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TEMPOROMANDIBULAR DISORDERS: AURAL SYMPTOMS AND CRANIOFACIAL
PAIN
Ramirez LM, DDS., MSD., Sandoval GP, MD., MSD., Schames J, D.M.D., James P Boyd, DDS.
Sarra Cushen, BS
In this review twelve different theories will be presented which have been
proposed by different researchers since 1920 until the present. These theories
offer a possible anatomic and embryologic link between the TMJ, the ear and
adjacent structures based on a neurological, vascular and muscular approach
connecting temporomandibular dysfunction (TMD) with aural and craniofacial
referred symptomatology.
INTRODUCTION
This paper will explore the ways in which
temporomandibular dysfunction (TMD) and otologic
and craniofacial symptoms are related.
In over 50% of patients with otic pain pathology of the
ear is not present.1,2 Otic symptoms such as tinnitus,
vertigo,
hearing
impairment,
otic
fullness,
retroauricular and/or preauricular pain, and popping
sensations3 are associated with functional and
inflammatory disorders of the Temporomandibular
joint
(TMJ)4
and
the
masticatory
muscles.
Investigations have demonstrated that in TMD muscle
hyperactivity can cause primary pain, referred pain,
and reflex muscular contraction that can generate
muscular dysfunction.5
TMD are a sub-classification of the muscle skeletal
disorders and they include a wide range of craniofacial
conditions with a multifactor etiology. They mask a
great variety of subjective otologic signs and
symptoms that are referred from the TMJ, the
masticatory muscles, the cervical muscles and
associated structures as much in adults as in
children.6,7,8,9,10 The prevalence of TMD is two times
higher in women than in men. 11,12,13
Bruxism plays a meaningful role in TMD and in
craniofacial referred symptoms. The closest relation
among a dysfunctional masticatory activity like
bruxism, TMD and stress is a cause-effect relationship
with the craniofacial disorders.
Okeson4 considers bruxism a microtrauma resulting
from a subconscious, non-functional clenching and
grinding of teeth that can exceed the structural and
physiological tolerance of muscles, teeth and
articulations. Kato et al.14 establish that bruxism is a
spontaneous
and
rhythmically
intense
motor
manifestation secondary to a sequence of physiological
changes observed as the increase of heart beating,
motor activity, cortex and respiratory activity
preceding the dental wearing. The sustained
microtruma and dysfunction that is produced by
bruxism is a precipitation as well as perpetuating
factor
of
TMD.
Green
and
Laskin15,16 have
demonstrated that psychological stress is the main
cause in the origin of TMD .
TMD manifests as signs and symptoms in the head,
neck and ear.17
These (symptoms) are also
associated with shoulder and back pain18,19 that can
generate referred craniofacial symptoms by involving
the anterior, lateral and suboccipital cervical muscles
in maximum occlusion. 20,21,22,23,24 Edmeads25 sets that
the referred pain to the head from the cervical zone is
generated through the facial and aponeurosis
connections sharing functional continuity among
shoulders, neck and pericranial muscles, so that the
spasm or tension of neck muscles activate the
neighboring pericranial muscles as well as the referred
pain. Mense26 state that muscle pain and tenderness is
not only perceived at the site of lesion but is usually
referred to other areas. TMD can occur as aural,
myalgic, articular, facial pain, and craniosinusal pain
as well as create cephalalgic symptoms.
Monson and Wright, in 1920, related the position of
the jaw and the TMJ with impairment of hearing in
adult and children populations. Goodfriend, in 1933,
related the aural symptoms with the TMJ.27 Costen28
in 1934 associated the auricular and craniosinusal
symptoms with articular disorders called Costen’s
Syndrome. Costen was the first one to describe otic
symptoms in total or partial edentulous patients and
the reflex muscular contraction29
of muscles
innervated by the trigeminal nerve (V3). Heteroptopic
projected pain is generated as a result of irritation and
compression of the sensorial branches of the
auriculotemporal nerve.
The functional and inflammatory disorders30 of the
TMJ4 in their acute states are recognized by patients as
“ear pain” 31, which can be explained by the proximity
of both of these structures to the neighboring
structures and the shared innervation by V3.27,32
Okeson4 states that 70% of the TMJ artralgias are
declared by patients as otalgic pain. Most people are
not aware of the possible relationship existing between
symptoms, such as headache and otalgia to TMD and
the masticatory system.
EMBRYOLOGY
Focusing on the articulation and the masticatory
muscles, as origin of TMD, and their aural effects, it is
undeniable that the embryological, physiologic and
anatomical proximity of the TMJ and the ear affect
each other.
In the human being the development of the TMJ and
structures such as the pharynges, the Eustachian tube,
and the tympanic cavity is complex and still a
controversial subject. Meckel’s cartilage, which is the
first branchial arch, forms the jaw and the maxillar;
the first and second arch forms the ossicle chain. The
malleus has a double origin: the anterior process
originates from mesenchimal cells (os goniale) through
intramembranous ossification, and the rest form
Meckel’s cartilage, through endochondral ossification.33
The middle auricular bones relate the malleus, also
called the hammer, to the condylar blastema and the
temporal blastema by fibrous connections passing
through the petrotympanic fissure that Rees34 named
the discomalleolar ligament in 1954. These fibrous
connections of the external pterygoid muscle in the
Meckel’s Cartilage form the interarticular disc by
mechanical stimulation of this muscle but Youdelis35
confirms the opposite.
