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.
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.