Temporomandibular Joint

The TMJ is a complex joint comprised of bone, ligament, and an articular disc. The bony components include the mandibular condyle and the glenoid fossa of the temporal bone. The mandibular condyle forms the lower part of the bony joint and is generally elliptical in shape, although variations are common.^5,6 The articulation is formed by the mandibular condyle occupying a hollow in the temporal bone (the mandibular or glenoid fossa). The S-shaped form of the fossa and eminence, as viewed sagitally, starts developing at about 6 years of age and continues into the second decade⁷ (Figures 10‐1 and 10‐2). The bony elements are enclosed and connected by a fibrous capsule.

The fibrous joint capsule is lined with synovial tissue, a vascular connective tissue which extends to the boundaries of the articulating surfaces. The synovial membrane consists of macrophage-like type A cells and fibroblast-like type B cells identical to those in other joints. The macrophage-like type A cells react with antimacrophage and macrophage-derived substances, including the major histocompatibility class II molecule, and show a drastic increase in their number in the inflamed synovial membrane.⁸ The joint cavity is filled with synovial fluid. Synovial fluid is a filtrate of plasma with added mucins and proteins. Its main constituent is hyaluronic acid. Fluid forms on the articulating surfaces and decreases friction during joint compression and motion.⁹ Joint lubrication is achieved by mechanisms described as weeping lubrication and boundary lubrication. Weeping lubrication occurs as fluid is forced laterally during compression and expressed through the unloaded fibrocartilage.¹⁰ As the adjacent areas become loaded, the weeping lubrication aids in reducing friction. Boundary lubrication is a function of water that is physically bound to the cartilaginous surface by a glycoprotein.¹¹ Collectively, the fluid dynamics depend on appropriate loading and unloading of the joint through normal function in order to maintain continuous lubrication as well as maintenance of the tissue health.¹²

Fibrocartilage, instead of the expected hyaline cartilage, covers the articulating surface of the joint. Fibrocartilage is less distensible than hyaline cartilage due to a greater number of collagen fibers including Type 1 collagen. The matrix and chondrocytes are decreased because of the larger irregular bundles of collagen fibers.¹³ The fibrocartilage found on the articulating surfaces of the TMJ is thought to provide more surface strength against forces in many directions while allowing more freedom of movement than would be possible with hyaline cartilage. This covering is thickest on the posterior slope of the articular eminence and on the anterior slope of the condylar head; these are the areas thought to receive the greatest functional load. The thinnest part of the fibrocartilage covering is on the roof of the mandibular fossa. Fibrocartilage has a greater repair capacity than hyaline cartilage which may affect how the TMJ responds to degenerative changes.^13,14

The TMJ articulation is a joint that is capable of both hinge-type movements and gliding movements. During wide mouth opening, the condyle rotates around a hinge axis and then translates as it glides, causing it to move beyond the anterior border of the fossa, which is identified as the articular eminence.¹⁵

Articular Disc

Dense fibrous connective tissue primarily made up of dense collagen of variable thickness is referred to as a disc and occupies the space between the fibrocartilage coverings of each of condyle and mandibular fossa (Figures 10‐3 and 10‐4). The disc consists of collagen fibers, cartilage-like proteoglycans,¹⁶ and elastic fibers.¹⁷ The disc contains a variable number of cells that resemble fibrocytes and fibrochondrocytes.¹⁸ Collagen fibers in the center of the disc (often referred to as the intermediate zone) are oriented perpendicular to its transverse axis functionally aligned with loading on that zone. The collagen fibers become interlaced as they approach the anterior and posterior bands, and many fibers are oriented parallel to the mediolateral aspect of the disc. Cartilage-like proteoglycans contribute to the compressive stiffness of articular cartilage.¹⁹ The disc is primarily avascular and has little sensory innervation. The disc is thinnest in the intermediate zone and thickens to form anterior and posterior bands represented as a “bow tie” in sagittal sections. This arrangement is considered to help stabilize the condyle in the glenoid fossa.⁵ Over time, discs may exhibit changes in this conformation; the central intermediate zone may become elongated or nonexistent, the anterior band may become thinner, or the posterior band may become either thinner or thicker. These conformation changes, while presumably affecting the ideal function of the disc in stabilizing the condyle during loading, are currently regarded as a variation on normal in the absence of any clinical manifestation of disordered function.²⁰

