To evaluate the presence of viruses and bacteria in middle ear and adenoids of patients with and without otitis media with effusion (OME). Adenoid samples and middle ear washes (MEW) were obtained from children with OME associated with adenoid hypertrophy undergoing adenoidectomy and tympanostomy, and compared to those obtained from patients undergoing cochlear implant surgery, as a control group. Specific DNA or RNA of 9 respiratory viruses (rhinovirus, influenza virus, picornavirus, syncytial respiratory virus, metapneumovirus, coronavirus, enterovirus, adenovirus and bocavirus) and 5 bacteria (S. pneumoniae, H. influenzae, M. catarrhalis, P. aeruginosa and S. aureus) were extracted and quantified by real-time PCR. 37 OME and 14 cochlear implant children were included in the study. At the adenoid, virus and bacteria were similarly detected in both OME and control patients. At the middle ear washes, however, a higher prevalence of bacteria was observed in patients with OME (p = 0.01). S. pneumoniae (p = 0.01) and M. catarrhalis (p = 0.022) were the bacteria responsible for this difference. Although total virus detection was not statistically different from controls at the middle ear washes (p = 0.065), adenovirus was detected in higher proportions in adenoid samples of OME patients than controls (p = 0.019). Despite both OME and control patients presented similar rates of viruses and bacteria at the adenoid, children with OME presented higher prevalence of S. pneumonia, M. catarrhalis in middle ear and adenovirus in adenoids when compared to controls. These findings could suggest that these pathogens could contribute to the fluid persistence in the middle ear.

Introduction: Cisplatin is an effective chemotherapeutic agent commonly used in the treatment of malignant tumours, but ototoxicity is a significant side effect.Objectives: To discuss the mechanisms of cisplatin ototoxicity and subsequent cell death, and to present the results of experimental studies.Material and methods: We conducted a systematic search for data published in national and international journals and books, using the Medline, SciELO, Bireme, LILACS and PubMed databases.Results: The nicotinamide adenine dinucleotide phosphate oxidase 3 isoform (also termed NOX3) seems to be the main source of reactive oxygen species in the cochlea. These reactive oxygen species react with other molecules and trigger processes such as lipid peroxidation of the plasma membrane and increases in expression of the transient vanilloid receptor potential 1 ion channel.Conclusion: Cisplatin ototoxicity proceeds via the formation of reactive oxygen species in cochlear tissue, with apoptotic cell death as a consequence.

The use of animal samples is important in otologic research and understanding the anatomy of their ears help make proper use of them in research projects. to study guinea pig's and rat's ears under light microscopy(LM) and scanning electron microscopy(SEM) and understand their anatomical advantages in basic otologic research. The temporal bones, tympanic bullas and cochleas from three albino guinea pigs and rats were photographed and analyzed under LM and SEM. Rats aren't as simple to handle as guinea pigs, and often present with otitis media. Rats have a fragile junction of the tympanic bulla, two and half turns in the cochlea, and their tympanic membranes do not seal off the entire external auditory canal. Guinea pigs have full bullas, their incus and malleus are fused and they have three and half cochlear turns. Under SEM, guinea pigs and rats have Tectori Membrane, Raissner's Membrane and the Organ of Corti. Only guinea pigs have Hensen's Cells. Guinea pigs were considered easy to handle for microdissection purposes because of the size and robustness of their temporal bones, and for surgical experiments involving the stapes, the oval window and the tympanic membrane. Under SEM there are similarities guinea pigs and rats, and both can be used in inner ear studies.

The most common etiologies of tympanic membrane perforation are infections and trauma. The objective of the present study was to assess the healing of traumatic tympanic membrane perforation in rats. The tympanic membrane from male Wistar rats was perforated in the anterior and posterior portions to the handle of the malleus. Five tympanic membranes were evaluated 3 days after tympanic perforation; 5 after 5 days; 5 after 7 days; 3 after 10 days; and 4 after 14 days. The tympanic membranes were submitted to histopathological evaluation after hematoxylin-eosin staining. Tympanic membrane closure occurred at about 7-10 days after injury and the healing process was complete by day 14. The proliferative activity of the outer epithelial layer was present close to the handle of the malleus and to the tympanic annulus. The spontaneous healing process of the tympanic membrane starts from the outer epithelial layer, with later healing of the lamina propria and the mucosal layer.