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37 Pathogenesis ofChronic Otitis Media andtheContinuum: TheBasics, Further andBeyond
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transformed, due to tubal obstruction, into a closed and
non- ventilated system. In fact, this pressure regulation mechanism seems to be very common in children [6]. Persistent
tubal obstruction would trigger a negative intratympanic
pressure cycle that, at rst, would try to be compensated by
the medial displacement of the tympanic membrane and the
consequent decrease in middle ear volume (Fig.37.5).
Thus, with the contraction of the continent (middle ear
space), the intratympanic pressure could be slightly modied
up to certain limits. Physiologically, this limit depends on the
total volume of the middle ear cleft and the speed with which
the tubal obstruction is established. At this moment, the process would reach a critical limit from which a series of events
could endanger the anatomical and physiological integrity of
the ear:
A. An air bolus would penetrate from the nasopharynx (NF)
toward the middle ear potentially carrying on contami-
Fig. 37.5 Tympanic membrane retraction due to negative pressure in
the middle ear
nated secretions from the nasopharynx (NF) rich in
microorganisms. Once installed in the middle ear, these
microorganisms would nd a favorable environment for
multiplication with the consequent development of acute
otitis media (AOM). This same process can be repeated
several times as long as the initial triggering factor is not
corrected: acute recurrent otitis media with a normal
middle ear between attacks (Fig.37.6).
B. If negative pressure is sustained, the subepithelial space
would react in a more or less uniform fashion, with vasodilation of small vessels by vascular engorgement caused
by the vacuum increasing its thickness. Consequently,
there would be an increase in intravascular hydrostatic
pressure and passive plasma outow from the vessels to
the subepithelial space and from there to the lumen of the
ME conguring the so-called otitis media with effusion
(serous) (Fig.37.7).
Since, even in this phase, there is the possibility of the
eustachian tube opening, the aspiration of NF secretions
could, from time to time, exacerbate this condition—
recurrent episodes of AOM with serous otitis media in
between (Fig.37.8).
C. The persistence of uid in the middle ear associated with
subepithelial changes and prolonged hypoxia would
expose and damage the middle ear mucosa which in turn
would react like any chronically attacked epithelium,
that is, going through a process of metaplasia. The epithelium that is normally cuboidal or squamous would
change into a secretory epithelium: pseudo-stratied
columnar rich in goblet cells and submucosal glands.
The mucus actively secreted by these glands would eventually ll the middle ear replacing the serous plasmatic
uid: secretory otitis media, mucoid, or glue ear
(Figs.37.9 and 37.10).
As we have pointed out, from this stage onward the
ME undergoes through a series of biological changes,
that is, the epithelium provoked by environmental aggressions engages in an active process of metaplasia. The
serous uid characteristic of SOM (transudate with a low
Fig. 37.6 Acute otitis media and normal middle ear in-between
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Fig. 37.7 Serous uid
(transudate) lling the middle
ear space
S. S. da Costa and M. M. Paparella
Fig. 37.8 Acute recurrent otitis media with middle ear uid in-between bouts
Fig. 37.9 Middle ear
undergoing epithelial
metaplasia and lled with
mucoid uid. Secretory otitis
media.
37 Pathogenesis ofChronic Otitis Media andtheContinuum: TheBasics, Further andBeyond
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Fig. 37.10 Tympanic membrane retraction, with changes in color typical of secretory otitis media and a temporal bone section with the same
ndings
protein concentration) would be progressively replaced
by a mucoid, thick secretion with high levels of proteins
(exudate), the transition between one phase and the next
is clinically difcult to determine.
Appropriate clinical therapy at any of these stages
could permanently reverse them as long as the triggering
factors are properly identied and treated (medical treatments or surgery like ventilation tubes insertion).
Spontaneous resolution could also occur at this stage.
D. It is possible that in some situations where there is an
apparent complete resolution of the process, the inammation always associated with it can inict changes in
the delicate structures of the ME/mastoid complex
(thickening of mucosal folds, ligaments, and tendons)
creating closed compartments or true "hypo-ventilated
islands" even after the ET function was reestablished.
