(1) The prerequisite for development of cholesteatoma is a cholesteatoma bed, that is a loose subepithelial connective tissue layer which acts as a nutrient bed and makes papillary growth of squamous epithelium possible. (2) The formation of cholesteatoma is facilitated by disturbed tubal function with reduced ventilation of the middle ear. (3) The progression of cholesteatoma, especially the bone destruction, is due to enzyme-activated cell groups. The epidermal layer in the postero-superior area of the tympanic membrane has a higher papillary content and during an inflammatory process there is a marked vascular reaction. This particular area has a special nutritional zone and the epidermis is especially well nourished [Lange, 1925]. The main artery to the tympanic membrane travels along the handle of the malleus and gives off branches. In our animal experiments epithelial cones grew into this well-nourished subepithelial zone and formed cholesteatoma. The importance of tubal function as regards cholesteatoma formation can be seen in everyday clinical practice. In stapedectomy patients, the lateral attic wall is usually removed to allow full visualisation of the stapes, but retraction pockets in this area are never seen at subsequent follow-up. However, if the lateral attic wall is removed during surgery for chronic otitis media, reconstruction with cartilage or ceramic is necessary to prevent retraction. This adds weight to the hypothesis that tubal dysfunction is an important aetiological factor in cholesteatoma. This is further supported by the 30 times greater incidence of retraction pockets in patients with cleft palate.