Medical Hypotheses 74 (2010) 710–718

Contents lists available at ScienceDirect

Medical Hypotheses
journal homepage: www.elsevier.com/locate/mehy

Stomatognathic adaptive motor syndrome is the correct diagnosis

for temporomandibular disorders
Carlos Roberto Douglas, José Luiz Villaça Avoglio *, Heloisa de Oliveira
Rua João Zappa 215, 12516 300 Guaratinguetá, SP, Brazil

a r t i c l e i n f o s u m m a r y

Article history: Temporomandibular disorder is a generic and inadequate conception to be used as a diagnosis. It fails to
Received 9 October 2009 express the etiology or the pathophysiology and it is mainly associated with the anatomical site. More-
Accepted 14 October 2009 over, the clinical condition presents a mandibular motor problem and not a joint problem. The hypothesis
presents the new diagnosis stomatognathic motor adaptive syndrome, which comprehend a motor
response and the adaptive processes it induces. Inadequate occlusal contacts cause the mandible to shift
in order to reach an ideal intercuspal position. The condylar displacements are proportional to such
movements. Temporomandibular joint (TMJ) receptors respond to the capsular mechanical stress and
the information reaches the trigeminal sensory nuclei. The mandibular modified position seems to be rel-
evant information and may interfere with catecholaminergic neurotransmission in basal ganglia. The
main motor responses comprise increased jaw muscle tone, decreased velocity of movements and inco-
ordination. The overload of muscle function will produce adaptive responses on many stomatognathic
structures. The muscle adaptive responses are hypertonia, pain, fatigue and weakness. Temporomandib-
ular joint presents tissue modification, disc alteration and cracking noise. Periodontium show increased
periodontal membrane, bone height loss and gingival recession. Teeth manifest increased wear facets,
abfraction and non-accidental fractures. The periodontal and teeth adaptive processes are usually iden-
tified as occlusal trauma. The altered stomatognathic functions will show loss of velocity during masti-
cation and speech. Fatigue, weakness in jaw muscle and difficulties to chew hard food are related to
hypertonia. Incoordination between stomatognathic muscles groups is found, causing involuntary ton-
gue/cheek biting and lateral jaw movements on speech. Otologic complaints, as aural fullness and tinni-
tus, are related to the tensor tympani muscle, innervated by the trigeminal nerve.
Ó 2009 Elsevier Ltd. All rights reserved.

Introduction have been used incorrectly as internal derangement, like osteoar-

‘‘Temporomandibular disorders (TMD) refer to a collection of
medical and dental conditions affecting the temporomandibular
joint and/or the muscles of mastication, as well as contiguous tis-
sue components” [1]. Under this concept various conditions, that
have no common etiology, are joined in the same diagnosis. Joint
diseases, facial or joint or muscle pain, headache, joint sounds, den-
tal wear, hearing disturbance and others are examples of condi-
tions aggregated on the same diagnosis.
The conflict of the prevailing concept is the admission of func-
tional, degenerative, autoimmune and inflammatory problems as
one pathology. In addition, there is a general acceptance of a joint
disease with subtypes. Many subtypes were suggested, and ranges
from myofascial pain, arthralgia, disc displacement to internal
derangements. Many of the diseases classified as subtype have
their own code on the International Classification of Diseases and
* Corresponding author. Tel.: +55 012 3125 1767.
E-mail address: dr.villaca@gmail.com (J.L.V. Avoglio).
thritis of the temporomandibular joint. The etiology were subject
of many consideration, but at moment may be considered as un-
known or not established. Consequently, there is a fully agreement
that just conservative and reversible therapies are recommended.
The concept in such diagnosis is based mainly on the anatomi-
cal site and not on the etiology or the pathophysiology. In this
sense, the belief that the etiology of TMD is multifactorial is not
applicable [2]. Various diseases are multifactorial, as lung cancer,
pneumonia and emphysema. Indeed, should Lung Disorders be
adopted as the diagnosis, there would be no way to prove that a
treatment was effective to all manifestations. It would not be pos-
sible to prove that chemotherapy, or antibiotic are effective treat-
ments. The diagnosis ‘‘temporomandibular disorder” jeopardizes
the comparison of clinical studies because the sample could not
be always homogeneous.
The stomatognathic system performs many physiologic func-
tions. They embrace mastication, speech mechanics, suction,
deglutition, spitting, blowing and vomiting, among others. In all
those functions there are mandibular motor request and, at the

0306-9877/$ - see front matter Ó 2009 Elsevier Ltd. All rights reserved.
doi:10.1016/j.mehy.2009.10.028
 C.R. Douglas et al. / Medical Hypotheses 74 (2010) 710–718 711

same time, movements of the tongue, hyoid, soft palate, lips and
other structures. All functions are motor events involving several
muscle groups that reach the neck, and maybe more. All these
tasks happen under the command of the central nervous system
and undergo the influence of peripheral inputs, allowing the har-
monious execution of all those events.
The mandible distinguishes in the system as the only movable
bone and by its role as support for the movement of other muscles
groups, in addition to its own muscles. Moreover, the mandible is
involved in the stabilization of the head and in the maintenance of
the postural equilibrium, because mandibular and hyoid muscles
are antagonist of the cervical musculature [3].
On the mandibular motor action, many demands of movements
and postural muscle tone occur simultaneously. During speech, for
example, mandibular movements are executed by isotonic contrac-
tion of the muscles, but with instantaneous increase of tone, when
the tongue is elevated and moved. These movements are the execu-
tion of central commands that continuously evaluate peripheral in-
puts in order to obtain the correct function performance.
Teeth have an effect on mandibular actions. The intercuspal po-
sition of maxillary and mandibular teeth is determinant to the jaw
movement envelope, especially while chewing. This primary man-
dibular action can influence all other tasks, because the occlusal
anatomy is closely related with the mandibular function. Noting
the mandible and teeth crowns evolution through the phylogene-
sis, such correlation is always preserved.
When some perturbation intervenes on the motor procedures of
the stomatognathic system, the organism uses various adaptive
processes to maintain the efficient execution of the different func-
tions. In case of depletion or insufficiency of such adaptive capac-
ity, the system will produce a failure in some point, which will be
manifested as a sign or a symptom, interpreted as a disease or as a
dysfunction. The aim of this paper is to propose a new hypothesis,
attempting to demonstrate that the problems nowadays diagnosed
as temporomandibular disorder are not a joint problem, but a mo-
tor problem. Such motor alterations involve all stomatognathic
system and its functions, and the signs and symptoms found in
these cases will be analyzed, explaining the pathophysiology re-
lated to those processes.
incorrect restoration among others, generically denominated as
inadequate occlusal contact in this paper.
When inadequate contact appears, the mandible is forced to
make minimal movements to obtain better intercuspal position,
because teeth and condyles have a fixed relation in the same bone
(Fig. 1). The TMJ capsular mechanoreceptors will fire impulses sig-
naling the altered mandibular position, with reflex response on
mandibular muscles.
Reflex muscular response is the first stomatognathic system
adaptive mechanism. Probably mediated by the basal ganglia,
there will be decreased mandibular movements, higher levels of
muscle tone and incoordination of mandibular movement and
other stomatognathic structures. It could be found involuntary
movements also.
Along the time, the overload of muscle response will activate
other stomatognathic adaptive mechanisms and cause modifica-
tions in other structures due to the over-solicitation. Such adaptive
changes will occur on TMJ tissues, periodontium, teeth and mus-
cles (Fig. 2). These dynamic processes can be named allostasis
and the organic reaction can be effective enough to sustain normal
clinical conditions or reach a situation of insufficiency.
