James Fricton DDS, MS
Essentials of Diagnosis
Several surveys of persistent orofacial symptoms indicate that approximately 7% of Americans (or 13 million Americans) suffer from an orofacial disorder causing face or jaw pain. Clinical subpopulations comprising those whose problems are sufficiently severe to prompt them to seek care include more women than men.
Neuropathic pain and headache pain are discussed in Chapters 10 and 12, respectively. Other causes of chronic orofacial pain are discussed under the section on differential diagnosis. Typical signs of chronic orofacial pain include joint noise, tenderness of masticatory muscles and joints, pain, and limitation and deviation in the range of motion of the mandible; the most common symptoms include jaw pain, facial pain, headache, distressing or disturbing joint noises, and difficulty with jaw function.
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Understanding the theories of the pathophysiology of temporomandibular joint (TMJ) disk displacements and masticatory myofascial pain are important to understanding the etiologic factors. These two disorders are the most common disorders of the temporomandibular structures.
TMJ disk displacements are classified by progressive stages of masticatory dysfunction involving anterior or medial displacement of the disk relative to the condyle (Figure 19-1). It is often characterized by TMJ clicking and pain in the early stages and jaw locking, limited range of motion, and degenerative joint changes in the later stages. The early stage TMJ disk displacement is the most common TMJ disorder and is characterized by reciprocal clicking of the joint on opening and closing from the impaired gliding function of the disk.
Although the exact etiology of TMJ disk displacement is unknown, one of the most common theories suggests that abnormal biomechanical forces on the condyle may cause the articular tissues to change in shape, form, and function. The friction created by malposition of the disk and jaw function may lead to further displacement and eventual morphologic changes to the form and function of the disk.
In addition, the pressure and strain from the condyle on the posterior attachment leads to inflammation, synovitis, and pain in the joint. Synovitis inhibits the synovial membrane's capacity to produce hyaluronic acid. With
time, the synovial fluid increases in viscosity, reducing its protective functioning. In a healthy joint, the side of the disk facing the condylar eminence is concave; during function, the condyle glides and expresses the synovial fluid out from this concavity, creating a negative relative pressure.
Figure 19-1. There are several stages of disk displacement relative to the temporomandibular joint. Each stage has different clinical characteristics.
The healthy synovial fluid viscosity, allows a “hyaluronic fluid film” under the disk and enables the synovial fluid to flow back into this concavity as the condyle retrudes. If the synovial fluid is viscous, fluid may not be able to refill the concavity and the disk acts like a suction cup and maintains the anteriorly displaced position. If the disk maintains this position or is displaced farther forward, adhesions will form between the eminence and the disk, locking it in this forward position. With each translation, the head of the condyle rides over the disk's posterior band causing clicking and eventually causing the disk to fold forward. Adhesions may then form between the folded portions of the disk and prevent it from ever assuming its normal shape. In addition, abnormal mechanical loading may impair synthetic functions in affected tissues of the TMJ. Chondroblast failure with excessive loading may be associated with disruption of specific cytoskeletal elements, factin, and tubulin, affecting protein synthesis and repair potential.
Masticatory myofascial pain, on the other hand, is a regional muscle pain disorder characterized by localized muscle tenderness termed “trigger points” and is the most common cause of persistent regional pain (Figure 19-2). The affected muscles may also display an increased fatigability, stiffness, subjective weakness, pain in movement, and slight restricted range of motion that is unrelated to joint restriction. Masticatory myofascial pain is frequently overlooked as a diagnosis because it is often accompanied by other signs and symptoms in addition to pain, coincidental pathologic conditions, and numerous
behavioral and psychosocial problems. As masticatory myofascial pain persists, chronic pain characteristics often precede or follow its development. Theories on the etiology of masticatory myofascial pain are based on a combination of peripheral and central theories.
Figure 19-2. The most common muscles associated with masticatory muscle pain include the temporalis and masseters with associated pain referral patterns. Left: Temporalis refers pain to temples and frontal, retroorbital, and maxillary teeth. Right: Masseter refers pain to the jaw, ear, and retromandibular and mandibular teeth. * = trigger point location; = referral patterns.