The connection existing between the aural symptoms
and the muscular and articular dysfunction in the head
and neck has been studied.1,2,44 It is not clear yet if
TMD contributes to tinnitus development or if they are
the same phenomenon.45 Lockwood and Col.46 find
some people alternate intensity of tinnitus with
voluntary muscular orofacial movement. Vergara47 also
found a solid relationship between facial and
masticatory muscular movements and the variations in
the quality of tinnitus. Morgan48 finds that when the
muscles of patients with aural symptoms are palpated
75% present trigger points, which affirms that TMD
can be one of the primary causes of tinnitus.
The neurological, vascular and ligament connection
between the TMJ and the middle ear persists in the
course of articulation development because of the
continuity in the Meckel’s Cartilage through the
petrotympanic fissure that in adults shows an
incomplete closing. The internal pterygoid muscle and
the tensor tympani develop from the temporal
blastema. These structures along with the tensor veli
palatini are innervated by V3 through the otic
ganglion, which innervates the masticatory muscles
coming from the mesoderm of the first branchial arch
in the same way.36 In this article we will develop the
evident embryological connection regarding the
innervation, the irrigation and the formation of
auricular, pharinge and articular structures including
the Eustachian tube.17,37,38,39,40,41,42
Rubinstein49 states that tinnitus is not a disease by
itself but it is a symptom in the otologic spectrum.
Rubinstein supports this idea by showing that patients
with chronic tinnitus respond less to treatment than
those with acute tinnitus. Vernon et al.50 assert that in
tinnitus the greater the quantity of different sounds
then the more complex this and TMD will be. Chole et
al. in 1992 widely demonstrated
(Chart 1) that
tinnitus and vertigo are highly associated with TMD.51
Lam et al.52 affirm that the prevalence of referred otic
pain and other aural symptoms of non otologic origin
in patients with TMD varies from 3.5% to 42%1,36 and
that the prevalence of tinnitus in patients with TMD
seems to be higher than that found in the general
population.23 The frequency of tinnitus in patients with
TMD varies from 33% to 76%.1,27,31,53 The prevalence
Researchers
Nº
Patients
%
Otalgia
%
Tinnitus
% Vertigo
% Hearing
Loss
91
400
1391
64
742
86
25
47
45
200
476
148
996
57
797
338
411
470
3
38
21
100
36
93
100
47
82
--50
--63
40
1.6
100
12-16
32
14
13
32
43
40
42
44
20
76
36
36
14
63
17
6.4
59
12-17
26
5
12
28
5
20
14
--26
33
40
40
15
41
8.7
1.6
70
--18
26
13
32
38
15
33
--24
80
35
38
14
25
26
7.6
----12
TMD
Goodfriend 1933
Costen 1934
Myrhaug 1964
Dolowitz et al. 1964
Gelb et al. 1967
Bernstein et al. 1968
Principato-Barwell 1978
Koskinen et al. 1980
Brookes et al. 1980
Gelb-Bernstein 1983
Cooper et al. 1986
Wedel-Carlsson 1986
Cooper et al.23 1993
Ogutcen Toller et al.90 1993
Ciancaglini et al.80 1994
Parker y Chole27 1995
Kuttila et al.1 1999
Lam et al.52 2001
%
Fullness
Ear
--6
--48
--62
--26
62
48
----30
5
----5-9
---
Chart 1. Chart modified from: Chole RA. MD, PhD, Parker WS. DMD,PhD. Tinnitus and vertigo in patients with
temporomandibular disorders. Arch Otolaryngol Head Neck Surg. 1992;118(8):817-21.
DIAGNOSIS
Patients with otologic symptoms present painful
muscles to the palpation more frequently than those
without otologic symptoms.1,2 The cause of otic pain in
individuals with TMD, but without a pathological
condition in hearing or the nasopharinx is explained by
the heterotopic referred pain of the masticatory
muscles, the TMJ and associated structures. 2,3,23,43
of dizziness in patients with TMD ranges from 40% to
70%51,52 and that of vertigo from 5% to 40%.28,45,54
Hazell55 reported that 39% of the patients with tinnitus
presented frequent tensional headaches with fatigue
and muscular soreness in facial and masticatory
muscles. 31 Bjorne and Col.56,57 assert that hearing
damage and auditive loss frequently associated with
tinnitus are strongly related to emotional tension
symptoms such as cephalalgia, cervical and pericranial
muscular tension, as well as dreaming disorders.