In fact, Proctor [14] demonstrated that, although the
middle ear is ventilated by the ET, the air passages within
the ME are narrow. A series of mucosal folds, part of the
ossicles and suspensory ligaments, known as the tympanic diaphragm (TD), practically separate the mesotympanum from the epitympanum and mastoid.
The components of this diaphragm are the head of the
malleus, the body of the incus, the lateral and medial
incudal folds, the anterior and lateral malleolar folds, and
the tensor tympani fold (Fig.37.11).
Only two narrow passages, the anterior and posterior
tympanic isthmus, perforate the diaphragm. The anterior
isthmus is larger and more consistent, lying medially to
the body of the incus, passing between the stapes and the
tensor tympani tendon. When a medial incudal fold is
present, a small posterior isthmus appears between this
fold and the posterior tympanic wall. When this fold does
not exist, the tympanic isthmus is a single passage. In
less than 10% of cases, the tensor tympani fold may fail
to develop, creating an additional passageway between
Fig. 37.11 Proctor´s tympanic diaphragm, its components, and main
routes of aeration
the mesotympanum and the anterior attic. The epitympanum communicates with the mastoid antrum through a
small triangular area known as the “aditus ad antrum”
[14].
The clinical importance of the TD is that its patency is
essential for ventilation of the epitympanum and whole
mastoid via aditus ad antrum [14].
The simple edema and thickening of the mucous folds
that constantly follow long-term or recurrent SOM,
MOM, or even AOM may block these tiny openings sealing the passages of air to the epitympanum and the mastoid with the consequent development of a new cycle of
localized negative pressure (Fig.37.12).
In such circumstances, the negative pressure can reach
extreme levels compromising the mucosa and especially
the ne endothelial structure of its rich capillary network
with consequent micro-bleedings randomly scattered in
the ME.As red blood cells break down, cholesterol in the
hemoglobin is released and the immune system reacts to
the cholesterol as a foreign body, producing an inammatory response and the consequent formation of cholesterol granulomas (Figs.37.13 and 37.14).
Another common response of the subepithelial
space is the development of granulation tissue (GT)
following a process of increasingly thickness due to
inammatory inltrates, vascular neoformations, and
inux of broblasts. The formation of GT in the middle ear space begins with a break in the basement
membrane of surface epithelial cells. Inammatory
cells in the underlying lamina propria traverse through
the broken basement membrane and enter the Iumen of
the middle ear space. This rupture may be caused by
bacterial toxins, inammatory mediators produced by
ruptured lysozymes, and the accumulation of subepithelial uid and vacuoles, all of which exert pressure
on the surface epithelium [15].
The second step in the formation of GT occurs when
a small piece of the lamina propria extrudes through the
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Fig. 37.12 Pathologically
created hypo-ventilated
micro-spots in the middle ear
S. S. da Costa and M. M. Paparella
Fig. 37.13 Hematoxylin-eosin-stained histopathology demonstrating
numerous cholesterol crystal clefts, surrounding multinucleate giant
cells, epithelioid histiocytes, and foamy macrophages, all of which are
consistent with a cholesterol granuloma
Fig. 37.14 Paparella´s "idiopathic hemotympanum”. Patient with a
history of long-lasting otitis media with effusion followed by cholesterol granuloma. The TM has a characteristic brownish color and
always with some degree of retraction
ruptured area of the epithelial cell surface. If the growth
of granulation tissue is vigorous and aggressive, polyps
can form (Figs.37.15 and 37.16). Both cholesterol granulomas and granulation tissue hold the strong potential to
Fig. 37.15 Human temporal bone section showing an intact TM (double arrows); the footplate (single arrow); and a mass of granulation tissues lling the oval window niche and the posterior recesses (GT)
Fig. 37.16 Right ear showing a polyp in a position corresponding to
the pars accida extending to the external auditory canal.
37 Pathogenesis ofChronic Otitis Media andtheContinuum: TheBasics, Further andBeyond
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cause bone and ossicular absorption, especially when
stimulated by inammation, local pressure, and specic
cytokeratins.
