Download bruxism, oclussion and tmd

TEMPOROMANDIBULAR DISORDERS AND REFERRED
SYMPTOMATOLOGY: ETIOLOGY, PATHOGENIA AND MANAGEMENT.
Ramirez LM, DDS., MSD., Sandoval GP, MD., MSD., Schames J, D.M.D., James P Boyd, DDS.
Sarra Cushen, BS
The concomitant reciprocity among the temporomandibular disorders and the referred
aural and craniofacial symptomatology is even more evident. The interdisciplinary
management that includes the dentist specialist in craniofacial pain gives major tools to
the medical staff in the conservative phase of these symptoms. This study relates the
temporomandibular disorders patophysiology as a cause and effect of other craniofacial
disorders. Even its therapeutic treatment is suggested, showing a proposal that reveals a
viable explanation of the etiology and pathogeny of the chronical tensional-vascular
headaches and the sustained therapeutic management with a new device that works in the
suppression of perypherical muscular activity.
INTRODUCTION
The aural and craniofacial symptoms have showed to be referred to manifestations of the
temporomandibular disorders (TMD) that can be confused with atypical facial neuralgia and psychogenic
pain due to the close similarity in the symptoms presentations.1 The understanding of the factors that
can generate anatomical and physiological changes in the referred pain behavior must be in advanced to
the diagnostic interpretation of the changes that happen in any pathology.
The TMD are complex pathologies that also have consequences which go from the chewing difficulty and
other oral functions to the acute, subacute and chronical pain. The TMD pain can be primary and
referred and can be expressed as aural symptoms, mialgia, arthralgia in the temporomandibular joint
(TMJ), facial pain, craniosinusal pain and headache.
TMD AND NEUROPHATIC PAIN
The primary and referred pain patterns in TMD depends on the intensity, localization and timing of the
perceived pain stimulus that can generate in its chronical states neurophatic pain in which the
pathophysiology and etiology is not clear and defined yet.2 The neurophatic pain is originated in the
pathological change of nociceptive afferent nervous fibers because of tissue injury generated in the
microtrauma or macrotrauma that produce inappropriate peripherical or central pain signals. 3 Vickers et
al.4 affirm that in chronical pain states there is frequently an involvement of the central nervous system
(CNS) and the perypherical nervous system (PNS) that both together are a dynamic system with a high
repair capacity. The neurophatic pain can be expressed in form of phantom tooth pain even dentate and
edentulous patients, orofacial burning sensation, hyperalgesic-dysestesic pain among other
manifestations that also can generate secondary TMD perpetuating the dysfunctional pain cycle.5,6,7
The relation of TMD in the neurophatic pain can be polemic, however the chronic lesion of minor
peripherical nociceptive nervous trunks and terminals can generate pain of neurophatic form because of
neuroplasticity originated peripherically in the TMJ and muscular mass in presence of macrotrauma,
microtrauma and chronic pain that generate sensitization and plasticity of the CNS.8,9 The mechanical
and chronical lesion of the auriculotemporal nerve in TMJ luxated discs10 can produce neurophatic pain
and autonomic symptomatology.11 The nervous lesion can be initiated from a minor anatomical level as
Willmore et al.12 explain through a studied process known like lipid peroxidation and how free radicals
are produced in the TMJ that happen to inflammatory disorders affecting primary afferent nervous fibers
to take them to a spontaneous ectopic activity and minor threshold pain respond because of perypherical
denervetion.
In the neurophatic pain Dubner and Ren13 propose a neuronal plasticity model in which the central
excitatory effect generates reversible adaptations and long term irreversible changes in CNS receptors
because of the presence of persistent pain. This contributes to the amplification of the perceived pain
and the beginning of the neurophatic pain influenced by pathologic alterations in the peripherical
nervous function. When the muscular dynamics is observed it is difficult to conceive the peripherical
nervous damage through organs that move constantly, however the nervous sensitization can be given
by isquemia and microspasms of little sectors in the squeletical muscles that can catch bordering
nerves.
Johansson and Sojka14 propose a pathophysiologic histochemical peripherical model for the muscle
dysfunction in which the sustained muscular contraction and isquemia sensitizes the muscle spindles and
the peripheric pain terminations due to the liberation of pain and inflammation mediators agents, that
maintain the pain through the increased sensibility to the stretching and relaxing. This high
intramuscular metabolites concentration plus the muscular sustained tension that impedes the normal
blood and oxygen supply converts the reduced peripheric circulation in another factor that contributes to
the TMD due to acidosis, anoxia and muscular fatigue. Mense15 affirms that all nervous lesion that
damages muscular primary afferent neurons involved in the nociception can produce neuropathic
muscular pain that will be extended to the region innervated by these neurons. Even he declares the
signals that converges in a neuron are not always constant because they can be influenced by a
peripheric lesion, then the muscular pain can form new CNS synapses that generate neurophatic pain.
MUSCULAR DYSFUNCTION AND REFERRED PAIN
People with TMD suffer chronic local muscle pain that affects the orofacial muscles and also produce
referred pain that can affect the cervical and the middle ear muscles with a varied symptomatology that
goes from vertigo, tinnitus, otic fullness to headache and neck pain.16,17,18,19,20,21,22,23,24,25,26 The muscle
dysfunction can be influenced in a central or peripherical way. The mialgia can be produced and
maintained in the fatigue and spasm of the chewing and accessory muscles.27 The dysfunction is
produced centrally by central excitatory effect because of a chronic pain or a deep one originated in a
toothache, mialgia, earache or an arthralgia. Peripherically it can be originated in the alteration of the
muscular function by trigger points effect,28,29 also can be originated by inflammation and local lesion.
Finally the muscle dysfunction must be perceived as alterable in the mood state and mental stress.30 The
etiology of the muscle dysfunction implies complex and alternative central and peripherical
mechanisms.31
The trigger points are found in the miofascial pain and are little hipersensitive and tense areas of the
squeletic muscle that involve the fibers, the fascia and the tendon that generates movement restriction
and can be in an active or latent state. The trigger points and the deep pain can develop a central
excitatory effect originated in a peripheric sensitization. The sensorial, motor or autonomic stimulation
depends on the nervous fiber type stimulated by the trigger point. In this way when the afferent nervous
branches are excited the heterotopic referred pain is expressed as mialgias, headaches, earache,
phantom tooth pain, artralgia and other referred symptoms in different zones from the origin of the
chronic pain.32,33,34 If efferent nervous branches are excited, a muscle protective co-contraction, satellite
trigger point and muscle reflex spasms will be provoked,21 these perpetuate the injured muscle state so
its diagnostic is more difficult.33 If the trigger points stimulate autonomous nervous fibers, changes can
be observed in the salivation, tearing, nasal flow, sweating, eye vascularization, muscular tone, heart
rhythm, and produce craneofacial pain included tensional and vascular headaches among others.
The TMD influence and can be influenced in the autonomous nervous system (ANS) function, relates to
the complex regional pain syndrome which the pain is maintained sympathetically. The complex regional
pain syndrome might be an atypical presentation of the miofascial pain according to
Melis et
al.6,11,29,35,36,37,38,39,40,41,42 Storrs11 shows how the mechanical irritation of the auriculotemporal nerve alters
the vasomotor and secretor presentation of the autonomous postganglionic efferent fibers that travel
with this nerve and produce paresthesia, temperature, sweat and color changes in the preauricular skin
in presence of food. This zone is innervated by the auriculotemporal nerve and its symptomatology can
be a presentation of complex regional pain syndrome. Arden et al.43 explain that the minor injury in
muscles, ligaments and soft tissues among other zones can produce sympathetic sustained pain that
makes part of the complex regional pain syndrome.
The pathophysiology of pain and inflammation in the TMD is undoubtless complex and a great amount
of inflammatory mediators interact and are involved in the presentation of this muscle-esqueletic
disorders.
BRUXISM, OCLUSSION AND TMD
The bruxism plays and important role in the TMD and in the referred craniofacial symptoms. Okeson29
considers bruxism as a subconscious microtrauma as a consequence of non-functional teeth grinding and
clenching that can exceed the physiologic and structural tolerance of the muscles, teeth and TMJ. 44 Kato
et al45 support that bruxism is a intense, spontaneous and rhythmic motor manifestation secondary to a
sequence of physiologic changes expressed in the increase of the heart rhythm, motor activity, cortex
activity and respiratory one that can precede the dental clenching or grinding. Catesby Ware and Rugh46
demonstrate how these night bruxistic episodes happen during the REM phase of the sleep and its
cause-effect relation with sleep disorders.45,47
Clark et al.48 found patients who exceeded the maximum conscious teeth clenching intensity during the
night subconscious bruxism phases. The intensity and duration of the clenching generated by the
temporal, internal pterygoid and masseter muscles domain the severity of the grinding which is done by
the external pterygoid muscles.36,37 The bruxism is a perpetual factor and at the same time an initiating
factor of the TMD because the sustained microtrauma and the unchained dysfunction.