Otorynolaryngological and odontological exams are
vital to set differential diagnosis of the craniofacial
symptoms by TMD.21,23,58 These should incorporate
both intraoral and extraoral muscle explorations of the
head neck59 as well as articular palpation of the
muscles. Also a physical and visual examination of
associated structures such as the pterygoid hamulus of
the soft palate, the estilohioid complex, the temporalis
tendon,
the
sphenopalatinum
ganglion,
the
estilomandibular ligament and the parotid gland, and
dental structures should be included as well as looking
for possible cervical lesions. These exams are
necessary to make a certain diagnostic approachment
because of the similarity to craniofacial symptoms. The
pain present in TMD is a subjective symptom which
possesses a relevant diagnostic difficulty, especially
under the absence of objective and unique signs which
is why the differential diagnosis with associated
structures
is
vital.4,25,60,61,62,63,64,65,6667,68,69,70,71,72,73,74,75,76,77
AURAL SYMPTOMS: THEORIES AND REALITY:
Theory of the Referred Muscular Spasm:
Myrhaug79 in 1964 suggested that neuromuscular
dysfunctions of the masticatory muscles may trigger
alterations in the sound-conducting apparatus. TMD
produce tension and contraction in the masticatory
muscles and a secondary reflex contraction in the
tensor veli palatini and tensor tympani muscles
generating aural symptoms. Bernstein et al.18 reported
that there could exist a neurological association
between the masticatory muscles, the suprahyoids,
the middle ear muscles and the Eustachian tube
muscles, based on the idea that V3 innervates the
masticatory muscles, the tensor tympani and tensor
veli palatini muscles.20,21,29,36,37,78,79,80,81,82,83 Myrhaug79
asseverates that in subjective tinnitus there is a
contraction reflex of the tensor tympani muscle and
that in objective tinnitus, where there is a rhythmical
opening and closing of the pharyngeal area of the
Eustachian Tube (palatal myoclonus), the contraction
reflex is present in tensor tympani and tensor veli
palatini muscles.84 Zipfel et al.85 affirms that the most
common mechanical causes of objective tinnitus are
palatal myoclonus and middle ear myoclonus
(rhythmic movement of the tympanic membrane
secondary to repetitive contraction of the tensor
tympani and stapedial muscles). They also states that
objective tinnitus is much less common that subjective
tinnitus.
Shapiro and Truex29 suggest a possible spasm by reflex
contraction of the tensor tympani and the stapedial
muscle to peripherally irritate the V and VII pair
(facial) respectively. This can originate in the loss of
the ability to hear low tones. It is worth mentioning
that the reflex contraction of the stapedial and tensor
tympani muscle is produced during high sounds and
immediately before speaking. 17,86 Kamerer87 declares
that the stapedial muscle improves external
vocalization too, reducing the masking effect of
autogenous sound. He also declares that the tensor
tympani responds to external stimuli activated by
vocalization, chewing, swallowing and the movement
of the facial muscles.88
Travell and Simons89 explain that unilateral tinnitus, in
the presence of trigger points in the ipsilateral
maseteric and external pterigoid muscles describe a
referred sensitivity phenomenon or a reflex muscular
spasm of the middle ear muscles.
Ogutcen-Toller and Juniper90 noticed that the
structures that lead to sound in the middle ear could
be affected by the reflexive contraction of the tensor
tympani muscle produced by TMD.18 Although they
referred to a spasm reflex as a cause of aural
symptoms, they performed an audiological evaluation
in patients with TMD and aural symptoms but did not
find a dysfunction of the middle ear or the Eustachian
tube, suggesting a more subjective hearing loss.
Schames et al.36 and Myrhaug79 affirm that the
dysfunction of the tensor tympani and tensor veli
palatini muscles
plays an important role in the
relationship of TMD and otic symptoms. They name
these muscles accessory masticatory muscles.21,31
Vergara47 describes the filogenetic and neurological
relationship of the middle ear muscles. He explains
that the tensor tympani muscle is a muscle of
mastication and that the stapedial muscle is a facial
muscle. These muscles are respectively innervated by
V3 and VII.
The normal function of Eustachian tube equalizes the
pressure of the middle ear. The Eustachian tube also
communicates with the nasopharinge by contracting
the tensor veli palatini muscle which is assisted by the
levator
palatini
muscle
during
velopharingeal
movements such as swallowing and the inhaling phase
of respiration.37,91,92,93,94 The alteration of its function
can generate tinnitus, vertigo, sensation of hearing
loss to low tones, otic fullness and otitis media with
effusion, specially in children, secondary to the reflex
contraction of the tensor tympani and the tensor veli
palatini muscles.95 Marasa and Ham96 as well as
Youniss8 assert that the Eustachian Tube dysfunction
plays and important role in otitis media with effusion.
Children are more susceptible to chronic otitis media
with effusion especially during respiratory system
infections because they have a short, horizontal and
wide lumen of their Eustachian Tubes.97
These complex neuromuscular interactions between
the masticatory muscles and the ear were named
“Otognatic Syndrome” by Myrhaug79 in 1964 and then
"otomandibular syndrome" by Bernstein in 196918 and
Arlen in 1977.98 The patients with otomandibular
syndrome present one or more aural symptoms,
without having pathology in the ear, nose or throat,
but with one or more muscles of the mastication in a
state of constant spasm.18 Bjorne and Col.56,57 find a
strong affinity among Meniere’s Syndrome and TMD,
showing how the craniofacial muscular pain and the
cervical spine disorders presented in TMD can produce
fluctuant impairment of hearing, vertigo and tinnitus,
supporting
Goodfriend,27
Ciancagliani80
and
Rubinstein53 findings. These findings show a strong
correlation among deafness and the TMD associated
with vertigo and tinnitus.
