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The Periosteum
With the exception of the tympanic membrane, Eustachian
tube, and round-window membrane, the middle ear and mastoid are surrounded by a bone with its periosteum facing the
connective tissue layer (Figs.5.3, 5.5, and 5.8).
The Tympanic Membrane
The tympanic membrane is a thin, elliptically shaped membrane situated between the medial end of the external meatus
and the middle ear cavity. Structurally, the membrane consists of three layers that are approximately 0.1 mm thick
(combined): These layers include:
1. An outer cutaneous layer of thin skin, which is continuous with the skin of the external canal
2. A middle layer of connective tissue consisting of the
following:
(a) A radiate brous layer, made up of bers radiating
peripherally from the umbo and manubrium of the
malleus
(b) A circular brous layer, made up of concentrically
arranged bers that are most prominent peripherally,
where they thicken to form a brocartilage ring or
annulus, attaching the membrane to the tympanic sulcus of the temporal bone
3. An inner layer of the mucous membrane continuous with
that of the middle ear cavity
M. V. Goycoolea et al.
Fig. 5.9 Middle ear opening of the Eustachian tube. (© Marcos
Y.Goycoolea 2023; all rights reserved)
The Eustachian Tube
The Eustachian tube extends from the anterior wall of the
tympanic cavity to its nasopharyngeal opening just posterior
to the dorsal end of the inferior nasal concha. Structurally,
the auditory tube consists of both cartilaginous and bony
components. The bony portion makes up approximately twothirds of the tube; it is widest at the tympanic orice and
gradually narrows throughout its length, with its anterior
extremity (the isthmus) being the most constricted portion of
the entire tube. The cartilaginous portion of the tube extends
from the isthmus to the nasopharynx. It is not totally cartilaginous. Its lower lateral and inferior walls consist of a
brous connective tissue overlying the tensor veli and levator
veli palatini muscles.
The lumen of the auditory tube, in the resting state, is a
closed, slit-like cavity. The pharyngeal end of the tube
strongly resists passage of air from the pharynx to the middle
ear. Passage from the tympanic cavity to the pharynx is much
easier.
The Eustachian tube is lined by a respiratory epithelium,
and, in addition to the opening function of the tensor veli
palatini muscle, there is seemingly some role of a surfactant.
The respiratory epithelium with its cilia and mucus secretion
are the basis of the mucociliary transport system of the middle ear (Figs.5.6, 5.7, and 5.9).
The Round-Window Membrane
The round-window membrane is located in the medial wall of
the middle ear, within the round-window niche. It consists of
three layers: an outer epithelium facing the middle ear, a core
of connective tissue, and an inner ear epithelium bordering
the inner ear. The outer epithelium consists of a single layer
of cells that are continuous with that of the promontory. The
5 Normal Histology oftheEustachian Tube, Middle Ear, andMastoid Complex: TheMucoperiosteum Concept
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55
cells are low cuboidal. Tight junctions are present near the
surface, and there is a continuous underlying basement membrane. The connective tissue layer contains broblasts, collagen, and elastic bers as well as blood and lymph vessels and
nerve bers. The inner epithelium is lined by squamous cells
with long lateral extensions that overlap each other.
Histological descriptions of the round-window membrane are
provided in this chapter of this book that discusses the use of
topical treatment and middle inner ear interaction (Chap. 31).
The Otitis Media Process
Once aggression occurs, the ear responds with histopathological defensive factors that are gradual, systematic and universal, and have variations, which are adaptations to the
different forms of insults. Their forms of presentation and
severity will depend on the balance between the aggression
and defense, with a direct inuence of the environment, the
genetic predisposition of the host, and the general defensive
conditions at the time of occurrence.
The result of the response of the ear to aggression is the
universal reaction of inammation. This is the starting point
of the sequential steps to be described. This inammatory
process involves all the walls, cavities, and anatomical structures that these contain as well as the mucoperiosteum that
lines these cavities and structures (Fig.5.10). With the under-
standing that the reaction is simultaneous at all levels, for
practical reasons, the epithelial changes will be initially
described.
Epithelial Changes
The epithelial cells participate in the inammatory reaction
by themselves and also as part of the mucociliary system.