The disc provides an interface for the condyle as it glides across the temporal bone. The disc is attached by ligaments to the lateral and medial poles of the condyle. The ligaments consist of both collagen and elastic fibers.²¹ These ligaments permit rotational movement of the disc on the condyle during mouth opening and closing. The disc and its attachments divide the joint into upper and lower compartments that normally do not communicate. The passive volume of the upper compartment is estimated to be 1.2 mL and that of the lower compartment is estimated to be 0.9 mL.²¹ The roof of the superior compartment is the glenoid (mandibular) fossa, whereas the floor is the superior surface of the disc. The roof of the inferior compartment is the inferior surface of the disc and the floor is the articulating surface of the mandibular condyle.²¹ At its margins, the disc blends with the fibrous capsule. Muscle attachments inserting into the anterior aspect of the disc have been observed in a relatively small number of individuals.²² Fibers of the posterior one-third of the temporalis muscle and of the deep masseter muscle may attach on the anterolateral aspect, and fibers of the superior head of the lateral pterygoid have been observed to insert into the anteromedial two-thirds of the disc.²²

Retrodiscal Tissue

Loose connective tissue occupies the space behind the disc and condyle. It is often referred to as the posterior attachment or retrodiscal tissue. The posterior attachment is a loosely organized system of collagen fibers, branching elastic fibers, fat, blood and lymph vessels, and nerves. Synovium covers the superior and inferior surfaces. The attachment has been described as being arranged in two lamina of dense connective tissue²³ but this has been challenged.²⁴ Between the lamina, a loose areolar, highly vascular, and well-innervated tissue has been described. Both superior and inferior lamina arise from the posterior band of the disc. The superior lamina attaches to the squamotympanic fissure and tympanic part of the temporal bone and consists primarily of elastin.^23,25 The inferior lamina inserts into the inferior margin of the posterior articular slope of the condyle and is composed mostly of collagen fibers.²³

Temporomandibular Ligaments

Capsular Ligament

The capsular ligament is a thin inelastic fibrous connective tissue envelope that attaches to the margins of the articular surfaces (Figure 10‐5). The fibers are oriented vertically and do not restrain joint movements. The medial capsule is composed of loose areolar connective tissue.²⁴ The capsule and the lateral discal ligament join and attach to the lateral aspect of the neck of the condyle.²⁶

Muscles of Mastication

The primary muscles of mastication are the paired masseter, medial and lateral pterygoids, and temporalis muscles (Figures ). Mandibular movements toward the tooth contact position are performed by contraction of the masseter, temporalis, and medial pterygoid muscles.²⁷

Masseter contraction contributes to moving the condylar head toward the anterior slope of the mandibular fossa (Figure 10‐6). The posterior part of the temporalis contributes to mandibular retrusion. Unilateral contraction of the medial pterygoid contributes to a contralateral movement of the mandible. The masseter and medial pterygoid muscles have their insertions at the inferior border of the mandibular angle. They join together to form a sling that cradles the mandible and produces the powerful forces required for chewing. The masseter is divided into deep and superficial parts. The deep masseter in some individuals overlaps the anterior aspect of the TMJ, such that pain localized to the pre-auricular region may be associated with masseter, TMJ, or both structures. The temporalis muscle is attached to the lateral skull and has been divided into anterior, middle, and posterior parts. The muscle fibers converge into a tendon that inserts on the coronoid process and anterior aspect of the mandibular ramus. The anterior and middle fibers are generally oriented in a straight line from their origin on the skull to their insertion on the mandible. The posterior part traverses anteriorly and then curves around the anterior root of the zygomatic process before insertion.

The lateral pterygoid is the main protrusive and opening muscle of the mandible. The inferior head is the main section responsible for lateral jaw movements when the teeth are in contact.²⁸ The lateral pterygoid is arranged in parallel-fiber units, whereas the elevator muscles are multipennate in structure. This differential arrangement allows greater displacement and velocity in the lateral pterygoid vs. greater force generation in the elevator muscles.²⁹

The lateral pterygoid muscle arises from two heads (Figure 10‐7). The inferior head originates from the outer surface of the lateral pterygoid plate of the sphenoid bone and the pyramidal process of the palatine bone. The superior head originates from the greater wing of the sphenoid bone and the pterygoid ridge. The fibers of the upper and lower heads course posteriorly and laterally, fusing in front of the condyle,³⁰ and inserting into the anteromedial aspect of the condylar neck. Although some of the fibers insert into the most anterior medial portion of the disc (or capsule), most of the lateral pterygoid fibers insert into the condyle.³⁰ The superior part of the insertion consists of an identifiable tendon inserting through fibrocartilage. The inferior part of the insertion consists of muscle attached to periosteum.³¹ Debate continues about the functional anatomy of the lateral pterygoid. The superior head is thought to be active during closing movements, and the inferior head is thought to be active during opening and protrusive movements.^32,33 However, substantial variability across individuals appears to account for some of the debate.^34,35 Translation of the condylar head onto the articular eminence is produced by contraction of the lateral pterygoid.