The development of trigger points is hypothesized to be a progressive process with a stage of neuromuscular dysfunction of sustained muscle hyperactivity and irritability that is maintained by numerous perpetuating factors and then followed by a stage of neurobiologic changes in the muscle bands with the trigger points. The characteristics of masticatory myofascial pain often outlast the initiating events, setting up a self-generating pain cycle of central sensitization that is perpetuated through lack of proper treatment, sustained muscle tension, distorted muscle posture, pain-reinforcing behavior, and failure to reduce contributing factors such as clenching or sleep disturbances.
The initiating events, including macro traumatic or micro traumatic events, may disturb the normal or weakened muscle through muscle injury (eg, whiplash, excess jaw opening) or sustained muscle contraction (eg, bruxism, muscle tension, postural habits). These traumas release free calcium within the muscle through disruption of the sarcoplasmic reticulum and, with adenosine triphosphate (ATP), stimulate actin and myosin interaction and local contractile and metabolic activity resulting in increases in noxious by-products. Substances such as serotonin, histamine, kinins, and prostaglandins sensitize and fire type III and IV muscle nociceptors, and a central sensitization is prolonged. These afferent inputs converge with other visceral and somatic inputs in the cells such as those of the lamina I or V of the dorsal horn on the way to the cortex, resulting in perception of local and referred pain.
These inputs may be facilitated or inhibited by multiple peripherally or centrally initiated alterations in neural input to this “central biasing mechanism” of the brainstem through various treatment modalities such as cold, heat, analgesic medications, massage, trigger point injections, and transcutaneous electrical stimulation. The cycle may be perpetuated by protective posturing of the painful muscle through distorted muscle posture and by avoiding painful stretching of the muscles. Any other perpetuating factors resulting in further sustained neural activity, such as continued muscle tension, poor postural habits, or inputs from pathologic viscera or dysfunctional joints, will support the reverbetory circuit.
With contractile activity sustained, local blood flow decreases, resulting in low oxygen tension, depleted ATP reserves, and diminished calcium pump. Free calcium continues to interact with ATP to trigger contractile activity, especially if actin and myosin are overlapping within the shortened muscle, and a self-perpetuating cycle is established. Sustained increases in local noxious by-products of oxidative metabolism then contribute to the beginning of the organic musculodystrophic stage with sensitization of nociceptors within the interstitial connective tissue at the trigger point and further disruption of the calcium pump. If normal muscle length is not restored and pain continues, functional, postural, and behavioral disturbances may further perpetuate the problem.
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Prevention of TMJ disk displacement and masticatory myofascial pain is based on reducing peripheral or central etiologic factors, or both. Peripheral factors that are most often cited as important in prevention of temporomandibular disorders includes oral parafunctional habits, occlusal dysharmony, and direct or indirect trauma to the jaw. These are among the numerous factors that drive the equilibrium of local tissues either toward normal or adaptive physiologic health and function or toward dysfunction and disease. However, peripherally based models of etiology do not address the issues of disparate findings in patients with similar objective findings or surgical treatments that fail.
Central factors that have been cited as important in the cause and progression of temporomandibular disorders include centrally mediated psychosocial factors (such as
depression and poor coping strategies) and problems with abnormal central modulation of pain (such as somatization and fibromyalgia). Because of the multifactorial nature of chronic orofacial pain, most experts believe that it should be conceptualized and prevented from a broader biopsychosocial model rather than the traditional medical model commonly used for acute problems.
Clinical Findings & Differential Diagnosis
Diagnosis of temporomandibular disorders relies on measurement of range of motion, assessment of TMJ function, and palpation of the muscles and joints using standard and reliable procedures.
Range of motion of the jaw is measured from incisal edge to incisal edge of the central incisor with a millimeter rule. Minimum normal jaw opening is considered to be about two finger widths at the knuckles of the patient's dominant hand, or approximately 40 mm. Lateral motion should be 7 to 10 mm to both the right and left. Normal protrusive range is between 6 mm and 9 mm. Limitation in range of motion may indicate any of the following conditions: contracture of one or more of the jaw closing muscles, a nonreducing anterior displacement of the disk (closed lock), coronoid process interference, fibrous ankylosis of the joint, a hematoma, neoplasm, infection, or a systemic condition (such as scleroderma).