The cells become taller and have increased secretion
(Figs.5.11 and 5.12). There is also new gland formation and
an increase in goblet cells.
Cells secrete different defensive substances such as lysozymes. The epithelial cells also have the capacity to synthesize the secretory piece of immunoglobulin (Ig)A (secretory
IgA) just like the intestine since both epithelia are of the
endodermal origin (Fig.5.13).
Fig. 5.11 An electron micrograph of the respiratory epithelium in
acute otitis media. Secretory granules and migration of polymorphonuclear cells toward the middle ear cavity. (© Marcos Y. Goycoolea
2023; all rights reserved)
Fig. 5.10 Middle ear cavity with middle ear effusion. The inammatory process involves all the walls, cavities, and anatomical structures
that these contain as well as the mucoperiosteum that lines these cavities and structures. (© Marcos Y.Goycoolea 2023; all rights reserved)
Fig. 5.12 An epithelial cell full of secretory granules and secreting
toward the middle ear cavity. (© Marcos Y.Goycoolea 2023; all rights
reserved)
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M. V. Goycoolea et al.
Fig. 5.13 Plasma and epithelial cells staining positive for IgA. (©
Marcos Y.Goycoolea 2023; all rights reserved)
All these secretions plus the cellular elements in the middle ear cavity develop middle ear effusion. In some areas and
depending on the degree of aggression, epithelial ruptures
occur. Cholesteatomas seem likely to develop because of
migration of the squamous epithelium of the tympanic membrane (and/or ear canal) rather than as a result of metaplastic
changes of the inamed epithelium (Goycoolea etal. 1999).
The Connective Tissue andPeriosteal
Changes
These are characterized as (Fig.5.10) follows:
1. Thickening, edema, and increased vascularity
2. Cellular changes: Gradual cellular inltration, changes in
the types and numbers of cells
3. Changes in the shape and numbers of bers
4. Inammatory reaction of the periosteum
5. Inammatory reaction of the underlying bone (osteitis)
In the early stages of the inammatory process, the initial
inltration is based on polymorphonuclears that respond rapidly and traverse the capillaries toward the connective tissue
(Fig.5.14). From there, some migrate through the epithelium
to the middle ear cavity (Fig.5.11). Their primary function is
engulfment of particles and microorganisms. The majority are
neutrophils, but there are occasional eosinophils. The second
cells to appear active are macrophages (Fig.5.15) and abundant
and active broblasts. Macrophages, despite being nonspecic,
mark the starting point toward a specic immunological reaction mediated by T and B lymphocytes. Macrophages play a
Fig. 5.14 Polymorphonuclears in the connective tissue of the promontory. (© Marcos Y.Goycoolea 2023; all rights reserved)
Fig. 5.15 Macrophages and active broblasts in the connective tissue
of the promontory. (© Marcos Y.Goycoolea 2023; all rights reserved)
role in processing antigens and interacting with B lymphocytes
(humoral immunity), which are the cells with a capacity for
specic recognition. B cells develop toward antibody-secreting
cells (plasma cells) (Figs.5.13 and 5.16).
The middle ear mucosa also has a local immunological
system via secretory IgA in which IgA is secreted by the
plasma cells (B cells) and the epithelial cells add the secretory piece. Both IgG and IgM are also synthesized by the
plasma cells and are secreted toward the mucosal surface.
Fibroblasts are also active since the early stages.
The middle ear defense system consists of:
1. An epithelium that is continuous, regenerative, and con-
stitutes a mechanical barrier
2. A mucociliary transport system (mucus, lysozymes, cili-
ated and secretory cells)
5 Normal Histology oftheEustachian Tube, Middle Ear, andMastoid Complex: TheMucoperiosteum Concept
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Eusion Formation
Effusion formation is dynamic and reects what is going on
in the mucoperiosteum in terms of the phase and type of an
inammatory process. Samples will eventually be helpful for
deciding treatments accordingly.
Changes intheMucosa asaWhole
The middle ear develops polypoidal changes with areas that
are prominent and areas that are depressed. Gland and blood
vessel formation occur.
