MOVEMENTS

Mastication, swallowing, and speech are associated with movements at the TMJs. The two joints move in unison and are limited and guided by dental occlusion during early opening and closing movements of the jaw. Therefore, the TMJs and teeth are often referred to as a tri-joint complex. However, later movements, beyond 2 mm opening, are guided by the musculoligamentous components of the TMJ and are not related to dental occlusion or bite. Movements at the TMJs have two components: rotation, which occurs during the very first stages of jaw opening, and translation, which occurs with wider opening. These movements are guided by the various components of the TMJ system and structure. The inferior compartment of the joint, between the mandibular condyle and the articular disk, functions as a hinge joint that allows mandibular rotation. The upper head of the lateral pterygoid muscle draws the disk anteriorly to prepare for condylar rotation. The superior compartment of the joint, between the temporal bone and the articular disk, acts as a sliding joint; it allows both disk and mandible to glide anteriorly, posteriorly, and laterally (left or right) along the slope of the articular eminence. The eminence is the primary functional area of the temporal bone during mandibular movement. Normal opening and closing of the mouth, a combination of rotation and translation movements, relies on function in both compartments of each joint. Further, it depends on a smooth sliding of the disk down the slope of the eminence. During mouth opening, the condyles glide forward over the articular eminence with the disk in between. Therefore, during mouth opening, the condyles rest on the articular eminences, and any sudden movement, such as wide mouth opening that might occur during yawning, and some forms of trauma may displace one or both condyles anteriorly and even past the articular eminence, a process that can lead to open lock of the mandible.

In the closed position, the mandible lies in the glenoid fossa, in contact with the posterior band of the disk (see Figure 9-1). In the resting position, the mouth is slightly open so that the teeth are not in contact. In centric occlusion occurs with maximal contact of the teeth, the position assumed by the jaw when swallowing.

TEETH

In humans, there are 20 deciduous—primary or “baby”—teeth, and 32 secondary, or permanent, teeth. Deciduous teeth are shed between the ages of 6 and 13 years. To identify or label the secondary teeth for the purposes of communication and treatment, their locations are divided into four quadrants: upper left (quadrant 1), upper right (quadrant 2), lower left (quadrant 3), and lower right (quadrant 4). When labeling or identifying deciduous teeth, the quadrants are continued so that deciduous teeth would be found in quadrants 5 through 8, with quadrant 5 being the deciduous “partner” of quadrant 1, used for secondary teeth and so on. In each quadrant, the teeth are numbered from 1 (most medial) to 8 (most distal). Therefore, a mandibular right first molar would be called tooth 4.6, or simply 46, and a first mandibular deciduous molar on the right side would be labeled tooth 8.5, or 85. Loss or restoration of teeth and malocclusion has been considered a major factor in the development of TMJ pain. Although this used to be considered a major risk factor for TMJ dysfunction, unless the occlusal changes are so great as to render the occlusion nonfunctional (e.g., no posterior occlusion at all), it is no longer considered as such (De Boever, 2000).

NERVE SUPPLY

The TMJs are innervated by the auriculotemporal and masseteric branches of the mandibular division of the trigeminal nerve.

INSPECTION

The TMJs are inspected for pain, swelling, redness, symmetry, clicking, crepitus, abnormal movements such as asymmetric translation, lack of movement, and hypermobility. Effusion of the TMJ manifests as a rounded bulge just anterior to the external auditory meatus. Arthritis of the TMJs, particularly rheumatoid (and not OA), can predispose to the development of an obvious anterior open bite, in which the patient cannot bring his or her anterior teeth together (e.g., to bite off a piece of thread). In children this might also result in the development of a disturbance of bone growth leading to a shortened, recessed lower jaw and excessive overjet. While excessive overjet may result from various causes, be they congenital or acquired, there are no studies revealing a conclusive relationship between factors of occlusion, such as overjet and overbite, with the development of temporomandibular dysfunction (TMD) (Gersh et al, 2004). It should also be recognized that other diseases can cause lysis or destruction of one or both TMJs, including neoplasia (benign or malignant), and these must be ruled out in the absence of a history consistent with adult or juvenile rheumatoid disease.