E. Cholesterol granuloma, granulation tissue, and ossicular
erosion are among the most prevalent irreversibly inammatory pathologic tissue encountered in the ME. The
presence of any of these ndings (in isolation or any
combination) focally or diffusely lling the middle ear
cleft in the presence of an intact tympanic membrane
congures a condition dened by as “silent chronic otitis
media” (SCOM). In these conditions, the intact TM may
display a spectrum of changes from grossly abnormal
aspect (retracted; atrophic of thickened) to, curiously a
near-normal appearance! So, the denition of chronic
silent otitis media is the presence of intractable inammatory-related disease focally or generalized in the ME/
mastoid complex associated with a non-perforated
TM.This innovative concept confronted the classic denitions of chronic otitis media that required the presence
of tympanic perforation (Fig.37.17). It is important to
highlight that the presence of the intact eardrum does not
exclude, in most cases, the detection of otitis media, particularly mainly if the diagnosis is supported by a careful
history and a good clinical examination. For this reason,
and to avoid the overuse of the term, SCOM has been
divided in two variants: undetected and undetectable.
This distinction is very important, because if the undetected SCOM may be due to a negligent investigation,
the undetectable SCOM is a clinical challenge to the
physician, who must be aware of the fact that a near-normal TM does not preclude the presence of active and
focal pathology in one or more of the ME multiple
compartments.
Regarding granulation tissue, it is well known its high
prevalence and generalized distribution throughout the
entire middle ear/mastoid complex. Only a handful of
Fig. 37.17 Section of a human temporal bone at mesotympanum level
showing the presence uid lling the anterior mesotympanum (yellow
star) concomitant with granulation tissue in the posterior recesses (red
star). Notice the presence of an intact TM (black arrows)
publications, however, mention the problem of some
patients who present with profuse and unremitting purulent otorrhea due to a large masses of granulation tissue.
Costa and Cruz [12] observed that the presence of small
masses of focal GT strategically distributed in the MEC,
especially in the region of the round and oval window
niches could be potentially responsible for audiovestibular symptoms presented by some patients.
In conclusion, GT can cause a series of signals and
symptoms like otorrhea, osteitis, ossicular necrosis, conductive and/or sensorineural hearing loss, and other
symptoms related to the posterior labyrinth. Granulation
tissue may also affect the homeostasis of the ME through
at least two mechanisms: (1) its own inammatory prole and (2) the possibility of blocking transitional areas
of the MEC (protympanum, isthmus and aditus), interrupting the natural airow inside the ME compartments,
compromising the ventilation and generating a vicious
cycle of additional pathological changes. Next to the
presence of effusion in ME, GT is the most prevalent
nding in SCOM. Expanding potential clinical
Implications of SCOM, there are two important concepts
to discuss: (1) hearing loss and bone pathology in COM;
(2) interaction between middle and inner ear.
The hearing loss associated with otitis media may
appear early or late during the process, varying considerably regarding the type and degree. As for the type, the
hearing loss may be conductive, sensorineural, or mixed.
As for the degree, depending on how aggressive and the
extension of the pathological process, they can vary from
mild, moderate losses (usually associated with the conductive type) even severe degrees with severe and profound losses (sensorineural).
As mentioned before, the mechanisms involved in
sensorineural hearing losses have been explained based
on the biological behavior of the round window, mainly,
and the oval one during the inammatory processes of
the MEC.This way, they could behave as true entrance
doors for toxins coming from the middle ear to arrive in
the inner ear conguring a legitimism interaction between
these two compartments. Several studies demonstrate an
association of the chronic otitis media to cochlear damage again pointing to the round window as the structure
responsible for the transmission of the pathological process to the labyrinth.
Costa et al carried out a study including 150 patients
with unilateral chronic otitis media and normal otoscopy
and normal hearing in the contralateral ear (CLE). The
main outcome measure was bone conduction threshold
averages calculated for frequencies of 500, 1000, 2000,
3000, and 4000 Hz, with comparison between the normal
ear and the ear with chronic otitis media. Thresholds
were examined separately for each frequency. The bone
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conduction threshold averages for the normal side were
lower than those for the ear with chronic otitis media.
The threshold shift was statistically signicant for each
frequency (P<0.0001, Student’s t test) clearly showing
that chronic otitis media may be associated with a
decrease in cochlear function.