Schwartz49 in 1955 affirmed that the cause of the TMD is focused on the muscle tension that is
generated in the subconscious bruxistic states in a way of dental clenching or grinding and emphasized
that the associated pain to the TMD was caused to a muscle with its primary etiologic factor in the
emotional tension. Clark et al.50 found in people with chronic tensional headaches that during the sleep
can exhibit electromyography levels fourteen times more intense in the temporal muscles than the
asymptomatic control group. They suggest that the elevated muscle activity in milagia and arthralgia as
a protective muscle activity can autoperpetuate the dysfunctional and pain presentation, in this way the
motor dynamic function is changed in presence of pain.25,51,52,53
It is still believed that many of the neural conditions that affect the oral motor control in the bruxism are
caused by dental problems as occlusion interferences and loss of the vertical dimension.54 The etiology,
pathogenics and effects of bruxism and their relation with TMD have been studied widely showing the
opposite.55
Greene and Laskin56 have demonstrated that the origin of bruxism is not related to morphofunctional
mechanical alterations as occlusal disharmonies57,58,59 because its primary cause is the psychological
stress and the TMD in a concomitant way. They affirm that the anxiety and depression produce bruxism
and then TMD and insist that these disorders should be understood from an orthopedic, anatomical and
physiologic approach for a true therapeutic handling.
It has traditionally been implied in the etiology of the TMD the association between the occlusal
interferences and the dysfunction.60,61,62,63,64,65 Other studies show a disagreement based on the little
scientific evidence without confirming this relation.19,66,67,68,69,70,71,72,73,74,75,76 However, the investigations
have in common that the muscular dysfunction plays an important etiologic role in the pathogenics of
TMD.77 The TMD have their origin in parafunctional or repeated dysfunctional forces of central origin not
in mastication or swallowing due to the functional contact of the teeth lasts about 17.5 minutes each 24
hours,78,79 which debates the primary cause-effect relationship of the occlusal disharmonies with the
TMD.
It is fundamental to warn that the dental occlusion is not an unique stable position and that is really
determined by the dynamic activity of its perioral environment and the gravity. The influence of the
cervical spine and its corresponding muscles in the masticatory system structures are frequently ignored
and they are given only an antigravitational activity when they also accomplish an important function in
the interarcade dental position. The mandibular position is influenced by the body position in the space,
the different postural changes in the head and neck generate different isolated tonic contractions in the
chewing muscles that are reflected in multiple interdental positions.80
Makofsky81,82 “Sliding Cranium Theory” explains how the changes of atlanto-occipital joint in the head
posture positions are able to produce changes in the muscle contact position and alter the dental
interarcade relation because of the change of the gravitational charge in the chewing muscles. The
craniofacial dynamics and its interarcade dental effect was also emphasized by Libin in his “Cranial
Theory” in which the cranio-mandibular-cervical position and the relation of the different cranial bones
delimited by their movable sutures influence the interarcade dental relation and can be modified in
different positions of the chewing cycle and cervical vertebras disposition in normal physiological
movements.83,84,85 Mohamed et al.86 study the interarcade postural relation in extension and flexion
cranial positions affirming that the head position is considerably dynamic and deserves clinic attention
due to the effects of its posture over the position of muscular and dental contact. Funakoshi et al.,
McLean et al., Goldstein et al., Darling et al., Rocabado et al., support that the cervical posture changes
can affect the mandibular closing trajectory, the mandibular rest or postural position and the chewing
muscle activity.87,88,89,90,91 It must understood the masticatory system as a morphofunctional unit that
integrates every cranio-cervical structure according to the physiological requirements. Manns 92 warns
that the mandibular movements must be developed over stables squeletic bases that fix cranial position
and the hyoid bone through indispensable distant muscles such as the neck and back ones that can act
in the mandibular simplest movements as postural retainers of this movable bone. Wallace et al.93
emphasized as a base the intimae neurological relation between the cranio-cervical structure and the
mandibular posture, influenced by complex muscular reflexes. They explain that the TMD are associated
not only with the relation between the cranium and the mandible, they also include supra and infrahyoid
structures, the cervical-toraxic and at last the lumbar-sacred spine that are related as a biomechanic
unit and can produce cervical pain.
Understanding the above it is comprehended that the mandible and teeth can express their multiple
territories in relation to the body and head situation in several circumstances -standing up, sitting
down, horizontal supine position, horizontal lateral and intermediate ones- in which the cranium
occupies a spatial extended, flexed or combined disposition with their direct effect over the interdental
relation. It must be substantially modified the static occlusion theories which are still worked in the
mechanic of an absolute and fixed maxilo-mandibular position because they are not practical neither
objectively possible. Reflexing and thinking about the postural position or mandibular equilibrium –
where all the functional mandibular movements start and finish – which ideally correspond to a standing
or sitting person sustaining his head in a way that the look targets the horizont, is to dogmatize and
limit the infinite craneofacial dynamics. It is more difficult to imply the mentioned factors in the
understanding of the traditional background of dental occlusion than keeping these philosophies like
paradigms. Is time to open the occlusion fields from a more efficient and physiological focus in which the
posture of the muscle-squeletic craniofacial and cervical complex harmonize and adjust the masticatory
cycle.
The preconceived occlusal concepts are based on specific and absolute morphologic ideals which leave
the individual physiologic needs in a second place.73 Multiple factors as functional- anatomical-structural
abnormalities, the muscular dysfunction induced by stress and deep pain and the articular overload due
to macro or microtrauma domain the horizons of the TMD and leave without clarity the occlusal factors.
The occlusal cause is a co-factor or co-variable of the TMD which mustn’t be overdimensioned or
overtreated. Some occlusal variations can be a consequence more than a cause of the
TMD.22,94,95,96,97,98,99 McNeill affirm that patients can be found totally asymptomatic with occlusal relations
far away from the ideal, in contrast patients with ideal and TMD.54
The masticatory system should have a harmonious relationship among the neuromuscular system, the
dental occlusion and the articulations for a healthy function.100,101,102,103
Patients that present
neuromuscular malocclusion with dental interferences can develop several accommodation degrees,
requiring tonic muscular discharges to allow the new posture or a habitual occlusion.29,54,104,105 These
might result in a dysfunction of the masticatory muscular system caused by the slight occlusal
instability, originated in the interferences; but it has not been possible to prove that it generates either
pain, TMJ dysfunction or bruxism.34,67
The engaged stability by the posterior dental absence can perturb the dynamic balance of the
stomatognatic system due to the components of the articular and muscular stability106 given by the teeth
would be affected in moderate or severely way for the unilateral, bilateral or total absence of these.
Witter et al.107 suggest in a study of short dental arches –without molars- that the occlusal stability in
the masticatory cycle can self-limit and adapt to a new masticatory equilibrium. In parafunction
presence this posterior absence can accelerate the evolving of articular degenerative disorders108 and
craneofacial disorders. Taking into account that the occlusal force magnitude and its linear increase from
anterior to posterior teeth is predictable by the close muscle relationship,109 it can be expected muscular
and articular disorders by major activity, inflammation110,111 or remodeling as a compensatory
mechanism112,113,114 thanks to the higher mechanic charge in dysfunctional activity.29,54,115,116,117
STRESS FISIOPATOLOGY IN DTM
The predisposing and initiating factors of the stress like anxiety, fatigue, rage, fear, frustration and
depression characterize the psychological domain of the TMD and influence its dynamics and the
interpretation of the painful experience.30,35,118,119 kinney et al.120 affirm that the psychological disorders
are the major concomitant factor in the TMD, originating and maintaining them, however Pierce121
affirms that the relation existing among the psychological variables and the dysfunctional expression is
more complex than a simple cause-effect relation motivated by the perceived stress.
Gatchel et al.122 reveal the psychological comorbility in patients with acute and chronic TMD showing how
the anxiety, depression, and the personality alterations domain this disorder in a complex way. They
also sustain that the stress and the psychologic perturbations affect the perception and the pain
behavior, the dysfunction and the treatment effectively. The development of a diagnostic criterion for
TMD that includes psychology status or Axis II of the patients in which the axis I or physic is daily
evaluated, avoid the diagnostic, therapy and prognostic limitants due to the anxiety disorders have an
impact on the TMD symptoms. The physic and psychological factors interact in a dynamic and
convergent way getting the psychological factors influence even cause pain.35, 123,124,125,126,127
Nishioka et al.128 consider the TMD like a psychological disorder and which is the pivotal cause of these
disorders in which an opening of a somatic-motor behavior is produced.
