This chapter focuses on the assessment and management of disorders of the masticatory system. The masticatory apparatus is a specialized unit that performs multiple functions, including those of suckling, cutting and grinding food, swallowing, and communication. The loss of these functions, particularly in association with pain, is characteristic of masticatory system disorders and causes significant distress that can be severely disabling.
The term temporomandibular disorder(s) (TMD) used in this chapter is a collective term embracing a number of clinical problems that involve the masticatory muscles, the temporomandibular joints (TMJs), and associated structures.1 These disorders are characterized by: (1) facial pain in the region of the muscles of mastication, TMJs, or both; (2) limitation or deviation in mandibular movements; (3) hyperalgesia of the musculoskeletal structures; and (4) TMJ sounds during jaw movement and function.2 “TMD” is not a diagnosis, but refers to any of many different disorders. Differentiating subtypes of muscle and joint disorders according to validated diagnostic criteria has often been sidestepped in favor of ad hoc assessment methods and ad hoc diagnoses. Adequate evidence supporting valid diagnostic approaches now exists3 and such approaches are recommended.4 In the past, disorders of the masticatory system were generally treated as one condition or syndrome, with no attempt to identify different muscle or joint disorders and link those to the chief complaint as well as targeted therapy. Use of a validated approach should lead to a better understanding of the natural course, more accurate predictions of prognosis, and more effective treatments. This chapter presents a general but evidence-based approach to the diagnostic assessment and nonsurgical management of the most common TMDs. Some of the less common disorders are also considered in order to better draw attention to the salient characteristics of the common disorders and why the general therapeutic guidelines for the common disorders remain the most sensible.4
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
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
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
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
Lateral Temporomandibular Ligament
The lateral temporomandibular ligament is the main ligament of the joint, lateral to the capsule but not easily separated from it by dissection. Its fibers pass obliquely from bone lateral to the articular tubercle in a posterior and inferior direction and insert in a narrower area below and behind the lateral pole of the condyle (Figure 10-5). However, various studies were unable to confirm a distinct structure separate from the capsule.21,26
The sphenomandibular ligament arises from the sphenoid bone and inserts on the medial aspect of the mandible at the lingula. The stylomandibular ligament extends from the styloid process to the deep fascia of the medial pterygoid muscle. It is thought to become tense during protrusive movement of the mandible and may contribute to limiting protrusive movement.5
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
Between 65 and 85% of people in the United States experience one or more symptoms of a TMD during their lives, but the symptoms are self-limiting for most individuals and resolve without professional intervention.39 Incidence of first lifetime onset of a painful TMD appears to be between 2–4% per annum.40–43 Although the prevalence of one or more signs of mandibular pain and dysfunction is high in the population, only about 5 to 7% have symptoms severe enough to require treatment.39,44,45Among those who develop a TMD, approximately 12% experience prolonged pain that results in disability,39 and more recent estimates indicate that between 25–50% of individuals with acute painful TMD develop chronic pain in the absence of appropriate intervention.46,47 In terms of symptom profile, individuals with a painful TMD are similar to those with headache and back pain with respect to pain intensity, frequency, chronicity, psychosocial distress, and pain-related disability.48,49 These profiles appear to be similar in individuals with TMDs across cultures; for example, Asian, Swedish, and American populations with TMDs share similar characteristics.50
Available evidence indicates that TMDs are most prevalent between the ages of 20 and 40 years, and that prevalence then decreases by age 60, after which it decreases substantially.51 The lower prevalence of TMDs in older age groups suggests that the disease course in a significant proportion of individuals with TMDs is strongly influenced by situational factors that resolve with aging. TMDs in the community occur at about twice the rate in females vs. males, yet females are eight times more common in the clinic population, compared to males. The reason why women make up the majority of patients presenting for treatment remains unclear. While the natural course of TMDs is poorly understood, gender apparently affects the disease course as well.52 For example, oral contraceptives and estrogen replacement in women over 40 years of age substantially increases the risk of developing a painful TMD.53
Signs and symptoms of masticatory muscle and TMJ dysfunction are also commonly observed in children and adolescents.54–56 Among adolescents in Sweden between the ages of 12 and 19 years, 4.2% reported TMD pain, and girls reported TMD pain approximately twice more frequently than boys, 6% compared with 2.7%.57 Surprisingly, a wide variety of painful TMD characteristics observed in adults also occur to largely the same extent in children and adolescents. For example, among a group of 40 children aged 10 to 16 years and presenting with signs and symptoms of a painful TMD, 14 (35%) were diagnosed as having acute reactive depression.58 Arthrography and computed tomography (CT) were performed on 31 children complaining of TMJ pain and dysfunction: 12 (39%) exhibited disc displacement with reduction, and 17 (55%) exhibited disc displacement without reduction.59 Among the 29 individuals with internal derangement, causation was attributed to previous injury in 12 individuals. Yet, in a survey of 1000 12-year-old children, only 1% had a maximum mouth opening of less than 40 mm, indicating that the norm for expected opening range is established prior to the final growth phase in adolescents. Despite this extent of abnormal findings, only a small proportion of children presented with clinical findings severe enough to warrant treatment.60
Etiology of the most common TMDs is unknown. The literature has been dominated by several hypothesized causes: occlusal disharmony, muscle hyperactivity, central pain mechanisms, psychological distress, and trauma.
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 cited85,86 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.
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.
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
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.
