| Co-Investigator(Kenkyū-buntansha) |
FUKUYAMA Hiroshi Kyusyu Dental College Professor, 教授 (60037546)
TAKAGI Thoru Tokyo Med. & Dent. Univ. Sch. of Dent.,Associate Prof., 歯学部, 講師 (20124696)
KUBOKI Yoshinori Hokkaido Univ. Sch. of Dent., Professor, 歯学部, 教授 (00014001)
NAGATSUKA Hitoshi Okayama Univ. Dental Sch., Assistant prof., 歯学部, 助手 (70237535)
TAKESHITA Nobuyoshi Okayama Univ. Dental Sch., Associate prof., 歯学部, 助教授 (00118275)
堤 啓 大阪医科大学, 検査部, 助教授 (10032864)
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| Budget Amount *help |
¥5,100,000 (Direct Cost: ¥5,100,000)
Fiscal Year 1992: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1991: ¥3,100,000 (Direct Cost: ¥3,100,000)
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| Research Abstract |
Odontogenic tumors are thought to be originated from epithelial and /or mesenchymal tissue of tooth germ, because of morphological similarities between these tumors and tooth germs. But the origin and histogenesis of most of the odontogenic tumors have been remained to be unproven. Amelogenin, an organic matrix of enamel in the early developmental stage, is well known to be proline rich glycoprotein with low molecular weight, distinct from keratins or collagen molecules(10-11). Since complete amino acid sequence of amelogenin was accomplished by Takagi et al (12) and Yeh et al (13), non cross-reacting monoclonal antibodies against amelogenin were developed. With these monoclonal antibodies, amelogenin was detected ultrastructurally, and merocrine secretion of amelogenin by late preameloblasts and secretory ameloblasts was elucidates. The detection of amelogenin was considered to be useful as a marker of functioning ameloblasts in clarifying the histogenesis of odontogenic tumors.
Immuno
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histochemical expressions of cytokeratin, amelogenin, and enamelin were studies in odontogenic tumors; ameloblastoma, adenomatoid odontogenic tumor, ameloblastic carcinoma. Four anti-cytokeratin monoclonal antibodies were used in this study: CK-1 to total keratin, SE-K to 56,56.5,58 and 68Kd,NSE-K to 52.5Kd,and 19K to 40Kd. Cytokeratin expression in follicular ameloblastoma was similar to that in tooth germ epithelia, and in plexiform ameloblastoma similar to that in fetal oral mucosa. Both types of ameloblastoma also showed slight immunoreactivity for amelogenin. In adenomatoid odontogenic tumor there was a difference between cytokeratin expression in central cells and in peripheral cells in the tumor nests. Moreover, cytokeratin expression in adenomatoid odontogenic tumor was completely different from those in ameloblastoma and tooth germ. Immunoreactivity for amelogenin and enamelin in adenomatoid odontogenic tumor was found in colloidal drops, calcified masses and lining cell membrane of ductlike structure. Therefore, it is possible that these tumor cells differentiate into enamel protein-producing cells, more than those of ameloblastoma do. Immunohistochemical results in ameloblastic carcinoma showed that this carcinoma is composed of undifferentiated odontogenic tumor cells. Also, an immunohistochemical study of localization of type I,II and III collagen were discussed in mandibular condylar cartilage compared with fibrillar bone. Bone matrix protein detected in osteogenic tumors. Less
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