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Year : 1998  |  Volume : 1  |  Issue : 1  |  Page : 5-16

Tympanic membrane retraction: Pathogenesis and management

Consultant University (U.Z.A), Temporal Bone Foundation, Brussels, Belgium

Date of Web Publication16-Jun-2020

Correspondence Address:
M.D., PhD B Ars
Consultant University (U.Z.A) Temporal Bone Foundation, Avenue du Polo, 68, 1150, Brussels
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-8491.286858

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Tympanic membrane retraction pocket is a clinical entity which results from a disease of the whole middle ear cleft.
Numerous causes are involved in the genesis of the retraction pocket; among which are the presence of an inflammatory process of the upper air ways mucosa, middle ear cleft negative pressure, tympanic membrane lamina propria atrophy and stratified squamous epithelium dysfunction. All these factors directly or successively are increased by the concomitant effect of local morphological factors which predispose to the genesis of the retraction pocket.
The management of tympanic membrane retraction pocket may be divided into two main methods. The preventive management consists of routine examination under the operating microscope and suction, if necessary, with the endoscope, as well as medico-surgical intervention intended to provide the appropriate treatment of the whole middle ear cleft mucosa inflammation. The curative management varies according to the developmental character of the pathological process. It is conservative at level I.
The stabilised retraction pocket of level II requires the insertion of an aerating tube and the excision of the atelectatic part of the drum. The destabilised retraction pocket corresponding to level III, needs replacement of the diseased membrane such as a total allograft myringoplasty, associated with a restoration of the volume of the mastoid air cells system.

Keywords: Tympanic membrane, Retraction pocket, Pars tensa, Pars flaccida, Pathogensis, Management.

How to cite this article:
Ars B. Tympanic membrane retraction: Pathogenesis and management. Saudi J Otorhinolaryngol Head Neck Surg 1998;1:5-16

How to cite this URL:
Ars B. Tympanic membrane retraction: Pathogenesis and management. Saudi J Otorhinolaryngol Head Neck Surg [serial online] 1998 [cited 2022 Nov 30];1:5-16. Available from: https://www.sjohns.org/text.asp?1998/1/1/5/286858

  Introduction Top

Classic works usually ascribe the pathogenesis of the tympanic membrane retraction pocket to Eustachian Tube dysfunction. [1] This mechanism is obviously not alone, but a part of a wide-ranging process.

This paper aims to show that the pathogenesis of the tympanic membrane retraction pocket is multi-factorial and brings to the fore, at least four main causes which have to be carefully taken into account when preventive or curative management of the retraction pockets is undertaken.

1- Definition

A Tympanic membrane retraction pocket consists of an invagination of a weakened tympanic membrane into the tympanic cavity.

It is the matter of the real disease of the middle ear cleft, which has to be considered above all and mainly, by the physician, in its anatomo-pathological character, even if the consequences upon the hearing take on, for the patient, primordial importance. These audiological repercussions will not be considered here.

2- Clinical Criteria

The tympanic membrane retraction pocket is a clinical entity that can be described by three different types: quantitative, qualitative, and topographical.

  • The quantitative criterion refers to the dimension : partial or total; depth; permitting regular control under the operative microscope and/or endoscopy.
  • The qualitative criterion consists of the behaviour of the pockct, whether it is self- cleaning or not; bone erosiveness, as for example, the lysis of the lenticular process of the incus, or of the tympanic bony frame [Figure 1]; the aggressive character of the pocket, fixed or non-fixed to the promontory and the surrounding structures. Clinical assessment of the fixation is performed either by : the Valsalva manoeuvre, which converts the non fixed retraction pocket into a ballooning tympanic membrane, [Figure 2] or by suction of the pocket which is ,however, a painful procedure. The presence of a secondary stimulus, irritating substances, [2] local additional inflammatory and/or infectious process like papillomavirus, may destabilise the status of the pocket.
  • Thirdly, the topographical criterion refers to the location: pars flaccida [Figure 3] or pars tensa.
Figure 1: Tympanic membrane postero-superior retraction pocket, non self-cleaning: Lysis of the lenticular process of the incus and erosin of the tympanic bone frame

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Figure 2: Tympanic membrane postero-superior non-fixed retraction pocket: The Valsalva maneouvre converts the non-fixed pocket (on the right). To a ballooning membrane (on the left)

Click here to view
Figure 3: Tympanic membrane retraction pocket involving the pars flaccida: accumulation of keratin

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These three types of clinical criteria namely the quantitative, qualitative and topographical, considered all together in an evolutive character, define three levelsfor management decision.