Reacting physiologically to the environmental stimuli, with an excessive muscular and cardiovascular
activity and altered breathing rhythms can prolong the TMD.127,129,130 The prolonged perception of painful
stimuli, such as stress and psychological components are known as some of the biggest activators of the
sympathetic nervous system. This autonomous activation in the limbic and hypothalamic systems is a
normal adaptive mechanism in front of the stress. 131,132
The psychological profile of bruxistic patients shows higher levels of hostility, anxiety, activity and
aggressiveness than psychological profiles of people without bruxism, suggesting a correlation between
the limbic and fusimotor system in bruxism.54 The muscles can be affected by the prolonged sympathetic
activity in its peripheral circulation and muscular tone. These can have the lowest physiologic and
structural tolerance and they will be the first ones in showing symptoms.29 The psychophysiologic
component and the TMD have a strong association.133,134,135 The number of episodes of night bruxism
increases in individuals under stress situations the day before.136
The stress, the dysfunction and the deep pain can alter the CNS in a afferent, efferent and/or
autonomous way. The increased emotional factor rebounds in the muscular function137 because the
centers of the emotion in the brain (reticular system, limbic system and hypothalamus) can influence the
muscular activity.138 The hypothalamus is activated by stress and can activate the intrafusal fibers from
the muscle spindle increasing the gamaefferent activity, sensitizing the muscular spindle that generates
reflex contraction and increased muscular tone. This influences the blood circulation in a negative way
and sustains the mialgic contractile cycle because of the presence of non-eliminated toxic products from
the muscular metabolism.14,22,25,29,35
TRADITIONAL ODONTOLOLIC BOARDING
The odontologic conventional conservative systems or splints, for the decrease of the muscular activity
and articular treatment have been diverse, depending on the type of therapeutic approach and
philosophy that are very vague and difficult to compare in an objective way. Among others, some of the
systems that have been used to treat the muscular disorder are: the occlusal splint, 139,140 hydrostatic
splint,141,142 anterior teeth deprogrammer -Lucia’s inclined plane-.143 These intervene the
mechanoreception caused in the interocclusal contacts, they diminish the muscular activity and modify
the position of the jaw in an more orthopedic and physiologic articular-muscular-ligament relationship,
redistributing and balancing forces on dental and TMJ level.
Dao et al.144 evaluate the therapeutical effects of occlusal splints finding them more as an adjunct
handling of pain for TMD than a definite therapeutic treatment. The conventional occlusal splints
minimize the effects of bruxism on teeth but they do not stop its cause, 140 because even thought it
produces a temporal suppression of the muscular activity in bruxism,145 patients start clenching in few
days with a higher intensity.144 Clark et al.146 sustain that the occlusal splints can affect the night activity
of muscles but not in a consistent and sustained way as time passes by. In the same manner they
sustain that effects are of short term and that the muscular activity can increase or stay invariable in
some patients.80,147
The occlusal splint give an efficient surface for the clenching by bruxism, thanks to a higher quantity of
occlusal contacts in a larger area.108 Ferrario et al.148 show a higher electromyographic activity in
presence of higher quantities of interocclusal contacts.149 An inconvenience of the conventional splints
and the anterior teeth deprogrammer is that the extension of the eccentric movements of the jaw during
grinding surpasses the bording line of the device.136 All the excursive mandibular positions should be
considered when the physician tries to suppress the muscular activity.150 Mandibular movements are not
limited to the interdental position, they also involve other boarding and extraboarding movements by
passive muscular tension limited in the TMJ ligaments.151
NTI-tss BOARDING
Boyd et al.36 discover a system of tensional suppression for nociceptive trigeminal inhibition or NTI-tss
that was developed one decade ago and it is approved by the FDA (510K-K010876) as a device to
suppress the intensity of the muscular pericranial activity in the TMD. This system of muscular
suppression (Photo 1) is a simple modification of the anterior teeth deprogrammer or Lucia's inclined
plane143 that provides support for all the extreme excursive movements of the jaw, avoiding the contact
of canine, premolars and molars in a minimum way; in this way the diurnal and nocturnal muscular
activity will diminish considerably.152
Photo 1- NTI-tss.
The NTI-tss system (Figure 5) takes advantage of the nociceptive arch reflex mechanism present in the
alveolar bone and in the periodontal ligament of the anterior teeth in situations of extreme that affect
the periodental integrity.153,154 The periodontal receptors don’t allow the high muscular contraction when
the pressure on tooth reaches a critic value or threshold generating an afferent discharge. This reflex of
closing inhibition (nociception) diminishes during sleep however keeps preventing the intense muscular
contraction.46,47,54 The system NTI-tss takes advantage in the day time of the protective reflex like a
biological feedback mechanism to stop the bruxism because of in presence of pain for compression of
the anterior teeth this reflex is activated inhibiting the agonist muscular masticatory activity and exciting
the muscles of jaw depression creating the reflex of mandibular opening.155,156
Manns et al.92,157,158,159,160,161 affirm that in anterior teeth the muscular activity inhibition can be controlled
efficiently thanks to the muscle modulatory and protective reflex. This already mentioned to the major
density of mechanoreceptors that the mouth offers in the anterior zone that includes teeth, lips and
periodental ligament. They manifest that the anterior teeth offer a lower sensitive threshold and a higher
biomechanic reception of the occlusal charges compared to the anterior teeth that present a minor
nervous density, a major sensitive threshold and a minor biomechanic perception due to a major root
area that better distributes the forces. The molar zone doesn’t have such fine sensorial functions
because they participate chewing the food with a great force. They show that the muscles generated
forces is greater in the posterior teeth than the anterior ones since the stomatognatic system works like
a class III lever, in this way the transferred pressure to the periodontal ligament of the anterior teeth is
used like an inhibitory feedback mechanism for protecting of non-physiologic charges. These alarm signs
are ruled by perypheric neuromuscular mechanism that prevent to clench beyond of certain threshold of
critic force protecting the morphofunctional integrity of the masticatory system. They explain that the
muscular activity modulation is controlled efficiently in the anterior teeth and it is partially supported in
the TMJ by propioceptors and nociceptors that use common afferent and efferent ways in the brain stem.
The TMJ receptors can modify the stimulation threshold of the motoneurons of the masticatory and
cervical muscles.80
Watanabe et al.162 recently introduced in an experimental way vibrating splints that stop the bruxism for
mechanoreceptive feedback without waking up the patients during sleep, which was an inconvenience
presented in sound feedback splints. This type of splints have an elaborated electro-mechanic device in
researching process. Although this type of device is not available yet, it shows that in the comprehension
of the etiologic factors of the TMD, the tendency is to understand the influence of perypheric sensorial
reception in the modulation of the muscular activity.
Figure 5- a. Anterior contact in the NTI-tss, b. Nociception in the periodental ligament, c. Trigeminal motor nucleus, d. Trigeminal spinal tract nucleus, e.
Inhibitory effect in mandibular closing muscles, f. Excitatory effect in mandibular opening muscles. Figure modified from: James P. Boyd, DDS, Wesley
Shankland, DDS, MS, PhD, Chris Brown, DDS, MPS, Joe Schames, DMD. Taming Destructive Forces. Using a Simple Tension Suppression Device.
PostGranduate Dentistry, November issue, 2000
The NTI-tss offers in a natural way the same mechanical feedback process and at the same time the
nociceptive protector reaction in the peripheral perception of this painful stimulus.161 This physiologic
feedback mechanism optimizes the functioning device lessening the muscular activity in a sustained
way, besides discouraging the bruxing patient over the device because the anterior teeth facing this
adverse biomechanics, activates the flexor protector reflex arch.
This system can be used as a prophylactic treatment in the reduction of the frequency and severity of
the headaches for migraine37 and associated tensional headaches,52,137 diminishing the heterotopic
referred symptoms by the reduction of the parafunctional neuromuscular activity, and the prevention of
the TMD.163
TMD AND HEADACHES
Sympathetically Maintained Spindular Dysfunction Theory
The etiology of headaches is not clear neither well understood, even the headaches study is still a
subjective area. It must be discarded inflammatory origins like an intracranial tumor, Eagle Syndrome,
Carotid Syndrome among other etyologies.29,164,165,166,167,168
The vascular and tensional headaches in TMD are common and highly associated since they share
common nociceptive ways.130,169 Some researches defend the hypothesis in which the tensional and
migraine headaches are two different presentations of the same pathophysiologic mechanism.35,37 The
traditional explanation of migraine as a hemicranial pulsate pain associated to prodrom, visual aura and
vomit is not a frequent form of this disorders. The muscular contraction that happens in the back and
mastication muscles occur either migraines as tensional headaches.170 Takeshima et al.171 warn
according to “Headache Severity Model” that tensional and migraineurs have a continuity and they are
not separate entities although with qualitative differences.172 Mikamo et al.173 suggest that tensional
headaches and migraine have a common etiology and both of them show irregular autonomic activity.
The belief that the migraine is a primary vascular phenomenon -Wolf encephalic vasospasm-174 has been
studied and does not have a firm foundation which has opened the etiology investigation a long time ago
in the relation among these and DTM through the night bruxism because 75 % of the migraine patients
suffer these attacks when they wake up.175,176 It also must be demonstrated that the encephalic vascular
changes are the cause of the symptoms or they are a secondary phenomenon in the migraine
patogenia.177
Moskowitz189 affirms that the trigeminal nerve gives the main afferent conduction in the pathophysiology
and the transmission of headache in humans. The ophthalmic and maxillary branches of trigeminal nerve
innervate the cerebral, cereberal posterior and basilar arteries also the dura and pial arteries, the medial
and anterior fossae. Taking into account that the sensitive cranial and cervical nerves can project pain
signs to the trigeminal nerve -subnucleous caudalis-178,179,180,181, and also to the meningeal arteries, the
dysfunctional peripheric muscular component as a cause of the TMD in the heterotopic pain such as the
tensional and vascular headaches can not be obviated. The chronical peripheral pain signs can be
adverse conditions to the trigemino-vascular neurons that generate alteration in the vascular brain flow
without an unique central origin that initiates the vascular events of these headaches. Hardebo182 explain
how neuron stimulation of the trigeminal nerve in the cornea, iris and around blood vessels derivate
from ciliary and conjunctival arteries cause vasomotor answers in the choroidal artery which increases
the intraocular pressure and the referred pain by effect of central excitation of trigeminal nervous.
