| Abstract|| |
Disk displacement of the temporomandibular joint (TMJ) is a clinically important condition, showing a high prevalence in both patient and non-patient populations. Despite its clinical importance, there is incomplete understanding of the etiopathogenic mechanisms leading to disk displacement. A number of possible risk factors have been identified. This article analyzes the etiopathogenesis from both the clinical and the biomechanical viewpoints and also reviews the literature on the association between disk displacement and the main risk factors (i.e., trauma, altered disk shape and/or dynamic properties, occlusal abnormalities, steepness of the articular eminence, hyperactivity of the lateral pterygoid muscle, joint hypermobility, etc.). According to our interpretation of available data, an impairment of joint lubrication may be a common finding in cases of disk displacement, thus suggesting the need for future studies addressing both local and systemic neuroendocrine aspects influencing the friction coefficient of the TMJ. A full comprehension of the etiopathogenesis of disk displacement is far from being achieved, and clinicians must take into account this consideration when treating patients with temporomandibular disorders.
Keywords: Disk displacement, etiopathogenesis, temporomandibular disorders, temporomandibular joint
|How to cite this article:|
Manfredini D. Etiopathogenesis of disk displacement of the temporomandibular joint: A review of the mechanisms. Indian J Dent Res 2009;20:212-21
Disk displacement of the temporomandibular joint (TMJ) was recognized as a clinically relevant problem more than a century ago.  Since then, there has been much research aimed at understanding the condition better, with attention mostly focused on the possible clinical and biomechanical consequences of disk displacement; relatively less attention has been paid to the etiopathogenic mechanisms.  Due to this, the factors involved in causing an abnormal disk position have not yet been fully understood.
|How to cite this URL:|
Manfredini D. Etiopathogenesis of disk displacement of the temporomandibular joint: A review of the mechanisms. Indian J Dent Res [serial online] 2009 [cited 2013 May 18];20:212-21. Available from: http://www.ijdr.in/text.asp?2009/20/2/212/51365
The present work is an overview of the current concepts regarding the etiopathogenesis of TMJ disk displacement. To get up-to-date information, an electronic search of the Medline database was performed to identify relevant English-language, peer-reviewed articles published before May 2006; the key terms used were: 'temporomandibular joint disk,' 'temporomandibular joint disk displacement,' 'temporomandibular joint disk displacement pathogenesis,' and 'temporomandibular joint disk displacement risk factors.'
| Biomechanics of the TMJ|| |
The articular disk has a biconcave shape, with a 2 mm thick anterior band and a 2.7 mm thick posterior band separated by a subtle (1.0-mm thick) intermediate zone. Histologically, the articular disk is a fibrocartilaginous structure constituted of dense connective tissue, with a few stratified chondrocytes. The extracellular matrix is made up of fibers of type I and II collagen with a peculiar distribution: fibers of the anterior and posterior bands are transversely (mediolaterally) oriented, and cross through those of the intermediate band, which are mainly sagittally oriented.  Elastic fibers are present in all areas of the disk, though mainly in the anterior and medial portions. 
In the closed-mouth position, the posterior band of the disk is located over the cranial portion of the condyle, the thinner intermediate band is positioned between the ventro-cranial profile of the condyle and the articular tubercle, and the anterior band lies in front of the condyle. ,,
The disk-condyle attachment is constituted both medially and laterally by transversely oriented collagen fibers of the posterior and anterior bands. From a biomechanical viewpoint, the retrodiscal area, the capsule, the medial and lateral ligaments, and the lateral pterygoid muscle are fundamental structures in the complex physiopathology of the disk-condyle relationship.
The retrodiscal area, commonly termed the bilaminar area,  fills up the dorsal area of the TMJ and is made up of a superior layer containing elastic and collagen fibers, fat, and vessels and an inferior layer of dense collagen fibers. Some authors have also described a vascular area composed of many vessels, fat, and nerves between the two main layers. In the open-mouth position, the vascular area fills with blood, rapidly increasing in volume. 
Collagen fibers of the bilaminar area are poorly organized and sagittally oriented; they connect with the posterior band of the disk, crossing the transverse fibers of the posterior band and the sagittal ones of the intermediate area. 
The superior layer of the bilaminar area is attached dorsally to the glenoid process, to the bony/cartilaginous structures of the acoustic meatus, and to the parotid. However, the insertion is characterized by considerable variability. 
The inferior layer is attached to the posterior part of the condyle and, according to most authors, it is fundamental for the stabilization of the disk position over the condyle, so much so that an excessive stress to this area has been postulated to be a cause for anterior disk displacement. ,
The articular capsule is a thin fibrous structure covering the joint. Capsular abnormalities may be risk factors for disk displacement, but this possibility needs to be further studied in view of the fact that anatomical studies have described many different types of condylar attachment.  The main function of the capsule is presently considered to be lubrication of the joint via secretion of synovial fluid, which is essential for the maintenance of a low friction coefficient during jaw movements. ,
The disk divides the articular cavity into two different cavities-the superior and the inferior-that are characterized by different friction coefficients. In the inferior part of the joint, i.e., the disk-condyle complex, only rotation movements are normally allowed; in the superior area, made by the articulation of the disk-condyle complex with the posterior part of the articular tubercle, only translation movements are normally allowed.
According to some authors, such differences might suggest that the TMJ is actually made up of two different joints, the temporodiscal and the disk-condylar ones,  which would be in accordance with the hypothesis that the TMJ originates from a twofold blastoma.  This hypothesis also suggests that each of the two parts of the TMJ complex has its own capsule. It might also explain some morphological and functional observations, such as the presence of blood vessels and nerves behind the capsule but not within it, and the attachment of the superior belly of the lateral pterygoid muscle to the disk, without a capsular involvement. A similar TMJ complex is also seen in other mammals. 
During the translation cycle of the jaw opening movement there is a combination of a rotation in the disk-condyle complex, with the condyle turning forward over the inferior concavity of the disk and the disk turning backward over the condyle, and a translation in the superior compartment, with the whole complex moving forward over the articular tubercle.  During this phase, the disk is stabilized by the condyle working in a ventro-cranial direction against its thinner intermediate band.
Previously, it has been suggested that the superior band of the lateral pterygoid muscle may drag the disk forwards, so hypothesizing that a lateral pterygoid hyperactivity was the main risk factor for disk displacement. ,, Actually, the biological plausibility of this hypothesis is still much debated, since most fibers of the superior band of the lateral pterygoid muscle are attached to the condylar neck and only a few fibers are attached directly to the posterior band of the disk. ,,,, Moreover, the superior band of the lateral pterygoid does not seem to be active during jaw opening; it advances passively in response to the activation of the inferior band.
The backwards rotation of the disk over the condyle is allowed by the properties of the superior layer of the bilaminar area, which belongs to the posterior attachment. This structure is elastic and is relaxed both in the resting position and in the closed-mouth position, becoming active only during the advancing phase of the translation cycle, when it retracts the disk backwards over the condyle.
