Otitis media is an inflammation of the middle ear cleft. It has been suggested that all types of otitis media represent different stages of a continuum of events, with the acute stage leading to a chronic stage.¹ In addition, one form of otitis media may resolve or lead to a more chronic stage of the disease. Although otitis media with effusion is characterized by the presence of a clear fluid in the middle ear cleft, there is no evidence of secretory cell proliferation at an earlier stage. Over time, the subepithelial space is widened by edema, vascular dilation, and the infiltration of host defense cells. With the reabsorption of watery components of the fluid, the increased density of goblet cells, and the formation of secretory glands, the middle ear effusion becomes mucoid and there are chronic inflammatory changes in the middle ear cleft.

Chronic otitis media (COM) has been clinically defined as a chronic discharge from the middle ear in the presence of a perforation of the tympanic membrane. Histopathologically, COM is defined when the inflammatory process has entered a chronic phase and permanent alteration of middle ear structures is seen (▶ Fig. 6.1; ▶ Fig. 6.2).² The pathologic changes in the tympanic membrane due to COM include perforation, retractions, myringosclerosis, pseudo-cystic spaces, and hemorrhage.³

The histopathological changes of the middle ear in COM are similar in the temporal bones with and without perforation of the tympanic membrane.⁴ The most frequently encountered pathological tissues in the middle ear of patients with COM are granulation tissue; osteitis; fibrous thickening of the mucoperiosteum; fluid; cholesteatoma; and cholesterol granuloma;² with granulation tissue being the most common.³

Throughout the course of COM, osseous changes, including osteitis, necrosis, reabsorption, and osteoneogenesis, are occurring in the middle ear cleft (▶ Fig. 6.3).² The bony involvement parallels the severity of the inflammatory process. In the generalized form of active COM, although all three ossicles can show chronic changes, the incus is the most commonly involved, being followed in frequency by the stapes, and then the malleus.²

6.2 Chronic Silent Otitis Media

The clinical definition of COM that requires a tympanic membrane perforation and/or drainage from the middle ear excludes a large number of cases that show chronic pathologic changes in the middle ear cleft. Paparella, Schachern, and Cureogluintroduced the concept of chronic silent otitis media on the basis of histopathologic evidence of chronic infection in the middle ear cleft in the absence of obvious ear-related symptoms and changes in the tympanic membrane (▶ Fig. 6.4).⁵ In 1999, Jaisinghani, Paparella, Schachern, and Le studied 150 temporal bones from 97 patients with COM to correlate the presence of middle ear pathologies with the changes in the tympanic membrane.³ Almost half of the temporal bones with middle ear pathology had no associated tympanic membrane pathology.

It has been stated that the incidence of COM associated with an intact tympanic membrane was four times more common than the incidence of COM with a perforated membrane.⁵ In addition, the otopathological changes of the middle ear cleft in COM are similar in patients with and without perforation of the tympanic membrane.⁵ In 1986, Paparella, Goycoolea, Bassiouni, and Koutroupas reported 10 temporal bones from 5 patients below the age of 2 years who died of Hemophilus influenzae meningitis.⁶ None of the patients studied had documented clinical manifestations of any ear pathology before the onset of meningitis. Temporal bone findings included acute inflammatory disease as well as chronic pathologies such as granulation tissue, fibrosis, and mononuclear cell infiltration. These chronic irreversible pathologies in the middle ear and the presence of labyrinthitis in all cases indicated that the otitis media had been present for some time, suggesting meningitis of otogenic origin (▶ Fig. 6.5).

Because the chronic pathology is undetected, there is a lack of clinical treatment of otitis media, increasing the risk of complications due to the underlying problems (▶ Fig. 6.6).⁵ As a result of the silent middle ear infection process, intratemporal problems, such as endolymphatic hydrops, labyrinthitis, facial palsy, and sensorineural hearing loss, and/or intracranial complications, such as meningitis or brain abscess, can be seen.^5,​7 The clinician should, therefore, be aware that an intact tympanic membrane does not necessarily preclude the presence of pathologic changes in the middle ear cleft.

6.3 Middle Ear/Inner Ear Interaction

The inner ear is intimately associated with the middle ear both functionally and anatomically. Functional changes of the middle ear mechanics affect the transmission of sound to the inner ear, whereas areas of anatomical connections allow for the passage of microorganisms, cytokines, toxins, or drugs from the middle to the inner ear, with potentially serious sequelae. The round window membrane, which is the only soft tissue barrier between the middle and inner ear and which lies within a niche and adjacent to the sinus tympani, facilitating the accumulation of pus, is vulnerable to toxic substances within the middle ear (▶ Fig. 6.6).

