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This article reviews the importance of the round-window membrane in exposing the labyrinth to or protecting it from the toxic effects of otitis media. Only in the last decades have the middle ear and the inner ear been recognized as valid and important immunocompetent structures [1]. The purpose of this article is to review the interrelations between the middle ear and the inner ear in otitis media and the role of bacteria, bacterial products, and inflammatory mediators as toxic agents acting through the roundwindow membrane. The middle-ear space is lined by a mucous membrane that in turn is covered by a layer of mucin (mucus) through which microorganisms must pass before they reach the mucosa itself (Table 1). Once the microorganisms have reached the epithelial surface of the mucous membrane, they must overcome the rapidly dividing mucosal cells and the superficial specific mucosal immune system [4].
If bacteria are able to overcome the mucus and epithelial layers of the mucosa, they must meet with both nonspecific and specific defense systems in the lamina propria. Once bacteria overcome the defense mechanisms of the middle-ear mucosa, damage to the inner ear can occur.
The conditions caused in the middle ear by bacteria - acute otitis media, chronic suppurative otitis media, and middle-ear effusion - now are accepted as representing different phases in the spectrum of the same pathological continuum of otitis media [11].
Bacteria that cause acute otitis media are predominantly aerobic, particularly Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis [13- 15]. Also related to inner-ear damage caused by otitis media is the role of inflammatory mediators. Round-window membrane anatomy and structural studies disclose three basic layers: an outer epithelium, a middle core of connective tissue, and an inner epithelium (Figs.
Ear Infections Infections can affect the outer part of the ear (Otitis externa), behind the ear drum (Otits media) or the inner ear. Ear Discharge and Perforated Ear Drum Recurrent or persistent discharge from the ear can be due to chronic infection, trapped skin (cholesteatoma) or a hole in the ear drum (perforation). Hearing Tests & Hearing Impairment Hearing is something we take for granted but people of any age can suffer from hearing loss.
Glue Ear & Grommets Grommets are tiny plastic ventilation tubes which sit in the ear drum.
Vertigo & Dizziness Vertigo or the illusion of movement is the medical term for dizziness. Characteristics of the immune system in the human middle ear and middle-ear mechanisms against bacteria are explained. One of the first and most important studies pertaining to the immunological aspects of the middle ear, published in 1974 [2], concerned the role of the secretory immune system in the middle ear and otitis media.
In this article, we emphasize the importance of continued investigations into the facilitative or protective contributions of the round-window membrane in inner-ear toxicity in the several forms of otitis media. Within the mucin are found substances that can either kill the bacteria or inhibit their growth: lysozyme, lactoferrin, and lactoperoxidase [4].
This specific defense system depends on the secretory antibodies, mainly secretory immunoglobulin A (IgA).


