Temporomandibular disorders and referred symptomatology: etiology, pathogenia and management

Download 226.81 Kb.
Date conversion02.12.2016
Size226.81 Kb.
1   2   3


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. Manns92 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
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
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


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


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 articular-muscular 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
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 self-regulation,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.
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 anti-inflammatory 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

2 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

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

7Graff-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):174-182

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

59Greene 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

62 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. 2nd 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):209-213, 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

124 Garofalo J. Predicting chronicity in acute temporomandibular joint disorders using the research diagnostic criteria. J Am Dent Assoc 1998;129:438-447

125 LeResche L. An epidemiologic evaluation of two diagnostic classification schames for temporomandibular disorders . J Prosthet Dent 1991;65:131-137

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;9:357-364

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 1974:1343-1350.
1   2   3

The database is protected by copyright ©dentisty.org 2016
send message

    Main page