Chronic ear disease with cholesteatoma is characterized by an intrusion of keratinizing stratified squamous epithelium into the middle ear manifesting bone resorption at the interface of the perimatrix. The aim of our study was to investigate the markers of a catabolic process associated with several chronic inflammatory states. We assessed the level of catabolism of glycoconjugates in assays of cholesteatoma extracts, quantifying two lysosomal exoglycosidases: α-mannosidase (α-MAN) and β-galactosidase (β-GAL). Cholesteatomas (n = 15) and normal adult postauricular skin served as controls (n = 15) were collected from the patients during surgery owing to chronic otitis media. To assess exoglycosidase activity, release of p-nitrophenol from p-nitrophenol derivatives of α-mannose and β-galactose was used. In 13 of 15 specimens, we observed significantly higher activity of investigated enzymes in cholesteatoma tissue compared with control tissue (postauricular skin). The mean activity of α-MAN from the cholesteatoma cells was 1.76 ± 1.10 nkat/g wet tissue and 0.61 ± 0.21 nkat/g wet tissue in the control probes. The mean activity of β-GAL from the cholesteatoma cells was 1.77 ± 1.07 nkat/g wet tissue and 0.87 ± 0.20 nkat/g wet tissue in the control probes. Catabolic reactions involving glycoproteins, glycolipids, and proteoglycans may play a role in cholesteatoma-related bone resorption. The present data indicating that the lysosomal exoglycosidases α-MAN and β-GAL are significantly and consistently elevated suggest the need to further correlations assessment between levels of α-MAN and β-GAL and cholesteatoma behavior. Further research should also evaluate the relative importance of these particular exoglycosidases in manifesting bone resorption in considering the spectrum of identified inflammatory mediators.
- catabolism of glycoconjugates
- normal postauricular skin
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