Fig. 5.16 Plasma cells in the connective tissue. (© Marcos
Y.Goycoolea 2023; all rights reserved)
3. A patent and functional Eustachian tube
4. An inammatory reaction of the connective tissue
5. Edema
6. Fibroblasts, collagen, and amorphous substance
7. Polymorphonuclear cells
8. Lymphocytes (small and large T and B cells,
respectively).
9. Plasma cells: immunoglobulins (IgA, IgG, IgE, IgM)
10. A complement system.
All structures are involved in the inammatory process.
The inammatory process is dynamic and so is the middle
ear effusion that tends to follow the histopathological
changes that occur in the middle ear mucosa. The different
forms of presentation of the otitis media process are therefore moments or instants of this dynamic process.
If otitis media is understood in this manner, it is much
more than classications and/or middle ear uid and an
inammatory process. The changes described are in reality a
reection of the stage of confrontation between the aggression and the defensive factors. Thus, one form may lead to
others in a dynamic way (Tables 5.1 and 5.2).
57
Table 5.1 Forms of otitis media
The form of presentation described in this table and the severity of the otitis media process will depend on
the balance between two opposing forces, namely, the aggressive factors and the defensive factors of the
middle ear. These are directly inuenced by environmental factors, genetic predisposition, and the status
of the defensive system of the host at the moment of aggression
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M. V. Goycoolea et al.
Table 5.2 Classication and continuum of otitis media with effusion
(OME)
POM, purulent otitis media; SOM, serous otitis media; MOM, mucoid
otitis media; COM, chronic otitis media; OM, otitis media
Complications andSequelae
In addition to the involvement of the mucoperiosteum of the
middle ear and mastoid as well as the Eustachian tube, there
are potential complications and sequelae in this disease process. A complication is a secondary disease or condition
developing in the course of a primary disease without being
part of it. It occurs when the inammatory process extends
beyond the mucoperiosteum. A sequela is an after effect of a
disease or injury. Herein, the term “sequela” refers to processes that remain within the mucoperiosteum (mucoperiosteal changes) and that have the capacity or potential to
develop a complication (Goycoolea and Jung 1991) [1, 2].
The line between complications and sequelae is at times
extremely tenuous. For example, the granulation tissue is a
sequela (active sequela), but erosion of bone by the granulation tissue is a complication. In addition, the overall consequences of a localized problem (e.g., ossicular disruption
causing conductive hearing loss) can have signicant effects
on a person and on their relationships with others (lack of
communication, isolation, learning problems, and so forth).
At the level of the epithelium, ruptures occur in some
areas of the mucosa (the degree of which will depend on the
magnitude and type of aggression).
These ruptures allow:
Pockets with serous content
The inamed connective tissue without epithelial covering
(granulation tissue) can migrate through these openings.
This tissue can persist or disappear. When it persists, it can
erode the neighboring bone (with or without an associated
cholesteatoma) and cause complications. It can disappear
or be covered with an epithelium and cause adherences,
which at times can serve as bridges for cellular migration
as is the case of cholesteatomas (Goycoolea etal. 1999).
References
1. Goycoolea M.Middle ear and mastoid. Chapter 1.4. In: Goycoolea
M, etal., editors. Atlas of otologic surgery and magic otology. New
Delhi: Jaypee Brothers Medical Publishers Ltd.; 2012. p.21–57.
2. Goycoolea M.Surgical procedures in different forms of otitis media.
Summary of concepts. Chapter 5.2.1. In: Goycoolea M, etal., editors. . New Delhi: Jaypee Brothers Medical Publishers Ltd; 2012.
p.463–89.
Further Reading
Friedmann I.The pathology of acute and chronic infections in the mid-
dle ear cleft. Ann Otol Rhinol Laryngol. 1971;80:390–6.
Goycoolea MV. Pathogenesis of otitis media. Dissertations Abstr Int.
1978;39(6):132–210.
Goycoolea MV, Jung TK.Complications of suppurative otitis media. In:
Paparella MM, Shumrick DA, Gluckman JL, Meyerhoff WL, editors.
Otolaryngology, vol. II.Philadelphia: Saunders; 1991. p.1381–403.