The accessory muscles of mastication are relatively smaller and their function is more indirect and perhaps complex. The digastric muscle is a paired muscle with two bellies. The anterior belly attaches to the lingual aspect of the mandible at the parasymphysis and courses backward to insert into the hyoid bone. Contraction produces a depression and retropositioning of the mandible. The mylohyoid and geniohyoid muscles contribute to depressing the mandible when the infrahyoid muscles stabilize the hyoid bone. These muscles may also contribute to retrusion of the mandible. The omohyoid muscle arises from the scapula and inserts on the hyoid bone and serves to lower and stabilize the hyoid bone. Together with the digastric muscle, the omohyoid muscle lowers the jaw when active and is not active in a jaw resting position (Figure 10‐8).³⁶ The buccinator attaches inferiorly along the facial surface of the mandible behind the mental foramen and superiorly on the alveolar surface behind the zygomatic process. The buccinator fibers are arranged horizontally; anteriorly, fibers insert into mucosa, skin, and lip. The buccinator helps position the cheek during chewing movements of the mandible and contracts in order to maintain the food bolus on the posterior teeth during chewing. The functional activity of these accessory muscles depends on simultaneous activation of the primary masticatory muscles for stabilizing the position of the mandible which, given the basal functions of the masticatory system, has implications with respect to the functional limitation and disability often associated with a TMD.

Vascular Supply of Masticatory System Structures

The external carotid artery (ECA) is the main blood supply for the structures of the masticatory system. The ECA leaves the neck and courses superiorly and posteriorly, embedded in the substance of the parotid gland, sending two important branches, the lingual and facial arteries, to the region. At the level of the mandibular condylar neck, the external carotid bifurcates into the superficial temporal artery and the internal maxillary artery. These two arteries supply the muscles of mastication and the TMJ. Arteries within the temporal bone and mandible also send branches to the capsule.⁵

Nerve Supply of Masticatory System Structures

The masticatory structures are innervated primarily by the trigeminal nerve, but cranial nerves VII, IX, X, and XI and cervical nerves 2 and 3 also contribute. The peripheral nerves synapse with nuclei in the brainstem that are associated with touch, proprioception, and motor function. The large spinal trigeminal nucleus occupies a major part of the brainstem and extends to the spinal cord. The spinal trigeminal nucleus is thought to be the main site for the reception of impulses from the periphery involved in pain sensation. The mandibular division of the trigeminal nerve supplies motor innervation to the muscles of mastication and the anterior belly of the digastric muscle. The auriculotemporal nerve, a branch of the mandibular portion (V3) of the trigeminal nerve, provides innervation of the TMJ (Figure 10‐9). The deep temporal and masseteric nerves supply the anterior portion of the joint. About 75% of the time, the masseteric nerve, a branch of the maxillary division of the trigeminal nerve (V2), innervates the anteromedial capsule of the TMJ. In about 33%, a separate branch from V2 comes through the mandibular notch and innervates the anteromedial capsule.³⁷ These nerves are primarily motor nerves, but they contain sensory fibers distributed to the anterior part of the TMJ capsule. The autonomic nerve supply is carried to the joint by the auriculotemporal nerve and by nerves traveling along the superficial temporal artery.³⁸

Occlusal Disharmony

The history of the dental occlusion, as related to TMDs, is long and complex within the dental profession. Managing occlusion is a major task within restorative dentistry and, not surprisingly perhaps, the focus on occlusion has often been at the boundary between clinical lore and scientific evidence. While deviations of the occlusion from the ideal—so-called occlusal disharmony—can be construed in many ways, operational features that clearly distinguish a “good” occlusion from a “bad” occlusion remain missing from the discussions; moreover, the persistent focus on occlusion and TMDs contrasts with the inadequate to poorly designed and executed research used to support that focus. A short history of these concepts will be followed by focusing on some of the major claims regarding the presumed importance of occlusion in relation to TMDs. That this section has been retained, if not expanded, over the past several editions of this book is telling in itself: dentistry is reluctant to abandon the evaluation and treatment of occlusion with regard to TMDs, perhaps to the point that occlusion becomes a cause célèbre.

