Chronic suppurative otitis media (CSOM) with and without cholesteatoma is regarded as chronic inflammation of the middle ear and mastoid mucosa that can be associated with the presence of granulation tissue and infection, which can lead to ossicular damage and hearing loss, but it is commonly known that cholesteatoma behaves aggressively.

Both lesions appear to contain a predominant population of inflammatory cells, among which proinflammatory cytokines secreting keratinocyte growth factor (KGF) and its receptor (KGFR). No clear difference was demonstrated between these entities.

The purpose of this study was to investigate the potential influence of KGF and KGFR in increased epithelial-cell proliferation of chronic otitis media (COM) with cholesteatoma in contrast to COM without cholesteatoma (CSOM), particularly in the granulated form, and to compare the rate of proliferation activity of epithelial cells using the Ki-67 epithelial proliferation marker expression.

Chronic suppurative otitis media (CSOM) with or without cholesteatoma represents a chronic inflammation of the middle ear and mastoid mucosa, in which the tympanic membrane (TM) is not intact and discharge is present. Usually, both types of lesions are associated with the presence of granulation tissue and infection,

These lesions can lead to ossicular damage and hearing loss, but it is commonly known that cholesteatoma behaves more aggressively, being able to cause fatal intracranial complications. Two main forms of the chronic otitis media are distinct: chronic suppurative otitis media with and without cholesteatoma.

Usually, not only do these two classic types differ in their clinical course and prognosis, but they also require different therapeutic strategies. Even though chronic otitis media without cholesteatoma is known as a benign disease with chronic irritating otorrhea, that can often be managed conservatively, in its granulated form the erosion of the bony labyrinth may occur.

Both forms of the chronic otitis media can be associated with granulation tissue and infection, with many interlinking mechanisms at the molecular level being responsive for bone resorption. Our results indicated that the abnormal behavior of the cholesteatoma epithelium seems to be induced by the paracrine interaction between KGF and KGFR.

Furthermore, they found that cholesteatoma expressing both KGF and KGFR had a high Ki-67 index, which correlated with its aggressiveness. These findings suggest that excessive KGF and KGFR synthesis may contribute to the hyperproliferative state in cholesteatoma and could explain the pathological difference between cholesteatoma and CSOM.