TMJ sounds may be detected by palpation of the joint during repetitive opening, closing, and lateral movements. They are common, and their presence does not imply the need for treatment. TMJ sounds may result from normal or pathologic mechanisms, including deviation in form or function of the disk, joint osteoarthritis, or anterior or medial TMJ disk displacement. Consider therapeutic intervention when limitation in movement or joint tenderness accompany joint pain.
Muscle and joint palpation is necessary to determine the presence of tenderness in the muscle, joint, and other soft tissue structures as the only sign found in masticatory pain disorders such as myofascial pain, myositis, TMJ synovitis, or capsulitis. Unfortunately, intra- and interexaminer reliability of muscle palpation is low and requires training and calibration to improve its consistency and replicability.
Imaging of the TMJ includes panoramic radiography; magnetic resonance imaging (MRI); and computed axial tomography (CT). Panoramic radiographic imaging of the jaw is convenient and inexpensive for TMJ screening. Although gross degenerative, traumatic, or dysplastic changes can be detected with panoramic radiographs, subtle condylar changes and abnormal disk/condylar/fossa relationships cannot be evaluated. Lateral open and closed mouth tomography or CT scans of the TMJ are usually recommended. MRI can provide a definitive diagnosis in most cases of suspected TMJ disk displacement. Patients with joint locking or restricted condylar motion, as demonstrated clinically or with lateral tomography, can be evaluated with MRI to determine disk position and morphology. In addition, MRI scanning can be used to detect joint effusions or altered circulation due to inflammation using gadolinium-DTPA enhancement. Dynamic MRI can also be used to determine the functional relationships between the condyle and disk during rotatory and translatory movement of the condyle. Limitations of MRI include the relative lack of definition of bony surfaces of the joint and restriction to patients without magnetic metallic implants.
Temporomandibular muscle pain disorders or masticatory myalgia are characterized by pain arising from pathologic or dysfunctional processes in the masticatory muscles. Pain is usually experienced over the involved muscle but is sometimes referred to distant structures, confusing the diagnostic process. There are several distinct types of masticatory muscle pain subtypes in the masticatory system.
Myofascial pain, the most common systemic muscle pain disorder, is characterized by regional pain associated with tender areas (trigger points) in taut bands of skeletal muscles, tendons, or ligaments. Although pain typically occurs over the trigger point, pain can be referred to distant areas (eg, the temporalis referring to the frontal area and the masseter referring into the ear). Reproducible pain upon palpation of the trigger point is diagnostic. Myofascial pain is the most common cause of masticatory pain, accounting for over 60% of all cases of temporomandibular disorders. Although the etiology of myofascial pain is unclear, current theories hypothesize that macrotrauma or microtrauma disturbs normal or weakened muscle through injury or sustained contraction (eg, bruxism or clenching). Such processes may induce peripheral and central changes that sensitize muscle nociceptors, resulting in tenderness and both local and referred pain.
Myositis is a less common acute condition involving inflammation of the muscle and connective tissue and associated pain and swelling. It may be septic or aseptic. Most areas of the muscle are tender, and there is pain within active range of motion. The inflammation is usually due to local causes such as acute overuse, local infection from an impacted third molar, pericoronitis, trauma, or cellulitis.
Muscle spasm is another acute disorder characterized by transient involuntary tonic contraction of a muscle. It can occur following overstretching of a previously weakened muscle, protective splinting of an injury, or acute overuse. A muscle in spasm is shortened and painful, producing limited range of jaw motion. Lateral pterygoid spasm on one side can also cause a shift of the occlusion to the contralateral side.
Muscle contracture is a chronic condition characterized by persistent shortening of the muscle. It can begin after trauma, infection, or prolonged hypomobility. If the muscle is maintained in a shortened state, muscular fibro-sis and contracture may develop over several months. Pain is often decreased by voluntary or involuntary guarding or by avoiding use of the muscle.
TMJ pain or arthralgia is usually due to capsulitis or synovitis, with associated joint inflammation, tenderness, pain, and fluid accumulation or effusion. The difficulty in diagnosing joint problems lies in determining whether pain in the area of the joint is due to muscle disorder, joint disorder, or a systemic disorder. Most TMJ arthralgias cause pain anterior to the ear, with occasional referral to surrounding (eg, temporal) regions; digital palpation and joint use are painful.