Inner ear sequelae that include labyrinthitis (▶ Fig. 6.1), endolymphatic hydrops (▶ Fig. 6.1),⁸ outer hair cell losses, and as a result, sensorineural hearing loss and vestibular disturbances can occur in both acute otitis media (AOM) and COM.^9,​10 In addition, a high-frequency sensorineural hearing loss can be clinically significant in cases of COM given that this denotes perilymphatic inflammation. The basal turn of the cochlea is the most common location of the pathologic changes in the inner ear during this middle ear interaction (▶ Fig. 6.7). This results in a temporary threshold shift, which may become permanent over time. Cureoglu et al showed loss of outer and inner hair cells, especially in the basal turn of the cochlea, and a decrease in the areas of the stria vascularis and spiral ligament in the basal turn of the cochlea of temporal bones with unilateral COM.¹¹

6.3.1 Serous (Toxic) Labyrinthitis

This is characterized by sensorineural hearing loss and vertigo that usually shows partial or complete recovery. It is usually a reaction to exotoxins rather than actual bacterial invasion (▶ Fig. 6.6).¹² The presence of vertigo in a patient with otitis media may indicate the presence of serous labyrinthitis. If it is diagnosed and treated before suppuration starts, the damage in the inner ear will be reversible. The histopathological markers of serous labyrinthitis can be described as endolymphatic hydrops, eosinophilic fluid staining due to increased proteinaceous content, and sero-fibrinous strands in the labyrinthine spaces without any associated host inflammatory cell invasion.¹³

6.3.2 Circumscribed (Localized) Labyrinthitis

The most common underlying problem of circumscribed labyrinthitis is cholesteatoma erosion. The erosion makes the membranous labyrinth sensitive to environmental changes such as temperature or pressure. The inflammation is localized to a bony surface of the labyrinth without the invasion of endosteum. If the patient starts to have sensorineural hearing loss in addition to a positional vertigo, treatment should be initiated for serous labyrinthitis to prevent suppurative labyrinthitis.

6.3.3 Suppurative Labyrinthitis

Hispathologically, suppurative labyrinthitis (▶ Fig. 6.8) has three stages; however, any intracranial complication may occur at any stage, and the patient may end up with a complete loss of labyrinthine functions.¹⁴

During the first stage, purulent effusion fills the perilymphatic spaces but spares the endolymph. The main symptoms are severe vertigo and hearing loss at this stage.

During the second stage, polymorphonuclear lymphocytes (PMLs) dominate in the area with fibrillar precipitates, especially in the perilymphatic space (▶ Fig. 6.9). Endolymphatic hydrops is also seen. This stage begins around 2 weeks after the onset of infection. Although vertigo subsides, sensorineural hearing loss progresses.

The third stage represents chronic labyrinthitis: fibroblasts predominate and small capillaries occur as a result of increased angiogenesis. Eventually osteogenesis may occur (in an animal model, around 2 months). After being stimulated by infection or inflammatory irritation following breakdown of cells, mesenchymal cells, which are located around capillaries, the undersurface of the basilar membrane, and endosteum that lines the perilymphatic space, rapidly differentiate into fibroblasts that produce collagen fibers, endothelial cells that form capillaries, and osteoblasts. The osteoblasts form trabeculae (lamellar or spongy bone) that join together and incorporate small blood vessels within them. Then, haversian canals form from the condensation of lamellar bone, which could be difficult to distinguish from the normal bone around it. Pathologic new bone formation within the otic capsule in response to inflammatory and/or destructive processes is called labyrinthine ossificans, which represents the terminal stage of repair of labyrinthitis. At early stages, only scala tympani of the basal turn of the cochlea is involved. Later, all parts of the inner ear are involved. In humans, it may take years to have a complete labyrinthitis ossificans (▶ Fig. 6.10; ▶ Fig. 6.11; ▶ Fig. 6.12).

6.4 Pathological Changes in the Middle Ear Cleft in COM

6.4.1 Granulation Tissue

Granulation tissue is the most common pathology encountered in chronic ears. It consists of vascularized connective tissue with a component of acute inflammatory exudation. The most common sites for granulation tissue are the epitympanum, mesotympanum, round window niche, and mastoid antrum (▶ Fig. 6.13).^2,​3,​5 During the formation of granulation tissue, the mucous membrane is thickened by edema, submucosal fibrosis, and infiltration with chronic inflammatory cells. Later, mucosal edema may progress to the formation of polyps.¹ With maturation, granulation tissue becomes more fibrous and less cellular, with increased collagen and reticular formation.² Granulation tissue may lead to adhesions or tympanosclerosis in the middle ear.¹ This activity, if unchecked, may lead to serious complications, including the destruction of the inner ear.

6.4.2 Cholesteatoma

Cholesteatoma can be described as a keratinized squamous epithelium in the middle ear cleft (▶ Fig. 6.14). It is classified as congenital or acquired based on its presumed etiology. The pathogenesis of cholesteatoma, outlined in Chapter 4, is multifactorial.

With acquired cholesteatoma, the pathogenesis is unclear and remains controversial. The most accepted theory is the invagination theory (also known as the retraction pocket theory) (▶ Fig. 6.15). Eustachian tube dysfunction creates negative pressure and causes loss of structural support for the tympanic membrane; eventually atelectasis results in retraction pockets (▶ Fig. 6.16). Keratin accumulates within these pockets and progresses to cholesteatoma (▶ Fig. 6.17).

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