In temporomandibular structures changes will happen in artic-
ular tissues, disc and cracking noises will appear. The periodon-
tium will show remodeling changes with or without tooth
hypermobility, bone loss and gingival recession. Teeth will reveal
wear facets, abfraction, and non-accidental crown or restoration
fractures. Muscle will evidence hypertonia, pain on palpation and
increased volume. Functional alterations will include incoordina-
tion, as intraoral involuntary biting while chewing (tongue and/

The hypothesis

Mandibular movements are governed by the central nervous

system. Several encephalic structures are involved in the control
of movements during the execution of varied functions, as can be
observed following electrical stimulation. Among them, the basal
ganglia seem to have an important role on selecting a determinate Fig. 1. Inadequate contacts force the mandible to make minimal movements to
obtain better intercuspal position, because teeth and condyles have a fixed relation
motor program and on the coordination of simultaneous activities
in the same bone.
carried out by several muscle groups. This control modulates the
magnitude of movements and tone, while executing the appropri-
ate motor program. The basal ganglia assess the relevance of
peripheral impulses and give an output to brainstem motoneurons
controlling mandibular movements and postural tone.
The intercuspal relation of the teeth has a relevant role on man-
dibular movements and postural tone. There is considerable con-
troversy about mandibular positions, but it is generally accepted
that there is a mandibular position independent of tooth contact
that represents the position of the condyle-disc complex in the gle-
noid fossa, denominated centric relation (CR). Another is the cen-
tric occlusion (CO), an intercuspal position independent of the
condylar position. These positions are not always ideally coinci-
dent, but constantly the receptors from periodontium and TMJ cap-
sule will fire to inform those positions.
Several dental conditions can cause those positions to show
anterioposterior difference, like caries, tooth loss, malocclusion, Fig. 2. Flowchart of the stomatognathic motor adaptive syndrome.
712 C.R. Douglas et al. / Medical Hypotheses 74 (2010) 710–718

Table 1 muscle activity were was noticed after capsule anesthesia even
Structure and the signs and symptoms related to stomatognathic motor adaptive with the mandible having being fixed [7].
syndrome.
Wyke [8] observed that capsule receptors are able to detect the
TMJ Tissues modification static and dynamic position of the condyle, as well as acceleration
Disc alteration and deceleration of movements and extreme posterior displace-
Cracking noise
ment. Those receptors are essential in the perception of TMJ struc-
Periodontium Increased periodontal membrane tures posture and motion and are the major contributors in the
Bone height loss
Gingival recession
reflex regulation of muscle tone, presumably operating through
the fusimotor system. He remarked that incidental observation
Teeth Increased wear facets
Abfraction
suggests that the articular receptors reflexes operate along poly-
Non-accidental fractures synaptic pathways and project to gamma system rather than only
Muscle Pain
to alphamotoneurons.
Hypertonia The mechanoreceptors from TMJ capsule are responsible for the
Fatigue proprioception of mandibular static position and dynamic move-
Weakness ment and act through reflex muscle tone. Experiments, where
Function Loss of velocity Mastication destruction or anesthesia of those receptors was performed,
Speech showed abnormalities on movements and reflex posture. Type I
Tone Fatigue
mechanoreceptors (see Wyke’s classification) continuously con-
Weakness
Difficulty to chew hard food tribute to isotonic and isometric changes in jaw muscles, while
Incoordination Involuntary tongue/cheek biting type II bring tone increase on acceleration and deceleration condy-
Lateral jaw movement on speech lar movements. The type III mechanoreceptors act as brake to limit
Otologic Aural fullness excessive posterior displacement of the condyles, causing inhibi-
complaints Tinnitus tion of musculature [8].
Experiments with TMJ mechanoreceptors performed by Clark
and Wyke reveal that generalized increase on motor activities of
or cheek), lateral movement and decreased speed on speech, fati- all mandibular muscles were found after anesthetic infiltration in
gue and difficulty while chewing hard food. Otologic complaints the posterior region of the capsule [6]. Electrocoagulation of the
maybe related to tonic changes in the tensor tympani and/or the TMJ anterior region expressed a significative reduction of the dy-
tensor veli palatini, since both receive trigeminal motor innerva- namic reflex activities in response to the passive opening, in all
tion (Table 1). muscles. Combined electrocoagulation of both anterior and poster-
It does not seem to have distinction between men and women ior regions of TMJ virtually abolished the dynamic reflex activities
about the pathophysiology described, but can be noted that wo- in both directions. The results of such experiments are evidence
men manifest more symptoms, especially muscle pain, while that capsular mechanoreceptors have crucial contribution to the
men show more dental signs. Another aspect of the problem is reflex control of motor activities of jaw muscles.
the emotional/behavioral condition interrelation with the motor Rapidly adapting responses were found in certain places of the
response. medulla and spinal trigeminal sensory nuclei obtained by opening
This hypothesis makes a pathophysiological model, where all and closing movements of the condyle, with corresponding activi-
signs and symptoms, nowadays diagnosed as temporomandibular ties on the homolateral trigeminal motor nucleus. This indicates
disorders, can be connected. The appropriate diagnosis should be that not only the muscle proprioception but also the inputs from
stomatognathic adaptive motor syndrome. TMJ participate on the control of muscle activities of the jaw [9].
The inadequate intercuspal relation of the teeth may result in
minimal mandibular positional changes and, in consequence, mod-
Physiology of the mandibular motor control ification on condylar position, causing alteration on capsular stress
pattern. This will cause changes on firing rate of the TMJ capsule
Mandibular movements and postural tone are performed by the mechanoreceptors [6]. Similar preparation suggested that TMJ
trigeminal motor nucleus that represents the lower motoneuron. mechanoreceptors operate through multisynaptic pathway, in con-
The operation of the lower motoneuron is controlled by upper trast with the monosynaptic nature of the miotatic masticatory re-
motoneurons, distributed throughout the central nervous system. flex [5].
Those neurons are found in motor cortex, basal ganglia, limbic sys-
tem, cerebellum and reticular formation. Mandibular movements Periodontal receptors
represent the action of central motor programs, but influenced
by many other variables, like head position, peripheral impulses Periodontal mechanoreceptors also influence the reflex control
and emotional/behavioral conditions. The relevancy of receptor of jaw muscles and participate on the regulation of the force ap-
information may affect muscle response in a wide range, from a plied over the occlusal surface by jaw muscles. Evidence of this
hypokinetic–hypertonic to a hyperkinetic–hypotonic pattern. observation is the improvement on brain control of mandibular
movements in patients that used conventional complete dentures,
TMJ capsular receptors but without melioration on occlusal force following rehabilitation
with dental implants [10,11]. Studies demonstrated that bite force
Temporomandibular capsular receptors are involved in reflex dramatically decreases with local anesthesia of the teeth. It can be
control of mandibular muscles. When there is a displacement of concluded that periodontal mechanoreceptors add an extra excita-
the condyle, the muscles contract in response. Studies with tion of the closing muscles and provide the essential information to
anesthesia of TMJ capsule showed great variation on amplitude avoid periodontal damage [12]. Those receptors could have lesser
and direction of mandibular movements following uni- or bilateral influence on movements, acting on the occlusal phase of the mas-
TMJ capsule anesthesia [4–6]. Mandibular rest position is under ticatory cycle. Nevertheless, in altered motor response this mecha-
control of neuromuscular reflex and determined by the tone of nism is connected with longstanding tightened occlusal contacts
supra and infra mandibular muscles, because an increase on mentioned in dental literature as occlusal trauma.