Integration of Etiologic Factors
The time period over which potentially etiologic events, from trauma to stress reactivity, occur as well as the latency between event and biological or behavioral consequences make assigning causation very difficult.51 The lack of a clear single cause of TMD is notable in the majority of individuals, and in such individuals, TMD is increasingly thought to emerge in response to multiple risk determinants: no one factor by itself is sufficient to cause the disorder, whereas multiple factors increase the risk. A final initiating event may even be relatively minor, but if it occurs in conjunction with other already active determinants, then critical thresholds can be exceeded and symptoms emerge. In other words, multiple factors often come together contributing to the initiation, aggravation, and/or perpetuation of the disorder. Given the available evidence, the factors that have supporting evidence and at least some biological plausibility are, from local to systemic, summarized as follows:
- TMJ hypermobility.148–150
- Trauma (e.g., dental procedures, oral intubations for general anesthesia, yawning, hyperextension associated with cervical trauma).145,147,151–156
- Parafunctional behaviors (e.g., sleep bruxism, tooth clenching, jaw guarding, lip or cheek biting).120–122,157–159
- Sleep disturbance.160,161
- Comorbidity in the form of other rheumatic, musculoskeletal, or pain disorders. 162,163
- Emotional distress.142,143,164,165
- Poor general health and an unhealthy lifestyle.166,167
The factors listed above vary in the strength of both evidence and association with TMD. Each factor can occur, for the most part, along continua defined by magnitude (i.e., weak to strong), frequency (seldom to continuous), and duration (short term to enduring). The actual threshold by which each factor exerts an influence on a given individual likely varies according to their susceptibility to each factor for its potential to cause problems for the organism. Plus, each TMD would appear to have its own profile of risk factors. For example, myofascial pain with arthralgia and myofascial pain alone were associated with trauma, clenching, third molar removal, somatization, and female gender.168 Emerging research will likely provide much better estimates regarding the relative significance of these and other factors.
Due to the uncertainty about etiology, the present diagnostic classifications of TMD have been based only on signs and symptoms. Whether this descriptive approach is a particular strength, given the complexity of etiology, or whether this is a weakness, given the emerging data regarding types of pain169 and pain processing models,170 remains to be determined. Substantial evidence is now emerging regarding the myriad factors that predict the first lifetime episode of TMD,171 and collectively the evidence indicates that TMD is a complex disease. A complex disease is one that does not follow simple classical etiologic pathways, whereby a single necessary and sufficient etiologic factor exists; instead, epigenetic factors, phenotypic factors, and environmental factors are dynamic and interact over time. Part of this interaction may also include feedback loops, whereby the activity of a particular factor will facilitate its emergence again; for example, stress experience due to poor coping tends to progress in a downward spiral. This type of complexity requires multidimensional assessment and, correspondingly, multiaxial classification. See Tables Table 10‐1‐Table 10‐5.
Current perspectives on taxonomy development point to the inadequacy, both scientific and clinical, of classification systems for complex disease developed according to traditional methods. For the future, we envision the merger of genetics, pain medicine, neuroscience, psychology, and bioinformatics as underlying the next major diagnostic system for TMD.172–176 In addition, we envision that diagnostic systems designed for each domain (jaw, head, back, etc.) will be integrated into one system based on a standard set of rules.177 Yet, it is also likely that the traditional taxonomic approach based on signs and symptoms will continue to be used, despite the limitations inherent in that approach, because the need for identifying the disorder at the local tissue level will continue to have clinical utility. For example, the present validated system for the common TMDs3 minimizes false positive diagnoses and thereby unnecessary treatment. And this will continue to be a major strength.
Table 10‐1 Taxonomic classification for temporomandibular disorders.
Source: Reprinted by permission of J Oral & Facial Pain and Headache, and Journal of Oral Rehabilitation.
|I. TEMPOROMANDIBULAR JOINT DISORDERS|
|1. Joint pain|
|2. Joint disorders|
|A. Disc disorders|
|1. Disc displacement with reduction|
|2. Disc displacement with reduction with intermittent locking|
|3. Disc displacement without reduction with limited opening|
|4. Disc displacement without reduction without limited opening|
|B. Hypomobility disorders other than disc disorders|
|C. Hypermobility disorder|
|3. Joint diseases|
|A. Degenerative joint disease|
|B. Systemic arthritides|
|C. Condylysis/Idiopathic condylar resorption|
|D. Osteochondritis dissecans|
|G. Synovial Chondromatosis|
|5. Congenital/developmental disorders|
|II. MASTICATORY MUSCLE DISORDERS|
|1. Muscle pain|
|1. Local myalgia|
|2. Myofascial pain|
|3. Myofascial pain with referral|
|5. Movement Disorders|
|A. Orofacial dyskinesia|
|B. Oromandibular dystonia|
|6. Masticatory muscle pain attributed to systemic/central pain disorders|
|A. Fibromyalgia or widespread pain|
|1. Headache attributed to TMD|
|IV. Associated structures|
|1. Coronoid hyperplasia|
In the late 1980s and early 1990s, TMD classification was influenced by several independent developments. The first developments emphasized concise symptom- and sign-based classification systems that were developed for use by the practicing clinician.178–180 The American Academy of Orofacial Pain (AAOP) published a more far-reaching general classification of disorders that was developed by a broad group of experts who applied available knowledge to the development of an acceptable and useful system for clinical practice,181 and emphasized multiple diagnoses which reflected clinical reality.182,183 This classification system was inclusive of all disorders a clinician might encounter but it was not highly reliable (due to its structure) and it was not assessed for validity. These developments, however, did not facilitate research, creating a large hole that was too often filled with poorly done etiologic and treatment studies. The Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) was published as a system “offered to allow standardization and replication of research into the most common forms of muscle and joint-related TMD.”184 This system was based on several core principles with enduring value for the field.185 The assessment of physical status (Axis I) was described in sufficient detail for standardized data collection, allowing reliable diagnoses and comparison of findings across investigators and clinicians. Because pain transcends a given organ system, the classification system also reflected psychological, behavioral, and social factors considered to be as important as an accurate description of the physical pathology. Consequently, the RDC/TMD classification contained a separate Axis II to assess psychosocial status and pain-related disability. The RDC/TMD was designed for research, and thereby permitted far more reliable diagnoses of the disorders the clinician encounters most often.