Most of the etiologic theories of the migraine now include a trigeminal explanation -vascular, muscular or
cortical- and recognize the muscular tension originated in the pericranial muscles such as the chewing,
neck muscles, and some of them recently found implications in the pathogenia of the cluster headache,
common and classic migraine since a peripheral muscle nociception which start them up.183,184 Olesen et
al.185 offer a common pathophysiologic explanation for the tension headaches and migraines in their
vascular-miogenic-supraspinal model in which integrate isolated explanations of this pathology such as
the trigemino-vascular, muscular and emotional mediated in the descended inhibitory or excitatory
supracortical effect because they use common nociceptive neurons –trigeminal subnucleus caudalis-.
These theories involve the central and peripheral mechanisms in which a central alteration exist in the
pain process generating a hypersensitive state. The implication of emotional factors, the articularmuscular deep pain the bruxism and the deep pain and the peripheral and central vascular changes
become more evident in the etiology of migraines and tensional headaches and they rid of the individual
models which have failed trying to explain the complexity of the clinic characteristics of this
disorder.47,79,186 The treatment strategy for migraines must be multimode which involve all the possible
etiologies.
Migraines affect one of five women and one of twenty men. The epidemiological information of the
tensional headaches is difficult to obtain because there is not an agreement in a precise classification of
this painful craneofacial disorder.187 It is still affirmed that the tensional headaches are not more than a
variant of the migraine.
Boyd et al.188 propose that the chronic tension or spasm of the intrafusal fibers of the skeletal muscular
spindles -trigger points-33 related to TMD is the etiologic factor of tensional headaches and migraines
since they sensitize ANS that innervates the intrafusal fibers.15 The intrafusal spasm, in the squeletic
muscle respond with pain, fatigue and local tension in the cervical and pericranial muscles that sensitize
the muscle nociceptors and autonomic fibers.189,190,191 The ANS dysfunction is important in the
pathophysiology of migraines. The pathology generated by TMD and their corresponding primary,
heterotopic and neurophatic pain are sympathetically maintained by stimulation of the autonomous
muscle component.25 Appel et al.192 describe the clear sympathetic instability that characterize the
migraines. Schor193 affirms that the headaches with vegetative characteristics have a connection with
the tensional and vascular headaches. The brain vascular regulation and the associated symptoms to the
migraine such as nausea, vomit, photophobia, phonophobia, temperature, thirst, sweat, cardiac,
appetite changes, sleep disorders, gastrointestinal and emotional disorders are presented by mayor
autonomic activity.194 Havanka-Kanniainen et al.195,196,197 affirm that the autonomic variations during
headaches are predictable and depend on inter and intraindividually. They also affirm that the failure of
ANS during migraine is mayor that it was believed and involves both the sympathetic and
parasympathetic divisions. The imbalance of the autonomous nervous signals from the muscle squeletic
fiber to the hypothalamus modulated by the serotoninergic activity is a possibility which must be taken
into account. The intrafusal fibers are innervated by the sympathetic nervous system, the conditions that
affect this system such as stress, food, brilliant light, hormonal changes, among others, generate
tension in the intrafusal fibers perpetuating the tensional disorder.198,199,200
ULTRACONSERVATIVE AND CONSERVATIVE THERAPHEUTIC MANAGEMENT
The boarding of these problems should be careful and conservative, 24,201 keeping in mind that the
irreversible treatment of the occlusal instability for interferences or premature contacts would not solve
in a therapeutic way the cause of the TMD and its craneofacial symptoms.139 Not implementing invasive
therapies and adopt an ultra-conservative treatment (NSAIDs,25,34,51,56,202, physical selfregulation,123,203,204 thermal and physical therapy29,35,205), and/or conservative (tensional suppression
system36,37 and selective grinding22,104,105,206,207,208,209) is/are the appropriate handling.210,211 The NSAIDs
can be useful in the initial treatment phase. The NSAIDs direct their action to the peripheral or deep
tissues where the pain is originated and sustained. A pharmacological handling using these drugs has
proved to be helpful in the safe therapeutic guide of the pain management and inflammation on TMD.51
The physic self-regulation can interfere the oral habits and maintain more relaxed muscles, avoiding the
isquemia and accumulation of algesic intramuscular and articular substances.14 Patients must have an
engagement with their physical treatment and with the management of their habits and behavior of their
TMD.66
Reversible therapies should be the first treatment election. Before considering the irreversible occlusal
therapy -crowns, onlays, inlays- as prophylactic treatment for the TMD. The understanding of these
disorders will be developed in a biopsychosocial model2,35,56,76,123,127,201,212,213 fusing the traditional
biomedic model with psychologic, social and behavioral dimensions of the patients due to and important
modulator of the TMD is the stress.209,214 In this way a multidisciplinary close is emphasized and the
traditional mechanical dental concept is avoided.127,215 A special effort must be done to avoid irreversible
therapies based on the clinical conception of an ideal functional relationship.
The NTI-tss system has been studied and approved against conventional splints216 for the successful
control of the pericranial muscular activity, TMD and the prevention of craneofacial pain by migraine. 36,37
In the migraine treatment the muscular component will be regulated by the NTI-tss system. The initial
conservative therapies include NSAIDs and physics theraphy to reduce pain. The elimination or reduction
of factors such as bruxism, inflammation and muscular hyperactivity have a vital importance in any
therapeutic treatment that gives to the body the opportunity of repairing and adapting.
This system suppresses the muscular hyperactivity as an "anterior teeth deprogrammer" but without its
inconveniences, allowing a stable muscle-skeletal position29 reducing the voluntary muscular intensity at
one third of the maximum and not allowing the bruxism through the nociptive reflex arch. 167 The anterior
teeth contacts reduce quickly the muscular pain in TMD because of the significant reduction of the
contractile muscular activity and at the same time the normalization of the peripheral muscular blood
flow.53 The possible TMJ microtrauma is reduced to diminish the muscular activity.54,162,,217,218,219
Williamson and Lundquist220 show electromiographically that the contact in posterior teeth and canines
activate the elevator muscles, depleting the classical belief proposed by D´Amico221 in 1958 in which the
canines contacts inhibited the muscular activity. This could be an important inconvenient if what is
pretended is diminishing the activity in the TMD with a canine guide in an occlusal device.
Nowadays there is a preconceived idea that the systems similar to NTI-tss like the anterior teeth
deprogrammer device caused in short term the extrusion of the teeth that were not in contact with the
device.208 The NTI-tss system should be taken off of the mouth to be able to eat. This daily stimulation of
the teeth during the mastication avoids its supraeruption or extrusion because of stimulation of the teeth
in its alveolus. It is important to mention that this system has been used during ten years without a
single report or clinical finding of dental extrusion.
DISCUSSION
The differential diagnosis is a difficult process where diagnostic error or omission produces treatment
failure. The diagnosis should be made by exclusion, making emphasis in the physical exam.
The goals in handling the TMD are similar to other orthopedic conditions like the reduction of pain,
reduction of an adverse mechanics and the improvement of the function to facilitate the capacity of cure
of the muscle-skeletal system. The TMD treatment protocol must precise over the base if they are
arthrogenic, miogenic, neurogenic or the combination of these. To restore the normal function
propitiating the adaptive and regenerative response to the pathophisiologic process are much more
important than returning the original articular-muscular anatomical morphology.
These raises a question: If the guide investigations to find a primary association between the TMD and
the occlusion do not explain the dental causal primary relationship, then why an intraoral device like the
NTI-tss solves the TMD and craniofacial symptoms therapeutically.
The peripheral neuromuscular mechanisms control and regulate the trigeminal motor units on the base
of a wide sensorial receptor information spectrum that modulates the fusimotor activity that is a final
determinant of the masticatory muscular efficiency. It must be understood that teeth are important in
the modulation of muscular activity in a central way from the peripheral sensitive reception present in
the periodontal ligament, bone, gum, mucous and pulp. The NTI-tss system carries out a central
function starting from an modified peripheral reception in the mechanorecepcion, propiocepcion and
nocicepcion. In the encephalic mass and brain stem, the muscular reflections, the movements controlled
in the central pattern generator and in the cortex lead the muscular activity starting from the peripheral
demands through the stimulation and sensitive mechanic reception to pressure, movement, position,
stretching and pain. The NTI-tss system is peripherically perceived in a different and minimal way without canine, premolar and molar contact- information that is processed in the brain stem and cortex
diminishing the functional-dysfunctional muscular activity and at the the same time the TMD and their
referred craneofacial symptoms. It is already understood that the sustained painful stimulus, the stress
with its emotional component, the muscular trigger points and the sympathetic-parasympathetic
stimulation in the TMJ and muscles activate the ANS. If the dysfunctional variable in the TMJ, muscles,
and deep pain is eliminated, unchained by the present pathology, it is deduced that the NTI-tss system
will also have and noticeable effect on the ANS.
