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Morphological Changes in the Temporal Bone and the Expression of Fas Ligand in Patients with Cholesteatoma

中耳膽脂瘤的顳骨骨質變化與Fas ligand的表現

摘要


背景 中耳膽脂瘤的特徵在於上皮細胞過度增生與角質碎屑堆積在中耳乳突腔中,引起顳骨骨質的破壞,這種細胞過度增生堆積的現象與膽脂瘤上皮細胞的凋亡作用有關。Fas ligand (FasL)爲上皮細胞凋亡作用的重要調控因數之一,並與骨細胞的活性有關。本研究除了藉高解析度顳骨電腦斷層掃描分析膽脂瘤患者的顳骨表現型態以外,分析膽脂瘤中FasL的表現情況,並討論FasL是否與骨質破壞有關。 方法 蒐集過去兩年間中耳膽脂瘤接受手術患者,回溯分析顳骨電腦斷層掃描的顳骨表現型態,手術時取出之膽脂瘤標本以傳統染色切片確定爲膽脂瘤,並利用免疫化學組織的方法檢測膽脂瘤中FasL之表現情況。 結果 針對過去未曾接受過耳部手術且有術前顳骨電腦斷層掃描的膽脂瘤患者共40名性18名,女性22名,平均年齡43歲。以電腦斷層掃描分析其顳骨表現形態,可以發現58%鼓室頂板或聽骨鏈磨損,乳突鼓室蓋磨損30%,耳囊磨損25%,骨質明顯硬化50%。免疫組織化學檢測則顯示耳後皮膚、膽脂瘤基質上皮細胞層以及基質表皮下發炎內芽組織FasL的表現均成陰性反應。 結論 膽脂瘤的顳骨表現型態鍚骨質破壞與骨質硬化或增生,前者的影響範圍以鼓室頂板及聽骨鏈最多;膽脂瘤上皮細胞及表皮下肉芽組織的FasL均呈陰性反應,由於FasL可以誘發導致細胞死亡的凋亡作用,因此膽脂瘤過度增生分化與死亡終極分化的凋亡作用不是經由FasL此一凋亡路徑,FasL與膽脂瘤常伴隨的骨質破壞可能無關。

並列摘要


Objectives The unique feature of cholesteatoma is the hyperproliferation and accumulation of keratin debris within the middle ear and mastoid cavity, a process that leads to destruction of the surrounding structures in the temporal bone. The proliferation of keratin and the resulting bony destruction in the cholesteatoma matrix are associated with apoptosis. FasL, when conjugated with Fas, is known to trigger apoptosis. This study aimed to analyze the temporal bone patterns in patients with cholesteatoma and the expression of FasL in the cholesteatoma matrix. Methods. From July 1999 to July 2001, all patients with cholesteatoma who received ear operations at the China Medical University Hospital were enrolled in this study. Surgical specimens from all patients were shown histopathologically to have cholesteatoma. The temporal bone patterns in these patients were reviewed by high resolution temporal bone computed tomography. Immunoperoxidase stain with a monoclonal antibody to FasL evaluated the expression of FasL in the cholesteatoma matrix. Postauricular skin, which was harvested during the same surgical procedure served as the control. Result& The temporal bone patterns in the patients were classified as blunted scutum (58%), ossicular chain erosion (58%), erosion of tegmen mastoid-tympanicum (30%), erosion of the otic capsule (25%) and marked sclerosis (50%). Expression of FasL was not detected in the postauricular skin, cholesteatoma matrix or subepidermal granulation tissue. Conclusions. The temporal bone patterns in the patients with cholesteatoma included bony destruction and new bone formation. No expression of FasL was detected in the cholesteatoma matrix or subepidermal granulation tissue. This indicates that apoptosis in the cholesteatoma matrix may not be through the FasL pathway. Therefore, the destruction of the temporal bone in patients with cholesteatoma may not be associated with FasL.

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