Firstly, the pocket begins to form and is safe and reversible; secondly, it is formed and stabilised; or, thirdly, it worsens and becomes destabilised and characterised by adhesion to the surrounding structures, by erosion of the ossicular chain and bony frame, by a loss of the self-cleaning property which leads to accumulation of keratin, and by the presence of moist mucous polyps, which indicates a local additional activity.

Classification is difficult and not universally accepted.

3- Pathogenesis of Retraction Pocket

There are numerous causes in the genesis of a tympanic membrane retraction pocket. The indisputable starting point is the presence of an inflammatory process of the upper air way and, more particularly of the middle ear cleft mucosa.

Middle ear cleft negative pressure, tympanic membrane lamina propria atrophy and stratified squamous epithelium dysfunction, are all factors which intervene directlyor successively and predispose to the formation of the retraction pocket. Additive contributor is the concomitant association of local morphological factors which constitutes a predisposition.

  3-A-Middle Ear Negative Pressure Top

3-A-I- Under normal conditions:

There are three main elements that govern the middle ear pressure : firstly the fibrocartilaginous Eustachian tube, the tympanic cavity and its mucosa and the mastoid air cells system. Each of these anatomical entities plays a specific role.[3],[4}

3-A-I-a- Role of the fibro- cartilaginous Eustachian tube:

The normal fibro-cartilaginous Eustachian tube consists of a highly sophisticated valve, through which gas-flow enters or leaves the middle ear cleft. This is a regular periodic active process of gas transfer. It is essential under well definite abnormal and pathological conditions .[5] However, the importance of the gas transfer via the Eustachian tube is quantitatively reduced under normal conditions, in favour of controlled gas exchanges between middle ear and blood compartment .[6] The amounts of gas introduced into the middle ear cleft is approximately : 1 microliter, 500 to 1000 times a day. The duration of the intermittent opening of the lumen of the Eustachian tube has been estimated at about 3 to 4 minutes a day (0.020sec X 1.000 = 3,3 min),[7] Under normal conditions,the Eustachian tube ensures intermittent supply of gas transfer into the middle ear cleft.

3-A-I-b- Role of the Tympanic cavity and its mucosa:

Oxygen and nitrogen are absorbed from the tympanic cavity, via the mucosa, C02 and water vapour are diffused from the blood compartment via the mucosa into the tympanic cavity.[8] The tympanic cavity contributes to the gas pressure balance in the middle ear cleft through two kinds of mechanisms : The first one (for sudden changes) is the compliance of the tympanic membrane lamina propria. [9] This is carried out in great part by the viscoelastic properties of the lamina propria and by the flexibility of the incudo-malleolar joint, which acts as a static pressure receptor, a tridimensional movement. [10],[11],[12],[13}

The second mechanism is the steady gas exchange through the mucosa.[14],[15]This diffusion depends on the functional properties of the cells of the mucosa, the specific diffusion rate of the gas, and the behaviour of the vascular system. [16],[17],[18]

The epithelium of the middle ear cleft is a continuation of the respiratory epithelium of the nasopharynx. Its morphological structure is not homogeneous as it is modified in different parts of the middle ear. The antero-inferior part of the middle ear cleft is lined with ciliated cells, secretary or non- secretary, principally devoted to muco-ciliary clearance function. [19],[20],[21],[22] While the postero-superior part, the epitympanum, aditus ad antrum, mastoid cavity and themastoid process, are covered by a richly vascularised cuboidal epithelium. The distance between blood vessels and basement membrane is reduced. This is a characteristic of respiratory epithelium performing the specific function of gas exchange.[23],[24]

The regular gases exchanges in-or-out of the tympanic cavity are an expression of the equivalence of the partial gas pressure in both compartments : tympanic cavity and mucosal lining tissue. [25] Gas exchanges of the tympanic cavity are dependent on the relative speed of gas diffusion: absorption or elimination, the specific diffusion rate of the gas (which is a constant value) and characteristic of the gas concerned. The behaviour of the vascular system also plays an important regulatory role in the physiologic balance of the middle ear gas pressure variations. [26],[27]