PALPATION

The TMJs can be located by placing the tip of the index finger just anterior to the external auditory meatus and asking the patient to open the mouth about halfway. The lateral poles of the TMJs will then become palpable by the tip of the examiner’s finger. The joint is palpated for warmth, tenderness, synovial thickening, effusion (a fluctuant mass), crepitus, or snapping or clicking with movement. With the patient’s mouth open, the TMJ can be palpated with the little finger placed in the external auditory meatus (fleshy part anteriorly). The patient is then asked to close the mouth when the examiner first feels the condyle touch the finger. With the mouth closed, the TMJs are in the resting position with a freeway space between the anterior teeth (normal range 2 to 4 mm) (Kerr, 1974). By palpating the condyle and noting its location within the mandibular fossa with the patient’s mouth closed, partially open, and wide open, the examiner can determine various degrees of dislocation.

When assessing for pain, one generally tries to maintain a consistent force of palpation. If tissues are clinically tender, it is generally recommended that the force needed to evoke a meaningful pain reaction is that which, when pressing the finger on a tabletop, the fingernail bed will blanch. If the pressure is too light, clinically tender tissues will not be identified; similarly, if too much force is applied, even normal tissues will be perceived as painful. For the purposes of standardization, it is also helpful to grade a patient’s pain reaction following palpation of the TMJs and surrounding musculature. In this case, a discontinuous but relatively reliable scale has been developed, as shown in Table 9-2.

RANGE OF MOVEMENT

Active TMJ movements include opening and closing of the mouth, protrusion, retrusion, and lateral or side-to-side excursions of the mandible. During opening (depression) and closing (elevation or occlusion) of the mouth, the two TMJs (inferior compartments) work in unison to produce a smooth, unbroken arc of movement without any asymmetry or sideways movement. Deviation of the chin to one side is generally caused by ipsilateral TMJ, severe degenerative changes that would generally be seen only in rheumatoid arthritis, physical trauma (e.g., fracture of the neck of the ipsilateral condyle), and, in some cases, spasm of the masseter or lateral or medial pterygoid muscles.

The range of vertical movement during opening and closing of the mouth is determined by measuring, with a ruler or calipers, the distance between the maxillary and mandibular central incisors during maximal unassisted or assisted opening (see the discussion that follows on passive movements of the TMJ). This range is often referred to as the interincisal range of opening (normal range 35 to 60 mm). Although this measurement is relatively reproducible, inaccurate measurements can be made in patients wearing dentures or in those who have otherwise lost maxillary anterior teeth that have then been replaced prosthetically. In hypomobile TMJs, the distance is less than 35 mm, and the displacement can be so severe as to be less than or equal to 1.5 cm, therefore only rotational movement of the condyles would be detected.

Protrusion and retrusion of the mandible occur at the superior compartment. Normally, the individual can both protrude the lower jaw out past the upper teeth and retract the lower teeth behind the upper teeth. Lateral or side-to-side movement of the mandible occurs at the superior compartment. This can be measured with a ruler, with the mouth partially open and the lower jaw protruded, as the range of movement of the midpoint of the mandible (i.e., the space between two central incisors) in relation to that of the maxilla (normal range 10 to 20 mm).

As alluded to earlier, jaw opening can be characterized as being assisted or unassisted. Unassisted opening is generally close to assisted opening in extent, when there is no pain or other disease associated with either the TMJs or their associated muscles, and it is measured by having the patient open his or her mouth to its widest extent or to the point where pain interferes with such movement. Assisted opening is measured, with the examiner wearing gloves, by placing the middle finger on the incisal edges of either the maxillary or mandibular teeth and the thumb on the incisal edges of the opposing incisors. The thumb and middle finger are then brought together gently and slowly, in a scissors movement, to determine whether it is possible to assist the mandible to open more than it did with unassisted opening. In these cases, there might be too much pain to even do this. However, in most cases this maneuver can still be done. Presuming no intraarticular disease, such as an anteriorly displaced TMJ meniscus without reduction, and as long as there is no extremely severe pain, the mandible can be coaxed to open, sometimes another 1 to 2 cm. This is also parallel to the concept of a springy feeling at maximal opening and would generally be consistent with a diagnosis of muscular pain and/or muscle trismus that is causing a restriction in unassisted opening. Alternatively, if the mandible can only be coaxed to open another 1 to 5 cm, a so-called hard feeling will be detected. The latter finding often suggests intraarticular disease, such as an anteriorly displaced TMJ disk without reduction. Another condition that could cause this type of finding might be TMJ ankylosis related to trauma or other bone/joint disease, including infection, and it may require surgical intervention (Straith, 1948). Conditions associated with TMJ disk position and shape will be discussed in more detail later (see Temporomandibular Joint Pain and History Taking).