 C.R. Douglas et al. / Medical Hypotheses 74 (2010) 710–718
Periodontal receptors have their cellular bodies on trigeminal
mesencephalic nucleus (Vmes) and on trigeminal ganglion
[13,14]. Most of periodontal receptors which somas are located
in the mesencephalic nucleus are distributed in apical region and
tend to have slowly adaptation, while the more coronal receptors
are innervated by neurons from trigeminal ganglion.
Trigeminal ganglion neurons show fast adaptation and burst
with tooth displacement [15]. Studies showed that those projec-
tions reach the supratrigeminal region, the interstitial system of
the spinal trigeminal tract, parvocellular reticular formation, as
well as the upper cervical spinal cord and cerebellum. This indi-
cates that those receptors collaborate on the control of jaw posture
by the forces generated on teeth intercuspal position.
Neurons from Vmes are related with mandibular reflexes and
are active on occlusal phase of masticatory cycle, since an increase
on the firing rate of these neurons are proportional to the mastica-
tory force.
For this reason it is possible to suppose that inadequate occlusal
contacts will produce motor responses that change the mandibular
position in relation to maxilla. This change is detected by the TMJ
mechanoreceptors with compensatory muscle repercussion. This
supposition explains the probable action of varied interocclusal
splints, which promote the elimination of teeth contacts allowing
the normalization of the condylar position.
Integration of peripheral inputs and motor response
Mastication and other functional jaw motions seem to be
sequential procedures activating motor areas, which may generi-
cally be called motor programs. There is a pattern of movements
with activation and inhibition of antagonist muscles and coordina-
tion with different muscle groups. Such movements take place in
all stomatognathic functions and are related with motor, emotional
and behavioral aspects.
Electrical stimulation of motor cortex, amygdala, hypothala-
mus, basal ganglia, and reticular formation evoke rhythmic jaw
movements. These movements are under the influence of periphe-
ral impulses that help the execution of the function. Experiments
of cortically induced mastication in anesthetized animals showed
that after inserting objects between teeth, the masticatory cycle
becomes significantly longer with mandibular deviation toward
the contralateral side during the occlusal phase. Similar prepara-
tion showed increased muscle activity proportional to the thick-
ness of plastic strips inserted between the teeth. The removal of
periodontal impulses by anesthesia or sectioning virtually abol-
ished these effects [13].
However, it there appears to be a difference in the action of the
peripheral impulse when related to the evaluation of food hardness
and when related to inadequate intercuspal relation. The former
could be associated with periodontal receptors and the latter with
capsular receptors. The capsular receptors suggest a long lasting
action, with the condition being added to the jaw motor program.
In another words, the inadequate intercuspal condition is merged
with the motor program while performing the mandibular
functions.
Evidences of that supposition will be discussed below, but it is
observable that alterations occur on speech movements even with-
out dental contacts on this function. Another is the involuntary
tongue/cheek biting while chewing. These functions also show de-
creased velocity of movements and increased tone.
The basal ganglia are supposed to participate on the selection of
the motor pattern and on the integration with other stomato-
gnathic structures movements (e.g. tongue). Lesions of basal gan-
glia are associated with alterations on planning, initiation and
execution of motor actions. Some authors accept the hypothesis
that basal ganglia act as a centralized selection mechanism [16],
713
allowing some motor solicitation and inhibiting others. The basal
ganglia operate essentially inhibiting the several motor solicita-
tions and, apparently, liberate the solicitation with most significant
priority. It is argued that in Parkinson’s disease there is incapability
to remove this inhibitory motor control and difficulties on the
selection mechanism. Other conditions may be related with failure
in the mechanism that suppresses the activities of other motor
solicitation, not having the mechanism that interrupts the motor
execution, like in Huntington’s chorea.
The lower motoneurons in brainstem are maintained under ba-
sal ganglia tonic inhibition output through GABAergic projections
from Globus Pallidus and Substantia Nigra. When a demand exists
for a motor action that inhibition is suppressed [17]. The selection
operates in memory-guided behavior, sequential procedures and
reward oriented behavior [18].
The neurons from striatum receive the basal ganglia incoming
inputs from different cortex regions [17]. In addition, the striatum
receive inputs form various thalamic nuclei. Spiny output neurons
from striatum are high threshold inhibitory (GABAergic) and re-
spond only to intense excitatory input. They tend to remain stabi-
lized, in hyperpolarized status (down state). However, in the
presence of dopamine (via D1 receptors) they reach an up state,
close to firing threshold. Most of these neurons project to output
neurons of basal ganglia (substantia nigra pars reticulata, globus
pallidus pars interna and ventral pallidum). When the striatum
neurons are activated, they will inhibit these output neurons and
then suppress the inhibition over brainstem motor centers, activat-
ing motor programs. Therefore, the motor control of basal ganglia
depends on cortical and thalamic excitatory impulses and the
dopaminergic system. The brain controls through the dopaminer-
gic system the voluntary movements by tone decreasing and
increasing contractility of skeletal muscles [19].
Electrical stimulation of the substantia nigra influences the con-
trol on movements and tone. The stimulation of the ventral portion
induced rhythmical activities on orofacial muscles. There are evi-
dences that mandibular movements are also mediated by the con-
nection from substantia nigra to superior colliculus [20].
Hikosaka suggests that basal ganglia control the movements
through projections to the brainstem motor areas and thalamus.
Particular patterns of movement like saccadic, chewing, vocaliza-
tion and swallowing are generated on brainstem, and the basal
ganglia involvement on these movements could be related with
the achievement of automatic control of these processes that fol-
low the voluntary movements [20]. The author emphasizes the sig-
nificance of the GABAergic projections to the mesopontine
tegmentum on tone and movements control. Therefore, the basal
ganglia control mandibular motor actions through the inhibition/
disinhibition of muscle tone and movement systems. These sys-
tems can be individually controlled because the lateral part of sub-
stantia nigra controls postural tone and the medial part controls
locomotion.
The striatum is involved on several mandibular motor aspects,
like rhythmical movements and muscle tone. Neurochemical
changes in this region were associated with occlusal interferences
in rats. Not only dopaminergic but also noradrenergic. Evidences
suggest that inadequacy on occlusal relation induces sensory stim-
uli to the central nervous system, through trigeminal path, which
may change the neurotransmission of dopamine in various regions.
Experiments with occlusal disharmonies in rats showed accu-
mulation of DOPA on the striatum that returned to control levels
after 14 days, except in the left striatum causing an imbalance be-
tween hemispheres. This study gave evidences of a central modu-
lation of catecholaminergic neurotransmission induced by
inadequate occlusal contacts. Moreover, the results appear to be
related to the nature of the occlusal alteration and the duration
of the problem. Long lasting inadequate occlusal contacts can
714 C.R. Douglas et al. / Medical Hypotheses 74 (2010) 710–718
cause modifications on mandibular motor patterns by this mecha-
nism [21]. Nevertheless, the experiment refers to an acrylic cap on
both incisors of rats, which probably influenced the mandibular
position, because the other groups of the study where the occlusal
alteration were just dental (incisal cut) the effects were not
significant.
Reflex modifications of jaw muscles pattern are also involved
with the antigravitational muscles of the head. Equilibrium is an
active process that keeps the extensor musculature under tonic
contraction, as consequence of the excitation of the gamma moto-
neuron, promoted by the vestibular complex. The vestibular nuclei
are excited by impulses from visual cortex, spindle from cervical
muscles, the vestibular sensory organs and cerebellar fibres [22].
