Altered regulation of cell surface peptidases in human cholesteatoma

Abstract

Cholesteatoma is a destructive process involving an accumulation of desquamated keratin arising from squamous epithelium that pathologically has invaded the middle ear or mastoid process. The clinical hallmarks of cholesteatomas, namely invasion of healthy tissues, migration, unrestrained proliferation, aggressiveness, recidivism, and uncoordinated differentiation predict the existence of defects in the normal biology and biochemistry of the cellular constituents that compose a cholesteatoma, as well as in the cellular interactions between these cells, the surrounding normal tissue, and the host. In the current report, we analyzed 11 cholesteatomas and matched healthy tissue for altered expression in four different cell surface peptidases, aminopeptidase A, aminopeptidase N, dipeptidyl peptidase IV, and neutral endopeptidase. We suggest that peptidases may modulate cell growth and differentiation by inactivating stimulatory signals (or conversely, by activating inhibitory signals).

Differential expression of S100 calcium‐binding proteins in epidermoid cysts, branchial cysts, craniopharyngiomas and cholesteatomas

“…As reported by Strunk, 10 aural cholesteatomas can be defined as skin growing in the middle ear cleft. This abnormal skin growth is characterized by a destructive process involving an accumulation of desquamated keratin arising from the squamous epithelium and pathologically affecting the middle ear or the mastoid process 11,12 . The unrestrained proliferation observed in cholesteatomas seems to relate, at least partly, to modifications occurring in the expression of the p53 phosphoprotein 13–16 .…”

Determination of the Levels of Expression of Sarcolectin and Calcyclin and of the Percentages of Apoptotic But Not Proliferating Cells to Enable Distinction Between Recurrent and Nonrecurrent Cholesteatomas

“…Although benign, cholesteatomas, nevertheless, exhibit aggressive biological behavior patterns that appear, particularly at clinical level, as the invasion of healthy tissues, including bones. The four most marked clinical hallmarks of cholesteatomas relate to unrestrained proliferation (with consequent aggressiveness and recidivism), uncoordinated differentiation, migration, and invasion 1 …”

Congenital Cholesteatoma of Temporal Bone with Bezold’s Abscess: Case Report

“…Cholesteatoma grows slowly with accumulation of desquamated keratin arising from the squamous epithelium and pathologically affecting the middle ear or the mastoid process [7]. Bone destruction caused by CC is thought to be caused by two predominant mechanisms: pressure induced bone resorption and enzymatic dissolution of bone by cytokine mediated inflammation [8].…”