The management of the generated craneofacial pain is sometimes frustrating due to the complexity of its
diagnose. The biopsychosocial factor and the behavior of the acute and chronic pain are on the base of
these disorders. Understanding it in that way is necessary because the meaningful implications over the
treatment success are more evident.
In general it is more difficult to find emotional predisposing factors than finding tangible clinical
discoveries but the therapeutic focus must include the emotional factors exam doing emphasis in the
treatment that involves and consientice the patient in the physical management and the behavior in
relation to his problem.
In the initial TMD management the NSAIDs have shown its effectiveness as analgesic and antiinflammatory agents and using them in the acute states function like an effective therapeutic support in
the treatment. Also the rest of the masticatory system for voluntary reduction of the muscular activity,
the recognition and regulation of the harmful habits and the conscious lifestyle changes that interfere
with the muscular hyperactivity must be implemented.
1
Calhoun KH, MD. Expert guide to otolaryngology. American College of Physicians. Philadelphia, Pennsylvania 2001
Klausner JJ. Epidemilogic of chronic facial pain: diagnostic usefulness in patient care: J Am Dent Assoc 1994, 125:1604-11
3
Dubner R. Topical capsaicin therapy for neurophatic pain. Pain 1991;47:247-8
2
4
Vickers ER. Analysis of 50 patients with atypical odontalgia. A preliminary report on pharmacological procedures for diagnosis and treatment. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod. 1998;85:24-32
5
Delcanho RE. Chronic paroxysmal hemicrania presenting as tootache. J Orofac Pain 1993;7:300-306
6
Kohjitani A.DDS, PhD. Sympathetic activity-mediated neuropathic facial pain following simple tooth extraction: A case report. The J Craniomand
Pract April 2002, Vol 20 (2):135-138
7
Graff-Radford SB.Atypical odontalgia. J Craniomandib Disord Facial Oral Pain 1992;6:260-6
8
Koelbaek JM. Generalised muscle hyperalgesia in chronic whiplash syndrome. Pain 1999;83:229-234
9
Asbury AK. Pain due to peripheral nerve damage: an hypotesis. Neurology 1984;34:1587-90
10
Johansson AS, DDS. A radiographic and histologic study of the topographic relations in the temporomandibular joint region. J Oral Maxilofac Surg
48:953-961, 1990
11
Storrs TJ. A variation of the articulotemporal syndrome. Br J Oral Surg;2:236, 1974
12
Willmore LJ. Iron-induced lipid peroxidation and brain injury responses. Int J Dev Neurosci 9:175, 1991
13
Ren K. Central nervous system plasticity and persistent pain. J Orofacial Pain 13(3):155-163
14
Johansson H, Sojka P. Pathophysiological mechanism involved in genesis and spread of muscular tension in occupational muscle pain and in chronic
musculoskeletal pain syndromes: A hypothesis. Med Hypothesis 35:196-203
15
Mense S. Nociception form skeletal muscle in relation to clinical muscle pain. Pain 1993;54:241-89
16
Shapiro HH, Truex RC. The temporomandibular joint and the auditory function. J Am Dent Assoc 1943;30:1147-1168
17
Myrhaug H. The incidence of the ear symptoms in cases of malocclusion and temporomandibular joint disturbances. Br J Oral Maxillofac Surg
1964;2(July):28-32
18
Schames J, Schames M. Trigeminal Pharyngioplasty: Treatment of the forgotten accessory muscles of mastication which are associated with
orofacial pain and ear symptomatology. American Jouranal of Pain Management Vol.12 No.3 July 2002
19
Candido dos Reis A. DDS, Takami H. DDS. Ear Symptomatology and occlusal factors: A clinical resport. J Prosthet Dent January 2000. Vol 83. 1:
21-24
20
Ciancaglini R, MD,DMD, Loreti P. MD,DMD. Ear, nose and throat symptoms in patients with TMD: The association of symptoms according to
severity of arthropathy. J Orofacial Pain 1994;8:293-297.
21
Campbell CD. Loft GH. TMJ symptoms and referred pain patterns. J Prosthet Dent April 1982 Vol.50(47).Num 4.
22
Bernstein JM. Temporomandibular joint dysfunction masquerading as disease of ear, nose and trhoat. Trans Am Acad Ophthalmol Otolaryngol
1969;73:1208-1217.
23
Eckerdal O. The petrotynpanic Fissure: A link connecting the tympanic cavity and the temporomandibular joint. The J Craniomand Pract. 1991 Vol
9(1):15-21
24
Greene C.S,DDS. The etiology of temporomandibular disorders: Implications for treatment. J Orofacial Pain soportados por evidencia científica Vol
15(2):93-105, 2001
25
Kopp S, DDS, PhD. Neuroendocrine, immune, and local responses related to temporomandibular disorders. J Orofacial Pain 2001;15:9-28
26
Kirveskari P. Association of functional state of stomatognatic system with mobility of cervical spine and neck muscle tenderness. Acta Odontol
Scan 1988;46:281-286
27
Gallo L.M, Salis S:S. Nocturnal Masseter EMG activity of healthy subjects in a natural enviroment. J Dent Res 78(8):1436-1444, August 1999.
28
Gelb H. Tarte J. A two-year dental clinical evaluation of 200 cases of chronic headache: the craniocervical-mandibular syndrome. JADA
1975;91:1230-6
29
Okeson JP, ed. Managment of temporomandibular disorders and occlusion. Ed 4, St. Louis: Mosby,1998
30
Kemper JT Jr.,DMD, Okeson JP, DMD. Craniomandibular disorders and headaches. J Prosthet Dent 1983 May;49(5):702-5.
31
Reid KL. The influence of time, facial side and location on pain, pressure thresholds in chronic miogenous temporomandibular disorders. J Orofacial
Pain, 1994;8:258-265
32
Hellstrom F., Thunberg J. Elevated intramuscular concentration of bradykinin in jaw muscle increases the fusimotor drive to neck muscles in the cat.
J Dent Res 79(10):1815-1822,2000
33
Travell JG, Simons DG: Dolor y disfuncion miofascial. El manual de los puntos gatillo, Mitad superior del cuerpo. Vol 1 Segunda Edición. Editorial
Panamericana 2002.
34
Clark GT.,DDS,MS. A critical evaluation of orthopedic interocclusal appliance therapy: design, theory and overall effectiveness. JADA Vol.108,
March 1984:359-363.
35
Okeson ,J.P.: Orofacial pain. Guidelines for assessment, diagnosis, and management. The American Academy of Orofacial Pain. Quintessence,
Chicago, 1996.
36
James P. Boyd, DDS, Wesley Shankland, DDS, MS, PhD, Chris Brown, DDS, MPS, Joe Schames, DMD.Taming Destructive Forces. Using a
Simple Tension Suppression Device. PostGranduate Dentistry, November issue, 2000
37
Shankland WE. Migraine and tension-type headache reduction through pericranial muscular suppression: a preliminary report. Cranio 2001
Oct;19(4):269-78
38
Melis M. Et al. Complex regional pain síndrome in the head and neck: A review of the literature. J Orofacial Pain 2002;16:93-104.
39
Rubinstein B, DDS. Prevalence of signs and symptoms of craniomandibular disorders in tinnitus patients. J Craniomandib Dis Facial Oral Pain
1990;4:186-192.
40
Jaeger B. Reflex sympathetic distrophic of the face. Report of two cases and a review of the literature. Arch Neurol Vol.43, July 1986: 693-695
41
Khoury R. Facial causalgia: report of case. J Oral Surg 1980;38:782-783
42
Hanowell ST. Phantom tonge pain and causalgia: Case presentation and treatment. Anesth Analg 1979;58:436-438
43
Arden RL. Reflex sympatethic dystrophy of the face: current treatment recommendations. Laryngoscope 1998;108:437-442
44
Major M. A controlled daytime challenge of motor performance and vigilance in sleep bruxers. J Dent Res 78(11):1754-1762, Nov 1999
45
Kato T, Rompre R. Sleep bruxism: and oromotor activity secondary to micro-arousal. J Dent Res 80(10):1940-1944, 2001
46
Ware JC. Destructive bruxism: Sleep stage relationship. Sleep 1988;11:172-181
47
Bailey DR. DDS,FAGD,FADI. Tension headache and bruxism in the sleep disordered patient. The J Craniomandib Pract April 1990, Vol.8(2):174182
48
Clark NG. Bruxing patterns in man during sleep. J Oral Rehabil, 11(2):123-7 1984 Mar
49
Schwartz, L. Laszlo. Pain associated with the temporomandibular joint. J Amer Dent Ass, 51:394-397 (Oct) 1955.