The relationship of so-called occlusal disharmony and TMD became the center of attention within the profession after Costen reported that a group of patients with multiple complaints associated with the jaws and ears improved after the occlusal–vertical dimension of their dentures was altered.⁶¹ Despite the lack of anatomic support for occlusal–vertical dimension as a mechanism,⁶² the occlusal hypothesis was nevertheless expanded to include other occlusal parameters, each believed to be responsible in addition to loss of vertical dimension for causing a TMD,^63,64 yet without evidence. During the 1950s and 1960s, a muscular cause not directly related to occlusion was proposed; the mechanisms were generic for similar pains elsewhere in the body, thereby highlighting the strong plausibility of the model.^65–67 In contrast, because this particular model ignored occlusion as a cause of TMD, the model proved to be very controversial within dentistry, setting the stage for ongoing controversy for any model that did not include occlusion as a cause. In the late 1970s, advances in diagnostic imaging resulted in a better understanding of intracapsular dynamics of the TMJ, and the focus was renewed upon so-called abnormalities of structure, now in the TMJ, as the “cause of TMD” and clearly evident via imaging.^68,69 The lack of a clear understanding with regard to cause, the existence of multiple hypotheses, and strongly held beliefs by some clinicians have resulted in a wide spectrum of views about what TMD constitutes, regardless of the absence of supporting evidence. This wide spectrum of views continues in the present, such that the transfer of science regarding TMDs to the clinical setting is often compromised, with inappropriate diagnosis and treatment as a consequence.

Clear and convincing evidence for so-called occlusal disharmony as a primary etiology of TMDs does not exist.⁷⁰ Research studying discrepancies between centric occlusion and maximal intercuspal position, nonworking side occlusal interferences, posterior crossbite, and Angle’s occlusal classification has not established a strong association in patients with myofascial pain compared with controls.^45,71,72 Significant differences in occlusal characteristics are not found between patients with myofascial pain compared with control subjects.⁷³ Overjet and overbite do not have a strong relationship with joint clicking, crepitus, pain, or limited opening.^74,75 A number of studies have been performed to investigate a possible relationship between orthodontic malocclusions and treatment and the development of TMD, but the results do not support a causal relationship.^76–80

A mainstay in the clinical lore regarding occlusion and TMDs is centric relation as an index for the position of the mandible relative to the maxilla. Centric relation is a position that has traditionally relied on guiding the condyles into a position to rotate around a stationary axis in the mandibular fossa, and it has served as both a highly idealized and a highly contentious anatomical point. The standard definition is “the maxillomandibular relationship, independent of tooth contact, in which the condyles articulate in the antero-superior position against the posterior slopes of the articular eminences.”⁸¹ This position of condylar rotation about a stationary axis can be reproduced and transferred to an articulator, and while that is useful clinically for restorative dentistry, a biological basis for the manipulated position has not been identified. A mandibular position usefully defined in operational terms for purposes of restorative dentistry should not be confused with necessarily having diagnostic or biological value beyond the operational definition. Evidence for centric relation as a diagnostic test or proxy for TMDs does not exist. Adjusting the maximum intercuspal position to be coincident with centric occlusion (the occlusion that exists when the mandible is at centric relation) has been strongly recommended by some clinicians to treat TMDs, but the biological evidence for this as a standard treatment is absent.⁸² In contrast, the available evidence indicates that the “stationary axis” is itself dynamic: for example, restoring a dentition for centric occlusion coincidence with maximum intercuspal position results in the development of a new centric occlusion over time,⁸³ implying that centric relation is a boundary of a zone used for normal movement. Moreover, such adjustments may actually increase risk for a TMD based on evidence suggesting that a gap in the maximal intercuspal position vs. centric occlusion is protective against TMD onset.⁸⁴ The biology associated with centric relation does not appear to support a causal linkage with TMDs.