Theory of the tensor veli palatini muscle origin
Rood and Doyle99 as a result of adult and fetal
cadaveric dissections found that the tensor veli palatini
was composed of a medial portion, which Gray named
the “tubae dilator” in 1918.100 They also found and
external portion of the same muscle composed by the
tensor veli palatini and an intratympanic zone
composed by the tensor tympani muscle that
intermingling its fibers with the external zone of the
tensor veli palatini muscle.94,101,102 The lateral zone of
the tensor veli palatini originates in the sphenoid
spine, scaphoid fossa, tensor tympani muscle and the
entire lateral osseous ridge of the sphenoid sulcus. The
medial zone of the tensor veli palatini originates in the
posterior and middle one-third of Eustachian Tube’s
lateral membranous wall. These muscles converge and
descend the hamular process in a strong tendon that
curves around this zone to insert horizontally in the
soft palate like an aponeurosis.
Rood and Doyle affirm that movement patterns such
as yawning, laughing, swallowing and coughing involve
pharyngeal and laryngeal muscles that activate the
tensor tympani muscle. Kamerer,87 in 1978, expresses
his astonishment that there is not a unified theory
dealing with this phenomena, even though there is a
close anatomical relationship between the tensor
tympani
and
the
tensor
veli
palatini
and
electromiographically
shows
that
they
work
simultaneously
during
swallowing
assisting
in
Eustachian tube ventilation, like an air pump.
Djupesland explained how the tensor tympani, during
its reciprocal contraction with the tensor veli palatini,
generates an inner deflection of the tympanic
membrane that breaks the seal among the mucosal
membranes of the Eustachian Tube isthmus. This
expels air and contributes to the venting of the middle
ear.88,97,103
Barsoumian, Kuehn and Col.104 corroborate Lupin’s
1969 findings and posteriously Rood and Doyle’s
findings by observing in adult cadavers how the fibers
of the most external zone of the tensor veli palatini
muscle and the fibers of the tensor tympani are joined
in the middle ear because of a small tendionous
portion, showing an anatomical connection in the
function of these muscles. Tensor tympani and tensor
veli palatini muscles act synergistically together and
temporary increase intra-tympanic pressure.88 These
findings affirm that the tensor veli palatini has an
additional bone origin in the manubrium of the
malleus. The dysfunction of the tensor veli palatini
muscle in TMD can either individually or in combination
modify the medial position of the malleus and the
tympanic membrane because of the insertion of the
tensor tympani muscle. Even the spatial disposition of
the oscicular chain can be modified by tension of the
tensor tympani muscle because of its continuity with
the tensor veli palatini muscle. In addition Schames
and Col.36 attribute the secondary miofibrotic
contraction to adhesions and trigger points of the
tensor tympani and tensor veli palatini muscles due to
dysfunction generated by TMD. This complicates the
anatomical and functional relationship between these
and aural symptomatology which is a consequence of
reduced muscle fiber length.
In 2002, Kierner et al.105 found the functional
connection amount the tensor veli palatini and the
tensor tympani muscles.106 They found this connection
through histological analysis of five human cadavers.
They affirm the re-confirmation of this finding and that
it represents an important step in understanding the
“functional unit” that these two muscles create in man.
Ligamental Biomechanical Theory:
Myrhaug79 affirms that the oscicular chain and the
middle ear muscles belong embryologically to the
chewing system. Posteriorly they become and serve as
the hearing sense.
Dissections of human adults and fetuses carried out by
Pinto,32,107
Komori108
and
other
researchers34,38,82,109,110,111,112,113,114,115 proved a specific
anatomical
link
between
the
TMJ,
the
sphenomandibular ligament and the middle ear made
by the discomalleolar and the anterior malleolar
ligaments that connect to the malleus separately in the
anterior process or processus gracilis to conform to the
previously described anterior ligament of the
malleus.100,116 The anterior malleolar ligament is a
continuation of the sphenomandibular ligament noted
by Burch117; these according to Komori et al.108 and
Ogutcen-Toller118 inserted on the ventral surface of the
hammer coming out to form a horizontal “V” with the
discomalleolar ligament in the petrotympanic fissure
(Figure 1). According to Pinto the discomalleolar
ligament is found more external and is inserted in the
medioposteriorsuperior border of the capsular ligament
and the disk. According to Komori et al. it is inserted
only to the medioposteriorsuperior zone of the
retrodiscal area and to the articular capsule. The
anterior malleolar ligament is more medial than the
discomalleolar
ligament
and
connects
the
sphenomandibular ligament along with the Chorda
Tympani nerve (VII). The sphenomandibular ligament
is inserted in the lingula or mandibular spix spine and
originates in the malleus, part of the sphenoid spine
and the most medial zone of the petrotympanic
fissure.119 The malleolar anterior ligament is an
embryological remainder of Meckel´s cartilage and the
disk-malleolar ligament is a remainder of the external
pterygoid muscle. Pinto and later, in more detail,
Komori show how the petrotympanic fissure in the Iter
Chorda Anterius is trespassed by the Chorda Tympani
and these two ligaments together within the Huguier
Channel, separated by a bone ridge of triangular base
on its path leaving the middle ear. The stretching of
these ligaments by functional and/or inflammatory
disorders4,120 affects the middle ear structures in some
patients. According to Eckerdal82 the range of
movement of these ligaments depends on the fibrous
connection in the walls of the petrotympanic fissure,
corroborating Coleman findings in 1970.121
Costen´s Theories -Neural Compression,
Muscular Spasm and Muscular Tone.