Inadequate occlusal contacts caused immediate electromyographic
changes in jaw muscles and sternocleidomastoid [23] and patients
treated by occlusal adjustment reported significant improvement
on headache symptoms [24]. Electromyographic alterations were
also found on jaw muscles when position of the head changed [25].
Centric relation and centric occlusion
There is an efficiency related situation between the intercuspal
position and the condylar position into the glenoid fossa. When
TMJ capsular ligaments sustain the condyle-disc complex while
displaced to posterior, the muscle solicitation to hold a mandibular
position is lesser. This observation is essentially valid to most syno-
vial joints.
This ideal condyle-disc complex position receives several
denominations. Centric relation is the most common, but it is also
known as terminal hinge axis [26]. However, there is an agreement
that centric relation is independent of tooth contact. It is a clini-
cally reproducible position by manipulation or using interocclusal
splints. It is also an anatomical position, because there is no poster-
ior osseous limitation in TMJ. Ligaments restrict extreme displace-
ment to posterior and type III mechanoreceptors inhibit the jaw
closer muscles when this position is reached [27–29].
However, when the intercuspal position does not happen in
centric relation and some tooth contacts occurs before the others,
there will be consequences on mandibular position. If an inade-
quate contact (e.g. cusp incline) occurs, the mandible will slide to
get the ideal intercuspal position. This new position, which seems
influenced by periodontal mechanoreceptors, is known as centric
occlusion. Therefore, when there is a difference between centric
relation and centric occlusion, there must be some degree of jaw
movement. This movement is always accompanied by muscle con-
traction [5]. On the other hand, this is a common event, found in
many patients, and does not necessarily causes clinical symptoms
[30], but the muscle response will signalize to adaptive processes.
Centric relation is a terminal or a boundary position and there is
still controversy if such position is utilized or not during the mas-
ticatory cycle. Although the reflex effects over jaw muscles are
undeniable when centric relation cannot be reached. Patients with
considerable centric relation and centric occlusion discrepancy
showed longer muscle activity in chewing cycles [31].
Not only mandibular position changes from centric relation to
centric occlusion are able to cause reflex muscle responses. Inade-
quate contacts can also act during mandibular motion. They have
been associated with pain and symptoms [32] and electromyo-
graphical alterations were observed in modifications of the occlu-
sal guidance [33].
The main clinical characteristic of the altered muscle response
in such situations is a decrease of movement speed. This is obser-
vable on the masticatory cycle and speech. The physiologic process
involved is the increased tone that appear to difficult the execution
of mandibular movements.
Overload and adaptation
Adaptive processes are associated with the relation between
damage and defense. When a perturbation intervenes on a system,
there will be an initial response to keep the functions running.
Usually, the initial response promotes the activation of adaptive
mechanisms in sites under overload. The composed response can
lead the situation to a balanced status even with higher level of en-
ergy consumption. When the resources of a site are insufficient or
ineffective, a failure will occur [34].
The inadequate occlusal contact initially produces the altered
mandibular position and the first response is muscular. Various
sites of the stomatognathic system will be put under overloaded
solicitation and will respond with adaptive processes that can lead
to a homeostatic situation and this maybe the reason because the
majority of individuals do not show any symptom. All these effects
are considered allostasis, defined as achieving stability through
change [35]. In case of depletion or insufficiency of such adaptive
capacity, the allostatic overload is characterized. The motor reac-
tion of the stomatognathic system to the altered mandibular posi-
tion keeps running while the inadequate contact is maintained,
regardless of other adaptive processes.
Studies where occlusal interferences were placed on animals
point to global organic reaction and not just on stomatognathic
system. Urinary cortisol excretion was significantly elevated in
monkeys that also presented increased teeth mobility [36]. Plasma
corticosterone and hypothalamic noradrenaline in the rat were af-
fected by occlusal disharmony [37]. Study with accelerated senes-
cence mice found increased plasma corticosterone levels and
hippocampal neuron loss [38]. All those studies however attrib-
uted these effects to the occlusal inadequacy without a specific ref-
erence to the capsular mechanoreceptor role.
A motor phenomenon should not be examined without consid-
ering the psychological aspects involved. On the other hand, that
aspect must be examined under a physiological critical view,
observing the emotional interrelation with motor activities. Con-
siderations about the chronic emotional process, magnification
and amplification are relevant. The involvement of the limbic sys-
tem and the emotion against pain, as well as how such variables
modify the motor response are largely unknown. About this aspect,
it is necessary to observe that different expressions may be found
between men and women’s responses.
Signs and symptoms
Hypertonia and pain
The initial reactive motor response affects the coordination of
movements and muscle tone. High level of tone may cause pain
symptoms. Evidence of such observation is the fact that patients
with hypertonic jaw muscles relate efficiency loss and fatigue,
becoming fatigued following chewing [39]. Comparative study on
patients relating jaw muscle pain showed that muscle altered re-
sponse might be related to a central mechanism and not with a
peripheral nociceptive mechanism, because increased activities
on electromyography were found in rest condition [40].
Dawson [26] relates that the removal of occlusal interferences
causes immediate relief of pain. Another report stated that the
insertion of orthodontic elastic separator caused the same effect
[41]. These effects provide evidence for minimal intercuspal posi-
tion changes affecting jaw muscles, due to changed condylar
position.
Women commonly present more muscle pain symptoms. This
observation may be related to muscle fibres composition, lesser
resistant to tone solicitation than men, because testosterone
 C.R. Douglas et al. / Medical Hypotheses 74 (2010) 710–718
causes great effect on jaw muscles myosin. Meanwhile, this may be
just one aspect of the problem, because phenotypic characteristics
may be involved in a magnified motor response, related to more
pain relevance.
Several theories have been proposed to explain muscle pain.
Most of them try to point the cause and the effect inside the muscle
and do not consider the painful contraction as a reactive apparatus,
commanded by neurons and with origin in another structures like
joints.
Muscle pain related to mandibular reactive altered function is
chronic, showing a regular behavior and sometimes is described
as headache or ear pain. There is little variation on pain localiza-
tion, usually related with the trigeminal mandibular branch der-
matome. The type of pain is reported as tightened, not pulsatile
or sharp. The intensity of pain shows less individual variation.
The duration on the same individual does not demonstrate much
variation. The most relevant characteristic is that there is not
increase on muscle pain caused by movements. It seems that there
is not chronic pain by depletion or algogenic substances
accumulation.
However, pain on palpation is easily observable and profusely
related in dental literature. Such observations suggest that the pain
relates more to posture than to jaw movement and that there is the
involvement of the fusimotor system. Gentle muscle palpation has
been used to identify intrafusal afferents fibres in laboratory ani-
mal preparations [42,43]. Another interesting study showed that
there is an increase in discharge rate of fusimotor neurons during
fatiguing contractions. When an arterial obstruction was produced,
the fusimotor discharge started early and was maintained until the
obstruction was removed [44].
It can be supposed that pain on palpation results from spindle
stretching in hypertonic muscles. This may also explain the further
incidence of muscle pain in women, which usually show less resis-
tance to tone solicitation than men. On the other hand, women
showed attenuated ATP reduction during repeated sprint exercise
[45,46].