Variations in the middle ear blood flow, associated with variations in the permeability of the vessels allow wide adaptations to normal gas pressure fluctuations. The normal wide variations observed in the middle ear cleft pressures during 24 hours appearing in a regular way, are among other factors, related to vascular adaptations required by the body position and sleep. [28],[29]

The transient variations in pressure in the tympanic cavity are normally coped with by the respiratory function of the adapted mucosa of the postero-superior part of the middle ear cleft, by the adaptation of the diffusion of the concerned gas and modulation of the vascular permeability and of the blood flow.

3-A-I-c- Role of the mastoid air cells system:

The mastoid air cells system contributes to the balance of gas pressure in the middle ear cleft by similar properties to those of the tympanic cavity, but the size of the air cells system and the extension of the mucosal area offered to the vascular system are of much more importance. As such these properties assign to the mastoid air cells system the role of a pressure buffer. There are numerous specific nerve endings and a considerable population of corpuscles which suggest the possible role of a pressure receptors .[30],[31] The size of the mastoid air cells shows a large range of variations. But whatever the cause, genetic determination of growth or environmental factors, there is unanimous agreement that a small mastoid air cell system is associated with pathologic situations. [32],]33],[34],[35],[36],[37]

The contributory effect of the size of the mastoid air cell system is significant. The smaller the system, the more rapid is the deviation from normal pressures. A slight negative pressure, created by the gas exchanges between the tympanic cavity and the blood compartment, via the local tissues is compensated by the gas contained in the mastoid air cells which act as an expansion barrel for the gas.

The mucosal surface area in relation to th vascular system is considerably increased by the high number of mucosal folds. These folds acting as mesenteries, providedby a high number of blood vessels, develop a sizeable mucosal surface. The vascularisation is particularly dense. The mucosal lining is single layered with a broad contact surface to the basal membrane.

3-A-II- Inflammatory and/or infectious process of the upper air ways mucosa :

A viral infection of the mucosa injures the epithelial cells, which provokes adhesion of the bacteria and keeps the inflammatory reaction going. The activation of the polymorphonuclear neutrophils releases gaseous metabolites, which are oxidising agents. Under high concentrations, these “free radicals” are capable ofkilling the cells. Under low concentration, they disturb both muco-ciliary clearance and the gas exchange functions of the cells. In addition, the inflammatory reaction increases both the number and diameter of blood vessels in the middle ear cleft, increasing as such the gas exchanges. [38],[39]

The normal slight compensated middle ear negative pressure increases and becomes pathological. This generates the formation of tympanic membrane retraction pocket.

3-B- Atrophy of the Tympanic membrane lamina propria.

The atrophy of the lamina propria never occurs as a sudden or isolated process. [47]

It always implies a more or less longstanding involvement. This tissue atrophy is explained by two kind of mechanisms: biochemical and biophysical.

The biochemical explanation is based on the rupture of the disulphate bridges, by collagenases, [48] which are liberated durning the inflammatory process.The biophysical explanation is based on the visco-elastic properties of the lamina propria .[49]

When subjected to constant stress, due to a negative pressure in the middle ear cleft, the tympanic membrane becomes strained to a degree which increases with time and is proportional to the stress forces. This change in strain is accompanied by changes in the internal structure. [50]

A typical arrangement of soft biological tissue is a network of load bearing fibres embedded in a gelatinous matrix. The fibres are cross-linked. Under the action ofexternal forces, the cross-links gradually break down causing further extension of the material. The volume of soft biological tissue is believed to remain constant under the action of external forces, and therefore, when the tympanic membrane is stretched, it will inevitably become thinner.

As a result of long-standing negative pressure in the middle ear cleft, the squamous epithelium (of ectodermal origin) and the mucous columnar epithelium (of endodermal origin) come closer together, and may even come into contact with each other. A local desintegration of the thinned lamina propria may take place, particularly in those area under highest strain.[51]

In the presence of the inflammatory process a local destruction of the mucous epithelium may occur causing a greater decrease of the tympanic membrane resistance. Those regions, which, as a result of their local elastic weakness Undergo the “greatest strain, induced by the negative middle ear pressure, are thus most likel to become the site of retraction pockets.