MUSCLE TESTING AND NEUROLOGICAL ASSESSMENT

Although there is no question that patients will present with jaw-associated pain because of TMJ disease, it must also be recognized that pain in the surrounding muscles can also cause pain; in most instances, this is in fact the case (Dworkin, 1990). Moreover, most patients present with both muscular and TMJ pain. In cases of combined joint and muscle pain, the overall symptom profile and responses to treatment suggest that it is the muscular pain that is of paramount importance as opposed to pain strictly in the TMJ (Hapak, 1994). Therefore in addition to assessment of the TMJ itself, it is critically important to also test for muscle pain. Furthermore, orofacial pain can arise as a consequence of dentoalveolar disease or neuropathy, which underscores the importance of carrying out an appropriate neurological assessment as well.

For neurological assessment, the patient is asked to close the jaws tightly for assessment of size, firmness, and strength of the temporalis and masseter muscles. Resisted isometric testing of the muscles that close the mouth is then performed, including the temporalis (innervated by facial or cranial nerve VII), the masseter (trigeminal or cranial nerve V), and the medial pterygoid (trigeminal nerve). This is followed by assessment of the muscles that open the mouth: the lateral pterygoid (trigeminal nerve) and the suprahyoid muscles—digastric (cranial nerves V and VII), mylohyoid (cranial nerve V), and geniohyoid (cranial nerve XII and the first cervical nerve, C1). Side-to-side movements of the mandible are a function of the medial and lateral pterygoids. Protrusion of the mandible is a function of the lateral pterygoids, whereas retrusion is produced by the posterior fibers of the temporalis. In patients with hypocalcemic tetany, tapping of the facial nerve, as it runs just in front of the tragus, produces a momentary spasm of the ipsilateral half of the face (positive Chvostek test). The jaw reflex is mediated by the trigeminal nerve.

When testing for pain in the muscles of mastication, it is important to examine the external muscles—masseter, temporalis, medial pterygoid at the angle of the mandible, and sternocleidomastoid—by palpation. The internal muscles must also be palpated; these include the masseter at its zygomatic attachment and the coronoid attachment of the temporalis. One can also palpate the medial pterygoid muscles, but this can also induce gagging, which makes it difficult to assess for pain reactions. The lateral pterygoid muscles are also palpated, but in reality, it is doubtful that they can actually be reached during a physical examination. The same amount of digital pressure on the muscles of mastication as described for palpation of the TMJs should be used. Similarly, the patient’s pain reactions can be gauged using the measurement system described in Table 9-2. Equally as important, as discussed with respect to examination of the TMJs, a patient might or might not feel pain following palpation; if the patient does feel pain, and the patient’s chief pain complaint has been exacerbated following palpation of the muscles of mastication, it can be concluded that the principal source of pain is muscular. That said, patients suffering from chronic muscle pain syndromes such as fibromyalgia, which is a common comorbid condition for patients with TMJ or associated pain in the muscles of mastication (Dao, 1997), might report severe pain following palpation; but their chief pain complaints might not be exacerbated. This latter type of finding should suggest a diagnosis of fibromyalgia, which would need further medical assessment, such as examination by a rheumatologist, neurologist, or physiatrist—three appropriate medical subspecialties concerned with these conditions.