As for the jaw closing movement, the most plausible mechanism explaining the posterior shift of the disk is condylar traction. In both opening and closing phases, the condylar excursion is wider and more rapid than the disk shift. This means that the disk, which during the closing phase is also subjected to a backwards traction due to the posterior attachment, must be held back by some forces acting in the opposite direction. Such braking forces are mainly provided by the masseter and the lateral pterygoid muscles, which are more active during the closing phase and, due to the characteristics of their insertions, are suitable to hold back the disk. Considering that the friction coefficient of the normal TMJ is quite low and similar to that of other joints, the intensity of the braking forces is also actually low, just sufficient to counteract the retrusive tension caused by the posterior insertion. When the condyle reaches its position under the disk, it drags the disk backwards passively, thanks to the concave shape of the disk.  According to this hypothesis, a disk which has lost its normal biconcave shape cannot be dragged, so abnormal disk morphology could be an important pathogenic factor for displacement during the translation phase of the closing movement.
An important contribution to disk stabilization during the final condylar rotation is provided by the inferior layer of the bilaminar area, whose stiffness counteracts a ventrally oriented force that is exerted on the disk in this phase.  For this reason, a stretching of the inferior layer of the bilaminar area, with or without flattening of the posterior band of the disk, is considered by many as an essential precondition for an anterior disk displacement. 
Normally, no shifts between the disk and the condyle are allowed to happen, thanks to the strong discal attachment to the condyle, which is reinforced both at the medial and the lateral poles by the TMJ ligaments. Like other ligaments, TMJ ligaments are nonelastic, only allowing a passive forwards-backwards movement of the whole disk-condyle complex. Another factor that prevents a disk-condyle shift is the biconcave shape of the disk, the maintenance of which is fundamental to its 'self-seating' capability.
| Definition and Epidemiology of Disk Displacements|| |
The use of the term 'disk displacement' implies the existence of a previous 'normal' or 'physiological' disk position. The correct relationship between the disk, the condyle, and the articular tubercle has been defined as the position that in the magnetic resonance (MR) imaging obtained with parasagittal projections is commonly known as the '12 o'clock position,' in which the posterior band of the disk is located over the cranial portion of the condyle.  This radiological criterion is based on the belief that disk positions other than '12 o'clock' are clinically appreciable due to the presence of typical 'click' noises, which indicate disk displacement. Actually, it has been shown that joints with a disk position which should be considered abnormal according to the '12 o'clock' criterion are asymptomatic in some cases. Therefore a strict observance of this definition easily leads to overestimation of the prevalence of disk displacement.  Based on these considerations and the existence of some discrepancies between clinical examination and the post-mortem observations in the assessment of the prevalence of an anteriorly positioned disk, it has been suggested that a distinction should be made between the concepts of 'disk displacement' and 'anterior disk position.' The latter term should indicate a physiological condition; [32,33] however, there are no reliable criteria by which one can accurately diagnose these conditions or discriminate between them.
Along with such taxonomic difficulties, reflected in the number of different terms adopted by various authors to indicate disk displacement, there are several other methodological shortcomings that make it hard to draw conclusions on the epidemiology of disk displacement based on the existing literature data. First of all, only a few studies have been done on large samples. ,,,, Moreover, most studies that have used MR imaging for evaluating disk position used only the sagittal projection; in fact, to the best of our knowledge, there are no epidemiological studies about the variability of disk position that have considered the localization of the sagittal tomograms on a mediolateral level.
Such limit is important if one considers the occurrence of a disk which is displaced on a mediolateral level only. This condition, termed 'partial displacement,' has also been described in the literature and its prevalence should not be underestimated.  Similarly, the possibility of a combination of disk displacement and rotation has also been recently emphasized. ,
Another concern is the high prevalence of asymptomatic disk displacements shown by some previous studies.  Numerous researches with autoptic, radiographic, and physical examination have shown abnormal disk positions in about 30% of asymptomatic subjects, thus supporting the hypothesis that an anterior disk position could be associated with a clinically silent joint and could therefore be considered a normal variation. ,,,
These observations, along with data reporting a higher prevalence in older subjects, made some authors suggest that disk displacement could be considered a physiologic process that increases with ageing.  According to this viewpoint signs such as a 'click' noise (in the absence of symptoms) could be considered a normal characteristic.  If one accepts these as 'normal variations,' disk displacement appears to be a much less frequent condition than is usually believed.
Otherwise, according to literature data, disk displacement has been found in about two-thirds of the patients requiring treatments for signs and symptoms related to the masticatory system.  In particular, studies investigating the prevalence of disk displacement in patients with painful joints reported a prevalence of 77-94%. ,, The incidence of painful disk displacements has a peak during the puberty: The risk for this condition in teenagers is four times higher than in older subjects. 
As regards asymptomatic subjects, the prevalence of MR-depicted disk displacement is about 6% in childhood,  about 34% in adolescence,  and 31-34% in adulthood. , Such high prevalence of disk displacement in asymptomatic joints made some authors suggest that this condition could represent a normal congenital anatomic variation.  On the other hand, a study on a sample of 60 TMJs of infants and children revealed no cases of displacement, which led the authors to claim that this is an acquired condition. 
Researches on autopsy specimens have shown that anteriorly positioned disks could also have a component of medial or lateral displacement. ,,, This introduced the concept of a disk undergoing an anteromedial or an anterolateral rotation.  One study investigating the variability of disk position on the various medial, central, and lateral levels, pointed out the tendency to a more anterior disk position in the more lateral tomograms of MR, both in asymptomatic subjects and in patients with painful disk displacement. 
| Tissue Modification in the Course of Disk Displacement|| |
Some researches have revealed that a more anterior disk position can excite several reactions in the discal and the retrodiscal tissues. , In particular, the adaptation capability of retrodiscal tissues in the case of an altered disk position makes it possible for them to assume a 'disk-like' function.
In the case of a chronic disk displacement, the anterior band can show atrophic signs or can bend down over the intermediate zone, while the posterior band tends to flatten and lengthen. Among the reactions in the retrodiscal tissues, an increase in fibrous connective tissue and a decrease in innervation and vascularization can be observed.
One interesting study showed that the mechanism of volumetric compensation provided by the retrodiscal tissues to balance intra-articular pressure during mandibular movements seems to remain intact even in the presence of a displaced and degenerated disk; this is because adaptive changes occur mainly in the anterior part of the retrodiscal tissues. 
In a postmortem histometrical study on 53 joints, a more anterior disk position was associated with an altered volume of the inferior synovial cavity; the superior cavity seemed to be less influenced. 
In a study in which the histological changes related to a more anterior disk position were assessed, it was found that degeneration of condylar and glenoid fossa surfaces seem to be age related and not to be influenced by the disk position. 
Another study revealed that morphological alterations of the disk's inferior surface were more frequent than those of the superior one. Moreover, no relationship between irregularities of the articular surface and disk position was described, even though the presence of a disk perforation was found mostly in joints with a displaced disk. 
According to some authors, such changes are an expression of a physiological adaptation to the increased load,  whereas others suggest that they represent pathological reactions to an altered load vector.  However, the same alterations were also found in elderly subjects, independently of the disk position,  and were not found in young subjects in joints with a more anterior position. , This suggests that changes in the retrodiscal tissues might be age related.
| Etiology of Disk Displacement|| |
According to some recent observations on TMJ friction, a joint with a physiologic disk-condyle relationship has an effective intra-articular lubrication mechanism that keeps the articular friction coefficient low.  An increase in the articular friction has been implicated as a cause of disk displacement. An excessive friction coefficient may reduce the fluency of movements and thus facilitate the onset of the complex processes leading to disk-condyle relationship alterations.