Several joint conditions can be associated with arthralgia. Disk displacement with reduction is characterized by clicking of the TMJ on opening and closing. The opening click reflects the condyle moving beneath the posterior band of the disk until it snaps into its normal relationship on the concave undersurface of the disk. The closing click reflects reversal of this process. The condyle moves under the posterior band of the disk until it snaps off the disk and on to the posterior attachment. The opening click occurs at a wider incisal opening than the closing click and at different points of incisal opening. Momentary dysfunction of the disk has been theorized to reflect articular surface irregularity, disk-articular surface adherence, synovial fluid degradation, disk-condyle incoordination as a result of abnormal muscle function, increased muscle activity around the joint, or disk deformation. As the disk becomes more dysfunctional, it begins to interfere with normal translation of the condyle and may even cause periodic jaw locking. An occasional patient has excessive opening due to ligament laxity and joint hypermobility and becomes at risk for open locking or subluxation of the joint.
Disk displacement without reduction is characterized by marked limited mouth opening due to interference with normal condylar sliding on the disk due to disk adhesion, deformation, or dystrophy. In this situation, the opening is usually restricted to 20 to 30 mm with a deviation of the jaw to the affected side on opening. Joint noise is minimal because little joint translation occurs. The masticatory muscles and joint frequently become tender and painful in response to the joint dysfunction. After the disk is permanently displaced, soft-tissue remodeling of the disk and associated ligaments in the joint occurs. After a permanent locking occurs, routine daily jaw function encourages the posterior attachment and collateral ligaments to accommodate to allow normal jaw opening and abatement of pain. Further adaptation within the joint includes remodeling of the surfaces of the condyle, fossa, and articular eminence, with corresponding radiographic changes. Disk perforation may cause degenerative changes and coarse crepitus upon opening and closing. Successful remodeling allows patients to regain normal opening with minimal pain, but joint noise often persists. Sometimes, however, bony degenerative changes progress with severe erosion, loss of vertical dimension, occlusal changes, worsened joint and muscle pain, and greatly compromised jaw function.
The genesis of disk disorders and TMJ arthralgia has been at least partially attributed to abnormal biomechanical forces on the condyle, which alter the shape, form, and function of articular tissues. Friction due to abnormal jaw function and malposition of the disk may exacerbate both jaw displacement and changes to the form and function of the disk. In other cases, a blow to the jaw, inadvertent biting of a hard object, or abnormal chewing may be inciting factors. Occasionally, whiplash injury contributes to TMJ arthralgia and disk displacement.
Disk displacements are common in the general population, but those affected generally function adequately without treatment. When a patient seeks help for asymptomatic TMJ noises, continued observation, education about the condition, and self-care are sufficient (Table 19-1). Pain, intermittent locking, and difficulty using the jaw mandate closer observation and possible intervention.
TMJ subluxation or dislocation with or without a disk displacement is characterized by hypermobility of the joint due to laxity of the ligaments. It may be provoked in the dental office when the mouth is held open for an extended period, particularly in patients with systemic hypermobility. The condyle is anteriorly dislocated with respect to the disk and articular eminence, unable to return to the closed position because normal posterior translation is blocked. In most cases, the condyle can be moved laterally or medially by the patient or clinician to disengage the locking and allow normal closure. If the lock cannot be immediately disengaged, jaw manipulation inferiorly and anteriorly may be required before it can glide posteriorly.
Osteoarthritis of the TMJ involves degenerative changes of the articular surfaces of the joint that cause crepitus, jaw dysfunction, and radiographic changes. In osteoarthritis, pain, inflammation, and tenderness of the joint accompany the degenerative changes. Osteoarthritis can occur at any stage of a disk displacement as well as after trauma, infection, and other insults to the integrity of the joint, or with rheumatic or other conditions that cause polyarthritis. The latter include disorders such as systemic osteoarthritis, rheumatoid arthritis, psoriasis, lupus erythematosus, scleroderma, Sjogren syndrome, and hyperuricemia. A rheumatology consultation
is indicated if the joint, consistent with other joints, are painful and swollen, red, stiff, or crepitant.