Goycoolea MV, Paparella MM, Carpenter AM, Juhn SK.A longitudinal
study of cellular changes in experimental otitis media. Otolaryngol
Head Neck Surg. 1979;87:685–700.
Goycoolea MV, Paparella MM, Juhn SK, Carpenter AM. The cells
involved in the middle ear defense system. Ann Otol. 1980;68(Suppl
89):121–8.
Goycoolea MV, Hueb MM, Muchow D, Paparella MM.The theory of
the trigger, the bridge and the transmigration in the pathogenesis
of acquired cholesteatoma. Acta Otolaryngol. 1999;119(2):244–8.
Hentzer E.Ultrastructure of the middle ear mucosa. Ann Otol Rhinol
Laryngol. 1976;85(Suppl 25):30–5.
Lim DJ.Functional morphology of the mucosa of the middle ear and
Eustachian tube. Ann Otol. 1976;85(Suppl 25):36–43.
Lim DJ, Klamer A. Cellular reactions in acute otitis media.
Scanning and transmission electron microscopy. Laryngoscope.
1971;81:1772–86.
Lim DJ, Shimada T.Secretory activity of normal middle ear epithelium.
Ann Otol. 1971;80:319–29.
Mogi G.Secretory IgA and antibody activities in middle ear effusions.
Ann Otol. 1976;85(Suppl 25):36–43.
Paparella MM, Sipila P, Jun SK, Jung TTK.Subepithelial space in otitis
media. Laryngoscope. 1985;95:414–20.
Paparella MM, Goycoolea MV, Jung TK.Otitis media with effusion. In:
Paparella MM, Shumrick DA, Gluckman JL, Meyerhoff WL, editors.
Otolaryngology, vol. II.Philadelphia: Saunders; 1991. p.1317–42.
Sadé J. Ciliary activity and middle ear clearance. Arch Otol.
1967;86:128–35.
Sadé J, Alufa I.Middle ear mucosa. Arch Otol. 1966;84:137–43.
Tos M.Production of mucus in the middle ear and Eustachian tube. Ann
Otol. 1974;83:44–58.
Tos M, Bak-Pedersen K.Goblet cell density in Eustachian tube of chil-
dren. Arch Otol. 1976;102:20–6.
1
This chapter is a summary of many of our previous reports that are
concentrated in two chapters of our Atlas of Surgical Otology.
2
All the gures are my own and represent some of my best in more than
40years of histological studies of temporal bones.
The
references include some of the classic reports of the otitis media
leaders, who, together with Michael Paparella and Steve Juhn, inspired
my work. I had the privilege of knowing those whose reports are quoted
and of learning from all of them—initially as a resident—and then in
many symposia of otitis media through the years.
My coauthors are young staff members who have contributed—as I did
initially—and, hopefully, they will also become inspired and improve
by far these studies to which all of us have contributed.
1
2
Understanding theAeration Avenues
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oftheMiddle Ear withtheAid
oftheEndoscope
AlessiaRubini, MargheritaBasso, NicolaBisi ,
PierfrancescoBettini, andDanieleMarchioni
6
Introduction
The study of the ventilation pathways of the middle ear, in
particular of the epitympanic diaphragm, has long been one
of the main interests of otologists, as, in the early 40s, it was
rst understood how its structure can affect the pathology of
the middle ear. The inter-attico-tympanic diaphragm, later
renamed the epitympanic diaphragm, was rst identied in a
histological study in newborns by Chatellier and Lemoine
[1]. They described a set of membranous structures that,
along with the incus and the malleus, shaped the oor of the
epitympanum. Their study was based on the previous histological description of the development of middle ear spaces
in fetuses at different stages of development by Hammar [2]
and on anatomical treatises, like the one by Prussak [3].
Palva etal. further dened this structure through studies of
microdissection of both healthy and diseased specimens,
focusing on the ventilation pathways and their implication in
the pathological processes of the middle ear. The epitympanic diaphragm divides the middle ear into two compartments: the epitympanum and the medial tympanum. It was
Palva et al. who underlined the association between the
blockage of the aeration pathways and the lesions of the
upper compartment, due to dysventilation [4, 5].
