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Tissular changes induced by Pseudomonas aeruginosa in an otitis media rat model with tubal obstruction

Conclusions. This is a suitable model for the study of different features of middle ear inflammation. This model allows manipulations inside the middle ear while preserving relevant structures such as the tympanic membrane, and provides a useful model for the study of interactions between bacterial...

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Published in:Acta oto-laryngologica 2007, Vol.127 (2), p.132-137
Main Authors: Trinidad, >Almudena, Ramírez-Camacho, Rafael, Ramón García-Berrocal, José, María Verdaguer, José, Vicente, Javier, Daza, Rosa
Format: Article
Language:English
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Summary:Conclusions. This is a suitable model for the study of different features of middle ear inflammation. This model allows manipulations inside the middle ear while preserving relevant structures such as the tympanic membrane, and provides a useful model for the study of interactions between bacterial infection and eustachian tube dysfunction. Objectives. Analysis of early and late histological features in an experimental model of Pseudomonas aeruginosa middle ear inoculation in the rat designed for the study of middle ear procedures. Materials and methods. Thirty Wistar rats were inoculated with Pseudomonas aeruginosa in the tympanic bulla followed by the cauterization of the eustachian tube. Culturing of middle ear effusion was carried out at 7 days follow-up and at sacrifice. Processing of the temporal bones for light microscopy was performed at 7, 14, 30 and 60 days. Results. Early cultures were positive in most cases, thus proving that middle ear inflammation was due to the presence of inoculated Pseudomona aeruginosa. Mucoperiosteal inflammatory changes similar to those observed in human middle ear infection were seen. Acute inflammatory cell infiltration was seen at 7 and 14 days, gradually decreasing to chronic inflammatory changes with fibroplasia at 60 days. Bone resorption was observed at 7 and 14 days, changing to a bony deposition at 30 and 60 days.
ISSN:0001-6489
1651-2251
DOI:10.1080/00016480600749994