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

本研究旨在建立一种实验动物模型，在该模型中，釉质发育不全发生在切牙和磨牙。对体重150-160 g的雄性Wister大鼠每天注射一次HEBP，持续一周。取上颌切牙及周围组织进行组织学检查和釉原蛋白mRNA原位杂交。牙本质-釉质交界处沿着形成若干个釉质岛，在这些岛之间观察到无釉质区。釉原蛋白基因在无釉区成釉细胞和釉岛成釉细胞中均有表达。在使用抗牛釉原蛋白抗体检测成釉细胞中的釉原蛋白的免疫组织化学检查中，提示在无釉区的成釉细胞中存在对抗体具有阳性反应的颗粒。这些结果表明，注射HEBP既不改变釉原蛋白基因的表达，也不合成的釉原蛋白肽在celles.In这项研究中，牙釉质低钙化的成釉性牙釉质发育不全的患者也进行了检查，使用免疫化学和生物化学技术。牙釉质中的釉原蛋白含量与未成熟的牛牙釉质相当。主要分子的大小被认为是约25 kDa，这与存在于分泌期釉质外层的牛24 kDa亲本釉原蛋白的大小几乎相同。这些结果表明，这种疾病可能是由于在成熟phase.The目前的数据表明，发育不全和hypocalcified类型的釉质缺损的过程中的降解和/或再吸收的过程中的干扰引起的牙釉质蛋白基因表达没有任何干扰。

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.