Table 10‐2 Diagnostic criteria for the most common pain-related temporomandibular disorders.
Source: Reprinted by permission of J Oral & Facial Pain and Headache.
|Myalgia (ICD-9 729.1)|
|Description||Pain of muscle origin that is affected by jaw movement, function, or parafunction, and
replication of this pain occurs with provocation testing of the masticatory muscles.
|Validity||Sensitivity 0.90; Specificity 0.99|
|Comments||The pain is not better accounted for by another pain diagnosis. Other masticatory muscles may be examined as dictated by clinical circumstances but the sensitivity and specificity for this diagnosis based on these findings has not been established.|
|Myofascial Pain with Referral (ICD-9 729.1)|
|Description||Pain of muscle origin as described for myalgia with referral of pain beyond the boundary of the masticatory muscle(s) being examined when using the myofascial examination protocol. Myofascial pain with referral is a subtype of myalgia.|
|Validity||Sensitivity 0.86; Specificity 0.98|
|Comments||The pain is not better accounted for by another pain diagnosis. Other masticatory muscles may be examined as dictated by clinical circumstances but the sensitivity and specificity for this diagnosis based on these findings has not been established.|
|Arthralgia (ICD-9 524.62)|
|Description||Pain of joint origin that is affected by jaw movement, function, or parafunction, and replication of this pain occurs with provocation testing of the TMJ.|
|Validity||Sensitivity 0.89; Specificity 0.98|
|Comments||The pain is not better accounted for by another pain diagnosis.|
|Headache attributed to TMD (ICD-9 339 4)|
|Description||Headache in the temple area secondary to pain-related TMD* that is affected by jaw movement, function, or parafunction, and replication of this headache occurs with provocation testing of the masticatory system.|
|Validity||Sensitivity 0.89; Specificity 0.87|
|Comments||The headache is not better accounted for by another headache diagnosis.|
|Footnote||* A diagnosis of painful TMD (e.g., myalgia, myofascial pain with referral, or TMJ arthralgia) is derived using valid diagnostic criteria.|
1 The time frame for assessing pain including headache is in “the last 30 days” since the stated sensitivity and specificity of these criteria were established using this time frame. Although the specific time frame can be dependent on the context in which the pain complaint is being assessed, the validity of this diagnosis based on different time frames has not been established.
2 The examiner must identify with the patient all anatomical locations that they have experienced pain in the last 30 days. For a given diagnosis, the location of pain induced by the specified provocation test(s) must be in an anatomical structure consistent with that diagnosis.
3 “Familiar pain” or “familiar headache” is based on patient report that the pain induced by the specified provocation test(s) has replicated the pain that the patient has experienced in the time frame of interest, which is usually the last 30 days. “Familiar pain” is pain that is similar or like the patient’s pain complaint.
4 The International Classification of Diseases 9th Edition (ICHD-9) has not established a specific code for Headache attributed to TMD; ICD-9 339 is for “other headache syndromes.” If a primary headache is present (e.g., tension type headache) then the headache can be classified according to the primary headache type.
Table 10‐3 Diagnostic criteria for the most common intra-articular temporomandibular disorders.
Source: Reprinted by permission of J Oral & Facial Pain and Headache.
|Disc Displacement with Reduction (ICD-9 524.63)|
|Description||An intracapsular biomechanical disorder involving the condyle-disc complex. In the closed
mouth position the disc is in an anterior position relative to the condylar head and the disc
reduces upon opening of the mouth. Medial and lateral displacement of the disc may also be
present. Clicking, popping or snapping noises may occur with disc reduction. A history of prior locking in the closed position coupled with interference in mastication precludes this diagnosis.
|Validity||Without imaging: sensitivity 0.34; specificity 0.92.
Imaging is the reference standard for this diagnosis.
|Imaging||When this diagnosis needs to be confirmed, then TMJ MRI criteria 2 are positive for both of the following:
|Disc Displacement with Reduction with Intermittent Locking (ICD-9 524.63)|
|Description||An intracapsular biomechanical disorder involving the condyle-disc complex. In the closed mouth position the disc is in an anterior position relative to the condylar head, and the disc intermittently reduces with opening of the mouth. When the disc does not reduce with opening of the mouth, intermittent limited mandibular opening occurs. When limited opening occurs, a maneuver may be needed to unlock the TMJ. Medial and lateral displacement of the disc may also be present. Clicking, popping, or snapping noises may occur with disc reduction.|
|Same as specified for Disc Displacement with Reduction. Although not required, when this disorder is present clinically, examination is positive for inability to open to a normal amount, even momentarily, without the clinician or patient performing a specific manipulative maneuver.|
|Validity||Without imaging: sensitivity 0.38; specificity 0.98.