Figure 1. Graphic of superior view of Ear and TMJ zone dissections: A. External
ear, B. Anterior Process of malleus, C. Chorda Tympani nerve, D. Tympanic
anterior wall, E. Discomalleolar Ligament, F. Sphenoid spine, G.
Posterosuperomedial retrodiscal and capsular zone, H. Anterior Malleolar
Ligament, I. Disc, J. Sphenomandibular Ligament, K. External pterygoid muscle
This ligament link between the TMJ and the middle ear
can be biomechanically subjected to a functional or
inflammatory articular disorder since the luxation or
displacement of the disk and the secondary edema by
inflammation,122,123,124,125 would generate additional
anterior tension on the discomalleolar ligament
because of the disk’s disposition and the increase of
intrarticular pressure.126 The malleolar anterior
ligament might be stretched by elongation of the
sphenomandibular ligament in extreme movements,
explaining the increase of tinnitus in exaggerated
intermaxilar positions.18,31 Libin127 in 1987 suggested
that the sphenomandibular ligament and the
retrodiscal bilaminar zone could be tensed in the
petrotympanic fissure under the normal physiological
movements of jaw opening or as a result of cranial
trauma to the temporal bone structures. Movements
named the “Cranial Mechanism” can have deep
implications in the movement freedom of the
discomalleolar ligament and malleolar anterior
ligament during jaw opening. Bernstein27 in 1933
observed how in extreme jaw movements some
patients could change the intensity and quality of
tinnitus. Burch128 researched the accessory ligaments
finding that the sphenomandibular ligament relaxed in
maximum jaw opening and it tensed in a position of
marked overbite.
Loughner et al.110 advise that in surgeries to the TMJ
where condyle distractions of more than 10 mm are
performed, the ossicular chain could be injured by the
extreme traction of these ligaments over the anterior
process of the malleus. They also suggest that in
presence of infectious otitis media, the TMJ can be
involved in generating capsulitis, especially in
newborns where the connection of the middle ear and
the TMJ is noticeable through the petrotympanic
fissure.111 Marasa and Ham96 explain that the
inflammation produced by inflammatory or functional
disorders of the TMJ can spread through the
petrotympanic fissure to the middle ear and generate
otitis media.
Reflex Vascular Spasm's Theory:
Merida-Velasco et al.129 affirmed Bleicker’s 193829
findings that in newborns small vessels of the anterior
portion of the middle ear cross the petrotympanic
fissure and reach the venous retrodiscal plexus that
drains into the retromandibular vein which is a part of
the articular vascular plexus. In adults the most
medial branches of the posterior group of the tympanic
anterior artery irrigate the tympanic cavity and the
external auditory meatus. They demonstrate how
these most medial branches are in intimate contact
with the discomalleolar ligament that enters the
middle ear through the petrotympanic fissure and with
the external ear through the most external branches in
the scamotympanic fissure. They show that the
intimate relationship between the TMJ and the middle
ear and in presence of secondary reflex vascular
contraction by functional or inflammatory articular
disorders could explain the referred otic symptoms.114
Reflex
One of Costen’s hypotheses28 associated otologic
symptoms with abnormal amounts of auriculotemporal
nerve (V3) compression by the TMJ in the posterior
and medial portion of the gleniod cavity. He confirmed
that its medial and posterior path to the condylar head
could project otic symptoms. The mechanical
compression exerted near the chord tympani (that
emerges from the medial area of petrotympanic fissure
and then unites the lingual nerve17,107,130) and the
symptoms referred to the tongue were equally related.
He postulated that aural symptoms were the result of
Eustachian tube’s compression because of the
relaxation of the superior head of the external
pterygoid muscle and the internal pterygoid muscle
that occurs with the posterior condylar movement that
then produces a loss of vertical dimension.28,29,131,132
Ash and Pinto32 explain that it cannot be excluded that
an abnormal anatomical position of the jaw secondary
to a diminished vertical dimension in dentate and
edentulous patients could indirectly occlude the
membranous area of Eustachian tube as a result of
compression of the muscular mass and associated
structures in relaxation or muscular hypotension.
Costen stated that the occlusion of the Eustachian tube
changes the intratympanic pressure that could
generate vertigo. Kelly133 found a relevant causal
association among vertigo, nausea, vomit and syncope
in 105 patients with over-closed dental relation and
found the complete resolution of their symptomatology
in 89% of these patients at increasing it.
In relation to the possible compression of the
retrodiscal structures because of the posterior
movement of the condyles, it is important to note that
in healthy articulation this posterior movement is
limited by the temporomandibular ligament (Figure 2).