Botulinum A toxin has been used on patients with muscle alter-
ations involving the mandible. Initially the effects were credited to
the termination of alpha motoneurons at the motor end plate. In-
deed, there are evidences that this substance also acts on gamma
motoneurons terminations, reducing thus the discharge to the al-
pha motoneurons. Evidences suggest that the results obtained
are related to not only motor paralysis, but also to reflex muscle
tone decrease, because there is improvement on pain, function,
mouth opening and sensibility to palpation [47,48]. The reaction
or adaptation to the increased muscle demand will cause more
than hypertonic and/or painful muscles. Various signs and symp-
toms may appear jointly.
Involuntary intraoral biting (tongue and/or cheek)
Involuntary biting of the tongue or cheek while chewing is a
common symptom in patients with altered mandibular functions.
It is also a neglected sign in dental literature. It indicates a non-
physiologic event and an incoordination of stomatognathic
muscles.
There is a reciprocal inhibition between the trigeminal mesen-
cephalic nucleus and the hypoglossal nucleus, in such a way that
when one is active the other is found inhibited. When the mandible
closes, the tongue comes to a centered position into mouth [49].
There also is reflex control of the genioglossus muscle by temporo-
mandibular receptors and the muscle becomes active as soon as
the mouth opens [50]. Lowe and Sessle demonstrated that the
mouth opening increases the activity of the genioglossus (respon-
sible for tongue protrusion) and the activity is maintained insofar
the mandible remains opened [51]. This response of the genioglos-
715
sus is abolished when the bilateral anesthesia of the TMJ capsule is
performed [52].
These physiological phenomena are essential for mastication
and the intraoral biting just only occurs when there are alterations
on mandibular function. Such alterations may be related to rostral
areas and not to brainstem.
The tongue motor control follows the extrapyramidal traject,
and there is not a monosynaptic connection between the cortex
and the hypoglossal nucleus in primates [53]. Although can be ob-
tained by cortical electrical stimulation, the tongue movements are
accomplished by intermediate relay in various brain structures
that includes the basal ganglia, cerebellum and reticular formation
[54]. Apparently, the mandibular modified position, influenced by
inadequate occlusal contacts, can interfere on the execution of mo-
tor patterns controlled by the basal ganglia, as observed, inducing
an incoordination between mandible and tongue (and/or cheek)
and causing such involuntary biting.
Speech mechanics
Difficulty on speech mechanics, in patients with modified man-
dibular posture, is another motor alteration and rises with more
intensity as loss of velocity on mandibular movement. This is com-
patible with muscle tone increase. In speech kinematics, the man-
dible moves to facilitate the generation of the phonemes and to
sustain tongue movements to produce the vowels [55]. According
to the articulation place, the mandible executes varied movements
of rotation and/or translation. The tongue adopts various positions
to generate the vowels, moving on vertical and sagittal directions.
Thus, there is instantaneous solicitation of jaw muscles tone to
support such tongue displacements.
In patients with altered mandibular motor patterns, the protru-
sive movements manifest more difficulty, especially on the /s/ pho-
neme with the vowel [i:] (e.g. ‘‘SEEm”). In many patients, the sound
‘‘[si:]” is generated with the approach of the canine teeth rather
than the incisors, so deviating the mandible from midline. This lat-
eral deviation is not a necessary movement on phonetics and,
when excessive, constitutes a functional alteration. Another obser-
vable phenomenon is that the lesser protrusive run of the mandi-
ble causes compensatory lip movement (e.g. phoneme/p/), and
lip wrinkle may be noted [56].
Otologic symptoms
Costen in 1934 related the correlation between otologic symp-
toms and the mandibular function [57]. The common related
symptoms are ear pain, tinnitus and aural fullness. Many hypoth-
eses were created to explain this correlation. In the context of this
paper, we will focus our attention on the innervation of the tensor
veli palatini and tensor tympani muscles, both from the trigeminal
nerve. The former is the main responsible for the opening of audi-
tory tube. The latter inserts on the malleus acting on the tympanic
membrane movement.
The presence of the tensor tympani inside the middle ear is ex-
plained by the evolution of the mandible in mammalians. In rep-
tiles, various bones compose the mandible and the joint is
between the articular (mandible) and the quadrate (cranium). In
mammalians, just the dentary bone forms the mandible and the
bones quadrate and articular become the incus and the malleus,
respectively [58]. It is relevant to observe that on the evolutionary
process changes also happened on teeth crown anatomy, with
narrow correlation between the mastication type and occlusal
shape [59].
There are evidences of a double system of muscle fibres in the
tensor tympani, with fast and slow fibres, filling the necessities
of movement and tone [60,61]. The motoneurons that innervate
716 C.R. Douglas et al. / Medical Hypotheses 74 (2010) 710–718
the tensor tympani appear to receive divergent impulses, both
auditory (upper olivary complex) and sensory (trigeminal) and lo-
cated separately from the trigeminal motor nucleus [62,63]. How
much such motoneurons are influenced by the motor alteration
described here remains to be explored.
However, tinnitus appears to be a generic diagnosis, describing
a symptom, but may represent a manifestation with different path-
ophysiology. In some situations, the tinnitus seems to be involved
with jaw muscle problems and responds to occlusal treatment. It
was observed that an increase in tinnitus occurs when the individ-
ual bite with strong force for more than a minute [64]. The occlusal
treatment that corrected the mandibular position in a patient with
otologic symptoms caused the relief of symptoms [65].
Periodontal and teeth reaction
The hypertonic functional state of jaw muscle causes effects on
teeth and periodontium in some individuals [12]. The excessive
force on tooth contact – related as occlusal trauma – is in fact a
muscle action, commanded by the trigeminal motor nucleus. As
the other signs, it is possible to find slight manifestation or large
destruction of the tissues. Patients can show two types of reaction.
One is when the mandible execute rhythmical movements as seen
in bruxism and the characteristic situation is huge occlusal and
incisal wear but with minimal repercussion on periodontal tissues.
The second is when the movements are fewer but a strong bite
force manifests. These dental signs are abrasion, wear facets,
abfraction, and non-accidental tooth or restoration fractures. The
periodontium will show remodeling changes with or without tooth
hypermobility, non-inflammatory bone loss and gingival recession.
These reactions may be considered as allostasis [66–70].
Periodontium presents a dynamic remodeling ability to react to
forces applied on tooth crown. Examples of this physiological abil-
ity are the orthodontic movements and the tooth migration follow-
ing extraction. Not just the tooth movement can be found, but also
hypermobility and widening of the periodontal ligament space
[66]. This phenomenon shall occur by increasing pressure when
excessive forces are delivered to periodontium [71]. The same
forces carried out cause decrease in marginal gingiva blood flow,
due to the tooth displacement [67], presumably facilitating the
incidence of gingival recession in a long lasting condition.
Finite elements study with the application of eccentric occlusal
loads on filled tooth showed increased cervical stress, due to cusp
flexure, especially under lateral forces. This relates to the loss of
dental hard tissue at the cementoenamel junction, known as
abfraction [68]. Excessive occlusal forces interact with chemical
corrosive reactions to cause stress corrosion at tooth cervical re-
gion [72]. This study refers to piezoelectricity – electric charge gen-
erated by deformation of loaded tooth – as a contributing factor to
the dental substance loss. Dental restorative materials may gener-
ate piezoelectric charges and causes pain under mechanical action
of masticatory forces [73]. Hypothetically, the piezoelectric
charges may reach pulp and/or periodontal receptors leading to ac-
tion potentials and causing jaw muscle reflex to avoid these teeth
contact. If true, this event may be a powerful originator of condi-
tioned reflex but investigations on this matter are unknown.