The morphologically weaker areas of the membrane, in the adults, are the pars flaccida and the postero-superior quadrant of the pars tensa. Both regions show a delay during maturation of elastic fibres and such a delay could lead to the weakness of the tissues. Both regions are the most vascularized regions and the inflammatory processes are most focussed in the more vascularized tissues.

Weakness of ths pars flaccida:

The notch of Rivinus corresponds to the absence of the tympanic bone at the top of tympanic frame. There is annulus at this point. The tympanic bone, the an annulus and the lamina propria originate from the mesoderm which constitutes a barrier between the two epithelia of different origin. The structure of the lamina propria, at this spot, is not clearly organised and we have even noted congenital defects in these fibrous layers in 3.5% of normal adult temporal bones.[52]

Tissue culture studies, have shown that the tympanic membrane stratified squamous epithelium, after an initial slow growing phase, undergoes rapid “en masse” spread across the culture plate. The flow is performed by the pars flaccida which acts as a generation centre. [53] One may propose that the considerable strength of the stratified squamous epithelium could pouch and force the relatively weaker fibers of the lamina propria which may spread out or break down causing the development of a retraction pocket.

Weakness of the posterior part of the pars tensa:

Since its early development the posterior arm of the tympanic bone is the most delicate portion of this structure, thinner and shorter than the anterior arm. [54] The circular fibers of the lamina propria are more delicate and are seldom seen in this part.[55],[56] The area is thinner (about 60 microns) than those near the rim (about 90 microns). The strain must consequently be greater in those thinner parts.

The strain near the sulcus, which constitutes the rigid insertion of the membrane, is necessarily therefore smaller than in the other regions.

3-C- Tympanic Membrane Stratified Squamous Epithelium dysfunction

The stratified squamous epithelium is the site of two kinds of specific movements. [57],[58],[59],[60],[61],[62]

The centrifugal keratin dispersion process involves the superficial layers, and is particularly well suited to the cleaning of the external auditory canal. when disturbed it provokes an accumulation of keratin into pockets.

The centripetal epithelial migration process is conspicuous in some pathological cases such as the healing of tympanic membrane perforations. The centripetal movement involves the whole squamous stratified layer which lines the perforation. In this case two conditions are required: the presence of free-edges, and the presence ofa substratum able to give to the cells a specific directional impulse. This is the “contact-guidance” phenomenon explained by Weiss. [63] These two conditions do not exist when considering the retraction pocket.[64]

The time and reason for the transformation of a retraction pocket into cholesteatoma is crucial. The disruption in the keratin dispersion process is at the origin of this transformation. Clinical observation informs us about the “moment” when this transformation is carried out. This observationis essential and decisive for the choice of the therapeutic management. When the pocket becomes fixed to the surroundings structures, erosive for the ossicular chainand bony frame, no longer self-cleaning (showing accumulation of keratin), with signs of inflammation, in other words, when the pocket is truly destablised, cholesteatoma is evolving !

A histo-immuno-chemical process may be one of the main reasons for this transformation. In the early embyrogensesis the epithelium of the bottom of the external auditory canal is pushed forwards by an aggressive growth power. Parallel and concomitantly, this growth forwards is regulated by control processes which put a brake on this burning progression. A release of the normal regulation of the growth of the squamous stratified epithelium takes place at the bottom of the external auditory canal [65], due to the secondary presence of an additional local stimulus, as for example irritating substances [2], a local additional inflammatory and/or infectious process among others a papilomavirus. This concept is based on the interpretation of several recent studies.[66],[67],[68],[69],[70]

Results of experimental works on tissue culture prove that cholesteatoma is derived from the epithelium of the bottom of the external auditory canal. In both epithelium, of the bottom of the external auditory canal and at the level of the matrix of the cholesteatoma, we note the presence of identical scars or marks of the epithelial growth power (growth factors, similar reactions to markers of epidermal differentiation involucin, filaggrin, glycoproteins, and other factors like the cytokeratin expression...)

