Interaction between middle and inner ears in otitis media

Abstract

Middle ear infection is one of the most common childhood diseases that causes inner ear pathology, resulting in hearing loss and communication disorders. The presence of sensorineural hearing loss (SNHL) in the extended high frequency range (8–20 kHz) in children with otitis media histories has been well established.

Pathological changes of the cochlear lateral wall and the organ of Corti have been reported in animal models of experimental otitis media (OM). The results of inoculation of Streptococcus pneumoniae in the middle ear suggest that bacterial OM can produce damage of both outer and inner hair cells. This damage may be a significant factor in temporary and permanent SNHL associated with bacterial OM. Bacteria, bacterial products and inflammatory mediators crossing the round window membrane are known to cause structural as well as biochemical changes of inner ear tissues and lead to the functional damage of the inner ear through the disruption of inner ear homeostasis and auditory transduction system. Many factors, namely, cytokines, nitric oxide or other oxygen derived radicals, prostaglandins, leukotrienes, platelet activating factors and bacteria-derived toxins are all involved in the processes that lead to altered expression of proteins, structural damage and apoptotic changes in the inner ear. Moderate SNHL was reported in the higher and middle frequencies after placing of IL‐2 or IL‐8 on the round window membrane. More recently, leakage of Evans blue dye from the vessels in the cochlear lateral wall after intraperitoneal injection of LPS in chinchillas was reported, indicating the possible disruption of the blood labyrinth barrier.

An increased understanding of host and pathogen interactions as well as more detailed clarification of the mechanisms of inner ear tissue damage by inflammatory mediators and bacterial products is necessary for the better treatment of OM and prevention of SNHL.