The first system is made up of a complement system, phagocytes (macrophages and polymorphonuclear neutrophils), and transferrin.
Pathological events can be caused by a direct effect of the bacteria itself: Bacterial penetration of all three layers of the round-window membrane was demonstrated experimentally and resulted in bacteria entering into cochlear turns and neuronal pathways, causing nerve degeneration and edema and hemorrhage of the stria vascularis [8]. Experimentally, the same pattern of otitis media pathological changes were observed in the round-window membrane and in the mucoperiosteum of the middle ear. Even middle-ear effusion, often considered to be or described as a sterile condition, is now accepted as containing bacteria and bacterial products in a high percentage of cases [16,l7], and the predominant microorganisms are the same as those in acute otitis media [18,19]. Mediators are biochemical components produced by epithelial cells, infiltrating inflammatory cells, and endothelial cells, which mediate inflammatory reactions in a sequential manner [20]. Only after drilling the lateral edge of the round window niche is the round window membrane clearly visible. Photomicrograph of the normal human round-window membrane, which consists of an outer low cuboidal epithelium (left side of the image) , a middle core of connective tissue, and an inner simple epithelium (right side of the image). Para reproducir la musica que tendra que actualizar su navegador o actualizar el Plugin de Flash. A small suction tube is used under microscope guidance for a more gentle and complete cleaning of the ear.
The role of bacteria and bacterial products in inner-ear damage is detailed, and related pathological events are described.
The concept that the inner ear is capable of mounting an immune response dates back only to the 1980s [3].
Sialic acid-containing oligosaccharides of the mucin form another defense mechanism and appear to act as mucin receptors for the bacteria, preventing their adherence to the epithelial wall, thus modulating bacterial colonization [5]. This system depends on B cells derived from mucosa-associated lymphoid tissue (MALT), which consists of lymphoepithelial structures, such as those constituting Waldeyer's pharyngeal ring [6]. Bacterial products also were important: Instillation of a suspension of Escherichia coli endotoxin into the round-window niche in rats demonstrated an inner-ear disturbance using a frequency-specific auditory brain stem response technique [9]. These changes could account for modifications of permeability, rendering the membrane an easy pathway from the middle to the inner ear [12]. In chronic otitis media, the most common isolate is Pseudomonas aeruginosa, and other isolates include such aerobic organisms as Staphylococcus aureus, S.
Besides bacterial infections, endotoxins, exotoxins, and other bacterial products, inflammatory mediators could be involved in the development of sensorineural hearing loss, the more frequent complication attributable to interaction between the middle ear and the inner ear [21].
Initially, round-window membrane alterations induced by otitis media were thought to be restricted to or predominantly centered in the outer epithelium, but subsequent ultrastructural studies demonstrated that the three layers participate in the resorption and secretion of substances to and from the inner ear [30]. For easy identification of the membrane for the image, the membrane was disrupted, and the lumen of scala tympani then is clearly visible. The entire membrane might participate in the inner-ear defense mechanism , but structural changes in otitis media were confined mainly to the inner epithelium and connective ti ssue layers. Characteristics of secretory immune system in human middle ear: Implications in otitis media.


Binding between outer membrane proteins of nontypeable Haemophilus influenzae and human nasopharyngeal mucin.
Bacteriology of acute otitis media in a cohort of Finnish children followed for the first two years of life. Bacteriological findings and persistence of middle ear effusion in otitis media with effusion. Effect of prostaglandin, leukotriene, and arachidonic acid on experimental otitis media with effusion in chinchillas.
Effect of exogenous arachidonic acid metabolites applied on round window membrane on hearing and their levels in the perilymph. Cytokine profiles in a rat model of otitis media with effusion caused by eustachian tube obstruction with and without Streptococcus pneumoniae infection. Clinical aspects of round window membrane permeability under normal and pathological conditions. The hypothetical role of inflammatory mediators in bacteriainduced inner-ear toxicity is particularly emphasized.
Ciliary function is also important because it promotes drainage of mucus and secretions or pus from the middle-ear cavity through the eustachian tube. These MALT-induced B cells migrate through lymph and blood to target such tissues as the middle-ear mucosa, where they differentiate after extravasation to IgA-producing plasma cells. However, a large field of knowledge remains to be elucidated about the extent to which these roundwindow otitis media-induced alterations influence the permeability of the membrane [31].
Clinical conditions causing these events are detailed, and the most frequently involved microorganisms are mentioned.
The round-window membrane is permeable to many substances, including inflammatory mediators, and many studies have shown that these mediators can affect inner-ear function, as seen in auditory brainstem response, cochlear microphonics, otoacoustic emissions, and cochlear blood flow studies [20].
An equally important consideration is that at least part of the response to inflammation is protective [20]. Finally, roundwindow membrane macroscopic and microscopic anatomy is discussed, and considerations about the exact role of membrane inflammation - protection versus damage of the inner earare expressed. The exact role of inflammatory consequences of otitis media in protection of versus damage to the inner ear has yet to be determined.
Bacterial products generated by some of these microorganisms and involved in deleterious inner-ear effects were mentioned by Hellstrom et al.
The comprehension of these mechanisms is of fundamental importance to the development of measures to counteract inner-ear consequences of otitis media, particularly sensorineural hearing loss and tinnitus.



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