没有改变细胞中淀粉原蛋白基因的表达，也没有改变淀粉原蛋白肽的合成。在这项研究中，我们也用免疫化学和生化技术检查了低钙化无釉发育不全患者的牙釉质。牙釉质与未成熟的牛牙釉质一样含有淀粉原蛋白。主要分子的大小约为25 kDa，与存在于秘书期牙釉质外层的24 kDa亲本淀粉原蛋白的大小几乎相同。这些结果表明，这种疾病可能是由成熟阶段珐琅质蛋白降解和/或吸收过程中的干扰引起的。目前的研究结果表明，牙釉质发育不良和低钙化两种类型的牙釉质缺陷均可发生，但不影响淀粉原蛋白基因的表达。

The present study was undertaken to establish an experimental animal model in which enamel hypoplasia has occur in incisors and molars. The teeth suffered from enamel hypoplasia in this animal model has also been examined histologically and biochemically.Male Wister rats, weighing 150-160 g, were injected with HEBP once a day for a week. The maxillary incisors and surrounding tissues were dissected out and used for the histological examination and in situ hybridization of amelogenin mRNA. Several islets of enamel were formed along the dentino-enamel junction, and enamel free zones were observed between these islets. The amelogenin gene expression was detected in the ameloblasts in the enamel free zone as well as in the ameloblasts on the enamel islets. In the immunohistochemical examination for the detection of amelogenin in the ameloblasts using anti-bovine amelogenin antibody, the presence of the granules having positive reaction to the antibody was suggested in the ameloblasts in the enamel free zone. These results indicate that the injection of HEBP alters neither the amelogenin gene expression nor synthesis of amelogenin peptides in the cells.In this study, enamels from patients with hypocalcified amelogenesis imperfecta were also examined using immunochemical and biochemical techniques. The enamel contained amelogenin as much as immature bovine enamel. The size of the major molecules had been suggested to be about 25 kDa which was almost the same as that of the bovine 24 kDa parent amelogenin being present in the outer layer of secretary-stage enamel. These results suggest that this disease may be caused by a disturbance in the process of degradation and/or resorption of enamel proteins in the maturation phase.The present data indicate that both hypoplastic and hypocalcified types of enamel defects will occur in the teeth without any disturbances in the amelogenin gene expression.