Learning Objectives: The objective of this presentation is to understand the scientific basis for the etiology of aural cholesteatoma.
Over the last century, a number of theories have been proposed to explain the pathogenesis of acquired cholesteatomas. Several of these theories have experimental evidence in animal studies.
Support for the retraction pocket invagination theory is seen in Eustachian tube obstruction models in Mongolian gerbils. When Eustachian tubes of gerbils are ligated in middle ear (bulla) fills with fluid, then over time the pars flaccida retracts, accumulates keratin and forms cholesteatomas.
Support for the epithelial ingrowth theory had been documented in a number of animal models. When toxic materials are applied to the tympanic membrane, destruction of the tympanic membrane and ingrowth of keratinizing epithelium occurs. In infected gerbils cholesteatomas often rupture leading to epithelial ingrowth. Human temporal bone studies have also supported this theory.
The squamous metaplasia theory is not support by experimental evidence. The only demonstration of squamous metaplasia has been seen in vitamin A deficiency. When rats are deprived of dietary vitamin A, the middle ear mucosa changes to a multilayered squamous epithelium, but cholesteatomas have never been seen in this model.
Basal cell hyperplasia and ingrowth through the basal lamina has been observed in human temporal bones for many years. Ruedi first described this phenomenon. It has been observed in human temporal bone section and occurs in spontaneous in induced cholesteatomas and Mongolian gerbils.
The pathogenesis of cholesteatoma is complex and cholesteatomas may arise from various simultaneous mechanisms.
