Louw L
Department of Otorhinolaryngology, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa.
J Laryngol Otol. 2013 Jun;127(6):542-9. doi: 10.1017/S0022215113000601. Epub 2013 May 9.
Cholesteatoma is considered a benign, gradually expanding and destructive epithelial lesion of the temporal bone. The pathogenesis of different classifications of cholesteatoma is marked by similar underlying cellular and molecular processes. Stepwise explanations of the histopathogenesis have been described previously. The current paper focuses on expounding the molecular events of cholesteatoma.
Cholesteatoma pathogenesis encompasses a complex network of signalling pathways during: epidermal hyperplasia, perimatrix-matrix interactions and mucosal disease. This paper presents a review of the molecular events driven by inflammatory mediators and enzymes during: cholesteatoma growth (cell proliferation and apoptosis); maintenance and deterioration (angiogenesis and hypoxia, oxidative stress and toxicity); and complications (bone erosion and hearing loss). The cascade of molecular events applicable to atelectasis and cholesteatoma that coexist with chronic otitis media and bone erosion as sequelae is summarised.
The role of lipids in this disease is relatively unexplored, but there is evidence in support of fatty acid role-players that needs confirmation. Future directions in lipid research to delineate molecular mechanisms are proposed.
胆脂瘤被认为是颞骨的一种良性、逐渐扩张且具有破坏性的上皮病变。不同类型胆脂瘤的发病机制具有相似的潜在细胞和分子过程。此前已有对组织病理学发病机制的逐步解释。本文重点阐述胆脂瘤的分子事件。
胆脂瘤发病机制涵盖表皮增生、基质周围 - 基质相互作用和黏膜疾病过程中的复杂信号通路网络。本文综述了炎症介质和酶在胆脂瘤生长（细胞增殖和凋亡）、维持与恶化（血管生成和缺氧、氧化应激和毒性）以及并发症（骨质侵蚀和听力损失）过程中驱动的分子事件。总结了与慢性中耳炎和骨质侵蚀后遗症共存的肺不张和胆脂瘤相关的分子事件级联反应。
脂质在该疾病中的作用相对未被充分探索，但有证据支持脂肪酸参与者的作用，这需要进一步证实。提出了脂质研究中描绘分子机制的未来方向。
