B-ENT

E-cadherin expression in acquired cholesteatoma

1.

Department of Otorhinolaryngology, Otology Unit, Military Medical Academy, Belgrade, Serbia

2.

Institute of Medical Research, Division of Clinical Immunology, Military Medical Academy, Belgrade, Serbia

3.

Institute of Pathology, Military Medical Academy, Belgrade, Serbia

B-ENT 2013; 9: 241-246
Read: 697 Downloads: 533 Published: 12 February 2020

E- cadherin expression in acquired cholesteatoma.

Objectives: The epithelial cell adhesion molecule E-cadherin is important for maintenance normal tissue architecture and for cell-cell communication and immune cell migration. E-cadherin is also present in cholesteatomas. This study determined E-cadherin expression in acquired cholesteatomas and analyzed its expression according to cholesteatoma clinical and histological characteristics.

Methods: We investigated E-cadherin expression in 30 samples from operated patients with acquired middle ear ­cholesteatomas that were classified according to their clinical and histological characteristics. E-cadherin expression in cholesteatoma was determined immunohistochemically. A semi quantitative method was used to determine the index of expression of E-cadherin and t-tests, Mann-Whitney U tests and Spearman correlation analysis were used for statistical analysis.

Results: We found significant expression of E-cadherin on CD1, CD3 total, CD4 (p<0.05), high expression of E-cadherin on CD8 total and CD19/CD38 lymphocytes (p<0.01) and very high expression of E-cadherin on mast cells and antigenpresenting cells, including Langerhans cells (p<0.005). We graduated results as no statistically significant (p>0.05), statistically significant (0.05>p>0.01), highly statistically significant (0.01>p>0.005) and very highly statistically significant (p<0.005).

Conclusion: E-cadherin expression was the same in the cholesteatoma matrix in all samples. There were no differences in expression according to the clinical and histological characteristics of the cholesteatomas.

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EISSN 2684-4907