[Otitis nigra: etiologic pathogenetic and clinical aspects (author's transl)].

1979 
: The clinical picture of otitis nigra (idiopathic sero-hemmorrhagic otitis media) as independent clinical entity is shown, presenting 5 cases requiring mastoid surgery. Samples of mastoid mucosa were investigated by light- and electron-microscopy employing histochemical, immunofluorescent and virological techniques. Pathological changes of the small vessels in the subepithelial connective tissue with increased vascular permeability and extravasation of red blood cells and serum play a central role in the pathogenetic course of the disease. Disintegration of erythrocytes leads by catabolism of hemoglobin to formation of hemosiderin and ferretin, whereas by processing of phospholipids of the cell-membrane cholesterin cristals are deposited in the connective tissue. These cholesterin deposits in turn induce a foreign body reaction with formation of typical cholesterol granulomas. The mucosa shows secretory activity in intraepithelial secretory cells and glandlike structures in the subepithelial connective tissue. Neutral and acidic mucopolysaccharides are demonstrated in the secretory product. As possible cause for the vascular lesion that in turn sets off the pathomechanisme of otitis nigra a subclinical viral infection is discussed. This conjecture is supported by demonstration of virus-like inclusion bodies in macrophages and fibrocytes and of virus-like particles in antral smears. In addition myxoviruses of the parotitis-epidemica group could be identified in these smears by serological methods. Furthermore, the stimulation of the local immunological defense system, evidenced by the presence of numerous immunoglobulin-producing plasmacells in the tissue, is in concord with a viral infection. Therapy requires mastoidectomy in combination with posterior tympanotomy in order to eradicate completely the intractably diseased mastoid mucosa.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    0
    References
    0
    Citations
    NaN
    KQI
    []