During the last 10 years, the endoscope has gained
increasing importance, rst as a support to traditional microscopic surgery [6, 7] and then as a tool of its own, to carry out
surgical procedures [8, 9].
The endoscopic approach to the middle ear has provided
a unique way of evaluating its anatomy and disease, as it has
made spaces, which cannot be reached with the use of traditional microscopes, easily accessible; in fact, 30°, 40°, and
A. Rubini · M. Basso · N. Bisi (*) · D. Marchioni
Department of Otolaryngology-Head and Neck Surgery, University
Hospital of Modena, Modena, Italy
P. Bettini
ENT & Audiology Department, University Hospital of Ferrara,
Ferrara, Italy
75° endoscopes enable the surgeon to reach blind spaces in
the middle ear, without disrupting any anatomical structures.
While traditional approaches with a microscopic postauricular tympanomastoidectomy provide a limited access to the
attic, especially to its anterior portion, the endoscope allows
the surgeon to assess the integrity of the whole epitympanic
diaphragm [10].
Since 2009, Marchioni etal. have published several studies on the endoscopic anatomy of the middle ear and have
developed a nomenclature of the structures they identied.
This classication has made it possible to standardize surgical approaches to lesions that require careful exploration of
all the compartments of the middle ear, such as acquired or
congenital cholesteatoma [11].
Ventilation Pathways
Anatomy oftheEpitympanic Diaphragm
(Fig.6.1)
The epitympanic diaphragm, along with the malleus and the
incus, forms the oor of the epitympanum, and it consists of
the following folds (Fig.6.2):
• Anterior, posterior, and lateral malleal ligament folds
• Posterior incudal ligament fold
• Tensor fold
• Lateral incudomalleal fold [12]
The anterior malleal ligament fold denes the anterior
limit of Prussak space, as it extends from the anterior portion
of the malleus neck to the anterior attic bony wall.
The posterior malleal ligament fold inserts into the posterior portion of the malleus neck and extends into the posterior tympanic spine. von Tröltsch’s pouch is medially
bounded by the posterior malleal ligament fold.
The lateral malleal ligament extends from the lateral wall
of the malleus head to the medial wall of the scutum. It pos-
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
M. V. Goycoolea et al. (eds.), Textbook of Otitis Media, https://doi.org/10.1007/978-3-031-40949-3_6
59
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Fig. 6.1 The right ear. A
drawing showing the
epitympanic diaphragm seen
in a caudal-to-cranial
orientation and from a lateral
to a medial one. The tensor
fold is incomplete, showing a
possible further ventilation
pathway of the anterior
epitympanum. SLIM, superior
malleal ligament; IN, incus;
MA, malleus; IMLF, lateral
incudomalleal fold; MLF,
lateral malleal fold; PLFM,
posterior ligament of the
malleus; ALFM, anterior
malleal ligamental fold; TF,
tensor fold; LCS, lateral
semicircular canal; FN, facial
nerve; PE, pyramidal
eminence; S, stapes; RW,
round window; CP,
cochleariform process; ET,
Eustachian tube
A. Rubini et al.
teriorly turns downward and merges with the anterior portion
of the posterior incudal fold, whereas it anteriorly converges
with the posterior portion of the anterior malleal fold.
The incudomalleal lateral fold is superior to the lateral
malleal ligament fold, and it separates into two more
compartments: the upper and lower lateral attic spaces. This
fold has its insertion in the body of the incus and in the incudomalleal joint; it runs horizontally and extends to the medial
wall of the scutum. Anteriorly, this structure bends and
merges with the posterior margin of the lateral malleal ligament. During an endoscopic approach to the middle ear, the
lateral incudomalleal fold must be disinserted from the body
of the incus, to fully expose the upper lateral attic.
The anatomy of the tensor fold was dened owing to the
introduction of the endoscope; in fact, its orientation and
location make it undetectable through traditional retroarticular approaches. The tensor fold separates the supratubal
recess in the protympanum from the anterior epitympanum,
which is the space between the head of the malleus and the
anterior bony wall of the scutum [12]. The tensor fold can
appear as either complete or incomplete and can have three
different orientations: vertical, horizontal, or oblique [13].
