PubMed · 6598273
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J Sadé. 1984. Eustachian tube function.. https://doi.org/10.3109/00016488409122886
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OBJECTIVES: To characterize glycoconjugate expression in normal human eustachian tubes and study the alterations in glycoconjugate expression found in eustachian tubes with otitis media. STUDY DESIGN: Using lectin histochemistry, alterations in glycoconjugates were studied in three normal temporal bones, in four temporal bones with mucoid otitis media (MOM), and in five with serous otitis media (SOM). METHODS: Sections of previously processed temporal bones were decelloidinized, and then incubated with seven biotinylated lectins--WGA, SNA, MAA, BPA, PNA, UEA-1, and LcH--that reflect seven carbohydrate residues of glycoconjugates, respectively: GlcNAc/NeuNAc, NeuNAc alpha(2-6)GalNAc, NeuNAc alpha(2-3)GalNAc, Gal beta(1-3) GalNAc, L-fucose, and alpha-mannose residues. Control sections were incubated with inhibitory carbohydrates or without biotinylated lectins. RESULTS: In the normal temporal bones, five carbohydrate residues in goblet cells and cilia of the eustachian tube demonstrated moderate to strong activity--NeuNAc alpha(2-6)GalNAc, NeuNAc alpha(2-3)GalNAc, GalNAc, Gal beta(1-3)GalNAc, and L-fucose. Two residues demonstrated weak activity--GlcNAc/NeuNAc and alpha-mannose. Temporal bones with MOM revealed increases in sialic acid and alpha-mannose, and a decrease in L-fucose. Residues of carbohydrates in the cilia of bones with SOM were notably decreased, especially for GalNAc, Gal beta(1-3)GalNAc, and NeuNAc alpha(2-6)GalNAc. CONCLUSIONS: Glycoconjugates in the normal human eustachian tube are rich in GalNAc, Gal beta(1-3)GalNAc, L-fucose, and NeuNAc alpha(2-3/2-6) GalNAc, but low in alpha-mannose and sialic acid. Eustachian tubes from cases with SOM or MOM demonstrated alterations in glycoconjugate expression in cilia and goblet cells, which may reflect disorder of the carbohydrate metabolism during otitis media, especially in SOM.
In a gross anatomic study of 20 sides in 16 human head specimens, the tensor veli palatini, the dilatator tubae, and the tensor tympani muscles were studied. The tensor veli palatini was observed to insert onto the anterior one-third of the pterygoid hamulus, whereas the dilatator tubae rounded the middle one-third of the pterygoid hamulus without an insertion. Thus, the dilatator tubae, not the tensor veli palatini, could serve to tense the anterior velum. An insertion from the superior pharyngeal constrictor muscle onto the posterior one-third of the hamulus could provide a curbing function for the dilatator tubae muscle. Adipose tissue, located at the hamulus, could provide lubrication for the tendinous fibers of the dilatator tubae as they round the hamulus. The dilatator tubae was observed to attach to the hook of the eustachian tube and is accepted as the tubal dilator. Observed on 13 of 20 sides in 11 specimens, the bulk of the dilatator tubae remained distinct from the tensor veli palatini despite a connective tissue alliance and intermingling of some muscle fibers. On 5 of 20 sides in 5 specimens, fibers of the dilatator tubae intermingled extensively with the tensor veli palatini. Of the 20 dilatator tubae muscles dissected, 2 were observed to be deficient. The tensor veli palatini was observed to be continuous with the tensor tympani. Full color versions of the figures are available at the following website: http://www.shc.uiowa.edu/papers/tensor/.
To explore the silence nature of otitis media, the temporal bone slides from 306 ear with various types of otitis media were studied histopathologically under the light microscopy and their case histories were reviewed at the Otopathology Laboratory, the University of Minnesota Otitis Media Research Center U.S.A. The results showed that 80.97% of otitis media cases lacked clinical symptoms in pathologic process. The subnormal function status of the eustachian tube and the low-degree infection in pathologic process of otitis media probably are basic causes of silence nature of otitis media. The anatomic specialty of ventilation/drainage system of middle ear cleft and the inflammatory pathologic change causing obstruction of internal ventilation/drainage system and leading to the retention of effusion in posterior areas of middle ear cleft may be are important factors for the development of obstinate pathologic change and silence nature of pathologic process of chronic otitis media.