[Expression of PTKs CDK4 and p15 in the middle ear cholesteatomatous epithelium].

Objective: To explore the cells proliferation and its molecular regulating mechanisms of cholesteatomatous epithelium from the aspect of protein tyrosine kinases (PTKs) signal transduction and cell cycle control.

Method: The expressions of phosphated PTKs, CDK4 and p15 were investigated by immunohistochemical S-P method and computer image analysis in 30 specimens of the middle ear cholesteatomatous epithelium and 19 specimens of external auditory canal epithelium from patients with chronic otitis media with cholesteatoma. The expressive results of phosphated PTKs, CDK4 and p15 were determined in same epithelium of different slices of same specimen. Statistical analysis was performed by the connection with degree of subepidermal inflammatory cell infiltration and degree of bone destruction.

Result: The expression of phosphated PTKs was primarily staining in cell membrane, and the staining of CDK4 were located in the nuclei as well as the cytoplasm of cells, and the staining of nuclei was primary, but the staining of p15 was expressed only in the nuclei of cell. The expressions of phosphated PTKs, CDK4 and p15 in epithelium were clearly increased compared with that of external auditory canal epithelium (P < 0.01). The expression of phosphated PTKs and CDK4 tended to be strong in the epithelium with subepidermal inflammatory, and the expression of CDK4 tended to be strong in the epithelium with high level expression of phosphated PTKs (P < 0.01). The expressions of above investigated indexes were not significantly different under the different degree of bone destruction (P > 0.05).

Conclusion: The cholesteatomatous epithelium have a hyperproliferation ability, and also show a mechanism of inhibiting proliferation ability. The microenvironment with inflammatory cell infiltration has a tendency to greatly affect proliferation ability of cholesteatomatous epithelium.