The relationship between the tensor fold and the cog
(transverse crest) is important. The latter is a bony septum
that cranially detaches from the tegmen tympani and vertically descends just anterior to the cochleariform process; it
usually denes two compartments of the epitympanum: the
anterior epitympanic space and the posterior epitympanic
space. When the tensor fold has a vertical orientation, it is
inserted into the cog, thus leading to a large supratubal
recess. In this case, the cog does not separate the anterior
from the posterior epitympanic space, rather, it represents
the bony boundary between the supratubal recess and the
epitympanic space. In the majority of cases, the tensor fold
has an oblique orientation and attaches to the anterior tegmen tympani; therefore, the cog represents the division
between the anterior and the posterior epitympanic spaces.
When the tensor fold has a horizontal orientation and
attaches to the tensor tympani semicanal, the supratubal
recess is small or nonexistent. Thus, the anterior epitympanic space is large, and it is divided from the posterior epitympanic space by the transverse crest. As it is, the more
vertical the tensor fold is, the wider the supratubal recess
becomes.
Ventilation oftheUpper Unit
It is known that three main factors inuence the ventilation
of the middle ear: the Eustachian tube function, the buffer
mechanism provided by the mastoid, and the mucosal gas
exchange.
The Eustachian tube plays a role in providing equalization of the pressure between the middle ear and the outside
air. When the Eustachian tube fails, the pressure in the tympanic cavity becomes negative, causing a retraction of the
tympanic membrane. The pressure in the middle ear is also
related to the transmucosal gas exchange through the mas-
6 Understanding theAeration Avenues oftheMiddle Ear withtheAid oftheEndoscope
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Fig. 6.2 The right ear. An
epitympanic diaphragm from
a superior view. The malleus
is severed at different heights
to show the attachment levels
of the epitympanic
diaphragm. The incus is
sectioned at the level of its
upper body. IMLF, lateral
incudomalleal fold; MLF,
lateral malleal fold; ALFM,
anterior malleal ligamental
fold; TF, tensor fold; MA,
malleus; IN, incus; IS,
tympanic isthmus; S, stapes;
PE, pyramidal eminence; CP,
cochleariform process
61
toid mucosa. These two systems achieve a balance if the ventilation pathways in the middle ear are open [14].
Two separate areas can be identied for what concerns the
ventilation: an upper unit and a lower unit. The upper unit is
made up of the superior lateral attic, along with the medial
attic, and is connected to the mastoid. In case of a complete
tensor fold, the upper unit is only aerated through two narrow spaces called the anterior and posterior isthmus, as the
epitympanic diaphragm separates the epitympanum from the
mesotympanum. The inferior lateral attic, which is divided
from the superior one by the lateral incudomalleal fold, by
contrast, is the only compartment of the epitympanum,
which is aerated by the mesotympanic region [12].
The tympanic isthmus (Fig. 6.3) was rst described by
Chatellier and Lemoine; it was then outlined by Aimi as a
narrow passage between the upper tubotympanic cavity and
the atticomastoid space [15].
It is laterally bounded by the short process of the incus
and the malleus head, anteriorly by the tensor tympani tendon and posteriorly by the posterior incudal ligament. The
isthmus is divided into an anterior isthmus, which is the
space dened by the incudostapedial joint and the tensor
tympani tendon, and a variable posterior isthmus, which is
just behind the incudostapedial joint.
The tensor fold plays a key role in the ventilation of the
upper unit (Fig.6.4), as it provides a separation between the
anterior epitympanum and the protympanum. When the tensor fold is complete, the only ventilation pathway is through
the tympanic isthmus, whereas in case of an incomplete tensor fold, additional ventilation is created between the protympanum and the anterior epitympanum.
Ventilation oftheLower Unit
The lower unit is represented by Prussak space; it is located
below the epitympanic diaphragm, since its roof corresponds
to the lateral malleal ligament fold. Prussak space is inferiorly dened by the short process of the malleus and medially
by the malleus neck. The area is anteriorly bounded by the
membranous anterior malleal ligamental fold, and its lateral
wall is represented by Shrapnell’s membrane, whereas the
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Fig. 6.3 The right ear. An
epitympanic diaphragm seen
from above. The arrows
indicate the main ventilation
of the epitympanum through
the tympanic isthmus (one
arrow is for the anterior
epitympanum and the others
are for the posterior
epitympanum and mastoid).
