アブストラクト（34巻4号：神奈川歯学）

神奈川歯学

Japanese

Title　： 歯原性腫瘍の病理発生におけるbcl-2の発現とその役割
Subtitle　：
Authors　： 駒津栄雄, 槻木恵一
Authors（kana）　： こまつしげお, つきのきけいいち
Organization　： 神奈川歯科大学口腔病理学教室
Journal　： 神奈川歯学
Volume　： 34
Number　： 4
Page　： 193-208
Year/Month　： 1999 / 12
Article　： 原著
Publisher　： 神奈川歯科大学学会
Abstract　： アポトーシスは, Kerrら1), Wyllie2)によって提唱された生理的細胞死の概念である. 多細胞生物に備わった重要な機能の一つであるアポトーシスは不必要となった細胞の消去の役割を果たし, その誘導から実行, あるいは抑制に至る一連の過程が遺伝子によって巧妙に制御されていることが近年明らかにされた. 一方, Bcl-2タンパクはミトコンドリア外膜に存在し, 種々の刺激によって生じるアポトーシスに対し, 最終的にその実行因子であるカスパーゼを不活性化してアポトーシスを抑制するという生理活性をもつ. 山崎ら3)はヒト歯の形成過程ならびに顎骨内に遺残した歯原性細胞に発現するBcl-2タンパクの局在を免疫組織化学的に検索し, エナメル質基質形成時期のエナメル芽細胞や中間層細胞に発現するBcl-2タンパクの細胞死抑制機能がその細胞寿命を延長し, 歯冠エナメル質の形成に関与すること, また歯の萌出後, 歯原性上皮の顎骨内遺残の一因がこれらの細胞に発現するBcl-2タンパクのもつ抗アポトーシス作用による可能性を示した.
Practice　： 歯科学
Keywords　： bcl-2, 歯原性腫瘍, エナメル上皮腫, ヒト歯胚

English

Title　： Bcl-2 Expression and Its Role in Odontogenic Tumor Genesis
Subtitle　：
Authors　： Shigeo KOMATSU, Keiichi TSUKINOKI
Authors（kana）　：
Organization　： Department of Oral Pathology, Kanagawa Dental College
Journal　： Kanagawa Shigaku
Volume　： 34
Number　： 4
Page　： 193-208
Year/Month　： 1999 / 12
Article　： Original article
Publisher　： Kanagawa Odontological Society
Abstract　： The subjects studied were 28 cases of odontogenic tumor including 23 cases of benign odontogenic tumor and 5 cases of malignant odontogenic tumor. Furthermore, 3 specimens of fetal tooth germ were also prepared as control. All of these were investigated for assessing the expression of Bcl-2 protein immunohistochemically. Furthermore, the materials of several cases were selected to detect bcl-2 mRNA detection by RT-PCR method and clarified the involvement of bcl-2 apoptosis regulation in the pathogenesis of odontogenic tumor. In the experiment using the tooth germs collected from 19-week and 20-week human embryos, bcl-2 mRNA was detected by the experiment using RT-PCR method. DNA amplification band which indicated the message of bcl-2 mRNA was detected in the resected tooth germ tissues (one case). Nineteen ameloblastoma cases were selected to assess the expression of Bcl-2 protein. This protein appeared in the tumor cells obtained from follicular type, plexiform type, acanthomatus type, basal cell type, unicystic ameloblastoma and desmoplastic ameloblastoma. The expression of Bcl-2 protein, however, was not detected in the tumor cells of granular cell type; bcl-2 mRNA was evident in two ameloblastoma cases (follicular type and plexiform type). The expression of Bcl-2 protein was detected in the epithelial tumor cells in all cases of benign odontogenic tumor tested including one case of ameloblastic fibroma, two cases of ameloblastic fibro-odontoma and one case of odontogenic epithelial hamartoma. Bcl-2 protein was also confirmed in the tumor cells from malignant ameloblastoma which showed primary intraosseous carcinoma (2 cases). On the contrary, Bcl-2 protein was detected neither in squamous cell carcinoma originated from the oral cavity, esophagus and parotid gland nor in the normal mucosal epithelium. The expression of Bcl-2 protein was not recognized in the three cases of squamous cell carcinoma originating from the odontogenic keratocysts. These results show that the apoptosis regulation function of Bcl-2 protein which appears in the odontogenic epithelium in the processes of dental development may be involved in odontogenic tumorigenesis.
Practice　： Dentistry
Keywords　：