Abstract: External auditory canal cholesteatoma (EACC) is a chronic
inflammation of the external auditory canal and is composed of
hyperproliferative epithelium. The upward migration of the epithelial cells
requires permanent breakdown and reformation of intercellular connection. This
is established by the modulation of the adherent junctions consisting of an
E-Cadherin–β-catenin complex. Dissociated
β-catenin intranuclearly enables persistent activation
of downstream transcription and growth factors and decreases the integrity of
tissue. In our study we examined EACC and normal meatal auditory skin taken
from 16 patients between 23 and 74 years of age. Immunostaining for
β-catenin was used for semiquantitative description of
the specimens after assessing hematoxylin-eosin-stained slides.
β-catenin was expressed in all layers of AMS-epithelium,
whereas in EACC only basal layer of the matrix epithelium showed positive
immunostaining for β-catenin. In the suprabasal layer of
the epithelium only faint reactivity was detectable. The immunostaining was
restricted to the membrane of the cells. We assumed that either the content of
membranous β-catenin was decreased or
β-catenin was changed due to molecular modification. It
is known that stimulation of endothelial cells by certain growth factors,
β-catenin is maximally phosphorylated. In regard to the
increased loss of immunoreactivity for β-catenin in the
suprabasal layers of the hyperplastic EACC-matrix, we assumed bio-molecular
modification or loss of β-catenin decreasing the
cell-cell-integrity. Furthermore, this might result in desquamation of
keratinocytes and accumulation of dead keratin debrids. In sum, this study
should be understood as a descriptive analysis of
β-catenin expression in EACC.