According to Vennix [70] there is a particularly wide expression of cytokeratines 14 in the basal cells of the matrix of the cholesteatoma, similar to cytokeratines 6, 16 and 17 in the supra-basal cells. The cytokeratines expression being able to induce hyperproliferative cells reactions, at the level of the normal epithelium of the bottom of the bony canal, is identical to the expression in the cholesteatoma matrix.This expression is almost non-existent in the cartilaginous canal.

On the other hand, we know that cholesteatoma is the result of a conflict between stratified squamous and mucous epithelium. A similar conflict exists at the mucocutaneous junction of the tympanic perforation. [71]

Both situations coexist with an important localised accumulation of inflammatory cells, which means that the mucocutaneous junction is not stable and that the front may be considered as an epidermal defect which is continually renewed. The stimulating action of the inflammatory process constitutes the key for transformation of the retraction pocket into cholesteatoma. This process acts as stimulus to discharge the expression of cytokeratines of cell hyperproliferation. In other words the local additional inflammatory process triggers the keratinocytes of the bottom of the bony canal, leading to the cholesteatoma formation.

These is a small nosological imprecision;a tympanic membrane retraction pocket is a pathology of the middle ear cleft. Cholesteatoma has to be considered as a pathology of the bottom of the external auditory canal. It could, however, be a matter of two stages in the evolution of the same pathological process!

3-D- Local Morphological Predisposing factors:

Local morphological predisposing factors act as a catalyst for the pathogenic mechanism of the tympanic membrane retraction pocket. These predisposing factors are the result of the dynamics of the development of the whole temporal bone. These are the unlimited anatomical variants of the temporal bone and their consequences upon the physiology of the middle ear cleft.

Each constituent part ;tympanic bone, squama and petrous bone, plays an active role in the elaboration of the whole structure of the temporal bone.

It is a true “living puzzle”. Each piece has to develop itself, and at the same time, to fuse with the other pieces which are growing too, immersed in unstable surroundings. Just a minute delay or minuscule modification in the sequence of those programmed events and we note more or less severe modifications of thenormal morphology. This could generate torsions and tractions of the mucous folds, with effects upon clearance and pressure in the middle ear cleft, associated with nerve and blood supplies disturbances and subsequently interactions on the local metabolism.[36]

Ninty one per cent of the external auditory canals we have dissected out in tympanoplasty, for chronic otitis media show protruding lateral posterior bony crista. Weexplain this fact by a slight rotational shifting of the tympanic ring during its early development. Strange as it may seem, the most frequent types of retraction pockets involve anteriorly the pars flaccida and posteriorly the pars tensa. The rotation epicenter would be localised in the epitympanum.

The concomitant association of local morphological predisposing factors with the other causes, installs, potentiates and triggers the other pathogenic causes, namelymiddle ear negative pressure and both tympanic membrane lamina propria atrophy and stratified squamous epithelium dysfunction.[72]

The pathogenesy of the retraction pockets is multifactorial!

4- Management

The two main routes are preventive and curative management.

4-A- Preventive Management

There are three major precepts :

  1. Tympanic membrane examination : Tympanoscopy has to be performed routinely, under the operative microscope, and, if necessary, with the endoscope.
  2. Suction: Every crust, epithelial accumulation and mucous polyps, on the tympanic membrane, should be removed by suction.
  3. Medico-surgical intervention: Appropriate treatment of middle ear cleft and of the upper airway mucosa inflammation and/or infection should be undertaken, including adenoidectomy.

4-B- Curative management

Curative management of the tympanic membrane retraction pocket varies according to the evolutive character of the pathological process.

Three levels for decision are to be distinguished :

Level 1. The pocket begins to constitute and is safe and reversible.

Level 2. The pocket is formed and stabilised.

Level 3. The pocket worsens and becomes destabilised

4-B-l- The curative Management: level 1:

The curative management at level 1 is conservative. It consists of regular meticulous cleaning of the external auditory canal and of the tympanic membrane, by suction, under the operative microscope, and/or with the endoscope.

