The pathology of the ET may or may not be involved in the pathogenesis of otitis media, whereas the pathophysiology of the tubal system usually is.

The chapter includes

Pathologic changes that occur in the ET, primarily related to


           Cleft palate

           Effects of a tumor


Pathologic changes in the ET can be involved in the pathogenesis of otitis media and tubal dysfunction, but intrinsic (intramural, mural) or extrinsic (extramural) tubal pathology does not have to be present for the development of middle-ear disease. As previously described, the tubal system can either be too open (nonintact tympanic membrane) or too closed (nasopharyngeal obstruction at the pharyngeal tubal opening) at either end without any pathologic changes in the tube itself, which can result in middle-ear disease. Also, the tube may be functionally obstructed owing to failure of the opening mechanism (failure of tubal dilatation or tubal constriction on swallowing), without any direct evidence of pathology of the tubal mucosa or extramural disease1,2; thus, histopathologic studies of the ET may not show any pathologic changes even though disease is present in the middle ear and mastoid. Also, functional obstruction of the tube can be caused by diseases or disorders of the tensor veli palatini muscle distant from the tube, such as by tumor, trauma, or surgery involving the palate or base of skull, without any pathologic changes in the tube itself (see Tumors and Irradiation).

However, a previous study has shown that a viral upper respiratory tract infection can result in partial tubal obstruction, as evidenced by the development of ET dysfunction, diagnosed by manometric testing of the tube.3 Also, following viral challenge of the nose in adult volunteers, tympanometry identified middle-ear negative pressure, which was followed by the development of an effusion or infection in the middle ear (see Chapter 6, “Pathogenesis”).4–10 As described subsequently, there are many diseases and disorders that can affect the ET that can result in middle-ear disease, as demonstrated on human histopathologic temporal bone specimens. Most of these reports have been from the laboratory of the late Professor Isamu Sando at the Eye and Ear Institute of the University of Pittsburgh School of Medicine.

Effect of Inflammation on the Middle-Ear Cleft

Acute Otitis Media

The following are the generally accepted stages of inflammation that occur in the middle-ear cleft. In the initial stages of classic acute otitis media, the mucoperiosteum of the middle ear and mastoid air cells is hyperemic and edematous. This is followed by an exudation of polymorphonuclear leukocytes and serofibrinous fluid into the middle ear. The quantity of fluid increases until the middle ear is filled and pressure is exerted against the tympanic membrane. If the disease progresses, the bulging tympanic membrane may rupture spontaneously. The resultant discharge is at first serosanguineous but then becomes mucopurulent. Throughout the middle ear and mastoid, the mucosa becomes markedly thickened by a mixture of inflammatory cells, new capillaries, and young fibrous tissue. Tos and Bak-Pedersen described an increase in goblet cell population in the ETs and middle ears in temporal bone specimens from children and adults who had a middle-ear infection.11 In the rat model of acute otitis media, Cayé-Thomasen and Tos recently reported that goblet cell density and mucous gland volume in the ET increased up to 6 months following infection when the animal was inoculated with Streptococcus pneumoniae or Haemophilus influenzae; Moraxella catarrhalis did not induce the same degree of these inflammatory changes, which supports the belief that this bacterium is not as virulent in the middle ear as S. pneumoniae or H. influenzae.12–14 They postulated that these pathologic changes in the ET can compromise the ventilatory (pressure regulatory) and drainage (clearance) functions of the tube following an attack of acute otitis media. An earlier study from the same laboratory demonstrated in the rat model of acute otitis media that increased mucosal goblet cell density caused by H. influenzae can result in secretory otitis media that can progress to the chronic stage (see Otitis Media with Effusion).15

The acute middle-ear infectious process may become associated with blockage of the aditus ad antrum, resulting in inadequate drainage of the mastoid gas cells and a consequent mastoiditis. Extension beyond the mucoperiosteum may lead to intratemporal complications, such as facial paralysis, labyrinthitis, and petrositis, or intracranial complications, which may include lateral sinus thrombophlebitis, meningitis, otitic hydrocephalus, subdural abscess, epidural abscess, and brain abscess.16