On the other hand, it is well established that the conductive losses regarding COM includes a series of
changes in the tympanossicular system. Concerning the
tympanic membrane, the loss of substance (perforations), the atrophy (and the consequent retraction), and
the increase of its rigidity (because of tympanosclerosis
plaque) are some of the biggest causes of hearing loss.
The ossicles, however, may be affected by ossicular erosion (with the interruption of the chain as a consequence)
and ossicular xation due to tympanosclerosis, osteoneogenesis, and/or brosis.
Finally, the mass effects within the MEC by effusion,
cholesterol granuloma, cholesteatomas, and granulation
tissue can also compromise the vibratory ability of the
tympanossicular system. Furthermore, all these changes
may be found isolated or in several combinations in the
middle ear. For instance, gross erosions of the long process of the incus, as usual, follow the atrophy and retraction of the posterosuperior quadrant of the TM.Nowadays,
we believe the ossicular defects are a consequence of
active processes of bone reabsorption and not of ossicular necrosis. This theory presupposes the presence and
the participation of live cells in the mechanisms of
demineralization, erosion, and destruction of the bone. A
simply necrotizing bone can remain in situ for several
years without suffering reabsorption process.
All those dedicated to middle ear surgery agree that
during the step of the exploratory tympanotomy, a series
of different pathological ndings frequently are revealed
cohabiting the ME regardless of the TM status (retracted
or perforated). We will return to this relevant topic and
expand its clinical and surgical implications later in this
chapter.
F. The sum of all these components (effusion, hypoxia,
negative pressure, and mucosal metaplasia) completely
modies the environment of the middle ear and its relationships with neighboring structures, and the TM (being
the most fragile wall of the ME) is the rst to be damaged. Consequently, the pars tensa may undergo sectorial
or diffuse atrophy (Fig.37.18).
Functionally, these patchy atrophic areas could not be
clinically relevant; however, if the intratympanic process
aggravates or even in the event of a traumatic injury, the
atrophic and fragile regions then created could easily
rupture creating TM perforations of considerably larger
dimensions and more difcult to heal than those seen in
previously healthy ears.
S. S. da Costa and M. M. Paparella
Fig. 37.18 TM displaying different stages of atrophy and sectorial or
diffuse retractions
Fig. 37.19 Tympanic membrane atelectasis. The TM can be detached
from the promontory after efcient Toynbee or Valsalva maneuver.
Diffuse atrophy could also lead to total TM retraction,
with the membrane practically carpeting the structures of
the middle ear without, however, rmly attaching to them
(TM atelectasis) (Fig.37.19).
Another possible condition would arise when the
retraction is limited to the posterosuperior region. The
progression of this retraction may be followed by erosion
of the long process of the incus and xation of this TM
segment to the head of the stapes, regardless of the formation of cholesteatomas (myringostapediopexy).
Curiously, most patients with natural myringostapediopexy have clinically irrelevant conductive hearing loss as
it may work as a type III tympanoplasty (Fig.37.20).
G. Yet another situation may follow with retraction of large
portions of the pars tensa attaching the ossicles and ME
mucosa. In such conditions, the possibility of destabilization of ME homeostasis may cause capillary pressure
ab
cd
37 Pathogenesis ofChronic Otitis Media andtheContinuum: TheBasics, Further andBeyond
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ischemia, necrosis, and progressive atrophy of the TM
eventually leading to a loss of its integrity. The large perforations thus generated, as a rule, show clear signs that
they were preceded by TM retractions (Fig.37.21).
Fig. 37.20 Myringostapediopexy (notice the retraction of the posterosuperior portion of the TM with erosion of the long process of incus and
attachment of the TM to the head of the stapes.
In any of these situations, the resulting perforation
could be central or marginal. In the case of a marginal
perforation, there is a chance of the skin from the external auditory canal (EAM) to migrate across it gaining
access to the ME and generating a secondary cholesteatoma (Fig.37.2).
Regarding the accid pars, it is well known that its
composition renders it prone to retraction which may
evolve along stages: simple retraction, retraction pocket,
and primary cholesteatoma (Fig.37.22).