An increase in the friction coefficient may be the result of a series of events. For example, most cases of disk displacement seem to be related to chronic (microtrauma) or acute injuries (macrotrauma) directed against the TMJ.  Such trauma can cause the onset of the pathologic event only if it acts on a perturbed system and/or in a system presenting one or more predisposing factors for disk displacement. The presence of a disk with an altered shape and/or dynamic properties, some occlusal abnormalities, a steep articular eminence, hyperactivity of the lateral pterygoid muscle, and joint hypermobility have all been proposed as risk factors for disk displacement in the literature.
| Trauma|| |
Among the acute injuries, macrotrauma caused by an external source that provokes damage to the TMJ are often considered to be a risk factor for disk displacement. Among these are, for example, a strong blow to the mandible, a whiplash injury, or mandibular hyperextension. The hypothesis of a relation between TMJ disorders and such kinds of trauma seems to be supported by an epidemiological association and might also be explained by some plausible pathogenic mechanisms. For example, about 25% of patients with disk displacement reported a mandibular trauma before the onset of clinical symptoms, whereas 43% of patients with TMD-related symptoms reported a history of face or neck injuries. Independently of the direction of the impact, a trauma to the mandible can cause an inflammatory reaction in the retrodiscal structures and an injury to the temporomandibular ligaments, thus producing a condition that predisposes to disk displacement.
Several studies have demonstrated that a mandibular whiplash may occur concomitantly with a cervical whiplash injury. [67,68] In such cases, some authors suggest that the extreme hypertranslation of the condyle out of the glenoid fossa might lengthen or even stretch the posterior attachment and the ligaments, both at a medial and at a lateral level. This condition seems to be a predisposing factor for disk displacement. Some authors recognize the importance of direct facial trauma as well as of indirect trauma (i.e., whiplash) in the causation of TMJ disk displacement.,, However, many other studies in the literature have contested both the frequency of the involvement of the stomatognathic system after an indirect trauma and the actual link of cause-and-effect between whiplash and TMD, therefore suggesting the need for further works. ,
Microtrauma refers to repetitive minor injuries to the TMJ occurring over a long period. Bruxism represents the most frequent cause of microtrauma; it is a source of articular overload, although recent studies seem to relate parafunctional habits to muscle disorders rather than to disk displacement. , In case of overloading, articular remodelling, which represents the normal adaptive reaction of healthy tissues to the forces acting against the joint, can be supplanted by degenerative changes. The TMJ disk, lacking in blood vessels, cannot undergo cellular remodelling and seems to be more vulnerable to degeneration and deformation than the condyle and the glenoid fossa.
Among the causes of articular overloading, some authors also mention the loss of posterior occlusal support as a cause of discal and condylar deformation and degeneration.  Actually, from an epidemiological viewpoint, the loss of the posterior occlusal support does not seem to be associated with TMD.  In any case, degenerative changes of the disk alter its normal biconcave shape and so represent a risk factor for disk displacement.
| Disk Deformation|| |
A disk that has lost its normal shape is more likely to be displaced. Indeed, under normal conditions, the strong discal ligaments and the 'self-seating' wedge shape of the disk prevent any shift movement. In order that the disk may shift over the condyle, a deformation of its surfaces is needed, together with damage to the discal ligaments.
The posterior band of the disk is thinner than usual in many cases of internal derangement and thus allows disk displacement, which occurs mostly in an anteromedial direction. Because of the articular anatomy, the lateral discal ligaments are usually compromised earlier than the medial ones, thus explaining the medial component of the displacement. In rare cases, both the medial and the lateral ligaments may be involved and therefore result in a pure medial displacement.
In every kind of disk displacement, the posterior attachment stretches variably, resulting in functional damage.
| Occlusion|| |
In the recent years, the diffusion of the theories about the multifactorial etiopathogenesis of TMD has led to the occlusal factors losing importance as a risk factor for TMD, although researchers are yet to reach a consensus on this particular issue. Some authors still consider occlusal abnormalities to be a fundamental factor in the onset of TMD symptoms, ,, whereas others suggest that they only represent one of the numerous factors that might be associated with TMD. ,,,, Past studies have suggested that many occlusal factors have a relationship with TMD but until now none of them have been proved to be sufficient, by themselves, to cause TMD. For example, a crossbite often causes asymmetric muscle function but it does not seem to be a direct cause of TMD.  The effects of a wide overjet and a deep overbite are controversial. ,, A slide between retruded condylar position (RCP) and intercuspal position (ICP) seems to be weakly associated with some kinds of TMD. ,, The presence of mediotrusive interferences is considered by some authors to be a predisposing factor for disk displacement, , whereas others suggest that they can exert a protective action. , The presence of an anterior open-bite can be considered a consequence of articular remodelling rather than the cause.  No relationship has been found between the onset of TMD-related symptoms and the loss of occlusal posterior support.  The trials aiming to assess the efficacy of occlusal treatment in TMD patients are not enough in number to draw conclusions. ,
Actually, the debate seems to be more philosophical than clinical. In particular, the supporters of the occlusal hypothesis observe that the critics may have confused the concepts of 'sufficient cause' and 'causal factor.' 
Furthermore, according to the former, it is possible that longitudinal studies, in which artificial interferences were introduced in the occlusal pattern of healthy patients, underestimed the importance of the occlusal factors because healthy patients, being capable of tolerating their own natural interferences, also have a greater adaptability to artificial interferences. This hypothesis seems to be confirmed by a study in which a group of patients with regressed TMD symptoms demonstrated a weak adaptability to artificial interferences.  So, in the opinion of supporters of the occlusal hypothesis, the current empirical and scientific evidences are not sufficient to deny the existence of any cause-effect relationship between occlusion and TMD. 
On the other hand, in the opinion of the critics of the occlusal theory, it is impossible to design a trial to study the etiology of a multifactorial entity like TMD, because neither epidemiological-associative investigations nor longitudinal studies about the effectiveness of the different treatments can be conclusive.  Therefore, the question of whether occlusal abnormalities are a cause of disk displacement or not may be an academic one. Besides, the objective difficulties in defining the relative importance of the supposed etiologic factors limits the possibility of developing a true etiologic TMD therapy, and make conservative, reversible, non- occlusal therapy the treatments of choice for TMD. ,
Although the ultimate aim of most researches is to find ways to treat a disease, it is also true that the investigation of the etiology of the disease can be fascinating and worthwhile. In this sense, among the various forms of TMD, disk displacement is relatively easy to study, because from a biomechanical viewpoint the consequences of different types of occlusal patterns at the articular level may be more easily studied than those at the muscular level. The few well-designed studies in which the different occlusal variables were put in connection to the presence of disk displacement have been associative works adopting advanced statistic models. , From these studies, the association between the various occlusal characteristics and the presence of disk displacement seems to be weak.
From a biomechanical viewpoint, it is likely that dynamic malocclusions, such as a wide slide between RCP and ICP and medio/laterotrusive interferences, are more important risk factors than static malocclusions.