Otitis Media with Effusion

The pathologic findings associated with the serous and mucoid types of chronic middle-ear effusion are similar. Early pathologic changes include hyperplasia, differentiation of epithelial cells, and gland formation.17 There is an increase in the number of secretory cells, including glands and ciliated cells. Tos and Bak-Pedersen described the increase in goblet cells and gland density in biopsies obtained from children’s middle ears that had chronic otitis media with effusion.18 The lamina propria or connective tissue layer becomes thickened by edema and infiltration of numerous inflammatory cells consisting of lymphocytes, plasma cells, macrophages, and polymorphonuclear leukocytes. These changes are more striking in the presence of a mucoid effusion than for a pure serous effusion, in which tissue edema is the predominant finding in addition to the presence of chronic inflammatory cells. It is generally believed that mucoid effusions are mainly the result of secretion, whereas serous effusions are mostly transudates. Persistent atelectasis of the middle ear, chronic middle-ear effusions, or both are associated with a number of intratemporal complications and sequelae, including hearing loss, tympanosclerosis, adhesive otitis media, perforation with discharge, chronic mastoiditis, and cholesteatoma.19

Pathology of Post–Tympanostomy Tube Placement

It is assumed that middle-ear pathology caused by chronic otitis media with effusion is resolved in the majority of patients following myringotomy and tympanostomy tube insertion. Indeed, most clinicians would agree that the tympanic membrane and hearing are restored to normal following tympanostomy tube surgery. Also, I had the opportunity to operate on the middle ears of many children (e.g., exploratory tympanotomy for perilymphatic fistula) who had had tympanostomy tubes previously inserted for chronic otitis media with effusion in which the middle-ear mucosa appeared to be perfectly healthy when observed through the operating microscope. Despite this clinical experience, there is some evidence that chronic pathologic changes in the middle-ear mucosa occur even when tympanostomy tubes are in place. Takahashi and Sando reported on their histopathologic studies of 12 temporal bones from eight children who had otitis media with effusion and who had tympanostomy tubes in place and described chronic pathologic changes, such as effusion, granulomatous tissue, and even epidermal ingrowth.20 All of these specimens were from patients who had a terminal event. There is no question that otitis media can commonly occur in the middle-ear cleft following placement of tympanostomy tubes, especially in children who have an acute or chronic upper respiratory tract infection, which I consider to be the result of reflux of nasopharyngeal secretions through the ET and into the middle ear. (Also, the middle ear can be contaminated from water in the external auditory canal when tympanostomy tubes are in place.) The pathophysiologic explanation for reflux into the middle ear when the tympanic membrane is not intact is described in detail in Chapter 5, “Pathophysiology.” Complications of tympanostomy tubes are addressed in Chapter 9, “Role in Management of Middle-Ear Disease.”

Mucosa-Associated Lymphoid Tissue

Three studies identified the presence of mucosa-associated lymphoid tissue (MALT) in the ET in humans. Kamimura and colleagues examined histopathologic sections from 263 temporal bones of children with and without evidence of otitis media.21 Of the 65 specimens that had otitis media, MALT was present in 30 (46.2%) ETs and in 19 (29.2%) middle ears, whereas in the 98 cases in which no otitis media was present, MALT was relatively rare or nonexistent. In a follow-up study, Kamimura and colleagues concluded that MALT has a close relationship to otitis media and might be a local response to recurrent infection in the ET and middle ear.22 Employing similar histopathologic studies of temporal bones, with and without otitis media, in the same laboratory, Haginomori and colleagues hypothesized that cellular proliferation of MALT within the middle ear and ET might reflect the activity that produces immunoglobulin A against invasion of foreign antigens.23

