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Inflammatory, invasive and neoplastic features of primary and secondary cholesteatomas: immunohistochemical and histological findings

Presenting Author: Nadir Yildirim

Published online by Cambridge University Press:  03 June 2016

Nadir Yildirim ,
Ayşenur Deger ,
Onur Erdogan  and
Sinan Aksoy
Nadir Yildirim
Affiliation:
Dumlupinar Universitesi Medical Faculty
Ayşenur Deger
Affiliation:
DPU Medical Faculty Department of Pathology
Onur Erdogan
Affiliation:
DPU Medical Faculty Department of ORL-HNS
Sinan Aksoy
Affiliation:
DPU Medical Faculty Department of ORL-HNS
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Abstract

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Learning Objectives: Objective: Etio-pathogenesis of middle ear cholesteatoma has not been wholly understood. Acquired cholesteatomas are classified into epitympanic/primary (PAK) and mesotympanic/secondary (SAK) subtypes. Herewith, we aimed to investigate the expression of multiple inflammatory, invasive and neoplastic markers in cholesteatomas using immunohistochemistry (IHC) and hematoxylene-eosin (H&E) staining with special reference to the PAK and SAK.

Objective: Etio-pathogenesis of middle ear cholesteatoma has not been wholly understood. Acquired cholesteatomas are classified into epitympanic/primary (PAK) and mesotympanic/secondary (SAK) subtypes. Herewith, we aimed to investigate the expression of multiple inflammatory, invasive and neoplastic markers in cholesteatomas using immunohistochemistry (IHC) and hematoxylene-eosin (H&E) staining with special reference to the PAK and SAK.

Material-Method: We statistically compared 74 (33 primary, 41 secondary) cholesteatoma matrices and normal (control) skin samples harvested from operated cholesteatoma patients for 10 different markers within, and between the subgroups using IHC and H&E staining. Evaluating pathologist was blinded.

Results: Statistically, staining scores for IHC markers of Ki67, collagen type-4, Proliferating cell nuclear antigen (PCNA), keratinocyte growth factor (KGF), fibronectin (FN), interleukin1α (IL-1α), tumor necrosis factor-α (TNF-α); and staining with H&E for vascularization and lymphocyte numbers were significantly higher in cholesteatomas than control materials of both subgroups except for collagen type-7. However, no difference in significances was found between the subgroups.

Conclusion: These results indicate that acquired cholesteatoma is pathologically the same invasive, inflammatory and hyperproliferative disease at different locations, irrespective of their different etio-pathology. Non-expression of collagen type-7 in cholesteatoma might be related to its interfacing location in uninvolved part of the basal membrane.