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鼻窦胆脂瘤的发病机制。

Pathogenesis of sinus cholesteatoma.

作者信息

Sudhoff Holger, Tos Mirko

机构信息

Department of Otolaryngology and Skull Base Surgery, Addenbrooke's Hospital, Cambridge, UK.

出版信息

Eur Arch Otorhinolaryngol. 2007 Oct;264(10):1137-43. doi: 10.1007/s00405-007-0340-y. Epub 2007 May 30.

Abstract

UNLABELLED

The aim of the present study was to provide evidence for the establishment of sinus cholesteatoma, defined as postero-superior pars tensa retraction extending into the posterior tympanum and tympanic sinuses.

BACKGROUND

There is clinical evidence for formation of a retraction, but there is a lack of explanation for the transition from a retraction pocket to an active and expanding sinus cholesteatoma. Epidemiological studies on incidence of postero-superior retractions of pars tensa and follow-up studies on patients with similar pars tensa retractions were performed. Additionally, expression of proliferation marker and analysis of basement membrane were studied in samples of sinus cholesteatoma. The prevalence of pars tensa pathology was between 9.2 and 24% of investigated ears. In children with manifest secretory otitis there were some sinus cholesteatomas and 5-6% severe retractions, some of those became pre-cholesteatomas, requiring treatment and controls. Immunohistochemistry of sinus cholesteatomas showed that proliferating keratinocytes were very often found within epithelial cones growing towards the underlying stroma. These growth cones exhibit focal discontinuities of the basement membrane especially in areas of intense subepithelial inflammation. As a possible explanation based on clinical and immunohistochemical findings, we propose a four-step concept for pathogenesis of sinus cholesteatoma combining the retraction and proliferation theory: (1) The retraction pocket stage. (2) The proliferation stage of the retraction pocket, subdivided in (a) Cone formation, (b) Cone fusion. (3) Expansion stage of attic cholesteatoma. (4) Bone resorption.

摘要

未标注

本研究的目的是为鼻窦胆脂瘤的形成提供证据,鼻窦胆脂瘤定义为紧张部后上象限回缩延伸至鼓室后部和鼓窦。

背景

有临床证据表明存在回缩形成,但对于从回缩袋向活跃且不断扩大的鼻窦胆脂瘤的转变缺乏解释。对紧张部后上象限回缩的发病率进行了流行病学研究,并对有类似紧张部回缩的患者进行了随访研究。此外,还对鼻窦胆脂瘤样本进行了增殖标志物表达和基底膜分析。紧张部病变的患病率在被调查耳的9.2%至24%之间。在患有明显分泌性中耳炎的儿童中,存在一些鼻窦胆脂瘤和5%至6%的严重回缩,其中一些发展为胆脂瘤前期,需要治疗和监测。鼻窦胆脂瘤的免疫组织化学显示,在朝着下方基质生长的上皮锥内经常发现增殖的角质形成细胞。这些生长锥在基底膜处表现出局灶性中断,尤其是在强烈的上皮下炎症区域。基于临床和免疫组织化学结果,作为一种可能的解释,我们提出了一个结合回缩和增殖理论的鼻窦胆脂瘤发病机制的四步概念:(1)回缩袋阶段。(2)回缩袋的增殖阶段,细分为(a)锥形成,(b)锥融合。(3)上鼓室胆脂瘤的扩展阶段。(4)骨质吸收。

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