2000 Fiscal Year Final Research Report Summary
Pathogenesis of adhesive otitis media and study of mechanism of development into the pars tensa cholesteatoma
| Project/Area Number |
11671705
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | THE JIKEI UNIVERSITY SCHOOL OF MEDICINE |
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Principal Investigator |
MORIYAMA Hiroshi THE JIKEI UNIVERSITY SCHOOL OF MEDICINE OTOLARYNGOLOGY PROFESSOR AND CHAIRMAN, 医学部・耳鼻咽喉科, 教授 (60125036)
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| Co-Investigator(Kenkyū-buntansha) |
MITANI Yukie THE JIKEI UNIVERSITY SCHOOL OF MEDICINE OTOLARYNGOLOGY, ASSISTANT, 医学部・耳鼻咽喉科, 助手 (30233894)
SHIWA Masanori THE JIKEI UNIVERSITY SCHOOL OF MEDICINE OTOLARYNGOLOGY, LECTURER, 医学部・耳鼻咽喉科, 講師 (20235766)
KOJIMA Hiromi THE JIKEI UNIVERSITY SCHOOL OF MEDICINE OTOLARYNGOLOGY, LECTURER, 医学部・耳鼻咽喉科, 講師 (60234762)
TANAKA Yasuhiro THE JIKEI UNIVERSITY SCHOOL OF MEDICINE OTOLARYNGOLOGY,ASSISTANT, 医学部・耳鼻咽喉科, 助手 (40266648)
TSUJI Tomihiko THE JIKEI UNIVERSITY SCHOOL OF MEDICINE OTOLARYNGOLOGY, ASSISTANT, 医学部・耳鼻咽喉科, 助手 (30236880)
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| Project Period (FY) |
1999 – 2000
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| Keywords | proliferation and differentiation of epithelium / cholesteatoma / cytokine / keratinocyto / apoptosis |
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| Research Abstract |
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.
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