For example, a possible pathogenic mechanism in disk displacement is the posterior shift of the condyle of the same side as the RCP-ICP slide, with a consequent anterior disk displacement. This hypothesis, based on empiric clinical observations, needs to be verified by means of studies designed to investigate the relationship between disk displacement and different types of guide, mandibular kinematics and condylar movements. ,
| Dynamic Properties of the Disk|| |
Abnormal biomechanical loads, both compressive and tensive, produce structural changes within cartilaginous structures. ,, In the case of the TMJ disk, structural changes may alter its tissutal features and dynamic properties and may thus contribute to its displacement.
Many cartilaginous structures exhibit viscoelastic features, determined by the movements of the interstitial fluids inside a solid matrix.  A number of studies have been done to investigate if the TMJ disk shows such features ,,,,, and if there are regional differences within it. , Actually, the presence of tissutal differences within the disk was investigated in a mediolateral direction, and this represents the limit of the current knowledge, because disk morphology changes more in an anteroposterior direction than in a mediolateral one.  These last considerations suggest that modifications in tissutal features in an anteroposterior direction may influence the articular mechanics more than modifications occurring in a mediolateral direction. 
The intermediate zone is the most resistant to load. ,,, It allows an optimal load distribution in the less resistant zones by ensuring a steady deformation of the whole structure and preventing the concentration of excessive loads in any single area.
From a histological viewpoint, the weaker cross-linking between the collagenous fibers is seen in those oriented in a mediolateral direction, as demonstrated by the fact that after a trauma the separation lines over the disk surface lie in a dorsoventral direction.  Recent works have demonstrated that in the TMJ the translation of the stress distribution vectors occurs in a mediolateral direction.  This may be one of the causes of disk deformation, because it may contribute to emphasize the deforming effect of the transversal forces (shear stress).
| Inclination of the Articular Eminence|| |
The disk should rotate forward over the condyle to maintain the correct relationship during the movements, and therefore some authors have suggested that a steep articular eminence may be an etiologic factor for disk displacement.  The forward rotation needs to be more pronounced than normal in such cases and may put the disk in an anterior position with respect to the condyle, which may predispose to disk displacement. This biomechanical theory to explain disk displacement seems to be supported by studies that have demonstrated the presence of a steep articular eminence in subjects with disk displacement. , However, MR studies did not confirm this theory.  One MR study showed that the inclination of the articular eminence was greater in subjects having the disk in a normal position than in subjects having an anteriorly positioned disk. 
The most important objection raised against the biomechanical theory of disk displacement is that the relationship between the inclination of the eminence and the disk rotation level has not been elucidated as yet. Therefore, in the absence of definitive demonstration that the disk rotation grade during the movements does not increase with the inclination of articular eminence, the assumption at the basis of this theory is not acceptable. Moreover, a work based on pseudodynamic MR imaging showed that the disk-condyle complex rotates forwards during the opening motion, but the degree of condylar rotation is greater than the discal rotation  and so the disk rotates backwards with respect to the condyle. Furthermore, there is no evidence that the degree of forward rotation of the disk is greater in the joint with a steep eminence. So, the assumption that the condyle moves parallel to the eminence, on which many past works were based, is not correct; actually the condyle descends with a less steep inclination with respect to the eminence.
Even though the anatomical and structural factors influencing the onset of a disk displacement have not been clarified as yet, it appears obvious that joints characterized by a condyle centered in a well-shaped fossa of normal dimensions are the most resistant to disk displacement. , This suggestion was confirmed using multifactorial statistical models applied to the investigation of the hard tissues of the TMJ. In fact, multifactorial analysis showed that joints with a normally positioned disk are characterized by fossa shape and dimension and condylar position that are not extreme. ,
| The Role of the Lateral Pterygoid Muscle|| |
A widely diffused opinion is that abnormalities of the lateral pterygoid muscle can be responsible for many forms of TMD. ,, A hypo/hyperactivity of this muscle or a poor coordination of its two bellies are thought to be possible causes of functional imbalance of the TMJ because of the important stabilization task that the lateral pterygoid muscle plays within this joint. From a clinical viewpoint, tenderness to palpation of the lateral pterygoid muscle is an almost constant factor in TMD patients.  From an anatomical point of view, the lateral pterygoid muscle is unique within the stomatognathic system, because the distribution of the muscle fibers allows the development of mainly horizontal force vectors.  The muscle consists of an inferior cape that originates from the lateral surface of the pterygoid process and connects with the TMJ capsule and with the condylar neck, and a superior cape that originates in the intratemporal fossa and attaches over the condyle and over the disk-condyle complex. ,
The lateral pterygoid muscle is functionally heterogeneous because the two bellies exert different functions and also because within each individual cape there are areas or bands that could be activated selectively in order to generate special movements.  The recent demonstration of the functional heterogeneity of this muscle , provided an explanation for the controversial results of studies reported in the literature. According to some of these studies, for example, the superior cape seems to be active during the ipsilateral laterotrusive movements and during mouth closing and retrusion, ,, whereas in some others it was activated during protrusion and contralateral movements. ,
The lateral pterygoid muscle is commonly thought to be responsible for the anterior dragging and displacement of the disk respect to the condyle.  Actually, despite its functional heterogeneity it may allow the selective activation of the fibers that connect with the disk, without causing the whole disk-condyle complex to be dragged anteriorly; studies on autoptic specimens suggested that the manual traction of the superior cape causes a forward shift of the whole complex. ,,
| Joint Hypermobility|| |
The theory that some types of TMD, and disk displacement in particular, could have a high prevalence in subjects with articular hypermobility was based on some early studies pointing out an association between TMD and the generalized joint hypermobility syndrome (GJH).  The premise on which this assumption is based is that a hypermobile joint suffers overloads that could cause degenerative changes or bad positioning of the disk.  In fact, the authors of a recent systematic literature review concluded that on the basis of up-to-date evidences it is not yet clear that GJH and TMD are clinically associated conditions.  However, these conclusions seem to be due also to the small number of studies that have been done and to the poor methodological quality of most of them.
With regard to the problem of the association between ligamentous laxity and disk displacement, the number of published studies are even fewer, ,,,, and any conclusion can only be speculative.
Therefore, further researches are needed in order to analyse the clinical relationship between articular hypermobility and the various types of TMD.
| Conclusions|| |
Disk displacement of the TMJ is a common condition, the clinical significance of which as a pathological sign has been questioned in the recent years. An analysis of the available information on this condition becomes frustrating, expecially if one considers the supposed etiopathogenic mechanisms that could lead to an abnormal disk position with respect to the condyle. Many hypotheses have been proposed over the years in the attempt to explain the pathogenesis of disk displacement, and many structural factors were suspected as possible risk factors. According to the literature, the roles of morphological (i.e., occlusal abnormalities and inclination of the eminence) and functional factors (i.e., hyperactivity of the lateral pterygoid muscle) appear to be much less important than hypothesized in the past.
