Sensorineural hearing loss due to cochlear otospongiosis: etiology.
This presentation discusses the most valuable way to correlate specific morphologic changes in cochlear otospongiosis with sensorineural hearing loss. Both biochemical and vascular factors may be responsible for the association of far advanced otospongiosis and histopathologic changes. An enzymatic concept of the disease is proposed on the basis of experimental findings and cytoclinical correlations, and the spread of proteolytic enzymes from the bursting lysosomes in histiocytes of the otospongiotic microfoci of the lateral wall. In addition, according to Ruedi's vascular concept, abnormal vascular connections called "shunts", provoked by active foci breakiny oxygen. Such extensive otospongiotic bone transformation breaking the endosteum of the cochlear is much less frequent than the progressive cochlear component encountered by otologic surgeons in far advanced otospongiosis. It is for this reason that the authors believe that their enzymatic concept of otospongiosis may explain the most important part of the sensorineural impairment in cochlear otospongiosis.
D000328:Adult; D000368:Aged; D003638:Deafness / Q000209:etiology; D007758:Ear, Inner / Q000098:blood supply* / Q000648:ultrastructure; D006644:Histiocytes / Q000648:ultrastructure; D006801:Humans; D006867:Hydrolases / Q000378:metabolism*; D008875:Middle Aged; D010040:Otosclerosis / Q000150:complications / Q000201:enzymology* / Q000473:pathology; D012039:Regional Blood Flow
D006867:Hydrolases