Imaging is the reference standard for this diagnosis.
|Imaging||When this diagnosis needs to be confirmed, then the imaging criteria2 are the same as for disc displacement with reduction if intermittent locking is not present at the time of imaging. If locking occurs during imaging, then an imaging-based diagnosis of disc displacement without reduction will be rendered and clinical confirmation of reversion to intermittent locking is needed.|
|Disc Displacement without Reduction with Limited Opening (ICD-9 524.63)|
|Description||An intracapsular biomechanical disorder involving the condyle-disc complex. In the closed mouth position the disc is in an anterior position relative to the condylar head, and the disc does not reduce with opening of the mouth. Medial and lateral displacement of the disc may also be present. This disorder is associated with persistent limited mandibular opening that does not resolve with the clinician or patient performing a specific manipulative maneuver. This is also referred to as “closed lock.”|
|Maximum assisted opening (passive stretch) < 40mm including vertical incisal overlap.|
|Validity||Without imaging: sensitivity 0.80; specificity 0.97.
Imaging is the reference standard for this diagnosis.
|Imaging||When this diagnosis needs to be confirmed, then TMJ MRI criteria2 are positive for both of the following:
Note: Maximum assisted opening of < 40mm is determined clinically.
|Footnote||Presence of TMJ noise (e.g., click with full opening) does not exclude this diagnosis.|
|Disc Displacement without Reduction without Limited Opening (ICD-9 524.63)|
|Description||An intracapsular biomechanical disorder involving the condyle-disc complex. In the closed
mouth position the disc is in an anterior relative the condylar head and the disc does not
reduce with opening of the mouth. Medial and lateral displacement of the disc may also be
present. This disorder is NOT associated with limited mandibular opening.
|Criteria||HISTORY||Same as specified for Disc Displacement without Reduction with Limited Opening.|
|Maximum assisted opening (passive stretch) > 40mm including vertical incisal overlap.|
|Validity||Without imaging: sensitivity 0.54; specificity 0.79.
Imaging is the reference standard for this diagnosis.
|Imaging||When this diagnosis needs to be confirmed, then TMJ MRI criteria 2 are the same as for
disc displacement without reduction with limited opening.
Note: Maximum assisted opening of ≥ 40mm is determined clinically.
|Footnote||Presence of TMJ noise (e.g., click with full opening) does not exclude this diagnosis.|
|Degenerative Joint Disease (ICD-9 715.18)|
|Description||A degenerative disorder involving the joint characterized by deterioration of articular tissue with concomitant osseous changes in the condyle and/or articular eminence.|
|At least one of the following must be present:
1. Crepitus detected with palpation during opening, closing, lateral, or protrusive movements.
|Validity||Without imaging: sensitivity 0.55; specificity 0.61.
Imaging is the reference standard for this diagnosis.
|Imaging||When this disorder is present, then TMJ CT criteria 2 are positive for at least one of the following: Subchondral cyst(s), erosion(s), generalized sclerosis or osteophyte(s). Note: Flattening and/or cortical sclerosis are considered indeterminant findings for DJD and may represent normal variation, aging, remodeling or a precursor to frank DJD.|
|Subluxation (ICD-9 830.1)|
|Description||A hypermobility disorder involving the disc-condyle complex and the articular eminence: In the open mouth position, the disc-condyle complex is positioned anterior to the articular eminence and is unable to return to a normal closed mouth position without a specific manipulative maneuver. The duration of dislocation may be momentary or prolonged. When prolonged the patient may need the assistance of the clinician to reduce the dislocation and normalize jaw movement; this is referred to as luxation. This disorder is also referred to as “open lock.”|
|Although no exam findings are required, when this disorder is present clinically, examination
is positive for inability to return to a normal closed mouth position without the patient performing a specific manipulative maneuver.
|Validity||Without imaging and based only on history: sensitivity 0.98; specificity 1.00.|
|Imaging||When this disorder is present, then imaging criteria are positive for the condyle positioned beyond the height of the articular eminence.|
1 The time frame for assessing selected biomechanical intra-articular disorders is in “the last 30 days” since the stated sensitivity and specificity of these criteria was established using this time frame. Although the specific time frame can be dependent on the context in which the pain complaint is being assessed, the validity of this diagnosis based on different time frames has not been established.
2 Ahmad M, Hollender L, John M, Anderson Q, Kartha K, Ohrbach R, Truelove, E and Schiffman E. Research Diagnostic Criteria for Temporomandibular Disorders: Development of Image Analysis Criteria and Examiner Reliability for Image Analysis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009;107:844–860.
Table 10‐4 Imaging-based diagnosis of soft-tissue and hard-tissue TMJ disorders.
|Disc diagnosis for the TMJ, based on MRI *|
|Normal||Disc location is normal on closed and open-mouth images.|
|Disc displacement with reduction||Disc location is displaced on closed-mouth images but normal on open-mouth images|
|Disc displacement without reduction||Disc location is displaced on both closed-mouth and open-mouth images.|
|Indeterminate||Disc location is not clearly normal or displaced in the closed-mouth view|
|Disc not visible||Neither signal intensity nor outlines make it possible to define a structure as the disc in the closed-mouth and open-mouth views. If the images are of adequate quality in visualizing other structures in the TMJ, then this finding is interpreted to indicate a deterioration of the disc, which is associated with advanced disc pathology.|
|Osseous diagnoses for the TMJ, based on CT **|
|Indeterminate for osteoarthritis||
* Adapted from Table IV, Ahmad et al, OOOOE, 2009
** Adapted from Table II, Ahmad et al, OOOOE, 2009
Table 10‐5 Selected TM disorders and supplemental characteristics.