50
Clark GT. Waking and sleeping temporalis EMG levels in tension-type headache patients. J Orofacial Pain 1997;11:298-305
51
Svensson P. Craniofacial muscle pain: Review of mechanisms and clinical manifestations. J Orofacial Pain. 2001;15:117-145.
52
Moss RA,PhD. A structural imbalance/muscular hyperactivity interactional theory of common migraine pain. The J Craniomandib Pract January
1988. Vol.6(1):8788.
53
Nielsen IL, McNeill C, Danzig W, Goldman S, Levy J, Miller AJ. Adaptation of craniofacial muscles in subjects with craniomandibular disorders.
Am J Orthod Dentofacial Orthop 1990 Jan;97(1):20-34z
54
McNeill C, DDS. Science and practice of occlusion. Ed 1. Quintessence Publishing Co, Inc 1997
55
Lavigne G.J, Rompré P.H. Rhythmic Masticatory muscle activity during sleep in humans. J Dent Res 80(2):443-448,2001.
56
Greene CS, Laskin DM. Temporomandibular disorders: Moving from a dentally based to a medically based model. J Dental Res. 79(10):1736-1739,
2000
57
Cacchiottti DA, BS Bianchi P, BS. Signs and symptoms in samples with and without temporomandibular disorders. J Craniomandib Disord Facial
Oral Pain. 1991;5:167-172.
58
Seligman DA, DDS, Pullinger AG,DDS,Msc. Analysis of occlusal variables, dental attrition, and age for distinguishing healthy controls form female
patients with intracapsular temporomandibular disorders. J Prosthet Dent 2000;83:76-82
59
Greene CS,DDS, Marbach JJ, DDS. Epidemiologic studies of mandibular dysfunction: A critical review. J Prosthet Dent August 1982. Vol
48,2:184-190.
60
Katona T.R. The effects of cusp and jaw morphology on the forces on teeth and the temporomandibular joint. J of Oral Rehab, 1989, Vol 16:211-219
61
Watanabe M, Sasaki K. A role of occlusion in the etiology of TMD. Dentistry in Japan. Vol 36:62-65, March 2000
Baba K, PhD,DDS, Yugami K, PhD,DDS. Immediate effect of occlusal contact pattern in lateral jaw position on the EMG activity in jaw-elevator
muscles in humans. Int J Prosthodont 2000;13:500-505.
63
Giannini A.I, Melsen B. Occlusal contacts in maximum intercuspation and craniomandibular dysfunction in 16 to 17 year old adolescents. J Oral
Rehabilitation 1991. Vol.18:49-59
64
Moller B.M. Craniomandibular disorders and masticatory muscle function. Scand J Dent Res 1992;100:32-8
65
Posselt U. DMD. The temporomandibular joint syndrome and occlusion. J Prosthet Dent April, Vol.25(4),1971:432-438
66
McNeill C, DDS. History and evolution of TMD concepts. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997;83:51-60
67
Kahn J,DDS, Tallents R, DDS. Prevalence of dental occlusal variables and intrarticular temporomandibular disorders: Molar relationship, lateral
guidance, and nonworking side contacts. J Prosthet Dent 1999;82:410-5
68
Campbell J, PhD,FDS,DDO. Extension of the temporomandibular joint space by methods derived form general orthopedic procedures. J Prosthet
Dent Vol 7(3). May 1957.
69
Tsukiyama Y, DDS,PhD, Baba K, DDS,PhD, Clark G.T, DDS, MSc. An evidence-based assessment of occlusal adjustment as a treatment for
temporomandibular disorders. J Prosthet Dent, 2001;86:57-66.
70
Greene C.S,DDS. Long-term evaluation of conservative treatment for myofascial pain-dysfunction syndrome. JADA, Vol. 89, December 1.974.
71
Goodman. Response of patients with myofascial pain-dysfunction syndrome to mock equilibration. JADA, Vol 92, April 1.976.
72
Clark GT, DDS, MS. The validity and utility of disease detection methods and of occlusal therapy for temporomandibular disorders. Oral Surg Oral
Pathol Oal Endod 1997;83:101-6.
73
McNeill C.Management of temporomandibular disorders: concepts and controversies. J Prosthet Dent 1997 May;77(5):510-22
74
Roberts CA. DDS. Comparison of internal derangements of the TMJ with occlusal findings. Oral Surg Oral Med Oral Pathol 1987;63:645-50.
75
Magnusson T. Changes in clinical signs of craniomandibular disorders from the age of 15 to 21 years. J orofacial Pain, 1994;8:207-215
76
Greene CS, Mohl ND, McNeill C, Clark GT, Truelove EL. Temporomandibular disorders and science: a response to the critics. J Prosthet Dent 1998
Aug;80(2):214-5
77
Manzione JV, MD,DMD. Internal derangements of the temporomandibular joint. I Normal anatomy, Physiology and Pathophysiology. The Int J
Period and Restor Dentistry.4/1984:9-15
78
Graf H. Bruxism. Dent Clin North America 13:659 1969
79
Molina OM, DDS, MS. Prevalence of modalities of headaches and bruxism among patients with craniomandibular disorders. The J Craniomandib
Pract October 1997, Vol.15(4):314-325
80
Santander H, DDS, Millares R, DDS. Influence of stabilization occlusal splint on craniocervical relationships. Part II: Electromiographic analysis.
Cranio 1994 Oct;12(4):227-233
81
Makofsky H. The effect of head posture on muscle contact position: the sliding cranium theory. Cranio 1989 Oct;7(4):286-92
82
Makofsky HW. A multidisciplinary approach to the evaluation and treatment of temporomandibular joint and cervical spine dysfunction. J
Craniomandib Pract 1989;7:205-213
83
Libin BM. The cranial mechanism: Its relationship to craniomandibular function. J Prosthet Dent 1987;58:632-638
84
Libin B. Cranial-mandibular-cervical therapy. Int J Orthod 1982;20:13-9
85
Libin B. The cranial mechanism and its dental implications. Int J Orthod 1984;22:7-11
86
Mohamed SE. Mandibular reference position. J Oral Rehabil 1985;12:355-367
87
Darling DW. Relationship of head posture and the rest position of the mandible. J Prosthet Dent 1984;52:111-115
88
Goldstein DF. Influence of cervical posture on mandibular movement. J Prosthet Dent 1984;52:421-426
89
Funakoshi M. Relations between occlusal interference and jaw muscles in response to changes in head position. J Dent Res 1976;55:684-690
90
McLean LF. Effects of changing body position on dental occlusion. J Dent Res 1973;52:1041-1045
91
Rocabado M. Physical therapy and dentistry: An overview. J Craniomandib Pract 1982-83;1:47-49
92
Manns A., Diaz G. Sistema Estomatognatico. Sociedad Grafica Almagro Ltda. Universidad de Chile 1988.
93
Wallace C. Management of craniomandibular disorders. Part I: A craniocervical dysfunction index. J Orofacial Pain 1993;7:83-88
94
Moncayo S. y Col. Desordenes Temporomandibulares. 1 Ed, Diciembre 1998. Editorial Graficas Jes.
95
Pullinger A.G, DDS,MSc. Quantification and validation of predictive values of occlusal variables in temporomandibular disorders using
multifactorial analysis. J Prosthet Dent 2000;83:66-75
96
Schellhas K.P, MD, Keck R.J, DDS. Disorders of skeletal occlusion and temporomandibular joint disease. Northwest Dentistry. January-February
1989
97
Mongini F, MD,DDS. Habitual mastication in dysfunction: A computer-based analysis. J Prosthet Dent 1989;61:484-94.
98
Schellas KP, MD. Unstable occlusion and temporomandibular joint disease. J C O Vol.23(5)May 1989
99
Echeverri Enrique, Sencherman Gisela. Neurofisiología de la Oclusion. Ediciones Monserrate. 1ra Edición. 1984
100
Cooper BC, Alleva M. Miofascial pain dysfunction: Analysis of 476 patients. Laryngoscope 1986;96:1099-1106.
101
Dawson P.E,DDS. New definition for relating occlusion to varying conditions of the temporomandibular joint. J Prosthet Dent 1995;74:619-27
102
Hidaka O, Iwasaki M. Influence of clenching intensity on bite force balance, occlusal cantact area, and average bite pressure. J Dent Res
78(7):1336-1334, July 1999.
103
Dos Santos J. Jr. DDS,MS,PD. Vectorial analysis of the static equilibrium of forces generated in the mandible in centric occlusion, group function,
and balanced occlusion relationships. J Prosthet Dent 1991; 65:557-67.