A particularly contentious topic has been that premature occlusal contacts, such as faulty restorative dentistry, initiate sleep bruxism. This belief stems from research studies that are typically uncritically cited^85,86 but which were completely inadequate for any scientific conclusion. Premature occlusal contacts actually trigger the opposite in healthy individuals: a decrease in the activity of masticatory elevator muscles during sleep.⁸⁷ In contrast, the same premature occlusal contact in individuals with a TMD or a prior history of a TMD will cause increased activity of the masticatory elevator muscles during sleep.⁸⁸ Importantly, this increased muscle activity in those with a TMD is not evidence of causation. Rather, the impact of such premature occlusal contacts appears to depend on pre-existing trait anxiety and extent of oral parafunctional behaviors.⁸⁹

To date, as summarized elsewhere,⁷⁰ TMDs exhibit an association with only a very few attributes of a static occlusion, and the magnitude of the association is relatively small and inconsistent across studies. These associations are based on cross-sectional study designs, not longitudinal designs, and collectively suggest that the specific occlusal features have a complex relationship to TMD pain. The available evidence indicates that that complex relationship, pointedly, does not include a direct causal role. Just as the evidence has not supported occlusal attributes as cause of TMD, the research literature has not supported any efficacy of occlusal treatment for a TMD.⁹⁰ Overall, studies examining occlusal characteristics and TMD symptoms have failed to identify a strong association.⁹¹ Returning to the early work of Costen, the loss of occlusal vertical dimension has been (and perhaps continues to be) considered a cause of a TMD, but contemporary evidence for this remains lacking.⁹² Finally, the focus on static occlusal features sidesteps the potentially far more important dynamic aspects of the dentition where more force and greater instability occur: during mastication, when the teeth do not actually contact.

Complicating static and dynamic occlusion is where the teeth should be when the teeth do not need to touch and the mandible does not need to function. When the mandible is not functionally active, it adopts a so-called rest position in which the condyle occupies a relatively neutral position in the glenoid fossa with the teeth separated. The rest position is considered to be associated with minimum muscular activity and with the articulating surfaces of the mandibular teeth a few millimeters from the occlusal contact position with the opposing teeth.⁹³ “Rest position” is, however, somewhat of a misnomer since a wide range of activity in the masticatory muscles is observed, under the presumed condition of “rest,” across individuals as well as within individuals across time; the masticatory muscles seldom exhibit a reliable level of lowest activity, even among those who have no signs or symptoms associated with a TMD. Consequently, the muscle activity as well as mandibular position vary for a number of reasons (for example, head posture, emotion, cognition, pain) and “rest position” is not an exact position.⁹⁴ Clinical diagnoses that require an interpretation of rest position must be considered very cautiously.

It may be premature to completely dismiss occlusal attributes for possible causal roles in TMD; a substantial limitation in a majority of studies of occlusion as a putative cause of TMD are that terms such as “disharmony” are used without an adequate operational definition, leading to research that is not reproducible. Inappropriate focus on largely minor occlusal features may have resulted in insufficient attention to the most important attribute of occlusion: stability.⁹⁵ Illustrating that perspective, a relationship between tooth loss and osteoarthrosis has been observed in patients with TMD but not in nonpatient populations.⁹⁶ In contrast, incisal relationships, condylar position, and joint sounds do not reliably differentiate symptomatic individuals and nonpatient populations.^97–99 Finally, perspectives regarding the importance of occlusion in TMDs typically ignore behavior: premature contacts in one dental segment coupled with balancing interferences on that same side could be due to unilateral guarding behavior in response to the TMD pain. Moreover, a shift in the apex point of the gothic arch can be initiated by masseter pain induced by saline injections, suggesting that pain might be the critical factor in producing the occlusal changes that are sometimes reported by patients with TMD.¹⁰⁰ And, finally, patient reports of changes in their occlusion (either accompanying other signs or symptoms of a TMD, or not), often interpreted by dentists as indicative of a problem in the occlusion that must be addressed through alteration of the occlusion, may represent occlusal dysesthesia.¹⁰¹ Dysesthesia refers to alteration in sensory perception, which can be induced by a variety of mechanisms such as persistent pain or altered behavior. The occlusal sense—the feeling of the body state regarding how the teeth fit together and as mediated by periodontal proprioceptors and muscle spindles—can be altered such that even a stable occlusion may be perceived as unstable.

Muscle Hyperactivity

Masticatory muscle hyperactivity—muscle activity without functional purpose—has been proposed as a cause of myofascial pain, also using the diagnostic terms in this context myospasm, muscle spasm, and reflex splinting. The combination of muscle hyperactivity and the muscle pain disorder has been characterized as a “vicious cycle” of hyperactivity and pain mutually reinforcing each other.¹⁰² Muscle hyperactivity is usefully separated into sleep bruxism and waking parafunction, corresponding to the respective states. The favored hypothesis for over 50 years was that sleep bruxism is caused by abnormalities of occlusion, but this was based on heavily flawed research mentioned above.^85,86 Currently, evidence strongly supports sleep bruxism as a parasomnia type of sleep disorder; specifically, sleep bruxism events are related to microarousals during sleep.^103,104 While microarousals are a normal part of sleep architecture in everyone, microarousals selectively trigger bruxism events in those individuals with the disorder, and do not do so in individuals without the disorder—for reasons as yet unknown. The evidence to date is circular, and it does not support microarousals as the cause of sleep bruxism; rather, individuals at risk for sleep bruxism may be differentially primed to respond to microarousals with bruxism events.