Adapted from McNeill C.127
|Deviation in form
Note: Painless mechanical dysfunction or altered function due to irregularities or aberrations in the form of intracapsular soft and hard articular tissues. Does not require intervention.
|Disc displacement with reduction
Note: Clinical significance is related to pain associated with the noise, to mechanical locking, or interference in mastication or other functional activities.
|Disc displacement without reduction||
|Synovitis or capsulitis
Note: Inflammation of the synovial lining or loading of capsular lining. Difficult to clearly differentiate from arthralgia.
Note: Degenerative noninflammatory condition of the joint, characterized by structural changes of joint surfaces secondary to excessive strain on the remodeling mechanism. Distinguish from osteoarthritis, which is a secondary inflammatory condition. Both osteoarthrosis and osteoarthritis are subsumed within degenerative joint disease in the DC/TMD.
Note: Is a regional disorder, distinguishing it from fibromyalgia. When the pain is local to the area of stimulation, this disorder is termed myalgia in the DC/TMD in order to note the presence of hyperalgesia without spreading, referral, or autonomic reactions. The clinical significance of these additional characteristics is with differential diagnosis; the requirement for specific treatments when referral is present remains untested but anecdotally rich.
|Protective muscle splinting
Note: Restricted or guarded mandibular movement due to co-contraction of muscles as a means of avoiding pain caused by movement of the parts. Should be distinguished from fear-avoidance behavior by ruling out local nociceptive source, either by history or by examination.
Note: Chronic resistance of a muscle to passive stretch as a result of fibrosis of the supporting tendon, ligaments, or muscle fibers themselves.
MRI = magnetic resonance imaging; TMJ = temporomandibular joint.
The RDC/TMD classification was subsequently assessed in a multicenter study for validation and the findings and subsequent publications improved upon the RDC/TMD while retaining the core features described above.186 The publications included: Diagnostic Criteria for TMDs (DC/TMD);3 an overall taxonomy and draft criteria for the less common TMDs;187 and incorporation of both into the AAOP guidebook.1,188 In summary, reliable and valid diagnoses of the common TMDs are readily available for clinical and research use. The DC/TMD allows, for each individual, multiple TMD diagnoses: several pain diagnoses and, for each joint, pain, disc displacement, degenerative joint disease, and subluxation diagnoses. The terms used are clearly defined, the clinical examination procedures are completely specified, and the criteria required to meet the diagnosis are specific. The pain diagnoses exhibit excellent sensitivity and specificity. In contrast, the joint disorders, with one exception, exhibit unacceptable sensitivity and specificity based only on clinical assessment. The one exception among the joint disorders is disc displacement without reduction, with limited opening, which does have acceptable sensitivity and specificity from clinical examination procedures.
In clinical practice, it has been generally believed that rigidly adhering to the criteria of a system such as the DC/TMD may not be possible due to the assumption that the common TMDs, for example, exhibit a wide spectrum of signs and symptoms. However, recent evidence indicates that each of the common TMD has reliable characteristics; for the very large majority of patients, the stated criteria clearly define the disorder. The consequence is that the clinician, using the described clinical assessment methods, can reliably and validly provide diagnoses for most individuals with TMD pain. Imaging will be required to establish a disc disorder diagnosis such as “disc displacement without reduction.” The clinician should recommend diagnostic imaging as part of the assessment when the prognosis or choice of treatment might benefit. The reader is referred to the publication by Schiffman and colleagues for a full description of the DC/TMD, to the publication by Peck and colleagues for diagnostic criteria for the less common TMD, to the text by DeLeeuw and Klasser for a comprehensive guidebook to evaluation, diagnosis, and treatment, and to the website of the International Network for Orofacial Pain and Related Disorders Methodologies (INfORM; rdc-tmdinternational.org) for clinical examination specifications, training videos, and all patient assessment instruments. Consequently, a system such as the DC/TMD appropriately guides the clinician towards better diagnosis. Yet, despite these developments toward a well-operationalized, reliable, and valid physical examination, it is underutilized and the psychosocial assessment domain is similarly underutilized.189
Where sleep bruxism belongs within a TMD classification system was a challenge for the RDC/TMD authors—who omitted it from the classification—and similarly it is not part of the DC/TMD. Is sleep bruxism a disorder, or is it a process?190 Classification of sleep bruxism remains an ongoing question, as does whether sleep bruxism aggravates or contributes to the persistence of pain symptoms associated with TMD. While the cause of bruxism is not fully understood, the evidence strongly indicates that occlusal abnormalities are not the cause.191,192 Occlusal appliances may protect the teeth from the effects of bruxism but cannot be expected to prevent or decrease the bruxism activity.193 When bruxism is considered to be the cause or a factor of TMD symptoms, oral appliance therapy is often effective, but symptoms are likely to return when appliance therapy is withdrawn.194 In one report, nocturnal aversive biofeedback and splint therapy caused a decrease in the frequency and duration of bruxism, but bruxism activity returned after treatment was withdrawn.195 Occlusal splints worn during sleep have not been found to stop bruxism but do reduce the signs of bruxing.196 While oral appliances remain the treatment with the best evidence for sleep bruxism,197 it is notable that placebo intraoral appliances are equally effective for reducing myofascial pain.198 The efficacy of the placebo-type oral appliance for bruxism critically questions the nature of the problem that the traditional oral appliance is assumed to address.