ALFM, anterior malleal
ligamental fold; MLF, lateral
malleal fold; IMLF, lateral
incudomalleal fold; TF, tensor
fold; MA, malleus; SLIM,
superior malleal ligament; IN,
incus; IST, tympanic isthmus;
S, stapes; PLIN, lateral and
medial posterior incudal
ligaments
A. Rubini et al.
Fig. 6.4 The right ear. View of a complete tensor fold from a medial to
a lateral direction and the main ventilation pathway of the epitympanum, through the tympanic isthmus. The epitympanic diaphragm is also
seen in transparency as lateral to the incus and the malleus (dashed
line). The black arrows show the ventilation of the anterior and posterior epitympanum. AES, anterior epitympanic space; ET, Eustachian
posterior wall corresponds to the posterior pouch of von
Tröltsch.
The ventilation of Prussak space occurs through commu-
nication with the mesotympanum, represented by von
tube; TF, tensor fold; ALFM, anterior malleal ligamental fold; MLF,
lateral malleal fold; MA, malleus; SLIM, superior malleal ligament; IN,
incus; IMLF, lateral incudomalleal fold; IST, tympanic isthmus; ED,
eardrum; PES, posterior epitympanic space; PLIN, lateral and medial
posterior incudal ligaments; MCS, mastoid cell; CP, cochleariform
process
Tröltsch’s pouch, which is posteroinferiorly open, at the
level of the most cranial portion of the mesotympanum, and
it is laterally bordered by the pars tensa and the pars accida
of the eardrum and medially by the posterior malleal ligament
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Fig. 6.5 The right ear. Lower
and upper unit ventilation and
epitympanic diaphragm. The
tympanic membrane has been
partially removed both in the
pars accida (showing
Prussak space) and in the pars
tensa. The red arrows indicate
the main ventilation pathway
for the upper unit through the
isthmus and for the lower unit
(Prussak space) through von
Tröltsch’s pouch. IN, incus;
MA, malleus; IMLF, lateral
incudomalleal fold; MLF,
lateral malleal fold; ALFM,
anterior malleal ligamental
fold; PRS, Prussak space;
PLFM, posterior ligament of
the malleus; MA, malleus;
ED, eardrum; ET, Eustachian
tube
63
(Fig.6.5). The ventilation path of Prussak space is narrow
and can easily tighten until it completely closes [16].
Even if the lower unit is an important component of the
epitympanum, its aeration pathway can be blocked without
affecting the function of the compartments, which lie superior to the epitympanic diaphragm or the one of other middle
ear structures and the mastoid air system.
The Role oftheMastoid andTransmucosal
Gas Exchange
The aerated mastoid is one of the three main factors inuencing the ventilation of the middle ear.
Sadé and Ar [17] observed that the mastoid plays the role
of an air reservoir to buffer rapid pressure changes within the
middle ear (Fig.6.6). Since volume and pressure are inversely
proportional, a small, poorly aerated mastoid does not grant
an optimal buffer function, allowing for wider pressure variations in the tympanic cavity (Fig. 6.7). Consequently, a
largely aerated mastoid requires great changes in volume to
achieve the same pressure as a small mastoid [12].
Another buffer mechanism is performed by the tympanic
membrane since, and, if it is mobile enough, it has the possibility of bending inward and outward according to the pressure changes of the middle ear. Conversely, if the tympanic
membrane is rigid and cannot bend properly, then the dilution of the pressure changes entirely depends on the aerated
areas of the mastoid.
Since a small mastoid is most vulnerable to pressure
changes, compensatory buffering mechanisms may develop,
such as additional tympanic membrane retraction or middle
ear volume reduction through uid accumulation. A correlation exists between a poorly pneumatized mastoid and pars
accida retraction, with a wider risk of atelectasis and subsequent cholesteatoma formation [18]. In the same way, it has
been observed that children with recurrent otitis media, also
complicated with cholesteatoma formation, usually have
more sclerotic (less pneumatized) mastoids than do healthy
children [19]. These examples provide further evidence of
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