As pointed out before, the same process may develop
in posterior–superior quadrant of the TM where the
retractions are aggravated by overlapped bouts of infection with consequent irritation and hyperplasia of cells in
the basal layer generating streams of squamous cells
toward the middle ear.
This sequence of events may not necessarily follow a
unidirectional pathway. In fact, it can be modied by
several factors extrinsic and intrinsic to the ear, with a
deceleration of the inammatory reaction and formation
of tympanosclerosis and bone new bone (Fig.37.23).
Two last issues that still remain to be addressed are
the non-healed traumatic tympanic perforations and
those perforations related to acute necrotizing otitis
Fig. 37.21 Signs of retraction associated with tympanic perforation.
(a) Medialization of the malleus handle, including touch in the promontory (black arrow). (b) Tympanic remnants lying over the promontory,
black arrows are indicating the TM transition from the usual position
until the promontory. (c) Erosion of the ossicular chain and tympanic
remnants over it, with the black arrow pointing to the stapes without the
incus (and tympanostapedopexy), showing an area of the eardrum
medialized concerning its usual position until it touches the ossicular
chain. (d) Otoscopy in which the tympanic retraction and perforation
are almost indistinguishable: white arrow showing medialization of TM
up to the promontory, black arrow pointing MT over the ossicular chain
and signicant thinning of the incus long process, over the medialized
malleus.
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Fig. 37.22 Evolution from simple retraction to retraction pocket and cholesteatoma
clinical set. It is quite common in some patients, even after a
complete workup we cannot come to the conclusion of which
form of otitis media we are dealing with. This difculty is
due to the constant dynamic behavior veried in this pathological process.
The Continuum: Animal Studies
As we mentioned before, the rst experiment involving the
idea of the continuum was carried out by Paparella in 1970
employing the monkey as animal model. Later in 1977, the
group by the University of Minnesota presented to the
American Otological Society in Boston, the results of longitudinal and parallel animal and human studies that supported
this theory. These studies focused on the chemical and pathologic evaluation of three essential components of otitis
media: (1) ME effusion; (2) ME epithelium; and (3) ME subepithelial space.
Goycoolea etal. [16] and Junh et al. reported further
Fig. 37.23 Dry TM perforation with diffuse plaques of
tympanosclerosis
media. In these rare situations, TM perforation is usually
central and kidney-shaped and associated by few changes
in the ME.
Otitis Media: Further
The Continuum: AnOperational Model
forthePathogenesis ofChronic Otitis Media
As we have discussed above, when we try to mix clinical,
pathological, and temporal aspects to obtain a rational classication of otitis media, we do not come up with crystal
clear and denitive concepts. On the contrary, interconceptual superpositions are frequent feeding more discussion and controversy.
This difculty is not limited as an academic issue, but it is
also intrinsic to our daily work with deep implications on the
animal studies demonstrating the continuum of events
from serous or purulent effusion to mucoid effusion and,
nally, becoming chronic or deaccelerating and turning
into sequelae. Furthermore, they indicated that acute
inammatory changes are usually seen in patients with
purulent otitis media and serous otitis media, whereas
chronic inammatory changes are more severe in temporal
bones with mucoid and chronic otitis media. Finally, these
studies showed overlaps in histopathologic ndings among
the various types of otitis media that suggested a steady
progression from the acute purulent stages to mucoid and
eventually chronic otitis media. Chemical and cellular
activity in the effusion, the epithelium, and the middle ear
subepithelial space underlies all forms of otitis media, and
the extent of involvement in each of these compartments
dictated the form of otitis media present in the middle ear
cleft.
Recently, Bauer etal. [17] evaluated otoendoscopies of
Mongolian gerbils after cauterization of the eustachian tube
and found a steady increase in the sequence: effusion, retraction, and cholesteatoma in relation to controls.
S. S. da Costa and M. M. Paparella
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The Continuum: Human Histopathology
Studies
The 1990 human histopathology study was conducted by
Yoon etal. [3] revealing that epithelial and subepithelial layers of the mucoperiosteum of the middle ear are actively
involved in all stages of otitis media. A very important observation drawn from these and other classic histopathological
studies is that that they dene chronic otitis media regardless
of its association with drumhead perforations, otorrhea, or
even prolonged temporal evolutions. More simply, chronic
otitis media is dened as a condition associated with, focal or
generalized, irreversible tissue pathology within the middle
ear cleft.