This is a strong ligament without elastic fibers that
maintains the condyle, disc and temporal bone firmly
opposed, even restricting the most posterior condylar
position in the TMJ. This ligament is composed of
horizontal and oblique portions. The horizontal portion
restricts the posterior movement of the condyle and is
assisted partially by the oblique portion.4 In situations
in which the partial and total edentulism and the
advanced tooth attrition permit the abnormal closing
of the jaw, the condylar movement could generate
mechanic compression of the auriculotemporal nerve
(transits posteroinferior to the condyle) in abnormal
articulations by elongation of this ligaments.
Figure 2. A. Horizontal Portion to Condyle and Disc of the Temporomandibular
Ligament, B. Oblicous Portion of the Temporomandibular Ligament , C.
Auriculotemporal Nerve.
Modified from: Okeson JP. Managment of temporomandibular disorders and
occlusion. 4th Ed, The CV Mosby Publishers, St. Louis, MO, 1998. Page 15
In 1943, Sicher,134,135 among other anatomists, argued
that these hypotheses were incorrect, although they
didn’t deny the possibility of considering them. More
than half a century later, in 1990, Johansson123 carried
out histological and radiographic studies that
corroborated not only the compression of the
auriculotemporal nerve in luxated disk articulations,
but also the probable compression of the masseteric
nerve, the branches of the deep posterior temporal
nerves and the possible compression of the lingual and
inferior alveolar nerves in some luxated articulations.
In articulations with disc luxation, the retrodiscal
vasculo-nerve plexus is compressed where the
auriculotemporal
nerve
is
included.
The
auriculotemporal nerve profusely innervates the
articulation as well as innervating the tympanic
membrane, the anterosuperior zone of the external
ear, the tragus and the external part of the ear upon
it, among other structures. The retrodiscal zone has
been extensively studied136,137,138,139 and similarly
confirms that adaptive inflammatory changes occur
because of discal luxation and the presence of
mechanical force in the retrodiscal vascular and
nervous system.
In his study Johansson123 explained that in the nervous
entrapment etiology is important not only to
anatomical mobility and bone deformities but also
inflammation of vascular and muscular structures that
can injure closely situated nerves117 since inflammation
can alter and reduce the normal contour and size of
the anatomical passages.
Theory of Hypertonicity:
In relation to the muscular dysfunctional spastic
contraction Marasa96 in 1988, and Youniss8 in 1993,
suggested that the internal pterygoid muscle
hypertonicity observed in TMD could externally
compress the tensor veli palatini muscle, as well as
cause anatomical interferences of the normal function
of Eustachian tube, generating audiologic symptoms.
Normally the Eustachian tube is maintained closed by
the collapsing pressure of the external mass which is
composed of structures like the internal pterigoid
muscle in the lateral zone, the levator palatini muscle
in the inferior zone and the Ostmann’s fat pad in the
internal zone. Under normal conditions the contraction
of the tensor veli palatini muscle opens the lumen of
the Eustachian Tube while it presses laterally the
internal pterygoid muscle.140 If the internal pterygoid
muscle is hypertonic, it interrupts the contraction of
the tensor veli palatini muscle causing difficulty in
opening the Eustachian Tube.141
If the mastication muscles are hypertonic because of
TMD, it is also possible that the tensor veli palatini is
hypertonic as well because of the common innervation
by the of V3. As the tensor veli palatini remains
spastic, its normal function of opening and closing the
Eustachian Tube will cease.
High, Narrow, Arched Palate Theory
Marasa and Ham96 in 1988 proposed that the long,
high, narrow palate concavities in children contribute
to anatomical changes like internal rotation of the
palatini and maxilar bones that modify the peripherical
muscular efficacy and its relation with the Eustachian
Tube, generating aural symptoms and otitis media
with effusion. The higher the separation and extension
of the pterygoid plate and the pharingeal tubercle in
high, narrow and arched palates, because of internal
rotation of the palatini and maxillar bone, the higher
the tension in the superior fibers zone of the superior
pharingeal constrictor muscle that tightens
the
pharynx concavity by elevating it in relation to the
Eustachian Tube. This raises the inferior and medial
pressure generated over the Eustachian Tube,
producing a blockage in the Eustachian Tube.
Consequently they suggested that in high, narrow
arched palates the contraction of the tensor veli
palatini will have to be higher to move the palatine
aponeurosis due to the longer axial length that
reduces the efficacy of this muscle to open the
Eustachian Tube. They state that the nasopharyngeal
constricted airway seen in high vaulted palate of
thumb-sucking children (initiating and perpetuating
habit in TMD)could narrow it, also the presence of
enlarged tonsils and adenoids, can block the
Eustachian Tube.
Otic Ganglion's Theory:
An auriculotemporal nerve lesion not only involves the
preganglionar sensorial fibers of this nerve but also the
secretomotor component of the parotid gland which is
generated by parasympathic postganglionic fibers of
the glosopharingeal (IX). It also involves the
sympathic postganglionar component of the blood
vessels and sweat glands in the skin, which are
innervated by this component. The sympathetic fibers
in the TMJ also contribute to the articular inflammation
increasing the activity of these postganglionic
sympathetic nervous fibers in TMD.142
Ash and Pinto32 relate the aural symptomatology,
explaining that the parasymphatic nervous fibers of
the otic ganglion that come from the glosopharingeal
nerve (tympanic plexus) through the small petrosal
nerve, reach the TMJ in its route with the
auriculotemporal nerve. When this is irritated it can
produce a reflex vascular spasm in the labyrinthine
system of the internal ear, which is secondary to
abnormal stimulation of these fibers to the tympanic
plexus and is associated with TMD.82,143,144
Since
1934,
Costen28
related
the
neuralgic
glosopharingeal etiology in articular pathologies to the
irritation of its sensorial connections in the IX pair of
the otic ganglion.
