Louw Louise
Department of Otorhinolaryngology, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa.
J Laryngol Otol. 2010 Jun;124(6):587-93. doi: 10.1017/S0022215109992763. Epub 2010 Feb 16.
Since Virchow's first, 1855 publication on cholesteatoma, this disease has been the subject of extensive debate. The pathogenesis of acquired cholesteatoma is repeatedly explained on the premises of the migration, hyperplasia and metaplasia theories, but proof for the latter theory remains limited. In retrospect, there is progress toward better understanding of all the pathological mechanisms involved, as expounded in this review.
The triggers for cholesteatoma onset are diverse, and may involve tympanic membrane trauma (i.e. perforation, displacement, retraction or invagination), tympanic membrane disease, and/or tympanic cavity mucosa disease. Research has revealed that cell migration is replaced under inflammatory conditions by hyperplasia, which triggers the onset of cholesteatoma. Lately, the hyperplasia theory gained prominence and circumscription of the papillary cone formation concept provided insight into cholesteatoma progression (growth and expansion). Diseased mucosa can contribute to the development of retraction pockets and cholesteatoma. The type of cholesteatoma trigger and the role of chronic inflammation during disease progression and recurrence are important in guiding clinical intervention.
自1855年维尔肖首次发表关于胆脂瘤的文章以来，这种疾病一直是广泛争论的主题。后天性胆脂瘤的发病机制多次依据迁移、增生和化生理论进行解释，但后一种理论的证据仍然有限。回顾过去，正如本综述所阐述的，在更好地理解所有相关病理机制方面已经取得了进展。
胆脂瘤发病的触发因素多种多样，可能涉及鼓膜创伤（即穿孔、移位、内陷或内翻）、鼓膜疾病和/或鼓室黏膜疾病。研究表明，在炎症条件下，细胞迁移被增生所取代，这触发了胆脂瘤的发病。最近，增生理论受到关注，乳头锥形成概念的界定为胆脂瘤的进展（生长和扩展）提供了见解。患病黏膜可促使内陷袋和胆脂瘤的形成。胆脂瘤触发因素的类型以及慢性炎症在疾病进展和复发过程中的作用对于指导临床干预很重要。