In his textbook, Schucknecht [18]meticulously describes
the prole of chronic otitis media breaking it into two stages:
active (increased vascularization of the mucosa and submucosa, acute inammatory inltrate, ulcerations of the mucosa,
and granulation tissue) and scarred (brosis and neo-bone
formation). Though all these authors agree that the drumhead perforation (and the otorrhea—its most common clinical manifestation) are included in this group of irreversible
pathological ndings they are not “sine qua non” ndings for
the denition of this condition.
We agree that those episodes of COM associated with
drumhead perforations and otorrhea express themselves
more dramatically, but many well-designed histopathological studies, retrospectives in human temporal bones (HTBs),
and prospective in animals have demonstrated inammatory
irreversible tissue pathology in the middle ear cleft independently of rigid temporal parameters and, much more importantly, regardless of the presence of a tympanic membrane
perforation [2, 11, 12, 19, 20].
With these concepts in mind, we conducted a study in the
temporal bone lab of the University of Minnesota with 144
HTB with indisputable inammatory irreversible tissue
pathology (granulation tissue, ossicular changes, cholesteatoma, cholesterol granuloma, tympanosclerosis, and tympanic membrane perforation).
The middle ear cleft was topographically divided into ten
different sites, so we mapped it completely in terms of kind
and location of pathology. Temporal bones were further
divided into two groups: those with intact tympanic membranes (group I) and those with perforated tympanic membranes ( group II). Both groups had their ndings statistically
compared through the chi-square test.
Granulation tissue (97.9% of the temporal bones), ossicular changes (91.6%), tympanosclerosis (24.3%), tympanic
membrane perforation (19.4%), cholesterol granuloma
(13.8%), and cholesteatoma (10.4%) were the ndings most
frequently encountered within the HTB.
Surprisingly, the comparative analysis of temporal bones
with and without tympanic membrane perforation indicated
that both groups were similar. When one considers granulation tissue, ossicular changes and cholesterol granuloma
were found in both groups with a difference in frequency not
statistically signicant. Cholesteatoma and tympanosclerosis were identied more frequently in the temporal bones
with tympanic membrane perforations (group II) [2]. The
conclusion of our study clearly shows that chronic middle
ear inammation may be underestimated using conventional
denitions of COM.
In short, chronic otitis media has been dened under clinical and pathological criteria. Both denitions share some
common aspects, but they differ deeply regarding the presence of the TM perforation. We believe that our responsibility is to shift the clinical criteria (very restrictive in our
opinion) to the more encompassing and broader eld of the
pathological denition. Perhaps, aware of this possibility, we
will investigate, understand, and work more properly some
ear symptoms that appear, at the rst sight, obscure, and
unexplainable. In our opinion, to neglect these concepts is a
big medical mistake. It could be interpreted as we were much
more concerned about either plugging or poking holes upon
the tympanic membrane than actually disclosing and treating
middle and inner ear pathology.
The Continuum: Human Clinical Studies
In the above paragraphs, we reviewed a series of studies
where the Continuum has been consistently replicated in animal models. Strong evidences also pointing to the same
direction came from elegant researches employing HTB with
otitis media. For obvious reasons, the process cannot be
studied longitudinally in the clinical set, since it would be
ethically unacceptable to only contemplate the classic evolution of the disease from early stages of serous and mucoid
effusion to the development of irreversible inammatory
pathology.
Still the ear surgeon can witness many irrefutable evidences of this march of events whenever performing middle
ear and mastoid surgery for COM.It is not rare to nd during
middle ear exploration a myriad of different pathologies
dwelling the same ear: cholesteatoma in the attic and antrum;
cholesterol granuloma in the tip of the mastoid and the oval
and round window niches; granulation tissue over the posterosuperior quadrant and promontory; thick mucoid uid in
the protympanum and tympanic orice of the eustachian
tube and tympanosclerosis patches all over the TM not rarely
involving and xating the ossicular chain and the cochleariform process (Fig.37.24).
