しん出性中耳炎の病態 最近の知見から

Abstract

Recent investigations on the pathophysiology of otitis media with effusion (OME) were summarized from several points of view.(1) Experimental study of OME: The long-standing mucoid type of OME was induced for the first time by the impairment of eustachian tube active function and the administration of immunosuppressant drugs.(2) Bacterial adherence to nasopharynx: In vitro experiments on adherence of nontypable Haemophilus influenzae and Streptcoccus pneumoniae to nasopharyngeal epithelial cells clarified the significance of bacterial adherence to the nasopharynx in the pathogenesis of OME in children: a secretory immunoglobulin (IgA) in nasopharyngeal secretions is related to a decrease of bacterial adherence.(3) Lipid A in the middle ear: The instillation of lipid A component of endotoxin into the middle ear cavity can induce inflammatory changes with middle ear effusion. The lipid A interacts with glycoconjugates on the epithelial surface and with secretion from goblet cells. Excess secretion from the goblet cells to exclude endotoxin from the middle ear cavity seems to play an important role in the pathogenesis of OME.(4) Pressure regulation in the middle ear: Middle ear pressure is thought to be regulated not only by active opening of the Eustachian tube but also by transmucosal gas exchange in the middle ear cavity. In addition to poor dynamic tubal function, impaired transmucosal pressure regulation due to mucosal inflammation is thought to be related to the pathoetiology of OME.(5) Size of the mastoid pneumatization: The suppression of mastoid pneumatization is closely related to a persistent state of middle ear inflammation. Patients with OME can be treated by conservative therapy or by tube insertion based on the degree of mastoid pneumatization seen on x-ray films. Patients with a well-pneumatized mastoid air system can be managed with conservative treatment alone.