Pathogenesis of otitis media was studied in humans and various animal models primarily from a pathological and chemical point of view. Findings were correlated and interpreted for various forms of otitis media in longitudinal and parallel studies, including acute purulent otitis media (POM), serous otitis media (SOM), mucoid or secretory otitis media (MOM), and chronic suppurative otitis media (COM), especially as regards the continuum or interrelated changes of various groups. Purulent otitis media was produced in chinchillas by direct inoculation of less than 100 pneumococci into the middle ear space. Serous otitis media was produced in chinchillas and cats following Eustachian tube obstruction with silicone. Mucoid otitis media followed the development of SOM in cats after two to four weeks of tubal occlusion. Samples of middle ear effusion (MEE) and serum, obtained from children with SOM and MOM after myringotomy for ventilation tube placement, were evaluated. The three components studied were MEE, epithelium and the subepithelial space (SES). Inflammatory changes in the SES were significant for all forms of otitis media, but especially for POM and SOM. Epithelial metaplasia to secretory cells was most prominent in MOM. Chemical factors involved in pathogenesis and defense were studied. Lactic dehydrogenase and lysozyme, chemical indicators of inflammatory activity, were greater in POM and MOM than in SOM. Immunoglobulins (A, G, & M) were greater in MOM than in SOM. The similarity of findings between the groups suggests a strong relationship between them. The ability of certain types of otitis media to evolve into another substantiates the concept of the continuum for some patients. Pathogenesis is dependent upon various extrinsic factors of etiopathogenesis, while the form that otitis media takes seems to rely mostly on relative activity of the SES and the epithelium.
Bibliographical noteFunding Information:
From the University of Minnesota, Minneapolis, Minnesota. This research was funded by a grant from USPHS (NS 07823-08). 7 1977 86 4 481 492 © 1977 SAGE Publications 1977 SAGE Publications