Cochlear Associated Innervation Theory
Vass and Col.145 found that in animals the trigeminal
innervation of the vascular system controls the
cochlear and the vestibular labyrinth. This innervation
is found specifically in the modiolar artery and in the
septum interscala giving a rich vascularization to the
stria vascularis, where the endolymph that maintains
the ionic and fluid balance of the cochlea is produced.
They also found this innervation in the ampullar crest
of the vestibular labyrinth but neither in its
neuroepithelium nor in the semicircular canals. The
projection of the ophtalmic fibers of the trigeminal
Gasser ganglion to the cochlea, through the basilar
and anterior inferior cerebella arteries, can play an
important role in its vascular tone in quick
vasodilatatory responses of the inner ear face to
metabolic stresses like intense noise. Inner ear
pathology which produces aural symptoms such as
sudden hearing loss, vertigo and tinnitus can originate
from the reduction of the cochlear blood flow because
of the presence of abnormal activity in the trigeminal
ganglion in patients with herpes zoster, migraine or by
central excitatory effect caused by chronic or deep
pain. The authors also found that the trigeminal
sensorial innervation plays an important role in the
regulation and balance of the cochlear vascular tone
and in the vestibular labyrinth canal that can be
responsible of the symptomatic complexity of some
cochlear diseases related to inner ear blood flow. They
also state that cephalalgia in cluster headaches,
tinnitus, hearing loss, vertigo and Meniere’s Syndrome
can have a similar relation (and can be explained by
this innervation.
Articular Inflammatory Pattern's Theory:
Myers,124 in 1988, suggests that in articulations with
luxated disks chronic inflammation is generated.125
Inflammation is generated because of vascular
damage that produces edema, vascular leakage and
fibrosis that extends into neighboring areas following
the patterns of smallest resistance generated in the
activity of the muscular masses, especially in medial
and anterior-medial areas of the TMJ (Figure 3). When
edema takes place in the anterior-medial area,
localized between the internal and external pterygoid
muscles, it can cause inflammatory compression of the
alveolar, lingual, chord tympani nerves and the middle
meningeal artery.
Figure 3. Possible Medial Inflammatory Paths from the TMJ in Inflammatory
Disorders.
Modified form: Myers LJ, DDS. Possible inflammatory pathways relating
temporomandibular joint dysfunction to otic symptoms. The J Craniomand Prac.
January 1988, Vol. 6(1): 65-70
When edema moves to the medial area it can take two
patterns. One pattern runs posterior, surrounding the
styloid process following the facial tissues in a distal
and caudal direction to the area of the internal carotid
artery, the jugular vein and the hypoglossal and
glosopharyngeal nerves (carotid sheath region). The
second pattern is directed to the carotid sheath,
generating fibrosis and adhesions that produce tension
in the carotid sheath with the jaw and neck
movements. This tension is transmitted to the jugular
foramen and to the endolymphatic sack, generating
pressure over the hair cells of the cochlea producing
tinnitus and vertigo.
A third pattern is described which passes between the
origin of the levator palatini muscle and the tensor veli
palatini muscle, which form a space along with the
apex of the isthmus of the Eustachian tube, allowing
edema and fibrosis to go toward the most vulnerable
area (isthmus) because of its narrow lumen that can
be pressed, lightly closing the isthmus and generating
otological symptoms of fullness and otitis media.
Myers demonstrates the fragility of the extrabony
extensions of the middle ear in the Eustachian tube
and of the internal ear in the endolymphatic sack. He
suggests
that
Meniere's
Syndrome
(increased
endolymphatic pressure) involves the transitory or
permanent impairment of hearing, tinnitus and vertigo
and has an etiologic explanation in this theory.
Heterotopic Pain Theory - Convergence Miller and Wyrwa43 demonstrate that in the "theory of
the convergence," studied by Sessle,146,147,148,149 the
pain referred to the ear, secondary to a orofacial
pathology150 and a chronic painful stimuli alters the
normal physiologic functioning of the brain and
sensitizes the Central Nervous System (CNS) from the
sensitization of the Peripheral Nervous System (PNS).
The sensorial innervation of the ear and periaural
region is derived form cranial nerves V, VII, IX, X, C2,
and C3. These nerves receive peripheral nociceptive
impulses to the second-order neurons through the
trigeminal subnucleus caudalis.120 The neurons of the
spinal nucleus of the trigeminal nerve in the brain
stem, particularly in the subnucleus caudalis and the
transition zone between caudal and interpolar
subnucleous, receive these craniofacial afferents
nociceptive signals.22,151 The central sensitization also
involves spinal motor neurons, the thalamus and the
somatosensorial cortex. The “convergence” of these
afferent nerves toward the spinal nucleus of the
trigeminal and lately the thalamus and the cortex can
confuse the brain in the appreciation of the sources of
peripheral chronic pain by the sensation of afferent
interneurons not related.