104
Ramfjord S, LDS,MS,PhD, Ash MM, BS,DDS,MS Occlusion, 3rd ed W.B Saunders Company. 1983
105
Dawson PE. Evaluation, diagnosis and treatment of occlusal problems. 2 nd ed.St Louis: CV Mosby Co, 1988
106
Gallo LM. Stress-field translation in the healthy human temporomandibular joint. J Dent Res 79(10):1746, 2000
107
Witter DJ. Occlusal Stability in shortened dental arches. J Dent Res 80(2):432-436, 2001
108
Tallents RH. Prevalence of missing posterior teeth and intraarticular temporomandibular disorders J Prosthet Dent January 2002, Vol. 87, No. 1
109
Mansour RM. In vivo occlusal forces and moments: I. Forces measured in terminal hinge position and associated moments. J Dent Res Jan-Feb
1975, Vol.54(1):115-120
110
Quinn JH, DDS. Pathogenesis of temporomandibular joint chondromalacia and arthralgia. Oral and Maxillofacial Surgery Clinics of North America
Vol.1, No. 1, September 1989:47-57
111
Bewyer DC. Biomechanical and physiologic processes leading to internal derangement with adhesion. J Craniomand Disord: Facial & Oral Pain.
1989;3:44-49
112
Moffett BC. Articular remodeling in the adult human temporomandibular joint. Am J Anat ,115:119-142
113
Beek M. Dynamic properties of the human temporomandibular joint disc. J Dent Res 80(3):876-880, 2001
114
Mongini F. MD,DDS, PhD. Condylar remodeling after occlusal therapy. J Prosthet Dent May 1980 Vol.43(5):568-577
115
Costen , J.B. A syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomandibular joint. Ann Otol 43:1 March
1934:1-15
116
Taddei C. Effects of complete denture waering on temporomandibular joints: A histomorphometric study. J Prosthet Dent 1991;65:692-8
117
Huang Q, Opstelten D. Experimentally induced unilateral tooth loss: Histochemical studies of the temporomandibular joint. J Dent Res 81(3):209213, 2002
118
Goddard Greg DDS. TMD Prevalence in rural and urban native american populations The J Craniomandib Pract APRIL 2002. Vol 20(2):125-128
119
Lobbezoo Frank, DDS, PhD. Topical review: modulation of trigeminal sensory input in humans: Mechanisms and clinical implications. J Orofacial
Pain 2002;16:9-21:9-21
120
Kinney RK. Major psychological disorders in chronic TMD patients: Implications for successful management. J Am Dent Assoc 1992;Oct
123(10):49-54.
121
Pierce CJ. Stress, anticipatory stress, and psichologic measures related to sleep bruxisms. J Orofacial Pain, 1995;9:51-56
122
Gatchel RJ et al. Major psychological disorders in acute and chronic TMD: An initial examination.
123
Molin C. From bite to mind: TMD--a personal and literature review. Int J Prosthodont 1999 May-Jun;12(3):279-88
62
124
Garofalo J. Predicting chronicity in acute temporomandibular joint disorders using the research diagnostic criteria. J Am Dent Assoc 1998;129:438447
125
LeResche L. An epidemiologic evaluation of two diagnostic classification schames for temporomandibular disorders . J Prosthet Dent 1991;65:131137
126
Dworkin SF. Orofacial pain of psycogenic origin: Currents concepts and classification. J Am Dent Assoc 1987;115:565-571
127
Dworkin SF. Perspectives on the interaction of biological, psychological, and social factors in TMD. J Am Dent Assoc 1994;125:856-863
128
Nishioka GJ. Masticatory muscle hyperactivity in temporomandibular disorders : Is it and extrapyramidally expressed disorder?. J Am Dent Assoc
1988;116:514-520
129
Moody PM, Calhoun TC, Okeson JP. Stress-pain relationship in MPD syndromes patients and non-MPD syndromes patients. J Prosthet Dent
1981;45:84-88
130
Pogacnik T, MD,PhD. Autonomic function testing in patients with tension-type headache. Headache 1993;33:63-68
131
Guyton AC, may JE. Textbook of Medical Physiology, ed 9. Philadelphia, PA:Saunders,1996
132
Beaton RD, PhD. Self-reported symptoms of stress with temporomandibular disorders: Comparisons to healthy men and women. J Prosthet Dent
1991;65:289-93.
133
Niemi P, PhD, Le Bell Y. Self-reported symptoms of stress in finnish patients with craniomandibular disorders. J orofacial Pain 1993;7:354-358.
134
Parker MW, DMD. Personality characteristics of patients with temporomandibular disorders: Diagnostic and therapeutic implications. J Orofacial
Pain 1993;7(4):337-344.
135
Weinberg LA, DDS,MS. The etiology, diagnosis, and treatment of TMJ dysfunction-pain síndrome. Part I: Etiology. J Prosthet Dent December
1979. Vol.42 Num 6.
136
Holmgren K. Effect of full-arch maxillary occlusal splint on parafucntional activity during sleep in patients with nocturnal bruxism and signs and
symptoms of craniomandibular disorder. J Prosthet Dent 1993;69:293-7
137
Suk Kim H, DDS. Pain-pressure threshold in the head and neck region of episodic tension-type headaches patients. J Orofacial Pain 1995;9:357364
138
Weiner S, DDS. Electromyofraphic activity in the masseter muscle resulting form stimulation of hypothalamic behavioral. J Orofacial Pain
1993;7:370-377
139
Clark G.T,DDS, Tsukiyama Y,DDS.PhD. Sixty-eight years of experimental occlusal interference studies: What have we learned? J Prosthet Dent
1999;82:704-13
140
Dylina TJ, DDS. A common-sense approach to splint therapy. J Prosthet Dent 2001;86:53945
141
Lerman MD. The hydrostatic appliance: a new approach to treatment of the TMJ pain-disfunction syndrome. JADA Vol 8 December 1974:13431350.
142
Lerman MD. A complete hydrostatically derived treatment procedure for the TMJ pain-disfunction syndrome JADA Vol 89. December 1974. 13511357.
143
Lucia VO. Modern Gnatholoci concepts, Sabt Louis, The C.V.Mosby Co.,1961
144
Dao TTT. The efficacy of oral splints in the treatment of myofascial pain of the jaw muscles: a controlled clinical trial. Pain 1994;56:85-94
145
Okeson JP, Kemper JT, Moody PM. A study of the use of occlusion splints in the treatment of acute and chronic patients with craniomandibular
disorders. J Prosthet Dent 1982 Dec;48(6):708-12
146
Clark GT, et al, Nocturnal electromyographic evaluation of myofascial pain dysfunction in patients undergoing occlusal splint therapy, J Am Dent
Assoc, 99(4):607-11 1979 Oct
147
Gibbs CH, Mahan PE, Wilkinson TM, Mauderli A. EMG activity of the superior belly of the lateral pterygoid muscle in relation to other jaw
muscles. J Prosthet Dent 1984 May;51(5):691-702
148
Ferrario VF. Relationship between the number of occlusal contacts and masticatory muscle activity in healthy young adults. The J Craniomandib
Pract APRIL 2002. Vol 20(2): 91-98
149
Canay S. Abdullah C.Effect of muscle relaxation splint therapy on the electromyographic activities of masseter and anterior temporalis muscles.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 85(6):674-9 1998 Jun
150
Borromeo GL. A comparison of the effects of group function and canine guidance interocclusal device on masseter muscle electromyographic
activity in normal subjects.J Prosthet Dent 1995;74:174-180
151
Koolstra JH, Naeije M. The three-dimensional active envelope of jaw border movement and its determinants. J Dent Res 80(10):1908-1912, 2001
152
Becker Irwin, DDS. Effects of a prefabricated anterior bite stop on electromyographic activity of masticatory muscles. J Prosthet Dent 1999;82:22-6.
153
Yamamura C, Kosugi S, Ono K, Shimada K. Patterns of jaw reflexes induced by incisal and molar pressure stimulation in relation to background
levels of jaw-clenching force in humans. Jpn J Physiol 1993;43(1):87-102
154
Yang J. , Türker K. S. Jaw Reflexes Evoked by Mechanical Stimulation of Teeth in Humans. The Journal of Neurophysiology Vol. 81 No. 5 May
1999:2156-2163
155
Tsai CM, Chiang CY, Yu XM, Sessle BJ. Involvement of trigeminal subnucleus caudalis (medullary dorsal horn) in craniofacial nociceptive reflex
activity. Pain 1999 May;81(1-2):115-28
156
Tsai CM.The caudal subnucleus caudalis (medullary dorsal horn) acts as an interneuronal relay site in craniofacial nociceptive reflex activity. Brain
Res 1999 May 1;826(2):293-7
157
Manns A, DDS, Millares R. DDS. Influence of variation in anteroposterior occlusal contacts on electromyographic activity. J Prosthet Dent 1989
May;61(5):617-23
158
Manns A.,DDS, Rocabado M., RPT. The immediate effect of the variation of anteroposterior laterotrusive contacts on the elevator EMG activity.
