Background Chronic otitis media(COM) is a significant clinical problem.Understanding the mechanisms of COM is critical for its control and treatment.However,little is known of the processes leading to COM as a result of lack of animal models of N-ethyl-N-nitrosourea(ENU) induced mutations in otitis media with effusion(OME).Methods Otoscopy and auditory brain response(ABR) evaluation were carried out under sedation in Nmf391nmf/nmf mice of 2,4,6 and 8 months of age.The mice were killed for study of middle and inner ear pathology.Results Tympanic membrane visualization and ABR thresholds in 1-to 8-month-old Nmf391nmf/nmf mice showed spontaneous OME and inner ear diseases in approximately 100% of the animals.The significant elevation of ABR thresholds suggested a sensorineural component in hearing loss in addition to the conductive loss.Middle and inner ear histology showed various degrees of outer hair cells loss and middle ear inflammation in all the mice,but no inflammation cells in the inner ear.The ABR threshold at 32 kHz was significantly elevated.Conclusions This study shows histopathologic changes in the Nmf391nmf/nmf mouse model of COM with effusion that have not been reported in human COM.This ENU induced mutation model of COM will be valuable for the characterization of middle ear inflammation and inner ear disease processes that are induced by middle ear infections.We propose that COM with effusion in this ENU induced mutation model is the cause of the cochlea hair cells damage. Background Chronic otitis media (COM) is a significant clinical problem. Understanding the mechanisms of COM is critical for its control and treatment. However, little is known of the processes leading to COM as a result of lack of animal models of N-ethyl- N-nitrosourea (ENU) induced mutations in otitis media with effusion (OME). Methods Otoscopy and auditory brain response (ABR) evaluation were carried out under sedation in Nmf391 nmf / nmf mice of 2,4,6 and 8 months of age. mice were killed for study of middle and inner ear pathology. Results Tympanic membrane visualization and ABR thresholds in 1-to 8-month-old Nmf391 nmf / nmf mice showed spontaneous OME and inner ear diseases in about 100% of the animals. The significant elevation of ABR thresholds suggested a sensorineural component in hearing loss in addition to the conductive loss. Mid and inner ear histology showed various degrees of outer hair cells loss and middle ear inflammation in all the mice, but no inflammation cells in th e inner ear. ABR threshold at 32 kHz was significantly elevated. Confclusions This study shows histopathologic changes in the Nmf391 nmf / nmf mouse model of COM with effusion that have not been reported in human COM. This ENU induced mutation model of COM will be valuable for the characterization of middle ear inflammation and inner ear disease processes that are induced by middle ear infections. We propose that COM with effusion in this ENU induced mutation model is the cause of the cochlea hair cells damage.