Type II Collagen Mediated Autoimmune Middle Ear Disease: Eustachian Tube Disease, Otitis Media with Effusion and Tympanosclerosis

Intact Eustachian tube and tympanic cavity functions are essential for normal middle ear physiology. Type II collagen is an essential component of ear tissue. Autoimmune response to this type II collagen produces sensorineural hearing loss, vestibular dysfunction, endolymphatic hydrops, otospongiosi...

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Veröffentlicht in:Auris, nasus, larynx nasus, larynx, 1985, Vol.12, p.S91-S93
Hauptverfasser: Yoo, Tai-Jun, Sudo, Naohiro, Tomoda, Koichi, Yazawa, Yoshiro, Ishibe, Tsukasa, Takeda, Teizo, Floyd, Rachael
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Sprache:eng
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Zusammenfassung:Intact Eustachian tube and tympanic cavity functions are essential for normal middle ear physiology. Type II collagen is an essential component of ear tissue. Autoimmune response to this type II collagen produces sensorineural hearing loss, vestibular dysfunction, endolymphatic hydrops, otospongiosis"like lesions, Eustachian tube inflammation and Eustachian tube chondritis. In addition, these autoimmune responses occasionally produce otitis media with effusion (not infectious). Tympanosclerosis, which is a frequent sequelae of otitis media with effusions, was also induced by type II collagen immunization together with surgical incision of the tympanic membrane. The exact mechanisms of this type II collagen autoimmune mediated middle ear disease are not clear. However, the animals thus induced have higher antibody titers and cell mediated immune responses to type II collagen. The tympanic membrane showing tympanosclerosis also had C3 and Ig deposits. All the animals with otitis media with effusion induced by type II collagen immunization also had Eustachian tube disease. This could be due to a mllfunction of the Eustachian tube. Thus, this model might provide a rational approach for the study of otitis media with effusion associated with vasculitis. Further studies are needed to elucidate the immunologic mechanism involved in the pathogenesis of otitis media with effusion.
ISSN:0385-8146
1879-1476
DOI:10.1016/S0385-8146(85)80112-7