The critical question raised by placebo oral appliances is extended when medication treatments are considered. Reports of bruxism and symptoms of facial pain, earache, and headache associated with the use of selective serotonin reuptake inhibitors (SSRIs) have been published.199 Symptoms of bruxing resolved when the dosage was decreased or when buspirone was added.200 Buspirone has a postsynaptic dopaminergic effect and may act to partially restore suppressed dopamine levels associated with the use of SSRIs. Tan and Jankovic injected severe bruxers in the masseter muscles with botulinum toxin in an open-label prospective trial and reported significant improvement in symptoms and minimal adverse effects.201 Botulinum toxin exerts a paralytic effect on the muscle by inhibiting the release of acetylcholine at the neuromuscular junction. The treatment effect lasted approximately 5 months and had to be repeated. The implications of this research, whereby the end organ response of the motor cortex signal is blocked, remain for future investigators.
The most valuable aspect of the diagnostic assessment is a thorough history;202 pain disorder diagnoses rely predominantly on the history, and the diagnosis of some pain disorders, such as headache, relies exclusively on the history.203 For some disorders such as headache, the history serves to rule out other forms of pathology; for TMD, the examination is confirmatory for a pain diagnosis but remains only suggestive for most of the joint disorders. An examination for a particular disorder (e.g., the comprehensive examination of TMD, as described),204 must be supplemented by examination procedures as indicated for a differential diagnosis; for example, ruling out odontogenic causes of regional masticatory system pain. In contrast to the situation 30 years ago when TMD diagnostic tests were not validated or standardized,180 the clinical tests most needed for the assessment of a person with a TMD are now standardized, reliable, and valid.3,205 In contrast, diagnostic tests such as ultrasonography of joint sounds, thermography, jaw tracking, and EMG, all of which exhibit high measurement reliability and precision, do not offer the assurance of a more accurate diagnosis or better treatment outcomes.206 These devices were reviewed for their diagnostic value in assessing patients with temporomandibular complaints, and were judged 30 years ago to not have the necessary sensitivity and specificity for a valid diagnosis.202 No additional supporting evidence has emerged over the past several decades. Claims that they are adjunctive tests must nevertheless be accompanied by the same evidence as required for any diagnostic test; if an adjunctive test is to be useful, incremental validity must be demonstrated. Incremental validity refers to the ability of an additional test to provide unique information that improves the sensitivity or specificity of the information obtained prior to the additional test. For example, analysis of TMJ synovial fluid is an active area of research but has not yet become a standard procedure in diagnosis or the selection of treatment. These tests require sophisticated instrumentation that would increase health care costs to the patient that, for the present, are not justified.
Consequently, history, clinical examination, and imaging when indicated remain the recommended diagnostic approach for most patients.4,179 Diagnostic imaging is of value in selected conditions but not as a routine part of a standard assessment. Diagnostic imaging can increase accuracy in the detection of internal derangements207 and abnormalities of articular bone.208 The clinical meaningfulness of such tests, however, must be determined prior to ordering the test; a special test should be preceded by a clinical hypothesis (differential diagnosis) that the test will be able to answer, and the clinical hypothesis should be related to a particular course of action. For example, if treatment for what appears to be a painful recurrent mechanical joint problem will proceed in one direction if the problem is a disc displacement, but in another direction if the disc is normal, then imaging would be well-justified. If, on the other hand, both treatments for this stated example would be pursued, each for 4–6 weeks and with no or minimal risk of adverse effects, then the treatment trial without imaging may be more prudent, thereby not unnecessarily expending health care resources and not adding imaging information that may only confuse rather than clarify. A painful clicking joint should be treated, regardless of whether the problem is due to an internal derangement or not.209 If the choice of treatment depends on a more accurate diagnosis, then imaging would be indicated.
Similarly, other tests should be ordered when the differential diagnosis warrants further diagnostic exploration. Examples follow. Facial pain similar to the pain of a painful TMD may be associated with serious undetected disease. Muscle or joint pain may be a secondary feature of another disease or may mimic a TMD. A diagnosis of a more serious condition may be missed or delayed.210,211 Severe throbbing temporal pain associated with a palpable nodular temporal artery, increasingly severe headache associated with nausea and vomiting, and documented altered sensation or hearing loss are all indications of serious disease requiring timely diagnosis and management. In short, TMD diagnosis (and management) requires ongoing use of clinical decision-making skills.
The most common symptom related to TMD is pain, and it is the overwhelming reason people seek care. Pain may be present at rest, may be continuous or intermittent, and characteristically increases with jaw function such as chewing or opening wide. Other chief complaints in relation to seeking care for a TMD include restricted jaw movement, painful or loud TMJ clicking or crepitus, and jaw locking.
Pain severity or intensity is a subjective measure provided by the patient and can be rated in several ways.212 A rating scale can be either numeric or verbal. A numeric scale asks the patient to rate pain by identifying a number, typically between 0 and 10, that best reflects pain intensity. Verbal descriptors such as no pain, mild pain, moderate pain, and severe pain can also provide an equally valid assessment. If an estimate with greater precision is needed, a visual analogue scale (VAS) has high sensitivity to change and better independence when using repeated measures. A VAS uses a 10-cm line anchored on the left side with the descriptor of “no pain” and on the right an extreme descriptor such as “the worst pain ever experienced.” The patient is asked to mark his or her pain intensity by placing a mark on the line, and the score is obtained by measuring from the left end to the mark.