TEMPOROMANDIBULAR ARTHRITIS

Temporomandibular (TM) arthritis can be caused by trauma, infection, OA, rheumatoid arthritis (RA), psoriatic arthritis (PsA), ankylosing spondylitis (AS), juvenile idiopathic (rheumatoid) arthritis (JIA), or crystal-induced arthritis—such as gout, and even pseudogout—or calcium pyrophosphate dihydrate deposition arthropathy (Pritzker, 1994). In some rare cases, TM arthritis may be caused by malignant metastatic or primary disease. The pain of TM arthritis may radiate to the teeth, face, or ear, and it is made worse by jaw movements during eating, chewing, and speaking. With regard to OA, pain usually occurs once there is loss of the fibrous articular joint surface. As a result, the loss of this protective layer exposes the innervated and vascularized osseous tissue to the effects of movement and forces that result in pain (Okeson, 2005). Rheumatoid arthritides (including JIA) occur as a result of proliferation of inflamed synovial membranes onto the articular surfaces (Okeson, 2005). Other symptoms include stiffness, restriction of movement with inability to fully open the mouth, swelling, clicking, and sometimes locking. Local tenderness, swelling, synovial thickening, effusion, fine or coarse crepitus, and sometimes a palpable click are the main findings. In chronic arthritis, excessive play of the TMJ is common.

TEMPOROMANDIBULAR DISORDER SYNDROME

Temporomandibular disorder syndrome (TMDS) is currently referred to as temporomandibular disorder (TMD) in recognition of the fact that this condition can be caused by TMJ pain and muscle pain, as well as combined TMJ and muscle pain as described previously. When the condition is predominantly caused by pain in the muscles of mastication, it can also be referred to as myofascial pain and dysfunction (MPD). The first descriptions of this condition were made by Costen in 1934. TMD is a relatively frequent cause of chronic head and neck pain associated with dysfunction of the masticatory muscles. The pain is dull, achy in character, rarely relieved by analgesics, and when associated primarily with the muscles of mastication, is fairly diffuse. This is in contrast to TMJ-associated pain from one of the arthritides mentioned previously, in which the pain is typically localized to the joint area (i.e., just anterior to the external auditory meatus, also often mistaken for otitis media). The pain of TMD related to joint disease is often unilateral and is aggravated by jaw movements, but it is independent of any local oral, nasal, dental, or ear disease. Tenderness of the muscles of mastication can be identified, too; but if the condition is related mainly to joint disease, palpation of the joints, not the muscles, would be expected to exacerbate the patient’s chief pain complaints.

INTERNAL DERANGEMENTS

The disk displacements discussed previously are also referred to as internal derangements. The etiology is not understood fully, but impaired lubrication due to TMJ overloading has been implicated. Known causes include direct or indirect trauma (blow to the jaw, endotracheal intubation), abnormal functional loading of the joint (bruxism, chronic teeth clenching), and OA. It is noteworthy that internal derangement is so common that it has been suggested that, unless associated with pain or severely restricted opening, it is more a variation of normal as opposed to true disease.

Clinically, there is a painless incoordination phase initially, during which the patient experiences a momentary catching sensation on mouth opening. This is followed by the clicking and popping associated with anterior disk displacement and reduction into the normal position with mouth opening. Some patients may subsequently develop restricted jaw movements with intermittent or permanent locking caused by anterior disk displacement without reduction on attempted mouth opening. The common factor here is that in such cases, almost all patients would have reported prior TMJ noises with jaw opening and/or closing (a reciprocal click) prior to the development of closed lock. Furthermore, on development of a closed lock caused by anterior displacement without reduction, the patient will also report that the clicking is no longer present. The diagnosis of internal derangement can be confirmed by magnetic resonance imaging (MRI); but in fact, history and clinical examination are just as sensitive (Romanelli et al, 1993).

