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  • Title: Eustachian tube goblet cell density during and after acute otitis media caused by Streptococcus pneumoniae: a morphometric analysis.
    Author: Cayé-Thomasen P, Tos M.
    Journal: Otol Neurotol; 2003 May; 24(3):365-70. PubMed ID: 12806285.
    Abstract:
    BACKGROUND: Prior investigations have shown that the number of mucus-producing goblet cells in the middle ear mucosa is highly increased during and up to at least 6 months after experimental acute otitis media. This may, in conjunction with deteriorated eustachian tube function, predispose to subsequent development of secretory otitis media. One reason for the deteriorated tubal function after acute otitis media has been suggested to be an excessive accumulation of mucus secretions, blocking the tube and thereby clearance of the middle ear. This investigation determines the density of the mucus-producing goblet cells in the eustachian tube during and up to 6 months after experimental acute otitis media. METHODS: Middle ear inoculation of Streptococcus pneumoniae in 25 rats. Groups of five animals, killed on Days 4, 8, 16, 90, and 180. Dissection and decalcification of the eustachian tube, followed by paraffin embedding and serial transverse sectioning, periodic acid-Schiff/Alcian blue staining and morphometric determination of the goblet cell density in every 20th section, using a light microscope. RESULTS: The goblet cell density was increased on Day 8 and later in the tympanic orificium, in addition to the tympanic and midportion third of the tube. Increased goblet cell density was seen in the pharyngeal third on Days 8 and 16, whereas no changes were registered in the pharyngeal orificium. Pathologic intraepithelial glands formed after the infection and goblet cells were found in mucosal areas normally devoid of these. CONCLUSIONS: The eustachian tube goblet cell density is increased during and up to 6 months after acute otitis media. Indicated excessive secretion of mucus by more goblet cells may contribute to the deteriorated eustachian tube function found after acute otitis media and thus predispose, sustain, or aggravate middle ear disease.
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