It is probable that the correct approach to the study of the pathogenesis of disk displacement should begin with improving the understanding of the mechanisms of joint lubrication and their impairment.
| References|| |
|1.||Annandale T. On displacement of the interarticular cartilage of the lower jaw and its treatment by operation. Lancet 1887;1:411-4. |
|2.||Nitzan DW. The process of lubrification impairment and its involvement in temporomandibular joint disc displacement: A theoretical concept. J Oral Maxillofac Surg 2001;59:36-45. |
|3.||Scapino RP, Canham PB, Finlay HM, Mills DK. The behaviour of collagen fibres in stress relaxation and stress distribution in the jaw-joint disc of rabbits. Arch Oral Biol 1996;41:1039-52. |
|4.||Nagy NB, Daniel JC. Distribution of elastic fibres in the developing rabbit craniomandibular joint. Arch Oral Biol 1991;36:15-23. |
|5.||Korioth T, Romilly D, Hannam A. Three-dimensional finite element stress analysis of the dentate human mandible. Am J Phys Anthropol 1992;88:66-96. |
|6.||Beek M, Koolstra JH, van Ruijven LJ, van Eijden TM. Three-dimensional finite element analysis of the human temporomandibular joint disc.J Biomech 2000;33:307-16. |
|7.||Tanaka E, Rodrigo DP, Tanaka M, Kawaguchi A, Shibazaki T, Tanne K. Stress analysis in the TMJ during jaw opening by use of a three-dimensional finite element model based on magnetic resonance images. Int J Oral Maxillofac Surg 2001;30:421-30. |
|8.||Rees LA. The structure and function of the mandibular joint. Br Dent J 1954;96:125-33. |
|9.||Mills DK, Fiandaca DJ, Scapino RP. Morphologic, microscopic and immunohistochemical investigations into the function of the primate TMJ disc. J Orofac Pain 1994;8:136-54. |
|10.||Wilkinson TM, Crowley CM. A histologic study retrodiscal tissues of the human temporomandibular joint in the open and closed position. J Orofac Pain 1994;8:7-17. |
|11.||Scapino RP. Histopathology associated with malposition of the human temporomandibular joint disc. Oral Surg Oral Med Oral Pathol 1983;55:382-97. |
|12.||Eriksson L, Westesson PL, Macher D, Hicks D, Tallents RH. Creation of disc displacement in human temporomandibular joint autopsy specimens. J Oral Maxillofac Surg 1992;50:869-73. |
|13.||Wilkinson FM, Crowley CM. A histologic study of retrodiscal tissues of human temporomandibular joint in the open and closed position. J Orofac Pain 1994;8:7-17. |
|14.||Bermejo-Fenoll A, Gonzαlez Sequeros O, Gonzαlez Gonzαlez JM. Histological study of the temporomandibular joint capsule: Theory of the articular complex. Acta Anat 1992;145:24-8. |
|15.||Teng SY, Xu T. Biomechanical properties and collagen fibre orientation of TMJ discs in dogs: Part 1, Gross anatomy and collagen fibre orientation of the discs. J Craniomandib Disord Facial Oral Pain 1991;5:28-34. |
|16.||Nitzan DW. Intra-articular pressure in the functioning human TMJ and its alteration by uniform elevation of the occlusal plane. J Oral Maxillofac Surg 1994;52:671-9. |
|17.||Bermejo-Fenoll A, Panchoz-Ruiz A, Gonzαlez-Gonzαlez JM, Gonzαlez Sequeros O. A study of the movements of the human temporomandibular joint complex in the cadaver. Cranio 2002;20:181-91. |
|18.||Keith DA. Development of the human temporomandibular joint. J Oral Surg 1982;20:217-24. |
|19.||Bermejo A, Gonzalez O, Gonzalez M. The pig as an animal model for experimentation on the temporomandibular articular complex. Oral Surg Oral Med Oral Pathol 1993;75:18-23. |
|20.||Isberg A, Westesson PL. Steepness of the articular eminence and movement of the condyle and disk in asymptomatic temporomandibular joints. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;86:152-7. |
|21.||Juniper RP. Temporomandibular joint dysfunction: A theory based upon electromyographic studies of the lateral pterygoid muscle. Br J Oral Maxillofac Surg 1984;22:1-8. |
|22.||Juniper RP. The pathogenesis and investigation of TMJ dysfunction. Br J Oral Maxillofac Surg 1987;25:105-12. |
|23.||Hiraba K, Hibino K, Hiranuma K, Negoro T. EMG activities of two heads of the human lateral pterygoid muscle in relation to mandibular condyle movement and biting force. J Neurophysiol 2000;83:2120-37. |
|24.||Mahan PE, Wilkinson TM, Gibbs CH, Mauderli A, Brannon LS. Superior and inferior bellies of the lateral pterygoid muscle EMG activity at basic jaw positions. J Prosthet Dent 1983;50:710-8. |
|25.||Carpentier P, Yung JP, Marguelles-Bonnet R, Meunissier M. Insertions of the lateral pterygoid muscle: An anatomical study of the temporomandibular joint. J Oral Maxillofac Surg 1988;46:477-80. |
|26.||Wilkinson TM. The relationship between the disc and lateral pterygoid muscle in the human temporomandibular joint. J Prosthet Dent 1988;60:715-9. |
|27.||Heylings DJ, Nielsen IL, McNeill C. Lateral pterygoid muscle and the temporomandibular disc. J Orofac Pain 1995;9:9-16. |
|28.||Naidoo LC. Lateral pterygoid muscle and its relationship to the meniscus of the temporomandibular joint. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996;82:4-9. |
|29.||Luder HU, Bobst P, Schroeder HE. Histometric study of synovial cavity dimensions of human temporomandibular joints with normal and anterior disc position. J Orofac Pain 1993;7:263-74. |
|30.||Tasaki MM, Westesson PL. Temporomandibular joint: Diagnostic accuracy with sagittal and coronal MR imaging. Radiology 1993;186:723-9. |
|31.||Dijkgraaf LC, de Bont LG, Otten E, Boering G. Three-dimensional visualization of the temporomandibular joint: A computerized multisectional autopsy study of disc position and configuration. J Oral Maxillofac Surg 1992;50:2-10. |
|32.||Hellsing G, Holmlund A. Development of anterior disk displacement in the temporomandibular joint: An autopsy study. J Prosthet Dent 1985;53:397-401. |
|33.||Turell J, Gutierrez Ruiz H. Normal and abnormal findings in temporomandibular joints in autopsy specimens. J Craniomandib Disord 1987;1:257-75. |
|34.||Davant TS, Greene CS, Perry HT, Lautenschlager EP. A quantitative computer-assisted analysis of disc displacement in patients with internal derangement using sagittal view magnetic resonance imaging. J Oral Maxillofac Surg 1993;51:974-9. |
|35.||Drace JE, Enzmann DR. Defining the normal temporo-mandibular joint: Closed, partially open and open-mouth MR imaging of asymptomatics subjects. Radiology 1990;177:67-71. |
|36.||Hans MG, Lieberman J, Goldberg J, Rozencweig G, Bellon E. A comparison of clinical examination, history and magnetic resonance imaging for identifying orthodontic patients with temporomandibular joint disorders. Am J Orthod Dentofacial Orthop 1992;101:54-9. |