Cranio 1993 Jul;11(3):184-191
159
Manns A. Influence of group function and canine guidance on electromiographic activity of elevator muscles. J Prosthet Dent 1987;57:494-501
Manns A. Influence of vertical dimension on masseter muscle EMG activity in patients with mandibular dysfunction. J Prosthet Dent 1985;53:243247
161
Manns A. EMG, bite force, and elongation of the masseter muscle under isometric voluntary contractions and variations of vertical dimension. J
Prosthet Dent 42:674, 1979
160
162
Watanabe T., DDS,PhD. A vibratory stimulation-based inhibition system for nocturnal bruxism: A clinical report. J Prosthet
Dent. Vol.85(3) March 2001
163
Shankland W. Data from clinical trials observing the effects of the NTI-tss vs. a full-coverage occlusal splint on medically
diagnosed migraine and tension-type headache. (submitted for publication, June 2001). Public Internet Information.
164
Eagle WW. Symptomatic elongated styloid process. Arch Otolaryngol 49:490, 1949
Eagle WW. Elongated styloid process: Further observations and a new syndrome. Arch Otolaryngol 47:630, 1948
166
Eagle WW. Elongated styloid process: Report of two cases. Arch Otolaryngol 25:584, 1937
167
Eagle WW. Elongated styloid process: Symptoms and treatment. Arch Otolaryngol 67:172, 1958
168
Baddour HM. Eagle’s Syndrome. Oral Surg 1978;46:486-494
169
Lipchik GL. Central and peripheral mechanisms in chronic tension-type headaches. Pain 64(1996)467-475.
170
Raskin NH. On the origin of head pain. Headache 1988; 28:254-257
171
Takeshima T. The relationship between muscle contraction headaches and migraine. A multivariate analysis study. Headache1988;28:272-277
172
Featherstone HJ. Migraine and muscle contraction headaches: a continuum. Headache 1985;25:194-198
173
Mikamo K. Cardiovascular sympathetic hypofunction in muscle cantraction headache and migraine. Headache 1989;29:86-89
174
Moskowitz MA. Neurobiology of vascular head pain. Ann Neurol 1984;16:157-168
165
175
Steele JG. Occlusal abnormalities, pericranial muscle and joint tenderness and tooth wear in a group of migraine patients. J Oral Rehabil
1991;18:453-458
176
Ruff GA. Common migraine; a review and proposal for a non-vascular aetiology. J Oral Rehabil 1986;13:499-508
177
Bittar G. A retrospective study of patients with cluster headaches. Oral Surg Oral Med Oral Pathol 1992;73:519-25
178
Sessle BJ, Hu JW. Convergence of cutaneous, tooth pulp, visceral, neck and mussle afferents onto nociceptive and non-nociceptive neurons in
trigeminal subnucleus caudalis (medullary dorsal horn) and its implications for refered pain. Pain 1986;27:219-235
179
Sessle BJ. Acute and chronic craniofacial pain: Brain stem mechanism of nocicptive transmission and neuroplasticity and their clinical correlates.
Crit Rev Oral Biol Med 2000;11:57-91
180
Sessle BJ. The neurobiology of facial and dental pain, present knowledge, future directions. J Dent Res 1987;66:962-81
181
Sessle BJ. The neural basis of temporomandibular joint and masticatory muscle pain. J Orofacial Pain 1999;13(4):238-245
182
Hardebo JE. The involvement of trigeminal substance P neurons in cluster headache and hypotesis. Headache 1984;24:294-304
183
Dunn GF. Anatomical observation of a craniomandibular muscle originating from the skull base: The sphenomandibularis. The J Craniomandib
Pract April 1996, Vol.14(2):97-103
184
Shankland WE. The “Pre-Anterior Belly” of the temporalis muscle: A preliminary study of a newly described muscle. The J Craniomandib Pract
April 1996, Vol.14(2):106-112
185
Olesen J. Clinical and pathophysiological observations in magraine and tension-type headache explained by integration of vascular, supraspinal and
miofascial inputs. Pain 1991;46:125-132
186
Sakai S, Clark GT. Stress pain and temporalis muscle EMG in temporal headache subjects (ABSTRACT 347). J Dent Res 1989;68:225
187
Ochoa Amaya G, MD. Dolor craneofacial. 1996. Gente Nueva Editorial, Bogota Colombia.
188
Boyd JP. Sympathetically maintained spindular dysfunction : A hypothesis for the etiology of chronic tension-type headache and migraine. (Public
Internet Information).
189
Jensen R. Muscle tenderness and pressure pain thresholds in headache. A population study. Pain 1993;52:193-200
190
Jensen R. Mechanisms of spontaneous tension-type headaches: An analysis of tenderness , pain thresholds and EMG. Pain 1996;64:251-256
191
Bovim G. Cervicogenic headache, migraine and tension type headache. Pressure threshold measurements. Pain 1992;52:169-173
192
Appel S. Evidence for instability of the autonomic nervous system in patients with migraine headache. Headache 1992;32:10-17
193
Schor DI. Headache and facial pain: the role of the paranasal sinuses-A literature review. J Craniomandib Pract 1993;11:36-49
194
Arena JG. The role of personality in the etiology of chronic headaches. Headache 1985;25:296-301
195
Havanka-Kanniainen H. Autonomic dysfunction in adult migraineurs. Headache 1986;26:425-430
Havanka-Kanniainen H. Autonomic dysfunction in migraine: A survey of 188 patients. Headache 1988;28:465-470
197
Havanka-Kanniainen H. Cardiovascular reflex responses during migraine attack. Headache 1986;26:442-446
198
Marcus D. Interrelationships of neurochemicals, estrogen and recurring headache. Pain 1995;62:129-139
199
Isselee H. et al. Pressure-Pain threshold variation in temporomandibular disorder myalgia over the course of the menstrual cycle. J Orofacial Pain
2002;16:105-117
200
Dao TTT. et al. Gender Diferences in pain. J Orofacial Pain 2000;14:169-184
201
McNeill C.Paradigm shift. J Orofac Pain 1996 Winter;10(4):293-4
202
Dionne RA, Khan AA, Gordon SM. Analgesia and COX-2 inhibition. Clin Exp Rheumatol 2001 Nov-Dec;19(6 Suppl 25):S63-70
203
Carlson C,MA,PhD, Bertrand P.M, BS,DDS. Physical self-regulation training for the management of temporomandibular disorders. J Orofacial
Pain 2000;15:47-55.
204
Carlson C,MA,PhD, Okeson J.P, DMD. Stretch-based relaxation and the reduction of EMG activity among masticatory nuscle pain patients. J
Craniomandib Disord Facial Oral Pain. 1991;5:205-212.
205
Hodges J. Managing temporomandibular joint syndrome. Laryngoscope 1990;100:60-66
206
Garefis P,DDS,PhD. Effectiveness of conservative treatment for craniomandibular disorders: A 2-Year longitudinal study. J Orofacial Pain
1994;8:309-314.
207
Kerstein RB, DMD. Treatment of myofascial pain-dysfunction syndrome with occlusal equilibration. J Prosthet Dent 1990;63:695-700.
208
McHorris WH, BS,DDS,FACD. Occlusal adjustment via selective cutting of natural teeth. Part I. The Int. J Perio and Rest Dent. 5/1985:9-24
209
Eversole LR. Temporomandibular joint internal derangements and associated neuromuscular disorders. J Am Dent Assoc 1985:110:69-79
210
Arbree N.S, DDS, Campbell S.D, DDS,MMSc. A survey of temporomandibular disorder conducted by the Greater New York Academy of
Prosthodontics. J Prosthet Dent 1995;74:512-6.
211
Stiesch-Scholz M. Medical and physical therapy of temporomandibular joint disk displacement without reduction. The J Craniomandib Pract
APRIL 2002. Vol 20(2):85-90
212
Reade P.C, MDS, MDSc,PhD. An approach to the management of temporomandibular joint pain-dysfunction syndrome. J Prosthet Dent January
1984. Vol 51(1):91-96
213
Engel GL. The need for a new medical model: A challenge for biomedicine. Science 1977;196:129-136.
214
McNeill C, Mohl ND, Rugh JD, Tanaka TT. Temporomandibular disorders: diagnosis, management, education, and research. J Am Dent Assoc
1990 Mar;120(3):253-263
215
Takai A, DDS, Nakamo M, DDS. Influence of occlusal force and mandibular position on tooth contacts in lateral excursive movements. J Prosthet
Dent 1995;73:44-8.
216
Lamey PJ. Migraine: The effect of acrylic appliance design on clinical response. Br Dent J 1996:180(4) Feb:137-140
217
Long JH, DDS. Interocclusal splint designed to reduce tenderness in lateral pterygoid and other muscles of mastication. J Prosthet
Dent.1995;73:316-8.
218
Kerstein RB. Electromyographic and computer análisis of patients suffering from chronic myofascial pain-dysfunction syndrome: Before and after
treatment with immediate complete anterior guidance development. J Prosthet Dent 1991;66:677-86.
219
Wood WW, DDS.EMG response to alteration of tooth contacts on occlusal splints during maximal clenching. J Prosthet Dent 1984 Mar;51(3):3946
220
Williamson EH, Lundquist DO: "Anterior guidance: its effect on eletromyographic activity of the temporal and masseter muscles" J Pros Dent
49:816,1983
221
D’Amico, A. The canine Teeth – Normal functional relation of the natural teeth of man . J Southern Calif Dent Assoc 261:198,1958.
196