Because pain intensity associated with TMDs typically varies, including periods of no pain, assessing pain intensity only at one time point—for example, at the clinic consultation—can be misleading. Any of the pain intensity rating scales can be used to assess differing aspects of pain, such as current, minimum and maximum in the past, or average pain ratings. Consideration of time period is important: too short, and meaningful variability may be lost; too long, and memory and relevance become potential problems. For the temporal reference frame regarding whether pain has been present or absent, the DC/TMD (Diagnostic Criteria for Temporomandibular Disorders)3 explicitly uses the “last 30 days” for two reasons: memory for prior pain is better with shorter time periods, and, in general, the last 30 days appears to be sufficient for an active chief complaint of pain. For assessing pain intensity, the DC/TMD utilizes the pain measurement scales from the Graded Chronic Pain Scale,213 in order to determine a characteristic pain index, based on current and, over the prior 30 days, average and worst pain.
As defined by the DC/TMD, regional masticatory system pain should be influenced by mandibular function, or an alternative diagnosis should be suspected. Table 10‐2 indicates that pain aggravated by function is a criterion for a diagnosis of either myalgia or arthralgia. Mandibular functions shown to reliably increase or trigger myofascial pain include chewing hard or tough food, opening the mouth, or moving the jaw. Table 10‐6 lists questions that are useful parts of the history for assessing mandibular function.
A pain drawing that contains the full body is helpful in defining the extent of pain; the recording of other body regions helps identify patients who have multiple sites of pain, which suggests a more systemic or generalized disorder. A pain drawing completed at initial evaluation may also be used to assess treatment progress of the TMD. Following the initial evaluation, a pain diary can be a useful tool for identifying events or times of increased and decreased pain; it may also serve to identify behaviors or situations that are contributing to the persistence of symptoms.214
|Where is the pain located? Is there pain in any other areas of the body?
When did the pain first begin? What has been the pattern over time; have there been notable periods of remission, or notable periods of exacerbation, and what were the circumstances?
|How often do episodes (or, if pain is continuous: flareups) occur, duration, temporal pattern to the bouts (time of day, day of week), and how managed?|
|When is pain at its worst (morning [on awakening] or as day progresses [toward evening])?|
|What aggravates the pain (e.g., when using the jaw such as opening wide, yawning, chewing, speaking, or swallowing; stress or deadlines; postural positions)?
What alleviates the pain (e.g., rest, analgesic, holding the jaw rigid in specific positions)?
[If other pains such as headaches, earaches, neckache, or cheek pain are present] When did the other pain(s) begin, did they worsen when the jaw pain worsened, did they respond to treatment for the jaw pain?
|Is there pain or thermal sensitivity in the teeth? Does biting on any teeth cause pain?|
|Do jaw joint noises (clicking, popping, grinding, or crepitus) occur when moving the jaw or when chewing?|
|Does the jaw ever hesitate, get stuck, or lock when trying to open or when trying to close from a wide open position?|
|Does jaw motion feel restricted?|
|Has the jaw ever been injured?|
|Has there been an abrupt change in the way the teeth meet or fit together? Does the bite feel “off” or uncomfortable?|
|What treatments have been provided? What was the outcome? What was the compliance with treatment requirements?|
* Miscellaneous symptoms sometimes reported in association with TMD-related include: dizziness; nausea; fullness or ringing in the ears; diminished hearing; facial swelling; redness of the eyes; nasal congestion; altered sensation such as numbness, tingling, or burning; altered vision; and muscle twitching.
Table 10‐7 Problem list of domains and specific factors contributing to persistence and symptom amplification in temporomandibular disorders.
Source: Adapted from Fricton J.163
|Lifestyle||Emotional Factors||Cognitive Factors||Biologic Factors||Social Factors|
|Diet||Prolonged anger||Negative self-image||Other illnesses||Work stresses|
|Sleep||Anxiety||Unrealistic expectations||Past trauma||Unemployment|
|Alcohol||Excessive worry||Inadequate coping||Past jaw surgery||Family stresses|
A range of other symptoms sometimes reported in association with a TMD include dizziness, ear symptoms of fullness, ringing, or earache. Altered occlusion and jaw misalignment are also commonly reported.215 Some patients, especially those with stress related disorders, report additional symptoms such as swelling and numbness, which are functional in nature. Functional symptoms are reported physical abnormalities which are not detected on a careful clinical examination.
Assessment for psychological distress and pain-related disability is frequently an important component of a TMD evaluation. Some TMDs evolve into a chronic pain disorder, resulting in psychological distress, disruption of interpersonal relationships, and an inability to perform daily activities, including work. Psychosocial factors are considered more important than physical factors in predicting treatment outcome.216 The lack of a direct relationship between physical pathology and intensity of pain to subsequent disability emphasizes the need to assess the psychological and behavioral effects of the disorder in order to better understand: (1) the reported pain and not assume that as-yet undetected physical pathology is responsible; (2) anticipated barriers to successful treatment; and (3) the potential for relapse.
Table 10‐7 lists multiple potential contributing factors, organized by domain, to TMD pain often reported in the pain research literature. No one health care professional can be expected to manage the physical pathology of the temporomandibular structures along with all of the various lifestyle, emotional, cognitive, and social issues that may affect the individual with chronic pain. Chronic TMDs with a significant emotional component are best managed in a multidisciplinary setting.
Cluster models have provided replicable insights into the different constellations of factors important for chronic pain. Rudy et al. classified TMD patients based on psychosocial and behavioral parameters into three unique subgroups: dysfunctional, interpersonally distressed, and adaptive copers.217 Patients with painful TMD exhibited psychosocial and behavioral profiles similar to those of patients with back pain or with headache.6 Similarly, Bair et al. also classified individuals with a painful TMD into three unique subgroups: adaptive, pain sensitive, and dysfunctional categories,218 overall very similar to those identified by Rudy and colleagues. These findings highlight the substantial overlap in important characteristics exhibited by patients with a variety of chronic pain disorders. Clinical evaluation of patients with TMD complaints which do not include consideration of emotional factors often result in incorrect diagnosis, a persistent belief on the part of the patient that a cure is imminent, and unsuccessful treatment.