|37.||Kircos LT, Ortendahl DA, Mark AS, Arakawa M. Magnetic resonance imaging of the TMJ disc in asymptomatic volunteers. J Oral Maxillofac Surg 1987;45:852-4. |
|38.||Silverstein R, Dunn S, Binder R, Maganzini A. MRI assessment of the normal temporomandiboular joint with the use of projective geometry. Oral Surg Oral Med Oral Pathol 1994;77:523-30. |
|39.||Foucart JM, Carpentier P, Pajoni D, Marguelles-Bonnet R, Pharaboz C. MR of 732 TMJs: Anterior, rotational, partial and sideways disc displacements. Eur J Radiol 1998;28:86-94. |
|40.||Chen YJ, Gallo LM, Meier D, Palla S. Individualized oblique-axial magnetic resonance imaging for improved visualization of mediolateral TMJ disc displacement. J Orofac Pain 2000;14:128-39. |
|41.||Chen YJ, Gallo LM, Palla S. The mediolateral temporomandibular joint disc position: An in vivo quantitative study. J Orofac Pain 2002;16:29-38. |
|42.||Raustia AM, Tervonen O, Pyhtinen J. Temporomandibular joint findings obtained by brain MRI. Cranio 1994;12:28-32. |
|43.||Westesson PL, Eriksson L, Kurita K. Reliability of a negative clinical temporomandibular joint examination: Prevalence of disk displacement in asymptomatic temporomandibular joints. Oral Surg Oral Med Oral Pathol 1989;68:551-4. |
|44.||Tallents RH, Hatala M, Katzberg RW, Westesson PL. Temporomandibular joint sounds in asymptomatic volunteers. J Prosthet Dent 1993;69: 298-304. |
|45.||Morrow D, Tallents RH, Katzberg RW, Murphy WC, Hart TC. Relationship of other joint problems and anterior disc position in symptomatic TMD patients and in asymptomatic volunteers. J Orofac Pain 1996;10:15-20. |
|46.||Pereira FJ Jr, Lundh H, Westesson PL. Morphologic changes in the temporomandibular joint in different age groups. Oral Surg Oral Med Oral Pathol 1994;78:279-87. |
|47.||Stegenga B, De Bont LGM, Boering G, Van Willigem JD. Tissue repsonses to degenerative changes in the temporomandibular joint: A review. J Oral Maxillofac Surg 1991;49:1079-88. |
|48.||Isacsson G, Linde C, Isberg A. Subjective symptoms in patients with temporomandibular disc displacement versus patients with myogenic craniomandibular disorders. J Prosthet Dent 1989;61:70-7. |
|49.||Ribeiro RF, Tallents RH, Katzberg RW, Murphy WC, Moss ME, Magalhaes AC, et al . The prevalence of disc displacement in symptomatic and asymptomatic volunteers aged 6 to 25 years. J Orofac Pain 1997;11:37-47. |
|50.||Paesani D, Westesson PL, Hatala MP, Tallents RH, Brooks SL. Accuracy of clinical diagnosis for TMJ internal derangement and arthrosis. Oral Surg Oral Med Oral Pathol 1992;73:360-3. |
|51.||Katzberg RW, Westesson PL, Tallents RH, Drake CM. Anatomic disorders of the temporomandibular joint disc in asymptomatic subjects. J Oral Maxillofac Surg 1996;54:147-53. |
|52.||de Bont LG, Dijkgraaf LC, Stegenga B. Epidemiology and natural progression of articular temporomandibular disorders. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997;83:72-6. |
|53.||Paesani D, Salas E, Martinez A, Isberg A. Prevalence of temporomandibular joint disk displacement in infants and young children. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;87:15-9. |
|54.||Kurita K, Westesson PL, Tasaki M. Diagnosis of medial temporomandibular joint disc displacement with dual space anteroposterior arthrotomography: Correlation with cryosectional morphology. J Oral Maxillofac Surg 1992;50:618-20. |
|55.||Liedberg J, Panmekiate S, Petersson A, Rohlin M. Evidence-based evaluation of three imaging methods for the temporomandibular disc. Dentomaxillofac Radiol 1996;25:234-41. |
|56.||Schwaighofer BW, Tanaka TT, Klein MV, Sartoris DJ, Resnick D. MR imaging of the temporomandibular joint: A cadaver study of the value of coronal images. Am J Roentegenol 1990;154:1245-9. |
|57.||Katzberg RW, Westesson PL, Tallents RH, Anderson R, Kurita K, Manzione JV Jr, et al . Temporomandibular joint: MR assessment of rotational and sideways disc displacements. Radiology 1988;169:741-8. |
|58.||Holmlund AB, Gynther GW, Reinholt FP. Disk derangement and inflammatory changes in the posterior disk attachment of the temporomandibular joint: A histologic study. Oral Surg Oral Med Oral Pathol 1992;73:9-12. |
|59.||Luder HU. Articular degeneration and remodeling in human temporomandibular joints with normal and anterior disc position. J Orofac Pain 1993;7:391-402. |
|60.||Kondoh T, Westesson PL, Takahashi T, Seto K. Prevalence of morphological changes in the surfaces of the temporomandibular joint disc associated with internal derangement. J Oral Maxillofac Surg 1998;56:339-43. |
|61.||Isberg A, Isacsson G. Tissue reactions associated with internal derangement of the temporomandibular joint: A radiographic, crymorphologic, and histologic study. Acta Odontol Scand 1986;44:160-4. |
|62.||Scapino RP. The posterior attachment: Its structure, function, and appearance in TMJ imaging studies: Part 1. J Craniomandib Disord 1991;5:83-95. |
|63.||Pereira Júnior FJ, Lundh H, Westesson PL. Age-related changes of the retrodiscal tissues in the temporomandibular joint. J Oral Maxillofac Surg 1996;54:55-61. |
|64.||Solberg WK, Woo MW, Houston JB. Prevalence of mandibular dysfunction in young adults. J Am Dent Assoc 1979;98:25-34. |
|65.||Pertes RA, Heir GM. Chronic orofacial pain: A practical approach to differential diagnosis. Dent Clin North Am 1991;35:123-40. |
|66.||Harkins SJ, Marteney JL. Extrinsic trauma: A significant precipitating factor in temporomandibular dysfunction. J Prosthet Dent 1985;54:271-2. |
|67.||Hacke W, Hausberger K, Sailer R, Ulmer H, Gassner R. Prevalence of cervical spine injuries in patients with facial trauma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92: 370-6. |
|68.||Garcia R Jr, Arrington JA. The relationship between cervical whiplash and temporomandibular joint injuries an MR study. Cranio 1996;14:233-9. |
|69.||Friedman MH, Weisberg J. The craniocervical connection: A retrospective analysis of 300 whiplash patients with cervical and temporomandibular disorders. Cranio 2000;18:163-7. |
|70.||Goldstein BH. Medical legal considerations in temporomandibular disorders. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88:395-9. |
|71.||Kronn E. The incidence of TMJ dysfunction in patients who have suffered a cervical whiplash injury following a traffic accident. J Orofac Pain 1993;7:209-13. |