Table 19-1. Self-Care for Masticatory Arthralgia and Myalgia.a
Other temporomandibular joint disorders include ankylosis, traumatic injuries and fractures, neoplasms, and developmental abnormalities. Ankylosis or total lack of joint movement can be due to osseous or fibrous attachment of the condyle to the fossa. Extracapsular conditions, such as coronoid process interference or muscle contracture, can also cause significant jaw limitation. Traumatic injuries usually result in either a contusion with joint hemorrhage, a sprain with tearing of the joint capsule and ligaments, or a fracture of the condylar neck or head or of the external auditory canal. TMJ injuries are usually accompanied by pain and limited range of motion. Developmental abnormalities, primary benign and malignant tumors, myxoma, fibrous dysplasia, and metastasis or local extension of neighboring malignancies to the TMJ can also occur but are rare.
Periodontal ligament pain is characteristic of deep somatic pain of the musculoskeletal type and is from repetitive strain to the periodontal ligaments through clenching, gross occlusal prematurities, or trauma to the teeth. Periodontal ligament pain is generally a dull aching pain in and around the teeth and can affect multiple teeth. Inflammatory fluid accumulation may cause displacement of the tooth in its socket with a resulting acute malocclusion and pain. The most common sign is tenderness of the teeth to percussion in the absence of pulpitis or periapical or periodontal abscess. Treatment consists of placing a splint and reducing oral habits.
Neuropathic facial or dental pain is a continuous, daily pain often described as a burning or tingling that is limited to a specific nerve distribution. Historically, the pain usually begins following surgery or injury of the face, teeth, or gums but continues despite healing and the absence of a demonstrable etiology. Anesthetic nerve blocks can be used diagnostically to decrease the pain for the duration of the anesthetic. Anticonvulsants, tricyclic antidepressants, and other medications traditionally used for neuropathic pain can be of help.
Complete or incomplete tooth fractures can cause persistent tooth pain that is difficult to diagnose. Pain can result when the pulp is exposed from fractures to the enamel and dentin that become displaced when mechanical strain is placed on the tooth. Diagnosis is difficult, particularly if an incomplete fracture is present, but can
be made by visual inspection, exploration of the tooth for loose fragments, tooth mobility tests, tooth discoloration, and tooth provocation tests that cause pain when the fractured segment is moved. The pulps of these teeth may or may not respond to an electric pulp test or to thermal testing. Fractures need to be treated with temporary banding, crowns, or endodontic treatment.
Pulpitis and periodontal pathology can present a diagnostic dilemma if it refers pain to areas that are distant from the involved tooth. Although not common, patients may complain of a toothache in a tooth that responds normally to all available tests. Further pulp testing or radiographs reveal that an adjacent tooth or other distant tooth or periodontal structure is inflamed. Subsequent treatment to the inflamed tooth resolves the referred pain.
Sympathetically maintained pain is often characterized by a constant burning sensation that is frequently associated with a prior history of tissue damage. The main clinical features include pain described as burning and continuous, exacerbated by movement, cutaneous stimulation, or stress, with onset usually weeks after injury. Confirmation and treatment of early cases of sympathetically maintained pain of the tooth or facial area is achieved by stellate ganglion blockade of the sympathetic nerve input to the painful region. Chronic cases are often considered permanent with pain relief achieved by pharmacologic medications, such as tricyclic antidepressants, clonidine, gabapentin, or carbamezapine.
Burning mouth syndrome is typically characterized by a burning sensation as if the mouth or tongue were scalded or on fire and can accompany other oral complaints, including xerostomia and dysgeusia. The oral tissue often appears normal. There are many factors that can cause burning mouth syndrome, including candidiasis, painful geographic or fissured tongue as well as parafunctional habits, allergies, xerostomia, and injury following dental treatment. Systemic disease and medication side effects have also been shown to cause burning mouth either directly or indirectly from the resultant xerostomia that may be pre0sent. Thus, it is not as difficult to diagnose a condition as burning mouth syndrome as it is to identify the underlying cause that will suggest a treatment.
