Abstract
It has been well documented that sensorineural hearing loss with and without vertigo is sometimes associated with acute otitis media. In addition, there have been several reports that in cases of unilateral chronic otitis media, deterioration of the bone conduction threshold is significantly higher in the diseased ears than in the contralateral normal ears. Therefore, inflammation of the middle ear could influence the inner ear function or could cause inner ear damage. Otogenic inflammation in the inner ear is classified into two types; suppurative labyrinthitis and serous labyrinthitis based on the pathogenesis in the inner ear. Suppurative labyrinthitis is caused by bacterial invasion of the inner ear mostly via the round window membrane. It is characterized by infiltration of polymorphonuclear leukocytes in the perilymphatic space and eventually also in the endolymphatic space. Endolymphatic hydrops is also seen. In the later stage, fibrosis and new bone formation occurs in the labyrinth, resulting in profound loss of auditory and vestibular function. Serous labyrinthitis is defined as an irritation of the labyrinth caused by degradation of the tissue fluid environment of the inner ear by bacterial toxins and inflammatory mediators. When the disease is mild, recovery of function may be complete. Inflammatory mediators that have been detected in the middle ear, can pass through the round window membrane under physiological conditions as well as under pathological condition. Bacterial toxins such as LPS and pneumolysin, and mediators including PAF, cytokines and NO may alter the cochlear function, particularly disturbing the ion homeostasis maintained by fibrocytes in the cochlear lateral wall. The repeated invasion and persistent presence of toxins and mediators may lead to permanent morphological change in the sensory cells and stria vascularis of the inner ear.
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