CHOLESTEATOMA – ΧΟΛΟΣΤΕΑΤΟΜΑ
Is well known that the cholesteatoma sometimes clinically shows a non aggressive,mild behavior, remaining mainly silent, small in the epitympanum, which is called in the German literature as “EPITYMPANAL KOLESTEATOM”. We call this cholesteatoma "simple cholesteatoma"
On the other side sometimes the cholestatoma has an aggressive course , an aggressive development and shows an excessive infective character with pus an bad odor secretion.We call this cholestatoma "aggressive cholestatoma"
After our opinion we believe according our findings and research that this type of cholesteatoma is infected with HPV virus. Eventually this also is the main reason of the reappearance of the cholesteatoma after succesfull surgery even if the surgery is done by a competent surgeon.
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Correlation of clinical and surgical findings to histological features (koilocytosis, papillary hyperplasia) suggesting papillomavirus involvement in the pathogenesis of cholesteatoma. 2006
Abstract: BACKGROUND: The clinical course of cholesteatoma is rather unpredictable, as some cases show aggressive development, while others have a mild, more 'benign' nature. The aim was to correlate the clinical course and surgical findings of cholesteatomas with histological features. MATERIAL/METHODS: The study included 45 patients with cholesteatoma, 29 of whom had surgically aggressive and 16 simple (not surgically aggressive) cholesteatoma. All patients underwent mastoid surgery and the cholesteatoma specimens were sent for histological examination. RESULTS: The clinical course of the cholesteatomas had a statistically significant association (p < 0.001) with the 'aggressiveness' found in surgery, suggesting that clinical history correlates well with surgical findings. All 29 specimens of patients with surgically aggressive cholesteatoma had characteristic papillary hyperplasia of the epithelium and marked koilocytosis, suggesting papillomavirus-incduced lesions. In contrast, none of the specimens of the 16 patients with simple (non-aggressive) cholesteatoma had papillary hyperplasia and there was no marked koilocytosis, as few koilocytes could occasionally be found. The difference was statistically significant (p < 0.001). In situ hybridization for human papillomnavirus (HPV) was performed in 14 specimens (7 each with aggressive and simple cholesteatomna). Positive staining was found in three aggressive cholesteatomas. All seven simple cholesteatomas were negative for HPV. CONCLUSIONS: The results of the present paper suggest that papillomaviruses may play an important role in the pathogenesis of cholesteatomas. Further studies with controls and the development of new methods to identify known and unknown types of papillomavirus are needed to explore their exact role.