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The most significant complication associated with orofacial pain is the relationship between the development of chronic pain, depression, and related lifestyle problems. Recent studies show that some, but not all, patients with chronic pain are depressed, with over 30% having major depressive disorders. Thus, it appears that there is a subgroup of patients with chronic pain who are depressed and have severe pain and lifestyle limitations, such as difficulty using the jaw, home or work disability, task avoidance, and sleep disturbance. It is possible that depression may intensify pain and cause increased suffering, disturbances in lifestyle, and therefore be a risk factor for development of chronic pain.
Management of all patients with orofacial pain from temporomandibular disorders aims to (1) reduce or eliminate pain, (2) restore normal jaw function, (3) reduce the need for future health care, and (4) restore normal lifestyle functioning. Specific interventions and their sequencing parallel treatment of musculoskeletal disorders in general. A key determinant of success in chronic pain management is the success in educating the patient about the disorder to enhance adherence to the self-care aspects of management, including jaw exercises, habit change, and proper use of the jaw. The treatments included here are supported by randomized controlled trials.
Most acute temporomandibular disorder symptoms are self-limited and resolve with minimal intervention. Therefore, initial treatment for masticatory myalgia and arthralgia should be a self-care program (Table 19-1) to reduce repetitive strain of the masticatory system and encourage relaxation and healing of the muscles and joints. Most patients respond well to self-care in 4 to 6 weeks; if not, further assessment and treatment are indicated.
The two most common splints include the anterior positioning splint and the stabilization splint and both have evidence to support their efficacy. The anterior repositioning splint places a patient's mandible and TMJ into an anterior position so as to reduce a TMJ click that occurs on opening and closing of the jaw. The anterior repositioning splint is typically placed on the maxillary arch with an anterior ramp that first engages mandibular teeth on initial closure and shifts the jaw forward into
final closure, when all mandibular teeth contact the splint. The stabilization splint provides a flat passive occlusal surface that is adjusted with contact on all short-term posterior teeth to allow passive protection of the jaw and reduction of oral habits. Although both splints can reduce temporomandibular disorder symptoms, the indications for each differ somewhat.
Anterior repositioning splints can be efficacious for intermittent jaw locking with limited range of motion, especially upon awakening, or for persistent TMJ arthralgia not responsive to other therapy (including a stabilization splint). They are recommended only for short-term, part-time use, primarily during sleep, because they can cause occlusal changes if worn continuously or long term.
The stabilization splint is most efficacious for masticatory myalgia and TMJ arthralgia, especially if the pain is worse upon awakening. This type of splint can also be used during the day for oral habit management. Such splints are designed to provide postural stabilization and to protect the TMJ, muscles, and teeth.
Partial coverage splints may cause occlusal changes in some patients. All splints should cover all of the mandibular or maxillary teeth to prevent movement of uncovered teeth, with malocclusion. The splint's occlusal surface can be adjusted to provide a stable occlusal posture by creating single contacts in all posterior teeth in the habitual closure position.
Approaches to changing maladaptive habits and behaviors, such as jaw tensing and clenching and grinding of the teeth, are important in treating painful tissues. Cognitive-behavioral therapies, such as habit reversal, biofeedback, relaxation techniques, and stress management, can be effective alone or in conjunction with other treatments.
Behavior modification strategies, such as habit reversal, are the most common techniques used to change these habits. Although many simple habits are easily abandoned when the patient becomes aware of them, changing persistent habits requires a structured program that is facilitated by a clinician trained in behavioral strategies.
Habit correction can be accomplished by (1) becoming more aware of the habit, (2) knowing how to correct it (ie, what to do with the teeth and tongue), and (3) knowing why to correct it. When this knowledge is combined with a commitment to conscientious self-monitoring and a focus upon the goal, most habits will change. Supplemental behavioral strategies, such as biofeedback, may also be helpful.
Even when clenching is unconscious or nocturnal, correcting it during the day may help reduce it at night. Splints may also increase patients' awareness of oral habits. If muscle tensing is the inciting factor, biofeedback and relaxation techniques may be indicated. Another major issue to address is pacing or hurrying related to a busy day. For triggers such as depression and anxiety, psychological therapy can helpful. If the problem is a sleep disorder, sleep hygiene self-care can be instituted by the psychologist for nonpathologic sleep disturbances, or the patient can be referred to a sleep laboratory for more detailed evaluation.