A variety of studies have linked sleep bruxism to pain.^105–111 The common explanation is that the pain is simply due to overuse of the muscle during sleep, as in postexercise pain. Clinical observations have indicated, however, that severe sleep bruxism, as measured by extensive tooth wear, can occur without symptoms. Moreover, empirical data demonstrate that not only pain but TMJ clicking and masticatory muscle tenderness are unrelated to severe tooth wear from sleep bruxism.¹¹² These contradictory findings lead to an important paradox: how could the most severe form of a disorder not produce pain while the less severe form presumably does? Polysomnography-based measurement of jaw muscle activity during sleep demonstrates that sleep bruxism may have, at best, a weak relationship to pain on waking the following morning.¹¹³ In other words, individuals with TMD pain may simultaneously have evidence of sleep bruxism and report jaw pain on awakening, but the bruxism may not directly cause the pain.

Parafunction while awake has for more than 50 years also been regarded as a cause of TMD pain, but only recently has any substantial evidence emerged. Waking parafunction has classically been depicted as excessive tooth clenching, but waking parafunction appears to be a much more complex process in terms of a wide range of behaviors (e.g., bracing, pushing, guarding, pressing), a high frequency of occurrence, and generally lower forces than previously assumed. The duration of such behaviors necessary to cause pain appears to vary across individuals. As described previously, muscle activity at so-called rest does not differ between individuals with painful vs. nonpainful jaw-closing muscles,¹¹⁴ suggesting that jaw behavior is very dynamic across the span of a day.¹¹⁵ Waking behaviors, such as tooth clenching or muscle guarding, are remarkably concrete and reliable in how they manifest across persons with or without TMD.^116,117 Experimental evidence suggests that tooth clenching at a relatively low but sustained level might be a source of pain in some individuals.¹¹⁸ As primary evidence that parafunctional behaviors can cause pain, positive findings on muscle examination are more frequent in individuals who perform tooth-clenching activities.¹¹⁹ In addition, among individuals who have developed a first lifetime episode of TMD pain, parafunctional behaviors are reported at a much higher rate prior to the development of the painful TMD compared to those who do not develop TMD, demonstrating the potential of these behaviors to contribute to the development of painful TMD.¹²⁰ Oral parafunctional behaviors exhibit a substantial association with chronic TMD pain, suggesting that the parafunctional behaviors have both contributed to the persistence of the TMD and become a result of the TMD pain.¹²¹ Increasing frequency of such behaviors is also associated with presence of articular disc disorders;¹²² the contribution of parafunction over time to potential worsening of disc displacements remains to be evaluated.

The Pain-Adaptation Model has been proposed as an alternative to the “vicious cycle” hypothesis regarding pain and muscle hyperactivity. The Pain-Adaptation Model is based on observations that EMG activity and force output of the muscle are lower in patients with musculoskeletal pain.¹²³ The reduction in muscle activity is thought to be protective to prevent further injury, and for acute pain, this model is both sensible and clinically useful. The Pain-Adaptation Model and the vicious cycle hypothesis are not incompatible, however; experimental evidence indicates that persistent parafunctional behaviors occurring at low levels of contractile activity are sufficient to cause pain.¹²⁴ Moreover, in chronic pain, the Pain-Adaptation Model fails to have the same relevance in that adaptation and goal-oriented behavior can over-ride the model-specified inhibition in behavior; for example, a person will chew tough textured foods regardless of the pain if the food is desired. In recognition of this clearly observed discrepancy between clinical presentations and the Pain-Adaptation Model, Peck and colleagues provided experimental evidence demonstrating the limits of the Pain-Adaptation Model in understanding pain and behavior.¹²⁵ Overall, the available evidence provides strong support for parafunctional behaviors having a strong role in the etiology of TMD as well as a strong role as a contributing factor for persistence of TMD.