Okesson4 affirms that if the pain stimuli is continuous
it gives place to an accumulation of neurotransmitter
substance in the interneuronal synapses, leading to
the leakage of this chemical substance toward groups
of adjacent interneurons being modulated by the
action of these neurotransmitters, generating in the
brain the perception of these impulses like coming
from the same pain area. Explain that the excited
original neuron gives information about the real origin
of pain (primary pain), but the other neuron only
shows central excitement, then the pain perceived
from this neuron is a heterotopic pain, particularly a
referred pain.146
Woolf et al.152 assert that the pathogenicity of pain is
in part a reflex of the CNS neurons’ capacity to suffer
dynamic alterations in the properties of response and
that the nociceptive fibers can trigger this functional
plasticity. Chronic pain brings out, as a consequence, a
reduction in the threshold of the cutaneus afferent
ways and an expansion of the peripheral response.
The repeated peripheral stimuli of primary afferent
fibers, the pain receptors, produces a progressive
increase in the action potential discharge and in the
same manner a prolonged enlargement in the
excitability of spine and brain stem neurons posterior
to the deep and chronic pain stimulus. Coderre et al.153
sustain that it is possible that the normal pain
inhibition process154 in the brain stem is altered by
peripheral pain reception and the central sensitization
process generating expansion of the perceived
peripheral pain. Bjorne and Col.56,57 describe a type of
vertigo and tinnitus without a cochlear and labyrinth
origin. They assert that these symptoms can be
unchained in the facial and cervical muscular
dysfunction in TMD, which generates hypertonicity and
muscular spasm irritating nerves and blood vessels by
muscular trapping. When this compression develops in
the neck, it distorts the normal propioceptive reception
to the vestibular nucleus in the oculo-vestibular
muscle reflex that controls the postural position of the
head.132 They affirm that constant muscular tension is
associated with tinnitus and vertigo by neuroplasticity
originating in irritation and posterior peripheral
sensitization.
Theory of Lability in the Internal and Middle Ear
Stability:
In 1964, Myrhaug79 suggests a theory that states that
the equilibrium of the ossicular chain, tensor tympani
muscle and stapedial muscle (antagonistics) depends
on the normal functioning of the structures that lead
sound into the middle ear. He affirms that in TMD, the
sustained reflex contraction of these muscles can alter
the endolimphatic pressure through the transmitted
changes from the oval window to the labyrinth walls.
This can unchain and unbalance the vestibular
impulses and a symptomatologic reaction similar to
Meniere’s Syndrome can develop. He also affirms that
the tympani chord (VII) can be mechanically irritated
in its path between the hammer and the incus by an
existing reflex contraction of the tensor tympani
muscle and that it can modify the positions between
both of the oscicular structures, permitting the
episodic or sustained contusion of this nerve and its
corresponding sensorial expression projected to the
tongue as an alteration of tasting sensation, a metallic
taste and a burning sensation. It is important to
mention that the tympani chord contains preganglionar
parasympathic fibers of a secretor nature that
correspond to the submaxilar, sublingual and
accessories glands that when irritated can explain the
variable salivate flow observed in patients with TMD.
(Figure 4)
DISCUSSION
TMD in their acute and chronic states can come to
seriously affect social life, labor performance and life
quality.
and perpetuating causes increase the biomechanics
and the neuromuscular factors.
The interdisciplinary handling is mandatory in the
differential diagnosis of TMD and the golden rule for
the detection of these and related symptoms is the
oral clinical exam.
The pain present in TMD is like a mystery where the
symptoms characterize the clues and the current
epidemiological information and a good clinical exam
gives support for where this mystery is armed and
takes form.
Sometimes it is necessary to be ready to renounce
some of the procedures and theories accepted as
paradigms in professional practice. Only the flexible
use of refreshing new knowledge and adoption of a
new direction will benefit our patients, and diminish
the unavoidable uncertainty of our daily practice.
Many of these theories are not possible to prove using
measuring instruments, but in the daily clinical
practice they are constantly applied. Consten’s 1934
positions are regularly applied and seem to be the
correct vision of TMD and their causal association with
referred symptomology.
Even after 68 years these
theories seem applicable in the explanation of the
craneofacial symptoms. The investigators that lean on
anatomical and physiological exploration in their daily
clinical practice have given form to each one of these
theories. These theories should be kept in mind as
diagnostic tools as they are the best understanding we
currently have of the etilogy and pathogenicity of
these disorders.
A
B
The causal relationship of heterotopic pain (aural
symptoms, migraines, miofascial pain) to the
masticatory system is found in large numbers of adult
patients as well as in the infantile population.)
Although the cause-effect relationship has a significant
association in TMD, continuous study is still needed.
It seems that for the development of TMD is necessary
a multifactorial model centered in local, systemic and
recent psychological factors. Predisposition, initiator
Figure 4. A. Equilibrium of ossicular chain in middle ear zone. B. Incus and
malleus trespassed by the Chorda Tympani nerve.
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