These ndings not only have conrmed that the otitis
media inammation/infection complex is very dynamic but
also led to the development of new surgical techniques, especially designed to treat this ongoing process. The prototype
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Fig. 37.24 Multiple pathological ndings in the middle ear cleft: uid;
granulation tissue (GT) in the round window niche; polyp (star); cholesteatoma (arrow)
of these techniques is the exible tympanomastoidectomy
approach which was described in detail by Costa etal [19].
The so-called exible approach consists in is a stepwise
technique designed to methodically and systematically
explore all the contents of the middle ear cleft and in the
process to disclose, conrm, and treat the disease encountered. We strongly believe that this exible approach can be
best dened as a true pathology-guided, pathogenesisoriented surgery for the middle ear.
Besides the unequivocal ndings during chronic ear surgery, we have pursued other practical alternatives to study
the continuum in a human model.
For such we decided to transversally investigate the middle ear status of a series of patients with cleft palate [21]. The
rationale behind the study was the well-known fact that these
patients have a chronic eustachian tube (ET) dysfunction
which is not completely corrected by palate reconstruction.
As a consequence, the occurrence of middle ear disease
among patients with cleft lip and palate or cleft palate only is
extremely high [22, 23]. In this population, almost as a rule,
there is an anomalous insertion of the elevator and tensor veli
palatine muscles into the posterior margins of the hard palate. Besides, there is also muscle hypoplasia, which may
cause ET dysfunction [24, 25]. As pointed out before, ET
tube malfunction, when persistent, may cause a negative
pressure in the tympanic cavity, with the resulting transudation of uid from the intravascular to the interstitial space,
and from there to the lumen of the middle ear [26]. This is
one of the initial landmarks of the pathogenesis of otitis
media [27]. From this point, the subepithelium (and later the
epithelium) reacts to the adverse situation, and there is the
S. S. da Costa and M. M. Paparella
setup of histological alterations that may become irreversible
inside the middle ear, and that will dene the next pathologic
process [3, 27].
The goal of our study was to describe the pattern of middle ear alterations in 180 patients with cleft of lip and palate
or isolated cleft palate followed at a university hospital in the
South of Brazil with no previous otologic interventions.
Effusions in the middle ear were present bilaterally in 65
patients (37.6%) and unilaterally in 15. Cholesteatoma
(CCOM) was seen in 11 patients (6.4%) and in two patients
it was bilateral. Chronic otitis media without cholesteatoma
(NCCOM) was observed in nine patients (two of them
bilaterally).
When considering the type of abnormality, patients were
divided into three main groups taking into account the main
nding: effusion, moderate/severe retractions, and chronic
otitis media, with or without cholesteatoma. Sixty-seven
patients (38.2%) presented middle ear effusions as the main
nding, 24 patients (13.3%) presented with moderate to
severe retraction as the main nding, and 18 (10%) presented
with chronic otitis media, with or without cholesteatoma.
There was a statistically signicant association between
age and the occurrence of cholesteatoma. The higher the age,
the higher the prevalence of the disease (chi-square linear
trend, P=0.008). The distribution of NCCOM among different age ranges has also shown a linear association. The
higher the age, the higher the prevalence of this condition
(P=0.003). Increasing age has also correlated with the presence of retraction pockets on the tympanic membrane
(P<0.0001).
The presence of middle ear effusions exhibited a linear
association with age. Older patients tended to a lower prevalence of effusions (P<0.0001). Figure37.25 shows the linear trends in the distribution of the pathologies found:
effusions, moderate/severe retractions, CCOM, and
NCCOM.
In conclusion, the middle ear ndings of a group of
patients with theoretically known ET dysfunction supported
the concept of the continuum: across younger age ranges,
there is the predominance of middle ear effusions, whereas
in the older patients the prevalence of retractions and chronic
otitis media are predominant. Underlined the obvious limitations of our study, we rmly believe that the progression of
the severity of the ME ndings in the cleft palate population
through the years is in close analogy with the ndings derived
from many well-designed longitudinal animal studies.
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