Central Pain Mechanisms

In addition to local factors affecting muscle function, the results of a number of experimental studies of myofascial pain support the hypothesis that chronic pain is caused by altered central nervous system (CNS) processing.^126–130 However, these studies have not been able to distinguish whether the findings are a consequence of the pain rather than the cause of the pain. For example, altered CNS processing related to pain amplification occurs in response to having a pain disorder rather than contributing to the etiology of the disorder.¹³¹ Central pain mechanisms are also proposed as the mechanism underlying the increased risk conferred by a pain disorder for developing another pain disorder.¹³² As such, comorbidity with widespread musculoskeletal pain is likely to contribute toward the development of a chronic TMD. Individuals with fibromyalgia, a chronic widespread musculoskeletal pain disorder, have a significantly higher frequency of masticatory myofascial pain than the general population.^133,134 In a follow-up study on TMD patients, the group that self-reported the coexistence of fibromyalgia had a higher frequency of chronic TMD symptoms.¹³⁵ The presence of pain in other body sites in individuals with a TMD pain diagnosis is high ^121,136 and may indicate that a musculoskeletal problem affecting the jaws is part of a more generalized pain disorder, itself a reflection of central mechanisms.

Psychological Distress

The psychological distress hypothesis proposes that TMD evolves as a consequence of pre-existing problems in overall functioning, usually due to the individual’s stressful environment coupled with poor coping skills, which leads to distress in the form of depression, anxiety, or both. Two pathways by which the psychological distress leads to TMD have been proposed. The most common pathway in the TMD literature specifies that distress leads to oral parafunctional behaviors (as described above) that then result in muscle pain.^137–139 The second pathway, which is common in the general pain literature, specifies that psychological distress results in an overall increased risk for an individual to experience pain in response to some event (for example, a traumatic yawn). A challenge that is continually faced in the clinic when evaluating patients with chronic pain disorders is determining how much of the psychological distress is a cause or a consequence of chronic pain.¹⁴⁰ The weight of the evidence has suggested that the emotional distress is more likely a consequence than a cause of pain.¹⁴¹ That evidence has been, however, largely cross-sectional at the time of entry into the clinic, and prior functioning is assessed retrospectively. In contrast, recent evidence from a large-scale prospective longitudinal study indicates that psychological distress, in the form of depression, anxiety, and problems with stress and coping, exerts a long-term effect on the individual with respect to increased risk for subsequent development of a painful TMD and, consistent with the prior cross-sectional evidence, chronic TMD is associated with greater extent of distress.^142,143

Trauma

The role of trauma as a primary etiology for TMDs varies from self-evident (e.g., pain or mechanical TMJ problem, following direct blow to the jaw and associated with regional swelling) to purely inferential (e.g., onset of jaw pain 6 months after a motor vehicle collision). While the literature points to some trauma events as having greater likelihood of being a sufficient cause of a TMD and other trauma events as not sufficient on their own to cause a TMD, conflicting conclusions emerge from other studies. The best evidence to date may come from two studies using the same methods and conducted in parallel. In a case-control study, individuals with chronic painful TMD reported a high number of trauma events, compared to individuals with no lifetime history of a TMD.¹²¹ Further results from that study indicate that while reported injury, stemming from various injurious events, is a strong predictor of developing a painful TMD, most such instances of injury are without observable tissue damage and injury does not act alone.^144,145 For example, pain sensitivity, psychological distress, and oral parafunctional behaviors remain important contributors to TMD onset, even when injury has occurred. Regardless of whether trauma has a direct causal role for a TMD, traumatic response to any potential tissue-damaging event appears to be increased once painful TMD is present, and consequently trauma becomes a potent perpetuating factor when pain becomes chronic. Individuals with a TMD and a history of regional trauma may be less responsive to treatment and may consequently require more health care resources.^146,147 Collectively, the research suggests that unless a traumatic event has a self-evident relationship to symptom onset, a simple cause–effect relationship may not adequately describe the potential relationship between such events and TMD symptoms.

Mandibular Range of Motion

Mandibular range of motion (ROM) comprises three procedures in the vertical plane and three procedures in the horizontal plane. Measurements of vertical ROM are generally far more useful clinically, compared to those of the horizontal ROM. The three vertical ROM procedures include: maximal opening without pain, as wide as possible with pain, and after opening with clinician assistance; each of these is operationalized accordingly. These measures are termed in the DC/TMD pain-free opening, maximal unassisted opening, and maximal assisted opening, respectively. Vertical measurements are made with a ruler between opposing maxillary and mandibular incisal edges; the measurement can be corrected by the extent of vertical overlap of the teeth, if a measure of full mobility is desired. Mouth opening with assistance is accomplished by applying mild to moderate pressure against the upper and lower incisors with the thumb and index finger. All three of these measures exhibit excellent reliability (ICC > 0.90) among trained examiners, and therefore are excellent measures for monitoring status of the disorder over time.