4-B-2- The curative management: level 2 :

In cases of stabilised tympanic membrane retraction pockets, we perform an excision of the atelectatic part which has become redundant. This attitude is the result of investigations we carried out on area changes induced by changing the middle ear pressure. The tympanic membrane area becomes larger under middle ear negative pressure than at rest position or under positive pressure . [49], [73]

The surgical steps are the following: [Figure 4].
Figure 4: Surgical steps of the curative management at level 2

Click here to view

  1. Implantation of a ventilating tube through any part of the tympanic membrane that still appears to be covering an aerated part of the tympanic cavity.
  2. Progressive suction of the atelectatic tympanic membrane to convert the retraction pocket into a lateral sac.
  3. Pressure followed by:
  4. Cutting of the edges of the lateral sac, to prevent eventual recurrence after tube extrusion.

When the lateral sac is too flaccid, it is recommended to lift the tympanic remnants, and to dislocate the annulus out of the sulcus. [49] In less than eight days, the tympanic membrane closes just like a traumatic perforation.

4-B-3- The curative management: level 3

In cases of destablised tympanic membrane retraction pockets, the fundamental cause is lack of the lamina propria which constitutes a mesodermic barrier between two epithelia, which are different in origin. For this reason, lamina propria has to be reinforced, by cartilage, or, better, replaced. We replace it by a tympanic allograft.

The technique consists of a total myringectomy, followed by the implantation of the tympanic allograft. [74]

The myringectomy consists of the total excision of the tympanic membrane including the fibro- cartilaginous ring.

For this: the skin of the bony external auditory canal is completely dissected from the bone.

The annulus must be removed completely all around the sulcus. The handle of the malleus is meticulously freed from the tympanic membrane. The whole meatal cuff, tympanic membrane with the retraction pocket and annulus are lifted out like removing one’s hand from a glove, and the skin is rolled outwards through the canalso that it becomes completely free. Diseased tympanic membrane, annulus and unhealthy skin are then removed in their entirety.

When the pocket is very difficult to dissect out, we use two techniques : Before myringectomy the implantation of a ventilating tube, and/or the peroperative use of alpha- chemo-trypsine.

After myringectomy, we implant a tympanic membrane allograft. The advantage of the tympanic allograft is two folds, in this situation, a new structure for the laminapropria, which gives to the epithelial cells the fitting directional impulse; and rigidity of the membrane due to preservation in the formaldehyde which prevents recurrence of the pocket. [75]

The tympanic membrane retraction pocket acts by its presence, adherence and weight upon the underlying bony structures and may disturb their vascularisation, provoking necrosis.

The “two holes” ossiculoplasty and/or reconstruction of the posterior bony canal wall may consequently be necessary.

The remodelling of the incus can be undertaken either using the intact incus of the patient, or an incus obtained from a tissue bank.

For the reconstruction of the posterior wall, a piece of allogenic fresh cortical bone is always routinely removed as the first step during mastoid opening. The frame work of bone is inserted into the tympanic cavity and held in position with fibrin glue. [74]

Opening of the mastoid sets the problem of the restitution of the role of gas expansion bottle and pressure buffer performed by the normal mastoid air cells system.

Tri-dimensional reconstruction of the C.T. scan images, from now on, more common, allows appreciation of the spatial repartition of the volume of the gas. The C.T. scan is the best evaluation technique to appreciate the preoperative volume of the gas contained in the mastoid.

The mastoid is, at present, open mainly according to its C.T. scan status.

The ideal procedure is the delicate balance between drastic eradication of all the diseased mucous epithelium, while respecting the largest surface area available for the remaining or future healthy mucosa and restoration of the physiological volume of the aerated cells.

This last notion of “volume” of the mastoid air cells system is the answer to the question of a possible mastoid filling.

If, as we believe, what really matters is to preserve or to restore a bed, as wide as possible, for the healthy mastoid mucosa in the view to conserve the largest surface for gas exchanges then mastoid filling is not advisable.

The posterior wall of the bony canal has to be reconstructed [74]; it constitutes the edge the mastoid air cells system. Similarly simple mastoidectomy isnot sufficient. Antro- atticomastoidectomy must be performed with the of aim restoring to the postero-superior part of the middle ear cleft to its gas exchange function.

  Conclusions Top

The pathogenesis of the tympanic membrane retraction pocket is multi-factorial. The management depends on the character of the pathological process and must take into account the pathogenesis.

  References Top

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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