|72.||Bergman H, Andersson F, Isberg A. Incidence of temporomandibular joint changes after whiplash trauma: A prospective study using MR imaging. AJR Am J Roentgenol 1998;171:1237-43. |
|73.||McKay DC, Christensen LV. Whiplash injuries of the temporomandibular joint in motor vehicle accidents: Speculations and facts. J Oral Rehabil 1998;25:731-46. |
|74.||Molina OF, dos Santos J, Mazzetto M, Nelson S, Nowlin T, Mainieri ET. Oral jaw behaviors in TMD and bruxism: A comparison study by severity of bruxism. Cranio 2001;19:114-22. |
|75.||Manfredini D, Cantini E, Romagnoli M, Bosco M. Prevalence of bruxism in patients with different Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) diagnoses. Cranio 2003;21:279-85. |
|76.||Kirveskari P, Alanen P. Association between tooth loss and TMJ dysfunction. J Oral Rehabil 1985;12:189-94. |
|77.||Ciancaglini R, Gherlone EF, Radaelli G. Association between loss of occlusal support and symptoms of functional disturbances of the masticatory system. J Oral Rehabil 1999;26:248-53. |
|78.||Kirveskari P. The role of occlusal adjustment in the management of temporomandibular disorders. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997;83:87-90. |
|79.||Thilander B, Rubio G, Pena L, de Mayorga C. Prevalence of temporomandibular dysfunction and its association with malocclusion in children and adolescents: An epidemiologic study related to specified stages of dental development. Angle Orthod 2002;72:146-54. |
|80.||Alanen P. Occlusion and Temporomandibular Disorders (TMD): Still unsolved question? J Dent Res 2002;81:518-9. |
|81.||DeBoever JA, Carlsson GE, Klineberg IJ. Need for occlusal therapy and prosthodontic treatment in the management of temporomandibular disorders: Part I, Occlusal interferences and occlusal adjustment. J Oral Rehabil. 2000;27:367-79. |
|82.||DeBoever JA, Carlsson GE, Klineberg IJ. Need for occlusal therapy and prosthodontic treatment in the management of temporomandibular disorders: Part II, Tooth loss and prosthodontic treatment. J Oral Rehabil 2000;27:647-59. |
|83.||Greene CS, Laskin DM. Temporomandibular disorders: Moving from a dentally based to a medically based model. J Dent Res 2000; 79:1736-9. |
|84.||Tsukiyama Y, Baba K, Clark GT. An evidence-based assesment of occlusal adjustment as a treatment for temporomandibular disorders. J Prosthet Dent 2001;86:57-66. |
|85.||Landi N, Manfredini D, Tognini F, Romagnoli M, Bosco M. Quantification of the relative risk of multiple occlusal variables for muscle disorders of the stomatognathic system. J Prosthet Dent 2004;92:190-5. |
|86.||McNamara JA, Seligman DA, Okeson JP. Occlusion, orthodontic treatment, and temporomandibular disorders: A review. J Orofac Pain 1995;9:73-90. |
|87.||Seligman DA, Pullinger AG. The role of intercuspal occlusal relationships in temporomandibular disorders: A review. J Craniomandib Disord 1991;5:96-106. |
|88.||Celic R, Jerolimov V. Association of horizontal and vertical overlap with prevalence of temporomandibular disorders. J Oral Rehabil 2002;29:588-93. |
|89.||John MT, Hirsch C, Drangsholt MT, Mancl LA, Setz JM. Overbite and overjet are not related to self-report of Temporomandibular Disorder symptoms. J Dent Res 2002;81:164-9. |
|90.||Raustia AM, Pirttiniemi PM, Pyhtinen J. Correlation of occlusal factors and condyle position asymmetry with signs and symptoms of temporomandibular disorders in young adults. Cranio 1995;13:152-6. |
|91.||Seligman DA, Pullinger AG. Analysis of occlusal variables, dental attrition, and age for distinguishing healty controls from female patients with intracapsular temporomandibular disorders. J Prosth Dent 2000;83:76-82. |
|92.||Pullinger AG, Seligman DA. Quantification and validation of predictive values of occlusal variables in temporomandibular disorders using a multifactorial analysis. J Prosthet Dent 2000;83:66-75. |
|93.||Kirveskari P, Alanen P, Jδmsδ T. Association between craniomandibular disorders and occlusal interferences in children. J Prosthet Dent 1992;67:692-6. |
|94.||Tarantola GJ, Becker IM, Gremillion H, Pink F. The effectiveness of equilibration in the improvement of sign and symptoms in the stomatognathic system. Int J Periodont Rest Dent 1998;18:595-603. |
|95.||Minagi S, Watanabe H, Sato T, Tsuru H. The relationships between sounds in humans: Proposition of the concept of balancing side protection. J Craniomandib Disord 1990;4:251-6. |
|96.||Minagi S, Ohtsuki H, Soto T, Ishii A. Effect of balancing side occlusion on the ipsilateral TMJ dynamics under clenching. J Oral Rehabil 1997;26:57-62. |
|97.||Forssell H, Kalso E, Koskela P, Vehmanen R, Puukka P, Alanen P. Occlusal treatments in temporomandibular disorders: A qualitative systematic review of randomised controlled trials. Pain 1999;83:549-60. |
|98.||Le Bell Y, Jamsa T, Korri S, Niemi PM, Alanen P. Effect of artificial occlusal interferences depends on previous experience of temporomandibular disorders. Acta Odontol Scand 2002;60:219-22. |
|99.||Greene CS. Clinical research: Studying relationship between occlusion and TM disorders. Angle Orthod 1999;69:391-2. |
|100.||Stohler CS, Zarb GA. On the management of temporomandibular disorders: A plea for low-tech, high-prudence therapeutic approach. J Orofac Pain 1999;13:255-61. |
|101.||Greene CS. The etiology of temporomandibular disorders: Implications for treatment. J Orofac Pain 2001;15:93-105. |
|102.||Yang Y, Yatabe M, Ai M, Soneda K. The relation of canine guidance with laterotrusive movements at the incisal point and the working side condyle. J Oral Rehabil 2000;27:911-7. |
|103.||Yang Y, Yatabe M, Ai M, Soneda K. The relation of mandibular laterotrusion with ipsilateral TMJ clicking. J Oral Rehabil 2001;28:64-7. |
|104.||Tuominen M, Kantomaa T, Pirttiniemi P, Poikela A. Growth and type-II collagen expression in the glenoid fossa of the temporomandibular joint during altered loading: A study in the rat. Eur J Orthod 1996;18:3-9. |
|105.||Mao JJ, Rahemtulla F, Scott PG. Proteoglycan expression in the rat temporomandibular joint in response to unilateral bite raise. J Dent Res 1998;77:1520-8. |
|106.||Quinn TM, Grodzinsky AJ, Buschmann MD, Kim YJ, Hunziker EB. Mechanical compression alters proteoglycan deposition and matrix deformation around individual cells in cartilage explants. J Cell Sci 1998;111:573-83. |
|107.||Kovach IS. A molecular theory of cartilage viscoelasticity. Biophys Chem 1996;59:61-73. |
|108.||Teng S, Xu Y, Cheng M, Li Y. Biomechanical properties and collagen fibre orientation of TMJ discs in dogs: Part 2, Tensile mechanical properties of the discs. J Craniomandib Disord Facial Oral Pain 1991;5:107-14. |
