This review deals with the characteristics of various inflammatory mediators identified in the middle ear during otitis media and in cholesteatoma. The role of each inflammatory mediator in the pathogenesis of otitis media and cholesteatoma has been discussed. Further, the relation of each inflammatory mediator to the pathophysiology of the middle and inner ear along with its mechanisms of pathological change has been described. The mechanisms of hearing loss including sensorineural hearing loss (SNHL) as a sequela of otitis media are also discussed. The passage of inflammatory mediators through the round window membrane into the scala tympani is indicated. In an experimental animal model, an application of cytokines and lipopolysaccharide (LPS), a bacterial toxin, on the round window membrane induced sensorineural hearing loss as identified through auditory brainstem response threshold shifts. An increase in permeability of the blood-labyrinth barrier (BLB) was observed following application of these inflammatory mediators and LPS. The leakage of the blood components into the lateral wall of the cochlea through an increase in BLB permeability appears to be related to the sensorineural hearing loss by hindering K+ recycling through the lateral wall disrupting the ion homeostasis of the endolymph. Further studies on the roles of various inflammatory mediators and bacterial toxins in inducing the sensorineumral hearing loss in otitis media should be pursued.

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The blood-labyrinth barrier is a concept used to explain the stability of composition of the labyrinthine fluids in spite of systemic alterations in blood composition. This blood-labyrinth barrier concept was tested by injecting various test substances into the systemic circulation of experimental animals and recovering these compounds in perilymph. The concentration of each test substance in perilymph lagged behind that of serum, and the transport of a series of test substances was found to be inversely related to the molecular weight and diameter. Among the osmotic agents injected, glycerol and urea penetrated into perilymph to a considerable degree; however, mannitol did not enter perilymph in any significant amount. This may explain the clinical differences noted with these agents in testing for Meniere's disease. Furosemide, an ototoxic diuretic, was found to penetrate into perilymph after intravenous injection into chinchillas. The concentration of furosemide, measured by high pressure liquid chromatography, was fairly constant at the time of full recovery of endocochlear potential after doses of 50-200 mg/kg. The principle of correlating drug concentration in serum and in inner ear fluids with pathophysiologic effect may provide a prediction of threshold concentration of ototoxic effect by measurement of serum concentration of the drug. More extensive studies are necessary to clarify the role of the bloodlabyrinth barrier in the regulatory mechanisms which maintain the hemeostasis in the inner ear and the pathology which may follow when this homeostasis is disrupted.

The blood-labyrinth barrier is concept that has evolved based on marked difference in chemical composition between perilymph and blood. Studies reported here have been designed to manipulate physiologic, metabolic, and pharmacologic conditions in experimental animals in order to determine the characteristics of this regulatory mechanisms. Tracer studies of uptake of sodium, calcium, and albumin from blood into perilymph showed that these substances penetrate into inner ear fluids quite slowly. Injections of ototoxic substances (kanamycin, furosemide) show limited transport of these agents into perilymph. Administration of an osmotic agent (urea) resulted in a parallel but delayed elevation of perilymph concentration. The possible role of a alteration of blood-labyrinth barrier in inner ear disorders has been discussed.

Conclusion-Middle and inner ear interactions in otitis media can lead to cochlear pathology. More severe pathological changes observed in the basal turn of the cochlea are consistent with prevalence of sensorineural hearing loss at higher frequencies in patients with otitis media.Methods-Of 614 temporal bones with otitis media, 47 with chronic and 35 with purulent otitis media were selected following strict exclusion of subjects with a history of acoustic trauma, head trauma, ototoxic drugs, and other diseases affecting the cochlear labyrinth. Temporal bones with labyrinthine inflammatory changes were further evaluated for loss of hair cells and other histopathologic changes compared to age-matched controls.Results-In all, 19% of temporal bones with chronic and 9% with purulent otitis media showed labyrinthine inflammatory changes. In chronic otitis media, inflammatory changes were: 56% localized purulent, 22% localized serous, 11% generalized seropurulent, and 11% generalized serous. Inflammatory changes in temporal bones with purulent otitis media included 67% localized purulent and 33% were generalized seropurulent. Pathological findings included: serofibrinous precipitates and inflammatory cells in scala tympani of basal turn and cochlear aqueduct, significant loss of outer and inner hair cells, and significant decrease in area of stria vascularis in the basal turn of the cochlea, as compared to controls.