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.