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Recent Advances in Pathogenesis of Otitis Media

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대한이비인후과학회 부산,울산,경남 지부회 (The Busan, Ulsan, Gyeoungnam Branch of The Korean Society of Otolaryngology)|2009.11|임상이비인후과 (Journal of Clinical Otolaryngology)|제20권 제2호|pp. 141-148|DOI 10.35420/jcohns.2009.20.2.141

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키워드

이관기능장애·병원균유착·점막섬모수송체계이상·자연면역.E-tube dysfunction·Bacterial adherence·Mucociliary dysfunction·Innate immunity
주제분류이비인후과학

초록

The pathogenesis of otitis media is not clearly understood, and not much attention has been paid to it even though otitis media is one of the most common diseases in the otolaryngological field. Since Politzer (1862) first suggested that abnormal function of the eustachian tube appreared to be the most important factor in the pathogenesis of middle ear disease, there has been abundant epidemiological and clinical evidences in support of the idea that eustachian tube dysfunction is an important predisposing factor in the pathogenesis of otitis media. There are three requirements for otitis media to take place；1) bacterial adherence on nasopharynx；2) bacterial entry to the middle ear via the eustachian tube；and 3) bacterial replication in the middle ear. To understand the pathogenesis of otitis media, it is important to understand the mucosal biology of the eustachian tube that is related to the protection of the middle ear. Numerous laboratory and clinical data support the notion that local defense mechanisms, in addition to systemic immunity, protect the middle ear and eustachian tube from invading organisms. In recent years, a special interest has been focused on the mucosal defense system of the middle ear and eustachian tube which is comprised of；1) mechanical defense (e.g., mucociliary transporting system)；2) biologic defense (e.g., mucins, aquaporins, surface active substances, molecules related to innate immunity)；3) immunodefense (e.d., humoral and cellular immune system)；and 4) defense against invading organism (e.g., phagocytosis). In summary, when bacterial colonization on pharynx (or after viral infection) is done, mucociliary dysfunction and decreased innate immunity makes acute otitis media. Negative pressure in the middle ear cavity induces transudation, which makes otitis media with effusion. Formation of biofilm in the middle ear mucosa with or without eardrum perforation means the chronic state of otitis media. Disturbed mucosa gas exchange and impaired ventilation and pressure regulation of the middle ear makes retraction of the eardrum, which finally induces cholesteatoma. Sometimes it makes adhesion of the eardrum, which induces adhesive otitis media. (J Clinical Otolaryngol 2009;20:141-148)

Abstract

The pathogenesis of otitis media is not clearly understood, and not much attention has been paid to it even though otitis media is one of the most common diseases in the otolaryngological field. Since Politzer (1862) first suggested that abnormal function of the eustachian tube appreared to be the most important factor in the pathogenesis of middle ear disease, there has been abundant epidemiological and clinical evidences in support of the idea that eustachian tube dysfunction is an important predisposing factor in the pathogenesis of otitis media. There are three requirements for otitis media to take place；1) bacterial adherence on nasopharynx；2) bacterial entry to the middle ear via the eustachian tube；and 3) bacterial replication in the middle ear. To understand the pathogenesis of otitis media, it is important to understand the mucosal biology of the eustachian tube that is related to the protection of the middle ear. Numerous laboratory and clinical data support the notion that local defense mechanisms, in addition to systemic immunity, protect the middle ear and eustachian tube from invading organisms. In recent years, a special interest has been focused on the mucosal defense system of the middle ear and eustachian tube which is comprised of；1) mechanical defense (e.g., mucociliary transporting system)；2) biologic defense (e.g., mucins, aquaporins, surface active substances, molecules related to innate immunity)；3) immunodefense (e.d., humoral and cellular immune system)；and 4) defense against invading organism (e.g., phagocytosis). In summary, when bacterial colonization on pharynx (or after viral infection) is done, mucociliary dysfunction and decreased innate immunity makes acute otitis media. Negative pressure in the middle ear cavity induces transudation, which makes otitis media with effusion. Formation of biofilm in the middle ear mucosa with or without eardrum perforation means the chronic state of otitis media. Disturbed mucosa gas exchange and impaired ventilation and pressure regulation of the middle ear makes retraction of the eardrum, which finally induces cholesteatoma. Sometimes it makes adhesion of the eardrum, which induces adhesive otitis media. (J Clinical Otolaryngol 2009;20:141-148)

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