1995 Fiscal Year Final Research Report Summary
Experimental study on the induction of enamel hypoplasia
| Project/Area Number |
06672042
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
矯正・小児・社会系歯学
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| Research Institution | Tokyo medical and Dental University |
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Principal Investigator |
TAKAGI Yuzo Tokyo Medical &Dental University, School of Dentistry Department of Pedodontics Associate Professor, 歯学部, 助教授 (30124697)
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| Project Period (FY) |
1994 – 1995
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| Keywords | ENAMEL HYPOPLASIA / EXPERIMENTAL ANIMAL MODEL / RAT / HEBP / AMELOGENIN / mRNA / ANTI-AMELOGENIN ANTIBODY / AMELOGENESIS IMPERFECTA |
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| Research Abstract |
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 150-160g, 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 HEBE 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 layr 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.
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Research Products
(2 results)
