2006 Fiscal Year Final Research Report Summary
Study on elucidation of the mechanism of development and progression of acquired middle ear cholesteatoma and its prevention and treatment
| Project/Area Number |
16591728
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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 | Jikei University School of Medicine |
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Principal Investigator |
MORIYAMA Hiroshi Jikei University, School of medicine, Professor, 医学部, 教授 (60125036)
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| Co-Investigator(Kenkyū-buntansha) |
KOJIMA Hiromi Jikei University, School of medicine, Associate Professor, 医学部, 助教授 (60234762)
TANAKA Yasuhiro Jikei University, School of medicine, Lecturer, 医学部, 講師 (40266648)
YOSHIKAWA Mamoru Jikei University, School of medicine, Lecturer, 医学部, 講師 (50277092)
WADA Kota Jikei University, School of medicine, Research Assistant, 医学部, 助手 (20307482)
YAGUCHI Yuichiro Jikei University, School of medicine, Research Assistant, 医学部, 助手 (30307475)
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| Project Period (FY) |
2004 – 2006
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| Keywords | epithelium growth / differentiation and apoptosis / cytokine / epidermal growth factor / mucosal gas exchange / mucosal regeneration / pathogenesis of cholesteatoma |
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| Research Abstract |
We conducted a basic and clinical study in relation to the mechanism of development and progression of acquired cholesteatoma and simultaneously assessed the pathology of acquired cholesteatoma, surgical procedures, postoperative results, postoperative course, recurrence, factors related to hearing improvement, and selection criteria for appropriate surgery.
The mechanisms of development and progression are postulated to be based on three. stages. In the first stage, there is retraction in the pars flaccid, and it is due to accumulation of fluid associated with intractable otitis media, the development of negative pressure as a result of impaired mucosal gas metabolism caused by mucosal lesions, and repair of inflammation. Interaction between of narrowing of bone morphology around the epitympanic recess associated with suppression of air cell formation and the formation of mucosal folds also appears to be involved. However, cholesteatomas do not develop as a result of these morphologica
… More
l changes alone, and persistence of chronic inflammation in the epitympanic recess space is necessary as the second stage. In other words, as a result of thickening of the stroma due to the spread of the inflammation the lower surface of the depressed epithelium leads to the formation of complex narrow pockets. Following epidermal proliferation and granulation as a result of acute exacerbation of the inflammation, the depressed cyst wall partially collapses. As stratified squamous epithelium replaces the mucosal epithelium, it immigrates into the mucosal spaces and exhibits a complex morphology. In the third stage there is involvement by cytokines as a result of accumulation of debris and infection. Cholesteatomas presumably progress by a vicious cycle of inflammation in which epidermal proliferation is induced by cross talk between the subepidermal tissue, including the stimulation by subepithelial fibroblasts, etc., due to impairment of the barrier function of the cholesteatoma epithelium. Less
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Research Products
(14 results)