The three horizontal ROM procedures include: right and left lateral, and protrusive movements of the mandible, and all are executed “as far as possible, even if painful” while the teeth are slightly separated. Lateral movement measurements are made with the ruler measuring the displacement of the lower midline from the maxillary midline and adding or subtracting the lower-midline discrepancy. Protrusive movement measurement is made by adding the distance the lower incisors travel beyond the upper incisors to the horizontal distance between the upper and lower central incisors during full closure. All three of these measures exhibit acceptable reliability (ICC > 0.80) among trained examiners; these measures are less useful clinically.

Normal maximum mouth opening is ≥ 40 mm. In a study of 1160 adults, the mean maximum mouth opening was 52.8 mm (with a range of 38.7 to 67.2 mm) for men and 48.3 mm (with a range of 36.7 to 60.4 mm) for women.²²⁵ Normal lateral and protrusive movements are ≥ 7 mm.^226–228 Measures of the mandibular range of movement are similarly performed in children. The mean maximum mouth opening recorded in 75 boys and 75 girls aged 6 years was 44.8 mm.²²⁹ Similar values (a mean maximum opening of 43.9 mm, with a range of 32 to 64 mm) were observed in 189 individuals with a mean age of 10 years.²³⁰ The means of left, right, and protrusive maximal movements were each approximately 8 mm.

ROM assessments have two types of diagnostic significance. The first is that following each of the tests (with the exclusion of pain-free opening), the patient is asked if the movement caused pain, and if so, to point to the area of pain and to indicate whether that pain replicated pain of complaint (see section Palpation for pain for further explanation regarding pain replication). The second is by using maximal assisted opening for distinguishing within the disorder of disc displacement without reduction the subtypes of with vs. without limitation. More generally, observed findings from the three vertical measures, and sometimes the three horizontal measures, are evaluated in relation to the history and other clinical findings: are the ROM measures expected or unexpected?

There are several non criterion-based uses of the ROM measures, particularly when comparing findings across all three procedures. Passive stretching (mouth opening with assistance) is a technique that may assist in differentiating limitation due to a muscle or joint problem, but clinical judgment is needed to interpret. In performing maximal assisted opening, the examiner can evaluate the quality of resistance at the end of the movement. Muscle restrictions are associated with a soft end-feel and should result in an increase > 5 mm beyond the maximal unassisted opening. Joint disorders such as acute nonreducing disc displacements are described as having a hard end-feel and characteristically limit assisted opening to < 5 mm. However, limited movement in response to attempted assisted opening can be due to two other causes: muscle contracture and guarding behavior by the patient. The latter can be especially meaningful when considering other biobehavioral factors, such as fear avoidance or kinesophobia,^231,232 for the direction of treatment. It is difficult to operationalize guarding behavior for reliable assessment.

Noises

Palpation of the TMJs is first performed to detect irregularities during condylar movement, described as clicking or crepitus. The lateral pole of the condyle is most accessible for palpation during mandibular movements. In addition to joint noise, there may be palpable differences in the form of the condyle comparing right with left. A condyle that does not translate may not be palpable during mouth opening and closing. This may be a finding associated with an ADD without reduction. A click that occurs on opening and closing and is eliminated by bringing the mandible into a protrusive position before opening is most often associated with ADD with reduction, but this maneuver for eliminating reciprocal clicks does not assure a diagnosis of ADD with reduction.²⁰⁵

Palpation for Pain

The most widely used clinical test for the assessment of a TMD is applying pressure to muscles and joints in order to determine if pain is elicited by the stimulus, known as palpation pain. While this procedure is deemed fully valid and appropriate for the extraoral muscles, intraoral palpation of the lateral pterygoid muscle has been challenged because of its location and inaccessibility (Figure 10-10).²³³ In addition to poor reliability associated with its examination, the examination procedure is likely to cause discomfort in individuals without a TMD, diminishing the value of lateral pterygoid palpation as a diagnostic test.²³⁴ The fibers of the deep masseter muscle are intimately related to the lateral wall of the joint capsule, which may explain the frequent localization by patients of the pain complaint to the preauricular area broadly. This anatomic characteristic makes differentiating muscle and joint pain in this area difficult.^235,236