THE ROLE OF THE MASTOID IN MIDDLE EAR PRESSURE REGULATION
Introduction
The mastoid consists of a series of aerated cells lying mainly behind the middle ear (ME) cavity and the ear canal. These air cells are formed after birth by successive expansion from the antrum; the air cell system is fully developed by the age of 14 to 16 years.1 Since the air cells are all interconnected as well as connected to the ME cavity by the antrum, these structures are all connected both in terms of structure and function referred to as the ME cleft.2 The pressure of the ME cavity is identical to the mastoid, and thus, the mastoid is likely to participate in the overall regulation of ME pressure.2
The role of the mastoid in middle ear physiology is relatively unknown, which may partly be explained by its inaccessibility. However, during recent years more studies have reported more detailed descriptions of its structure, whereas functional studies are still few.
Mastoid structure
Studies on the mastoid structure based on 3D reconstruction of clinical CT scans have given valid estimates of its properties. A majority of these studies are limited by only determining the mastoid volume, while relatively few have undertaken the more complicated task of determining its surface area. Whereas the mastoid volume may be relevant for some of its functions, its surface area is important for the capacity of gas exchange across its mucosa.2,3 While the ME cavity exhibits a surface area and a volume of 7.7 cm2 and 0.7 cm3, respectively, the mastoid has corresponding values of 85 cm2 and 6 cm3 in normal ears.4 Thus, the mastoid surface area is much larger, and its area-volume-ratio is also larger than for the ME cavity (17 vs. 12 cm-1).4 However, the resolution of CT scans applied in a clinical context is limited to around 0.6 mm, so that smaller air cells may not be detected.
Micro-CT scanning has been applied for description of the human ME structures such as the ossicles,5 but no data have been reported yet for mastoid surface area and volume. Most recently, however, micro-CT scans of temporal bones have revealed a distinct set of numerous micro-channels connecting the exterior surface of the mastoid directly with its underlying air cells (Fig. 1).6 The dimension of these channels shows an average diameter of 150 μm, which coincides with a content of a venole and an arteriole. Based on the development of the mastoid from birth, its vascular supply would reasonably expand together with the air cells from the antrum;1 thus, this set of micro-channels seems to suggest an additional and separate vascular supply for the mastoid, but its role remains unknown.
The histological structure of the mastoid is different from the ME cavity itself, so that the surface epithelium is lower with flat or cuboidal cells, and the underlying connective tissue is more loose with an ample superficial vascular network.7 This results in a short diffusion distance as well as enabling a high perfusion; these properties, including its larger surface area, seem to indicate that the mastoid is adapted to gas exchange.3,4,7
Fig. 1. Micro CT-scanning of a human temporal bone (tangential view of lateral surface; the mastoid tip is seen at the bottom). Volume rendering enhances the transitional voxels, i.e., the surfaces between air and bone. Multiple micro-channels are seen connecting the surface of the bone directly with the underlying air cells; these micro-channels transverse the superficial compact bone (black area between surface and air cells).
Mastoid function – passive aspects
The larger part of the literature considers the functions of the mastoid to be merely passively related to its air volume. It has been suggested to act as a buffer for pressure changes or a gas reservoir for pressure regula-tion.8,9 In addition, its cellular structure may result in damping of acoustic pressures and act as an acoustic filter decreasing noise and increasing hearing sensitivity.10
The pressure regulation of the ME cleft has traditionally focused on the function of the Eustachian tube and gas exchange between its air and the mucosal blood of the ME cleft.11 In this context, its gas exchange has been considered passive, only driven by the differences in partial pressures of the gases.
Mastoid function – active aspects
Basically, the gas exchange depends on both the diffusion properties of the gases and the barrier as well as the perfusion of the mucosa.11 Whereas the diffusion itself is a passive process, there is also evidence that gas exchange may be dependent on the mucosal perfusion.12 Thus, changes in perfusion may be altered by vasomotor actions, which may alter the exchange of gases; this may ultimately alter the ME pressure. Altogether, this implies that mucosal perfusion may contribute in an active regulation of the pressure.
Recent clinical experiments on direct measurements on ME pressure have revealed two distinct patterns of systematic counter regulation of experimental pressure changes.13 These pressure changes consist of step-wise pressure changes towards ambient pressures explained by Eustachian tube openings,14 and gradual pressure changes explained by the mastoid found in both positive and negative directions.13 These latter changes cannot be explained by gas exchange only, since the experiments were performed in awake subjects, where the gas exchange normally would result in gas absorption (negative direction), therefore, other mechanisms seem to be involved.
An alternate hypothesis has been proposed for ME cleft pressure regulation, where changes in the congestion of the mastoid mucosa result in changes in the pressure.15,16 Diving mammals such as the hooded seal and the sea lion exposing their ME’s to high pressures, when diving to high depths of water, seem to employ such a mechanism; their ME mucosa is rich in sinusoids or cavernous venoles, which are thought to fill with blood during diving.16,17 Based on measurements of human mastoid surface areas and volumes,3 it has been calculated that a small change in mucosal thickness of only 6 µm can alter the ME pressure by 1 kPa.15 Therefore this mechanism seems very effective, and may contribute to pressure regulation also in humans. Since vasomotor action may control the congestion, this process may also be active, but in essence it may also be passively driven by the pressure gradient.16
We have recently found support for the hypothesis of mucosal congestion playing a role in pressure regulation by histological examination of the mucosa from the lateral part of the mastoid in a normal human ear (Fig. 2). The specimen has been immuno-stained with CD-31 displaying the endothelial cells, and a collection of broad venous structures are seen, which appear similar to sinusoid. Moreover, the connective tissue is loose, which may allow for expansion of the mucosa. Finally, the surface epithelium is low with flat cells, as well as the distance to the underlying vascular structures is short.7 Previous studies on the histological properties are few, and seem to be focused on the medial parts of the mastoid,7 whereas the lateral parts may exhibit specialized vascular structures represented by sinusoids (Fig. 2). This has not been reported earlier.
Fig. 2. Histological image of the mucosa at the lateral part of a normal mastoid (×40). The specimen has been immuno-stained with CD-31 coloring the endothelial cells with brown. The surface epithelial lining is thin with flat cells, while the subepithelial tissue contains a loose connective tissue with numerous broad venous structures.
Conclusions
The mastoid air cells are likely to participate in the overall regulation of ME pressure; passive buffering of the pressure may be obtained merely by its volume, but also gas exchange is facilitated by its structure with a large surface area together with the properties of its mucosa. In addition, congestion of the mucosa may play a role, and the distinct set of micro-channels at the lateral part of the mastoid implying an abundant separate blood supply together with a specialized vascular structures in the same area may represent an entity which seem important in ME pressure regulation. The systematic existence of such structures will have important functional implications for the role of the mastoid in normal and diseased ears.
References
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16.Stenfors LE, Sadé J, Hellström S, Anniko M. How can the hooded seal dive to a depth of 1000 m without rupturing its tympanic membrane? A morphological and functional study. Acta Otolaryngol (Stockh) 121:689–695, 2001
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Address for correspondence: Michael Gaihede, MD, Department of Otolaryngology, Head & Neck Surgery, Aarhus University Hospital, DK-9000 Aalborg, Denmark. mlg@rn.dk
Cholesteatoma and Ear Surgery – An Update, pp. 17–20
Edited by Haruo Takahashi
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