The occurrence of cusp and/or restoration fractures is another
effect of occlusal excessive force caused by hypertonic jaw muscle
condition. Studies report that non-accidental fractures are gener-
ally found with more incidences on lingual lower molars cusps
and buccal upper molars. More fractures are found in molars than
bicuspids and in teeth with restorations [74–76].
Such dental and periodontal adaptive processes appear to be re-
lated to strong muscle force applied on teeth occlusion. Patients
who manifest muscle pain tend to have lesser effects on these tis-
sues. Individuals with robust musculature ordinarily do not evi-
dence painful but hypertonic muscles and more effects on teeth
and periodontium, usually men. This observation explains why
women are thought to be more affecting when the diagnosis tem-
poromandibular disorders are is applied.
Temporomandibular joint tissues response
Adaptive processes runs continuously on TMJ articular tissues.
They relate to the main function of mandible: chewing. Governed
by the intercuspal relation, the changes respond to tooth loss and
food hardness [77]. The articular cartilage becomes, after growth,
an adaptive centre that responds to compressing forces and may
degenerate under overload. Soft diet and loss of occlusal support
caused diminution of cartilage thickness [78]. The TMJ fibrocarti-
lage may degenerate by ageing or by external factors response [79].
The remarkable characteristic of the temporomandibular carti-
lage is its capacity of adaptive remodeling in response to external
stimulation during or after growth [80,81]. The functional adapta-
tion activates chemical physiological processes that act on synovial
membrane, articular cartilage and disc and may lead to degenera-
tive conditions [82].
Anterior disc displacement
Anterior disc displacement has been studied more as a regular
disc out of position than a disc with degenerative alteration [83–
86]. At this point it is necessary to register that the insertion of a
muscle inside a joint is unique in the body and the lateral pterygoid
may be also designated as a discal muscle.
In patients with the motor response described herein, the lat-
eral pterygoid shall present high level of contraction, because the
mandibular positional changes imply in disc–condyle complex
movement. This muscle appears to have a modulator role of on
the closer jaw muscle, since it works in opposition to the jaw clos-
ers resultant force.
An interesting study showed that destabilized and uncoordi-
nated movement of the disc-capsule complex relative to the con-
dyle – presumably under action of the lateral pterygoid – might
result in degenerative disc changes. Such long lasting situations
were related to alterations on disc anterior band, enlargement of
blood vessels and connective tissues close to the lateral pterygoid
fibres insertion and hypertrophy of the synovial membrane. Bun-
dles of elastic fibres are seen in the anterior band going downward
beneath the lateral pterygoid muscle fibres. On an advanced stage
the bulbous shape deformation occurs, shortening of the disc, and
with the anterior part becoming curled up and pulled downward
[87]. The altered mandibular function, in addition to disc deforma-
tion, seems to induce modifications on condyle and articular emi-
nence [88], by the same mechanism that alters those structures
when ageing and/or teeth loss [78], that is, an adaptive process
or allostasis.
Articular sounds
Clicking TMJ is commonly found in patients with altered man-
dibular motor function. Joint clicking is a physiological event re-
lated to articular release of many body joints and is associated
with increased distance between articular surfaces and freedom
of motion [89]. Many theories have tried to explain such occur-
rences and different mechanisms may produce the various sounds
emanated from the TMJ [90]. However, there is not a completely
developed methodology to examine those sounds.
While the mandible moves, the relation between articular
superficies changes, with different concentration of mechanical
stress and dynamic variation of the intra-articular space [91].
 C.R. Douglas et al. / Medical Hypotheses 74 (2010) 710–718
Lateral deviation of the mandible from centric relation and centric
occlusion correlates positively with TMJ sounds [92].
Any fluid presents phase change (liquid to vapor) when submit-
ted to high temperature or low pressure. This characteristic is also
present in synovial fluid. Thereby, negative instantaneous pres-
sures inside TMJ may generate bubbles, a process known as cavita-
tion, or the formation of cavities inside a fluid. A cavitation event
represents the molecular diffusion with the creation of spaces
(void) that concentrate in bubbles; when the void or bubble col-
lapses, a sound occurs. This process appears to explain the cracking
from the vertebral column under manipulation.
In a study with metacarpophalangeal joint cavitation, the pres-
ence of such bubbles was demonstrated [93]. On these joints, how-
ever, an increase between articular surfaces is found after cracking.
On TMJ movements, there is not a joint release, or space creation,
because when the disc moves the internal pressure vary instanta-
neously. Studies about this phenomenon in TMJ are unknown, but
it seems that the cracking sound cannot be credited just to disc
movement, and even the disc participates [94].
Conclusion
The hypothesis presents the new diagnosis stomatognathic mo-
tor adaptive syndrome, structured on pathophysiological basis, for
the problems nowadays diagnosed as temporomandibular disor-
ders. As observed, the manifestations indicate a stomatognathic
motor reaction that induces adaptive changes in several stomato-
gnathic structures.
An appropriate diagnosis is the cornerstone to establish the
adequate treatment. Many improvements will derive from this
new concept. The homogeneity on research samples, the evalua-
tion of treatments currently applied the integrated treatment of
each manifestation, a rationale for new treatments and drugs.
Moreover, the determination of the etiology permits to reject the
assumption that only conservative treatments are indicated, but
the correct and necessary action now can be performed, whatever
it is. In addition, the diagnosis allows differentiating the effects of
systemic diseases, traumatic injuries, central nervous problems,
emotional reactions and drugs from the effects analyzed.
Conflicts of interest statement
None declared.
References
[1] National Institutes of Health Technology Assessment Conference Statement.
Management of temporomandibular disorders. National Institutes of Health
Technology assessment conference statement. J Am Dent Assoc
1996;127(11):1595–606.
[2] Rinchuse DJ, Kandasamy S, Sciote J. A contemporary and evidence-based view
of canine protected occlusion. Am J Orthod Dentofacial Orthop
2007;132(1):90–102.
[3] Douglas CR. Patofisiologia oral: fisiologia normal e patológica aplicada à
odontologia e fonoaudiologia. Säo Paulo; Pancast; 1998.
[4] Klineberg I. Influences of temporomandibular articular mechanoreceptors in
functional jaw movements. J Oral Rehabil 1980;7(4):307–17.
[5] Greenfield BE, Wyke B. Reflex innervation of the temporo-mandibular joint.
Nature 1966;211(5052):940–41.
[6] Clark RK, Wyke BD. Temporomandibular articular reflex control of the
mandibular musculature. Int Dent J 1975;25(4):289–96.
[7] Clark RK. Neurology of the temporomandibular joints: an experimental study.
Ann R Coll Surg Engl 1976;58(1):43–51.
[8] Wyke B. The neurology of joints. Ann R Coll Surg Engl 1967;41(1):25–50.
[9] Kawamura U, Majima T. Temporomandibular-joint’s sensory mechanisms
controlling activities of the jaw muscles. J Dent Res 1964;43:150 (Jan-Feb).
[10] Yan C, Ye L, Zhen J, Ke L, Gang L. Neuroplasticity of edentulous patients with
implant-supported full dentures. Eur J Oral Sci 2008;116(5):387–93.
[11] Fontijn-Tekamp FA, Slagter AP, van’t Hof MA, Geertman ME, Kalk W. Bite
forces with mandibular implant-retained overdentures. J Dent Res
1998;77(10):1832–9.
717
[12] Türker KS. Reflex control of human jaw muscles. Crit Rev Oral Biol Med
2002;13(1):85–104.
[13] Lund JP. Mastication and its control by the brain stem. Crit Rev Oral Biol Med
1991;2(1):33–64.