LOCAL ASPIRATION AND INJECTION/ARTHROSCOPIC TREATMENTS

When considering treatment of an inflamed TMJ, local aspiration and injection of the joint may be required, with a steroid and/or with hyaluronate. With the patient sitting or reclining and the head supported, the joint line is palpated as a depression located 1 to 2 cm anterior to the tragus, and the mandibular condyle is felt as it moves during mouth opening and closing. With the patient’s mouth open, a 27 gauge needle is inserted into the joint perpendicular to the skin and directed slightly posteriorly, medially, and superiorly, with care being taken not to inject directly into the intraarticular disk (Figure 9-2). The ease of injection and/or aspiration of fluid is the best guide to ensure that the needle’s point is within the joint cavity. Generally speaking, local anesthesia should be established as per routine when carrying out such procedures. More recent developments in this approach, and with arthrocentesis in particular, require a similar approach but also involve the development of a draining channel with a second needle. This allows for inflammatory cytokines (e.g., prostaglandins) to be flushed from the joint capsule, followed by placement of the steroid and/or hyaluronate. It should be noted that if a patient’s pain is not alleviated following local anesthetic administration into the joint, presuming the patient is in pain at the time of presentation, the patient’s pain is likely not emanating from the joint. This would mean that another source of pain should be considered; as alluded to earlier, this is likely to be muscular, presuming other sources of pain, such as dentoalveolar pain and otitis media, have been eliminated diagnostically. Therefore, injection of the TMJ is not only a possible therapeutic measure, it can be used for diagnostic purposes as well.

FIGURE 9-2 ARTHROCENTESIS OF THE TEMPOROMANDIBULAR JOINT.

Arthroscopic methods can be used to guide aspiration and injection along with surgical management of intraarticular disease. Interestingly, studies focused on the use of arthroscopic surgery have shown that surgical outcomes can be affected by the presence and/or severity of a psychopathological disorder (Freeman, 1997; Dworkin, 1994; and Murray, 1996). The various investigations have demonstrated that the biomechanical aspects of jaw function—as measured directly and objectively, as with maximal mandibular opening (MMO)—were unaltered following arthroscopic surgery. In parallel, the incidence and severity of TMJ sounds did not change following surgical treatment. However, there were marked reductions in pain (> 60%). Moreover, although there were no changes in the objective measurements of either MMO or joint noises, based on measurements made with visual analog scales, patients perceived at least 60% reductions in joint noises that also correlated with similar perceptions in their maximal jaw opening. These data suggest that although biomechanical function might be an important parameter insofar as joint function is concerned, pain might be the overriding symptom; when pain is reduced, patients seem to perceive that their biomechanical problems (i.e., maximal jaw opening) have improved to a similar extent.

INJECTION OF MUSCLES OF MASTICATION

When it is suspected that a patient’s symptoms are related to painful muscles of mastication, diagnostic, and in some cases therapeutic, injection of local anesthetics may be considered with or without a corticosteroid. As suggested for injection of the TMJ, the administration of a local anesthetic prior to placement of a steroid, if a steroid is to be used, should also lead to elimination or at least reduction in the patient’s chief pain complaints. These injections can be therapeutic (Wheeler, 2004) or at least diagnostic. Both internal and external muscles of mastication can be injected, depending on what muscles were shown to be tender to palpation; in general it is suggested that when the muscles are injected with a local anesthetic, it should be done without a vasoconstrictor. Dry needling has also been used, but its effectiveness is questionable (Furlan et al, 2003).

PREDICTION OF TREATMENT OUTCOMES FOR TMD AND ASSOCIATED MUSCULOLIGAMENTOUS PAIN CONDITIONS

Predicting treatment outcome in chronic pain cases, and with temporomandibular disorders in particular, is one of the most challenging aspects of managing these conditions. Unlike more conventional medical and dental models, in which the response to treatment is based on a number of well-defined interventions, chronic pain management provides numerous challenges not observed in other conditions. The biopsychosocial model used to explain the etiology of chronic pain may provide some insight into the variability of patient outcomes. Additionally, the originating trigger to the complaint, such as a motor vehicle accident, and other cofactors, including sleep disturbance and fibromyalgia, have been shown to play a significant role in determining the outcome of therapy.