Cleft Palate

I describe here the histopathologic findings from human temporal specimens from individuals who had cleft palate, but in Chapter 5, I describe how these congenital abnormalities are related to the development of middle-ear disease. The infant with an unrepaired cleft palate has been reported to have a universal incidence of a middle-ear effusion,24 which has been associated with a functional obstruction (failure of normal tubal dilation during swallowing) of the ET.25 It is my contention that understanding the underlying structural and functional abnormalities that lead to middle-ear disease in the child who has a cleft palate will aid in finding answers to the development of otitis media in children who have an intact palate. Indeed, there is some evidence that the tubal dysfunction identified by tubal function tests of patients who have a cleft palate26,27 is similar to that of children who have chronic otitis media with effusion but no cleft palate.28

Histopathologic Studies of Human Temporal Bones

Using extended temporal bone histopathologic specimens from infants with cleft palate, computer-aided three-dimensional reconstructions have shown anatomic differences between specimens with and without a cleft palate. Sando and colleagues described in detail the procedure of removing and processing these human extended temporal bone specimens.29 These findings help us understand the pathophysiology and pathology of tubal dysfunction and pathogenesis of middle-ear disease in infants who have a cleft palate. Table 7–1 is a summary of these findings from the late Professor Sando’s laboratory at the Eye and Ear Institute of Pittsburgh and from our other studies conducted in the Anthropology Department at the University of Pittsburgh.30–36

There are at least nine known abnormalities in the structure of the ET associated with cleft palate (compared with specimens without a cleft palate). The following have been identified from studies of extended histopathologic specimens taken from individuals with cleft palate:

       1.  ET length. Sadler-Kimes and colleagues and Siegel and colleagues compared the length of the tube between individuals with and without a cleft palate and found that the tube was shorter in specimens from infants and young children with a cleft palate than in age-matched controls. The significance of this finding is discussed later.30,31

       2.  Angle between the tensor veli palatini muscle and the cartilage. Sadler-Kimes and colleagues reported that the angle at which the tensor veli palatini muscle attaches to the ET cartilage was larger than control specimens without a cleft palate.30

       3.  Deformed cartilage. Shibahara and Sando described the angle between axial lines through the lateral lamina and the medial lamina of the cartilage as wide in the cleft palate specimens compared with age-matched controls.32 In a similar follow-up study, Sando and Takahashi examined three specimens from patients who had a cleft palate and found the cartilage deformed; the angle between lines along the upper half of the luminal side of the medial lamina of the cartilage and the luminal side of the lateral lamina of the cartilage was different than in specimens without a cleft palate.33

       4.  Cartilage cell density. Shibahara and Sando assessed the cross-sectional area of the cartilage between cleft and non–cleft palate specimens and reported it to be greater in cleft palate patients.32

       5.  Ratio of area of lateral and medial laminae of the cartilage. Matsune and colleagues measured the areas and ratio of the lateral and medial laminae of the tubal cartilage and reported that the ratio of the areas of the cartilage was smaller than in specimens with a cleft palate when compared with cases without a cleft palate.35 In a later similar study, Takasaki and colleagues evaluated the cartilage of the ET in 10 specimens with a cleft palate and compared them with 34 non–cleft palate cases.34 They found that the ratio of the lateral and medial laminae of the cartilage was smaller in the specimens with a cleft palate.

TABLE 7–1.  Summary of the Differences in Structures of the ET in Extended Temporal Bone Specimens from Infants and Young Children With Cleft Palate Compared With Specimens Without Cleft Palate

Abnormality Compared With Specimens Without Cleft Palate


Length of tube shorter

Sadler-Kimes et al., 198930; Siegel et al., 198831

Angle between cartilage and TVP larger

Sadler-Kimes et al., 198930

Cartilage deformed

Shibahara and Sando, 198832; Sando and Takahashi, 199033

Cartilage cell density greater

Shibahara and Sando, 198832

Ratio of lateral and medial laminae area of cartilage smaller

Takasaki et al., 200034; Matsune et al., 199135

Curvature of lumen less

Matsune et al., 199135

Elastin at hinge portion of cartilage less

Matsune et al., 199236

Insertion of TVP into tip of lateral lamina abnormal

Matsune et al., 199135

Insertion ratio of TVP to cartilage less

Matsune et al., 199135

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Jul 15, 2018 | Posted by in ABDOMINAL MEDICINE | Comments Off on Pathology
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