[14] Byers MR, Dong WK. Comparison of trigeminal receptor location and structure
in the periodontal ligament of different types of teeth from the rat, cat, and
monkey. J Comp Neurol 1989;279(1):117–27.
[15] Capra NF, Dessem D. Central connections of trigeminal primary afferent
neurons: topographical and functional considerations. Crit Rev Oral Biol Med
1992;4(1):1–52.
[16] Redgrave P, Prescott TJ, Gurney K. The basal ganglia: a vertebrate solution to
the selection problem? Neuroscience 1999;89:1009–23.
[17] Grillner S, Hellgren J, Ménard A, Saitoh K, Wikstrom MA. Mechanisms for
selection of basic motor programs – roles for the striatum and pallidum.
Trends Neurosci 2005;28(7):364–70.
[18] Takakusaki K, Saitoh K, Harada H, Kashiwayanagi M. Role of basal ganglia-
brainstem pathways in the control of motor behaviors. Neurosci Res
2004;50(2):137–51.
[19] Korchounov AM. Role of D1 and D2 receptors in the regulation of voluntary
movements. Bull Exp Biol Med 2008;146(1):14–7.
[20] Hikosaka O. GABAergic output of the basal ganglia. Prog Brain Res
2007;160:209–26.
[21] Areso MP, Giralt MT, Sainz B, Prieto M, García-Vallejo P, Gómez FM. Occlusal
disharmonies modulate central catecholaminergic activity in the rat. J Dent
Res 1999;78(6):1204–13.
[22] Douglas CR. Fisiologia do equilíbrio. In: Douglas CR, editor. Fisiologia aplicada
à fonoaudiologia. 2ª ed., Rio de Janeiro: Guanabara Koogan; 2006. p. 170–86.
[23] Ferrario VF, Sforza C, Dellavia C, Tartaglia GM. Evidence of an influence of
asymmetrical occlusal interferences on the activity of the sternocleidomastoid
muscle. J Oral Rehabil 2003;30:34–40.
[24] Karppinen K, Eklund S, Suoninen E, Eskelin M, Kirveskari P. Adjustment of
dental occlusion in treatment of chronic cervicobrachial pain and headache. J
Oral Rehabil 1999;26:715–21.
[25] Funakoshi M, Fujita N, Takehana S. Relations between occlusal interference
and jaw muscle activities in response to changes in head position. J Dent Res
1976;55(4):684–90.
[26] Dawson PE. Evaluation, diagnosis and treatment of occlusal problems. 1st
ed. St. Louis: C.V. Mosby; 1974.
[27] Keshvad A, Winstanley RB. An appraisal of the literature on centric relation.
Part I. J Oral Rehabil 2000;27(10):823–33.
[28] Keshvad A, Winstanley RB. An appraisal of the literature on centric relation.
Part II. J Oral Rehabil 2000;27(12):1013–23.
[29] Keshvad A, Winstanley RB. An appraisal of the literature on centric relation.
Part III. J Oral Rehabil 2001;28(1):55–63.
[30] Michelotti A, Farella M, Gallo LM, Veltri A, Palla S, Martina R. Effect of occlusal
interference on habitual activity of human masseter. J Dent Res
2005;84(7):644–8.
[31] Ingervall B, Egermark-Eriksson I. Function of temporal and masseter muscles
in individuals with dual bite. Angle Orthod 1979;49(2):131–40.
[32] Geering AH. Occlusal interferences and functional disturbances of the
masticatory system. J Clin Periodontol 1974;1(2):112–9.
[33] Okano N, Baba K, Igarashi Y. Influence of altered occlusal guidance on
masticatory muscle activity during clenching. J Oral Rehabil
2007;34(9):679–84.
[34] Selye H. Stress and the general adaptation syndrome. Br Med J
1950;1(4667):1383–92.
[35] McEwen BS, Wingfield JC. The concept of allostasis in biology and biomedicine.
Horm Behav 2003;43(1):2–15.
[36] Budtz-Jørgensen E. Occlusal dysfunction and stress. An experimental study in
macaque monkeys. J Oral Rehabil 1981;8(1):1–9.
[37] Yoshihara T, Matsumoto Y, Ogura T. Occlusal disharmony affects plasma
corticosterone and hypothalamic noradrenaline release in rats. J Dent Res
2001;80(12):2089–92.
[38] Kubo KY, Yamada Y, Iinuma M, Iwaku F, Tamura Y, Watanabe K, et al.
Occlusal disharmony induces spatial memory impairment and hippocampal
neuron degeneration via stress in SAMP8 mice. Neurosci Lett 2007;414(2):
188–91.
[39] Liu ZJ, Yamagata K, Kasahara Y, Ito G. Electromyographic examination of jaw
muscles in relation to symptoms and occlusion of patients with
temporomandibular joint disorders. J Oral Rehabil 1999;26(1):33–47.
[40] Bodéré C, Téa SH, Giroux-Metges MA, Woda A. Activity of masticatory muscles
in subjects with different orofacial pain conditions. Pain 2005;116(1–
2):33–41.
[41] Mintz AH. Buccal separators for relief of TMJ pain and symptoms. Angle Orthod
1988;58(4):351–6.
[42] Kato T, Kawamura Y, Morimoto T. Branching of muscle spindle afferents of jaw
closing muscles in the cat. J Physiol 1982;323:483–95.
[43] Goodwin GM, Luschei ES. Discharge of spindle afferents from jaw-closing
muscles during chewing in alert monkeys. J Neurophysiol 1975;38:
560–71.
[44] Ljubisavljević M, Jovanović K, Anastasijević R. Changes in discharge rate of
fusimotor neurones provoked by fatiguing contractions of cat triceps surae
muscles. J Physiol 1992;445:499–513.
[45] Esbjörnsson-Liljedahl M, Sundberg CJ, Norman B, Jansson E. Metabolic
response in type I and type II muscle fibers during a 30-s cycle sprint in
men and women. J Appl Physiol 1999;87(4):1326–32.
718 C.R. Douglas et al. / Medical Hypotheses 74 (2010) 710–718
[46] Esbjörnsson-Liljedahl M, Bodin K, Jansson E. Smaller muscle ATP reduction in
women than in men by repeated bouts of sprint exercise. J Appl Physiol
2002;93(3):1075–83.
[47] Filippi GM, Errico P, Santarelli R, Bagolini B, Manni E. Botulinum A toxin effects
on rat jaw muscle spindles. Acta Otolaryngol 1993;113(3):400–4.
[48] Freund B, Schwartz M, Symington JM. Botulinum toxin: new treatment for
temporomandibular disorders. Br J Oral Maxillofac Surg 2000;38(5):466–71.
[49] Douglas CR. Fisiologia do equilíbrio. In: Douglas CR, editor. Fisiologia aplicada
à fonoaudiologia. Rio de Janeiro: Guanabara Koogan; 2006. 2ª ed. p. 170–86.
[50] Dubner R, Sessle BJ, Storey AT. The neural basis of oral and facial function. New
York: Plenum Press; 1978.
[51] Lowe AA, Sessle BJ. Tongue activity during respiration, jaw opening, and
swallowing in cat. Can J Physiol Pharmacol 1973;51(12):1009–11.
[52] Lowe AA, Gurza S, Sessle BJ. Excitatory and inhibitory influences on tongue
muscle activity in cat and monkey. Brain Res 1976;113(2):417–22.
[53] Kuypers HG. Some projections from the peri-central cortex to the pons and
lower brain stem in monkey and chimpanzee. J Comp Neurol
1958;110(2):221–55.
