Pathogenesis of adhesive otitis media and study of mechanism of development into the pars tensa cholesteatoma

粘连性中耳炎发病机制及紧张部胆脂瘤发展机制研究

• 批准号: 11671705
• 负责人: MORIYAMA Hiroshi
• 金额: $ 2.24万
• 依托单位: THE JIKEI UNIVERSITY SCHOOL OF MEDICINE
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671705/
• 关键词: proliferation and differentiation of epithelium; cholesteatoma; cytokine; keratinocyto; apoptosis; 細胞周期関連因子

From our molecular biological studies concerning proliferation, terminal differentiation and apoptosis of keratinocystes (epidermis) in cholesteatoma, cholesteatoma is a result of a vicious circle of inflammations. Therefore, the treatment for cholesteatoma is either complete removal of cholesteatoma matrix and debris or the cutting off of the vicious circle.First of all, migration in retraction pocket is disturbed by infection, then inflammation persists and leads to proliferation of keratinocytes. As a result, keratine debris accumulates and epidermis and subepithelial tissue are activated. Various cytokines and other factors are involved in this reaction. In addition to it, autocrine and paracrine regulation of cytokines plays a key role in the growth of cholesteatoma epithelium.However, there is only a slight difference between the terminal differentiation and apoptosis of keratinocytes (epidermis) in the cholesteatoma and those in the normal skin.I surmise that the hyperproliferation of cholesteatoma epidermis is compensated by the full function of terminal differentiation and apoptosis, thus the balance is retained as opposed to malignant squamous neoplasias.

从我们对胆脂瘤角质细胞（表皮）增殖、终末分化和凋亡的分子生物学研究来看，胆脂瘤是炎症恶性循环的结果。因此，胆脂瘤的治疗要么是彻底清除胆脂瘤基质和碎片，要么是切断恶性循环。首先，回缩袋的迁移受到感染的干扰，炎症持续存在，导致角质形成细胞增殖。结果，角蛋白碎片积聚，表皮和上皮下组织被激活。该反应涉及多种细胞因子和其他因素。除此之外，细胞因子的自分泌和旁分泌调节在胆脂瘤上皮的生长过程中也起着关键作用。但胆脂瘤中角质形成细胞（表皮）的终末分化和凋亡与正常皮肤中的差异不大。 .我推测胆脂瘤表皮的过度增殖是通过终末分化和凋亡的完整功能来补偿的，因此保持了平衡，而不是恶性鳞状肿瘤。

项目成果

小島 博巳,他: "鼓膜緊張部の菲薄化、陥凹、癒着化 -上皮の増殖、分化、緊張部真珠腫の発症機序-"Otology Japan. 9:3. 202-210 (1999)

Hiromi Kojima 等人：“鼓膜张力区变薄、凹陷和粘连 - 张力区胆脂瘤的上皮增殖、分化和发病机制”Otology Japan 9:3 (1999)。

森山寛,上出洋介,小島博己 他: "真珠腫の病態と治療 その3-自然消退する先天性真珠腫?"耳鼻咽喉科展望. 42:3. 301-305 (1999)

Hiroshi Moriyama、Yosuke Kamide、Hiroki Kojima 等：“胆脂瘤的病理学和治疗第 3 部分 - 自发消退的先天性胆脂瘤？” 301-305 (1999)。

Miyamaki H, et al: "Terminal differentiation of epithelial cells in middle ear cholesteatoma : Investigation Of patterns of expression of protein kinase Cδand protein kinase Cη"Laryngoscope. 109:12. 1785-1792 (1999)

Miyamaki H 等人：“中耳胆脂瘤上皮细胞的终末分化：蛋白激酶 Cδ 和蛋白激酶 Cn 表达模式的研究”Laryngoscopy 109:12 (1999)。

Moriyama H, Kojima H, Tanaka Y, Miyazaki H, Aoki K.: "Pathogenesis and treatment for middle ear cholesteatoma-Pars flaccida retraction caused by congenital cholesteatoma of mastoid cavity (in Japanese)."ORL Tokyo. 42. 414-420 (1999)

Moriyama H、Kojima H、Tanaka Y、Miyazaki H、Aoki K.：“乳突腔先天性胆脂瘤引起的中耳胆脂瘤 - 松弛部回缩的发病机制和治疗（日语）。”ORL 东京。

辻富彦 他: "鼓膜癒着症の耳管機能-術前、術後の評価-"日本耳鼻咽喉科学会会報. 102:6. 818-824 (1999)

Tomihiko Tsuji 等人：“鼓膜粘连中的肠管功能 - 术前和术后评估”日本耳鼻喉科协会通报 102:6 (1999)。