In general, patients presenting with idiopathic TMD (iTMD)—those conditions not associated with a traumatic origin—recover in approximately 75% to 80% of cases (Brooke, 1977). Contrary to this observation, those patients presenting with signs and symptoms associated with a temporomandibular disorder with an onset in conjunction with a motor vehicle accident (pTMD) tend to do poorly in treatment and require more modalities of therapy than those patients that do improve. In fact, only about 48% of post-traumatic temporomandibular disorder sufferers suggest that they improved following conservative therapy (Romanelli, 1992). It has been suggested that those suffering from signs and symptoms associated with pTMD demonstrate a greater incidence of sleep disturbance, decreased energy level, mood swings, problems with cognitive functioning, and memory and concentration disturbances. These characteristics are similar to those seen in patients suffering from post-traumatic stress disorder (PTSD) (Afari, 2008). Yet in most TMD populations, there is no overt neurological deficit identified. Thus, it has been suggested that further characterization of these conditions, in particular those temporomandibular disorders that are more refractory to treatment, via the use of neuropsychological testing similar to that used in the post-traumatic TMD group may be helpful in not only assessing common features but may assist in formulating a more accurate diagnosis early in therapy.

A number of neuropsychological tests are available for assessment of cognitive functioning. However, some of the more common tests include a simple and complex reaction-time test, the California Verbal Learning Test, the Peterson-Peterson Consonant Trigram Test, and the Symptom Checklist-90 revised (SCL 90R). It has been suggested that individuals who have suffered from a head injury may develop difficulties with information processing. Therefore, the reaction-time tests and memory tests that assess the ability to encode information, including short and long-term memory function, may all be reflective of a cognitive deficit despite a normal neurological examination. It has been demonstrated by Goldberg et al (1996). that patients presenting with TMD symptoms associated with a motor vehicle accident did worse on reaction time and cognitive function tests compared to those suffering from a TMD of an idiopathic origin.

Following up on this work, it was suggested that neuropsychological deficits may play an integral role in mediating poor treatment outcomes in TMD patients. Accordingly, using various neuropsychological testing tools, as was done in the pTMD population, may provide some form of predictor in terms of poor treatment outcomes in the iTMD population. Although reaction-time testing was shown to be a poor predictor of treatment outcomes, other neuropsychological parameters described in the California Verbal Learning Test and the Peterson-Peterson Consonant Trigram Test were able to discriminate between responders and nonresponders in an iTMD population (Grossi, 2001). Conceivably, these tests might be utilized to predict poor outcomes and thereby funnel patients into therapies to improve memory and cognition, which may in turn improve outcomes overall. Similarly, it has been demonstrated that these findings may be extrapolated to other chronic pain conditions, such as irritable bowel syndrome, with consistent findings noted (Grossi, 2008).

One of the overriding factors associated with chronic pain, and with TMD in particular, is the presence of a sleep disturbance. Chronic diffuse myalgia, fibromyalgia, and chronic fatigue syndrome are just some of the conditions associated with chronic sleep disturbance (Moldofsky, 1993). Along with that, it has been demonstrated that post-traumatic TMD patients are more likely to claim to suffer from a sleep disturbance and other symptoms related to affect than a comparative nontraumatic TMD population (60% vs. 14%) (Romanelli, 1992). However, in those that are considered refractory to treatment, it was demonstrated that on average, the nonresponding TMD population performed worse on most cognitive tests than those TMD patients who responded to treatment. Additionally, results of the University of Toronto Sleep Assessment Questionnaire (SAQ) indicated that elements of a sleep disturbance may have been present in the nonresponsive TMD group, although the diagnosis of a sleep disturbance could not be definitively made (Grossi, 2001). Overall, however, studies on TMD and sleep disturbance are limited. It has been reported that as many as 77% of those suffering from orofacial pain suffer from a sleep disturbance (Riley, 2001). The sleep–pain relationship is complicated by mood (Menefee et al, 2000), with poor sleepers endorsing higher scores on measures of depression and anxiety (Haythornthwaite, 1991). In a sample of patients with orofacial pain, sleep quality was predicted by depressed mood or psychological distress and greater pain severity and less perceived life control (Yatani et al, 2002). However, in a study assessing psychological and cognitive variables that may be predictive of positive outcomes in TMD patients undergoing physiotherapy treatment, it was determined that neuropsychological test results, as well as sleep quality, were not able to predict treatment outcome in any meaningful way (Bielawski, 2008). Although many factors may contribute to the etiology and pathogenesis of TMDs, it is still beyond our ability to accurately predict those who will or will not respond to therapy, no matter which modality is utilized.