[54] Lowe AA. Neural control of tongue posture. In: Taylor A, editor.
Neurophysiology of the jaws and teeth. London: Macmillan Press; 1990. p.
322–68.
[55] Ostry DJ, Munhall KG. Control of jaw orientation and position in mastication
and speech. J Neurophysiol 1994;71(4):1528–45.
[56] Smith A. The control of orofacial movements in speech. Crit Rev Oral Biol Med
1992;3(3):233–67.
[57] Costen JB. A syndrome of ear and sinus symptoms dependent upon disturbed
function of the temporomandibular joint. Ann Otol Rhinol Laryngol, St. Louis
1934;43:1–15.
[58] Crompton AW, Parker P. Evolution of the mammalian masticatory apparatus.
Am Sci 1978;66(2):192–201.
[59] Mills JR. Evolution of mastication. Proc R Soc Med 1972;65(4):392–6.
[60] Fernand VS, Hess A. The occurrence, structure and innervation of slow and
twitch muscle fibres in the tensor tympani and stapedius of the cat. J Physiol
1969;200(2):547–54.
[61] Myrhaug H. The incidence of ear symptoms in cases of malocclusion and
temporo-mandibular joint disturbances. Br J Oral Surg 1964;2(1):28–32.
[62] Keller JT, Saunders MC, Ongkiko CM, Johnson J, Frank E, Van Loveren H, et al.
Identification of motoneurons innervating the tensor tympani and tensor veli
palatini muscles in the cat. Brain Res 1983;4;270(2):209–15.
[63] Friauf E, Baker R. An intracellular HRP-study of cat tensor tympani
motoneurons. Exp Brain Res 1985;57(3):499–511.
[64] Wright EF, Bifano SL. Tinnitus improvement through TMD therapy. J Am Dent
Assoc 1997;128(10):1424–32.
[65] Torii K, Chiwata I. Occlusal management for a patient with aural symptoms of
unknown etiology: a case report. J Med Case Reports 2007;12(1):85.
[66] Ishigaki S, Kurozumi T, Morishige E, Yatani H. Occlusal interference during
mastication can cause pathological tooth mobility. J Periodontal Res
2006;41(3):189–92.
[67] Yamaguchi K, Nanda RS. Blood flow changes in gingival tissues due to the
displacement of teeth. Angle Orthod 1992;62(4):257–64.
[68] Rees JS. The role of cuspal flexure in the development of abfraction lesions: a
finite element study. Eur J Oral Sci 1998;106(6):1028–32.
[69] Miller N, Penaud J, Ambrosini P, Bisson-Boutelliez C, Briançon S. Analysis of
etiologic factors and periodontal conditions involved with 309 abfractions. J
Clin Periodontol 2003;30(9):828–32.
[70] Page RC, Sturdivant EC. Noninflammatory destructive periodontal disease
(NDPD). Periodontol 2000. 2002;30:24–39.
[71] Palcanis KG. Effect of occlusal trauma on interstitial pressure in the
periodontal ligament. J Dent Res 1973;52(5):903–10.
[72] Grippo JO, Simring M. Dental ‘erosion’ revisited. J Am Dent Assoc 1995;126(5).
p. 619–20, 623–4, 627–30.
[73] Sjögren G, Bergman M, Johansson K. Piezoelectricity in dental materials, a
conceivable cause of postrestorative sensitivity. Acta Odontol Scand
1992;50(5):313–9.
[74] Fennis WM, Kuijs RH, Kreulen CM, Roeters FJ, Creugers NH, Burgersdijk RC. A
survey of cusp fractures in a population of general dental practices. Int J
Prosthodont 2002;15(6):559–63.
[75] Bader JD, Martin JA, Shugars DA. Incidence rates for complete cusp fracture.
Community Dent Oral Epidemiol 2001;29(5):346–53.
[76] Eakle WS, Maxwell EH, Braly BV. Fractures of posterior teeth in adults. J Am
Dent Assoc 1986;112(2):215–8.
[77] Hinton RJ. Changes in articular eminence morphology with dental function.
Am J Phys Anthropol 1981;54(4):439–55.
[78] Fanghänel J, Gedrange T. On the development, morphology and function of the
temporomandibular joint in the light of the orofacial system. Ann Anat
2007;189(4):314–9.
[79] Benjamin M, Evans EJ. Fibrocartilage. J Anat 1990;171:1–15.
[80] Shen G, Darendeliler MA. The adaptive remodeling of condylar cartilage–a
transition from chondrogenesis to osteogenesis. J Dent Res 2005;84(8):691–9.
[81] Robinson PD. Articular cartilage of the temporomandibular joint: can it
regenerate? Ann R Coll Surg Engl 1993;75(4):231–6.
[82] Douglas CR, Douglas NA. Patofisiologia geral da articulação Têmporo-
mandibular. In: Douglas CR, Cisternas JR, editor. Fisiologia clínica do sistema
digestório. São Paulo; 2004, p. 333–66.
[83] Bryndahl F, Eriksson L, Legrell PE, Isberg A. Bilateral TMJ disk displacement
induces mandibular retrognathia. J Dent Res 2006;85(12):1118–23.
[84] Orsini MG, Kuboki T, Terada S, Matsuka Y, Yatani H, Yamashita A. Clinical
predictability of temporomandibular joint disc displacement. J Dent Res
1999;78(2):650–60.
[85] Miyawaki S, Tanimoto Y, Inoue M, Sugawara Y, Fujiki T, Takano-Yamamoto T.
Condylar motion in patients with reduced anterior disc displacement. J Dent
Res 2001;80(5):1430–5.
[86] Emshoff R, Jank S, Rudisch A, Bodner G. Are high-resolution ultrasonographic
signs of disc displacement valid? J Oral Maxillofac Surg 2002;60(6):
623–8.
[87] Fujita S, Iizuka T, Dauber W. Variation of heads of lateral pterygoid muscle and
morphology of articular disc of human temporomandibular joint-anatomical
and histological analysis. J Oral Rehabil 2001;28(6):560–71.
[88] Kurita H, Uehara S, Yokochi M, Nakatsuka A, Kobayashi H, Kurashina K. A long-
term follow-up study of radiographically evident degenerative changes in the
temporomandibular joint with different conditions of disk displacement. Int J
Oral Maxillofac Surg 2006;35(1):49–54.
[89] Protopapas MG. Joint cracking and popping: understanding noises that
accompany articular release. In: Protopapas MG, Cymet TC, editor. J Am
Osteopath Assoc 2002;102(5):283–87.
[90] Prinz JF, Ng KW. Characterization of sounds emanating from the human
temporomandibular joints. Arch Oral Biol 1996;41(7):631–9.
[91] Gössi DB, Gallo LM, Bahr E, Palla S. Dynamic intra-articular space variation in
clicking TMJs. J Dent Res 2004 Jun;83(6):480–4.
[92] Egermark-Eriksson I, Carlsson GE, Magnusson T. A long-term epidemiologic
study of the relationship between occlusal factors and mandibular dysfunction
in children and adolescents. J Dent Res 1987;66(1):67–71.
[93] Unsworth A, Dowson D, Wright V. Cracking joints. A bioengineering study of
cavitation in the metacarpophalangeal joint. Ann Rheum Dis 1971;30(4):348–
58.
[94] Manfredini D, Basso D, Salmaso L, Guarda-Nardini L. Temporomandibular joint
click sound and magnetic resonance-depicted disk position: which
relationship? J Dent 2008;36(4):256–60 [Epub 2008 Feb. 13].