Histologic Changes in Eustachian Tube Mucosa of Rats After Exposure to Gastric Reflux
Objective: Reflux is thought to be a risk factor for middle ear disease, but the mechanism underlying this relationship is unclear. In this study, we evaluated the effects of reflux on the eustachian tube (ET) mucosa. Materials and Methods: Twenty‐two healthy 150 to 220 g Wistar rats with normal mid...
Gespeichert in:
Veröffentlicht in: | The Laryngoscope 2008-05, Vol.118 (5), p.849-853 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Objective: Reflux is thought to be a risk factor for middle ear disease, but the mechanism underlying this relationship is unclear. In this study, we evaluated the effects of reflux on the eustachian tube (ET) mucosa.
Materials and Methods: Twenty‐two healthy 150 to 220 g Wistar rats with normal middle ears were used. The animals were divided into three groups according to exposure time: 1‐, 3‐, and 12‐week exposures. Four rats were used as a control group. An experimental model of gastroesophageal reflux was induced under general anesthesia. After exposure, the animals were sacrificed, and cross sections of the ETs were prepared. The histologic changes in the ET mucosa were observed under a light microscope.
Results: The density of goblet cells, numbers of lymphocytes, polymorphonuclear leukocytes, and eosinophils, subepithelial edema, subepithelial vasodilatation, subepithelial gland formation, and intraepithelial gland formation were compared among the groups. The goblet cell density and numbers of lymphocytes and polymorphonuclear leukocytes were significantly higher in the three exposure groups compared with the control group.
Conclusion: Nasopharyngeal exposure to experimental reflux alters the ET mucosa histopathology, which suggests that gastroesophageal reflux has a role in ET dysfunction. |
---|---|
ISSN: | 0023-852X 1531-4995 |
DOI: | 10.1097/MLG.0b013e318164d0c0 |