Common medications used for temporomandibular disorder pain are classified as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, opioids, muscle relaxants, anxiolytics, hypnotics, and antidepressants. Analgesics are used to allay pain; muscle relaxants and anxiolytics for anxiety, fear, and muscle tension; hypnotics for enhancing sleep; and antidepressants for pain, depression, and with certain agents, insomnia.
Randomized controlled trials of NSAIDs for temporomandibular disorder suggest adopting a low threshold for their use as a supplement to self-care. Long-term NSAID use is best approached with caution due to their systemic and gastrointestinal effects. For more severe joint inflammatory symptoms, corticosteroids are effective in TMJ synovitis, either as brief, tapering oral doses (“dose packs”), injected, or given via iontophoresis. Injection of hyaluronic acid is as effective as corticosteroid injections without being associated with higher risk of degenerative joint disease. Repeated injections of corticosteroids can lead to chondrocyte apoptosis and acceleration of the degenerative process.
For myalgia, especially with limited opening, NSAIDs and benzodiazepines are effective. Cyclobenzaprine has also been shown, in clinical trials of muscle pain, to be effective in reducing pain and improving sleep.
In patients with chronic pain due to a temporomandibular disorder, tricyclic antidepressants, such as 10 to 25 mg of amitriptyline or nortriptyline at night with gradual titration, significantly ameliorate insomnia, anxiety, and pain. These medications can be used long term. Selective serotonin reuptake inhibitors should be used with caution in patients with temporomandibular disorder since these agents may increase masticatory parafunctional muscle tension and aggravate muscle pain.
Physical medicine interventions can be efficacious for patients with temporomandibular disorder (TMD) pain and restricted motion. Jaw exercise is the primary and often the only physical medicine treatment required. Jaw exercises include relaxation, rotation, stretching (range of motion), isometric exercise, and postural exercise.
Stretching exercises, together with cold or heat, are effective in reducing pain and improving range of motion. Their benefit is enhanced when incorporated into the patient's daily routine in conjunction with relaxation techniques and a relaxed posture to reduce strain from sustained jaw contraction.
If exercises are ineffective or worsen pain, other physical modalities can be considered: ultrasonography, shortwave diathermy, low-intensity laser, pulsed diathermy, iontophoresis, phonophoresis, superficial heat, cryotherapy (cold), and massage have all demonstrated efficacy. In the short term, such modalities can reduce jaw pain and increase range of motion, thereby allowing jaw exercises to proceed. When range of motion of the jaw is restricted by a TMJ disk displacement without reduction, short-term manipulation of the jaw by a physical therapist or self-mobilization by the patient can help in remodeling the disk to improve joint translation, range of motion, and pain.
If persistent pain is localized to the TMJ and is associated with specific structural changes in the joint, surgical intervention can be considered if comprehensive non-surgical care is unsuccessful. Muscle pain and associated contributing factors should be addressed and controlled prior to TMJ surgery. In general, the less invasive surgeries are as effective as those that are more invasive, so the health care provider should consider an arthrocentesis or arthroscopic procedure before more invasive interventions, such as diskectomy or disk repair. Postoperative management includes appropriate medications, physical therapy, splint therapy when indicated, and continued behavioral treatment as appropriate.
There is no consistent evidence from randomized controlled trials with persistent TMD that altering the occlusion through occlusal adjustment will benefit temporomandibular disorders. Likewise, other dental treatments, such as prosthodontic and orthodontic treatments, are not recommended as a primary treatment for the management or prevention of TMD. However, patients with TMD may require these procedures as part of normal dental care. In these cases, care should be exercised to minimize additional strain to the muscles and joints and aggravation of an existing TMD during these procedures.
As treatment approaches are better defined and validated through clinical trials, triaging patients to appropriate treatment strategies will most likely result in improved, more predictable outcomes. However, patients with similar diagnoses may have quite different histories, contributing factors, and outcomes. In some cases, the causative web of persistent pain is complex, and unraveling it may require a team that includes a dentist, physician, physical therapist, health psychologist, or other health professionals. Factors such as depression, fibromyalgia, and secondary gain may play a role in delaying recovery leading to chronic pain. Patients with chronic temporomandibular disorder, like others with chronic pain, bear witness to the fact that chronic pain is a disease whose remission depends on timely and appropriate application of drug and nondrug therapies.
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