Regardless of the pathogenesis of congenital and acquired cholesteatoma two questions seem to be fundamental: what is the origin of the keratinizing squamous epithelium, and what influences invasive and hyperproliferative behavior of the epidermis. The authors of this paper advance a hypothesis that the similar mechanism of the skin infection could exist in psoriasis and atopic dermatitis as well as in cholesteatoma. The retraction pocket leads to the loss of the defense mechanisms and development of planctonic bacteria. Direct and indirect signalings of bacterial products, such as endotoxin stimulate the cytokine cascade and therefore the hyperproliferation of the epithelium keratynocytes. The mobilization of the immunological system may an important role in the perimatrix development.
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