|109.||Chin LP, Aker FD, Zarrinnia K. The viscoelastic properties of the human temporomandibular joint disc. J Oral Maxillofac Surg 1996;54:315-8. |
|110.||Kuboki T, Shinoda M, Orsini MG, Yamashita A. Viscoelastic properties of the pig temporomandibular joint articular soft tissues of the condyle and disc. J Dent Res 1997;76:1760-9. |
|111.||Tanaka E, Tanaka M, Miyawaki Y, Tanne K. Viscoelastic properties of canine temporomandibular joint disc in compressive load-relaxation. Arch Oral Biol 1999;44:1021-6. |
|112.||Tanne K, Tanaka E, Sakuda M. The elastic modulus of the temporomandibular joint disc from adult dogs. J Dent Res 1991;70:1545-8. |
|113.||Lai WF, Bowley J, Burch JG. Evaluation of shear stress of the human temporomandibular joint disc. J Orofac Pain 1998;12:153-9. |
|114.||Beek M, Aarnts MP, Koolstra JH, Feilzer AJ, van Eijden TM. Dynamic properties of the human temporomandibular joint disc. J Dent Res 2001;80:876-80. |
|115.||Werner JA, Tillmann B, Schleicher A. Functional anatomy of the temporomandibular joint: A morphologic study on human autopsy material. Anat Embryol (Berl) 1991;183:89-95. |
|116.||DeVocht JW, Goel VK, Zeitler DL, Lew D. A study of the control of disc movement within the temporomandibular joint using the finite element technique. J Oral Maxillofac Surg 1996;54:1431-7. |
|117.||Nagahara K, Murata S, Nakamura S, Tsuchiya T. Displacement and stress distribution in the temporomandibular joint during clenching. Angle Orthod 1999;69:372-9. |
|118.||Gallo LM, Nickel JC, Iwasaki LR, Palla S. Stress-field translation in the healthy human temporomandibular joint. J Dent Res 2000;79:1740-6. |
|119.||Atkinson WB, Bates RE Jr. The effects of the angle of the articular eminence on anterior disk displacement. J Prosthet Dent 1983;49:554-5. |
|120.||Hall MB, Gibbs CC, Solar AG. Association between the prominence of the articular eminence and displaced TMJ disks. Cranio 1985;3:237-9. |
|121.||Kerstens HC, Tuinzing DB, Golding RP, Van der Kwast WA. Inclination of the temporomandibular joint eminence and anterior disc displacement. Int J Oral Maxillofac Surg 1989;18:228-32. |
|122.||Galante G, Paesani D, Tallents RH, Hatala MA, Katzberg RW, Murphy W. Angle of the articular eminence in patients with temporomandibular joint dysfunction and asymptomatic volunteers. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995;80:242-9. |
|123.||Ren YF, Westesson PL, Isberg A. Magnetic resonance imaging of the temporomandibular joint: Value of pseudodynamic images. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996;81:110-23. |
|124.||Pullinger AG, Seligman DA, John MT, Harkins S. Multifactorial modeling of temporomandibular anatomic and orthopedic relationships in normla versus undifferentiated disk displacement joints. J Prosthet Dent 2002;87:289-97. |
|125.||Pullinger AG, Seligman DA, John MT, Harkins S. Multifactorial comparison of disk displacement with and without reduction to normals according to temporomandibular joint hard tissue anatomic relationship. J Prosthet Dent 2002;87:298-310. |
|126.||Ai M, Yamashita S. Tenderness on palpation and occlusal abnormalities in temporomandibular dysfunction. J Prosthet Dent 1992;67:839-45. |
|127.||Van Eijden TM, Korfage JA, Brugman P. Architecture of the human jaw-closing and jaw-opening muscles. Anat Rec 1997;248:464-74. |
|128.||Murray GM, Orfanos T, Chan JY, Wanigaratne K, Klineberg IJ. Electromyographic activity of the human lateral pterygoid muscle during contralateral and protrusive jaw movements. Arch Oral Biol 1999;44:269-85. |
|129.||Phanacet I, Whittle T, Wanigaratne K, Klineberg IJ, Sessle BJ, Murray GM. Functional heterogeneity in the superior head of the human lateral pterygoid. J Dent Res 2003;82:106-11. |
|130.||Phanacet I, Whittle T, Wanigaratne K, Murray GM. Functional properties of single motor units in inferior head of human lateral pterygoid muscle: Task relations and thresholds. J Neurophysiol 2001;86:2204-18. |
|131.||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;51:691-702. |
|132.||Wood WW, Takada K, Hannam AG. The electromyographc activity of the inferior part of the human lateral pterygoid muscle during clenching and chewing. Arch Oral Biol 1986;31:245-53. |
|133.||Sessle BJ, Gurza SC. Jaw movement-related activity and reflexly induced changes in the lateral pterygoid muscle of the monkey Macaca Fascicularis. Arch Oral Biol 1982;27:167-73. |
|134.||Murray GM, Phanachet I, Uchida S, Whittle T. The role of the human lateral pterygoid muscle in the control of horizontal jaw movements. J Orofac Pain 2001;15:279-92. |
|135.||Widmalm SE, Lillie JH, Ash MM Jr. Anatomical and electromyographic studies of the lateral pterygoid muscle. J Oral Rehabil 1987;14:429-46. |
|136.||Wilkinson TM. The relationship between the disk and the lateral pterygoid muscle in the human temporomandibular joint. J Prosthet Dent 1988;60:715-24. |
|137.||Christo JE, Bennett S, Wilkinson TM, Townsend GC. Discal attachments of the human temporomandibular joint. Aust Dent J 2005;50:152-60. |
|138.||Dolwick MF, Katzberg RW, Helms CA. Internal derangements of the temporomandibular joint: Fact or fiction? J Prosthet Dent 1983;49:415-8. |
|139.||Dijkstra PU, de Bont LG, Stegenga B, Boering G. Temporomandibular joint osteoarthrosis and generalized joint hypermobility. Cranio 1992;10:221-7. |
|140.||Dijkstra PU, Kropmans TJB, Stegenga B. The association between generalized joint hypermobility and temporomandibular joint disorders: A systematic review. J Dent Res 2002;81:158-63. |
|141.||Bates RE, Stewart CM, Atkinson WB. The relationhip between internal deranegements of the temporomandibular joint and systemic joint laxity. J Am Dent Assoc 1984;109:446-7. |
|142.||Chun DS, Koskinen ML. Distress, jaw habits, and connective tissue laxity as predisposing factors to TMJ sounds in adolescents. J Craniomandib Disord 1990;4:165-76. |
|143.||Khan FA, Pedlar J. Generalized joint hypermobility as a factor in clicking of the temporomandibular joint. Int J Oral Maxillofac Surg 1996;25:101-4. |
|144.||Plunkett GA, West VC. Systemic joint laxity and mandibular range of movement. Cranio 1988;6:320-6. |
|145.||Westling L, Mattiasson A. Generalized joint hypermobility and temporomandibular joint derangement in adolescents. Ann Rheum Dis 1992;51:87-90. |
TMD Clinic, Department of Maxillofacial Surgery, University of Padova