It is difficult to determine the presence of active oral parafunction, such as bruxism. Direct interview will produce a high rate of false negatives due to the unconscious nature of the behavior. Patients are often unaware of tooth clenching or other behaviors associated with jaw hyperactivity during the waking hours. There are several methods that can improve this assessment. Use of a checklist that describes the common types of parafunctional behaviors appears to trigger intentional access to memory via the patient deciding to “test” each listed behavior in order to determine whether the behavior feels familiar (i.e., I must do this one) or not familiar (i.e., I probably don’t do that one). Field monitoring of daytime jaw activity, reports by friends and coworkers of observed behaviors (e.g., clenching with associated observable masseter contraction), and reports by a bedroom partner of tooth-grinding noises during sleep are helpful. Finally, teaching a therapeutic jaw relaxation posture will often uncover the otherwise denied or unknown behaviors via recognition, typically by both patient and clinician, that the target therapeutic behavior is very challenging.
Clinical characteristics that are indicators of the need for expert psychological evaluation of a person with TMD include the following:219
- The persistence of pain beyond the expected healing time and no clear physical explanation is identified.
- Inconsistent or poor response to usual treatments,
- Significant psychological distress, as revealed via self-reported instruments and confirmed through clinical interview,
- Disability greatly exceeds what is expected on the basis of the clinical findings.
- Excessive or inappropriate use of health care services, encompassing tests and treatments, including prolonged use or reliance on opioids, sedatives, minor tranquilizers antianxiety medications, or alcohol for pain control.
There is no single pathognomonic physical finding that can establish a TMD diagnosis. Historically, and as described previously for the AAOP Guidelines, a set of possible physical findings was listed for each type of TMD, but in the absence of clear data regarding what constituted a given problem, the diagnostic rubric was based on the presence of any of the findings. By extension, the more such findings occur, either the more severe the disorder or the more certain the diagnosis. For the common TMDs, as initiated by the RDC/TMD and now validly described in the DC/TMD,3 each disorder is defined by, or constituted by, specific characteristics, and all of them must be present in order for the putative diagnosis to correctly identify the problem. Table 10‐8 provides a general overview of the DC/TMD examination procedures. For the uncommon TMDs,187 each disorder is less strongly defined by the stated characteristics, simply because there are, at present, little data to empirically characterize each of those disorders. Distinguishing clinical decision-making when we have sufficient data versus when we do not is a critical function of being an expert: knowing when—and when not to—use the rules.220,221 In recognizing that the DC/TMD is not 100% accurate, the clinician must consequently know when exceptions to the rules are optimally invoked. Taking a history prior to the examination has a seminal role: serving as sufficient information by which the clinician has developed clinical hypotheses (i.e., differential diagnoses) and then knows what to look for in the examination. Unexpected findings should be appropriately followed up. A standardized examination routine (as defined by the DC/TMD and available as a full set of specifications204 from INfORM) and supplemented by a video for examiner training222 simplifies the task of the examiner: it provides a reference frame emerging from consistent examinations and better identifies unexpected findings. In general, the clinical features that distinguish patients from controls are decreased passive mouth opening,223 and masticatory muscle pain provoked by maximal mouth opening and palpation.224 Among all individuals with a TMD, masticatory muscle tenderness on palpation (see Figure 10‐10) is the most consistent examination feature.182 In contrast, the literature has described an uncorrected deviation on maximum mouth opening as characteristic of acute disc displacements without reduction.39 While that uncorrected deviation is perhaps common in the individual with an acute joint, such deviation is less reliable than assumed; such deviations in chronic conditions are far more variable as a finding. Moreover, uncorrected deviations require a differential diagnosis between disc displacement, unilateral contractures, and guarding behavior. Components of the physical examination that are discussed in this section are summarized in Table 10-8.
Table 10‐8 Physical examination of the masticatory system for TMD.
|Inspection||Facial asymmetry, swelling, and masseter and temporal muscle hypertrophy
Opening pattern (corrected and uncorrected deviations, uncoordinated movements, limitations)
|General palpation||Parotid and submandibular areas
|Mandibular range of motion (ROM)||Vertical jaw movements: pain-free opening, maximal opening with pain, and maximal assisted opening
Horizontal jaw movements: lateral and protrusive movements
Pain provocation, location, and replication are assessed with each movement
|TMJ noises||Any noise produced by vertical or horizontal movements, as reported by the patient and as identified as to type by the examiner (e.g., click vs. crepitus), any pain and replication with noise, and any locking|
|Palpation for pain||Masticatory muscles
|Additional provocation tests as indicated||Static pain test (no mandibular movement to pressure)
Dynamic pain test (active mandibular movement against resistance)
Pain in the joints or muscles with tooth clenching or unilateral biting
Reproduction of symptoms with chewing (wax, sugarless gum)
|Other systems||Cervical ROM
Palpation for pain of neck muscles and accessory muscles of mastication
Neurologic screening, sensory testing
|Intraoral examination||Signs of parafunction: cheek or lip biting, accentuated linea alba, occlusal wear
Dental pathology: tooth mobility, percussion, thermal testing, fractures of enamel and restorations
General soft tissue: scalloped tongue borders, parotid gland patency
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.
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