Temporomandibular Joint Disorders

CC

A 43-year-old Caucasian woman presents with a 6-month history of daily bitemporal headaches that worsen as the day progresses.

Temporomandibular joint dysfunction is a heterogenous group of disorders that includes myofascial pain dysfunction (MPD), which predominantly affects females.

HPI

The patient reports that the pain is dull and, while often present upon awakening, it continues to worsen throughout the day (characteristic of MPD). When asked to point to the regions of pain, she readily identifies the areas over her temporalis and masseter muscles. She has difficulty falling asleep and wakes up frequently throughout the night. The pain is worse when eating food, especially when chewing tough foods, such as steak (increasing pain and muscle fatigue during mastication are typical findings in MPD). She has modified her diet by excluding hard and chewy foods to reduce the pain and discomfort associated with eating. She reports no history of migraines but admits to a high level of stress at work (work- or home-related stress can exacerbate MPD). She denies any prior history of temporomandibular joint dysfunction and is not aware of any parafunctional habits such as bruxism. (Bruxism is grinding of the teeth. Many patients may be unaware of nocturnal bruxism, unless reported by their bed partner. Also, patients with nocturnal bruxism are characteristically worse on waking and improve over the course of the day).

PMHX/PDHX/Medications/Allergies/SH/FH

The patient's medical and dental histories are unremarkable. She is happily married and has one child. She denies any history of depression (depression is a risk factor for MPD). She works at a regional bank and was recently promoted to vice president, a job that she finds quite stressful (stress is a risk factor for MPD).

Examination

General. The patient is a well-developed and well-nourished, anxious woman.

Maxillofacial. There is no facial swelling or asymmetry. On palpation, there is tenderness of the temporalis, masseter, and sternocleidomastoid muscles bilaterally (temporalis and masseter muscles are most commonly involved in MPD). There is no TMJ capsular tenderness and no clicks or crepitus (making an intracapsular source of pain less likely). The patient has a maximal incisal opening of 28 mm (less than normal) with a soft end feel, which can be stretched to 39 mm with pain (limited opening due to muscle guarding that can be slowly stretched to a normal opening is consistent with MPD). Her left and right lateral excursions are 9 and 8 mm, respectively (normal condylar translation makes TMJ internal derangement less likely). The remainder of her physical examination is noncontributory.

Imaging

A panoramic radiograph is the initial screening examination of choice. Although it cannot diagnose MPD, it provides a general overview of the teeth and related bony structures to rule out other sources of pain. Magnetic resonance imaging (MRI) and computed tomography (CT) scans are ordered based on the clinical suspicions of pathology in conjunction with MPD (see the section on Internal Derangement of the Temporomandibular Joint). However, MRI and CT are not indicated when MPD is the sole clinical diagnosis.

The panoramic radiograph in the current patient reveals no odontogenic or osseous pathology.

Labs

Laboratory tests are not indicated in the work-up of MPD unless associated with other suspected or diagnosed medical conditions (e.g., rheumatoid arthritis or neuromuscular disorders). A suspicion of temporal arteritis would warrant further laboratory testing (erythrocyte sedimentation rate and C-reactive protein as markers of inflammation) and biopsy of the superficial temporal artery.

Assessment

Myofascial pain dysfunction (MPD) syndrome.

The diagnosis of MPD is largely based on the patient history, which is confirmed with a thorough clinical examination. MPD can occur alone (as in the current patient) or in association with internal derangement of the TMJ (see the section Internal Derangement of the Temporomandibular Joint , later in this chapter).

Treatment

The treatment of MPD begins with the correct diagnosis. The etiology of MPD is multifactorial; therefore, the management of MPD requires a multimodal approach. Initially, the patient should be reassured that the pain is purely myofascial and likely to be the result of increased muscle activity secondary to any of a number of entities. These may include stress, anxiety, bruxism, clenching, malocclusion, parafunctional oral habits, internal derangement of the TMJ, rheumatologic diseases (polymyalgia rheumatica), fibromyalgia, and vasculitis (e.g., temporal arteritis). Treatment must address the etiology; however, given the difficulty associated with correct diagnosis, the approach is often generic.

Conservative therapy is generally the first-line treatment unless other identifiable associated diagnoses (tumors, infection, severe internal derangements, degenerative joint disease) are present that are thought to exacerbate the symptoms of MPD. Treatment options include reassurance, stress management (relaxation exercises, biofeedback), occlusal splint therapy, physical therapy, application of heat to affected muscles, nonsteroidal antiinflammatory drugs (NSAIDs), muscle relaxants, and anxiolytics (anxiolytics should be prescribed with caution due to abuse potential). Conservative treatment often results in significant improvement in or resolution of the MPD.

Patients who do respond to conservative therapy with an occlusal splint and have a significant malocclusion may be considered for orthodontic treatment or orthognathic surgery (there is some evidence that malocclusion may be associated with MPD). These modalities may offer a long-term solution to MPD, but they are invasive and not without complications.

Trigger point injections may be beneficial in a select group of patients with MPD who are refractory to all conservative approaches. Typically, a local anesthetic (with or without a steroid) is injected directly into tender areas in the muscles. This can be repeated as often as necessary. It may also be possible to improve MPD with injection of botulinum toxin into the muscle to reduce muscle activity. This may need to be repeated every 3 to 6 months, due to the temporary effect of the botulinum toxin. Regeneration of the nerve endings at the motor end plate of the neuromuscular junction is responsible for cessation of the clinical effects. Excessive muscle activity alone may not explain the majority of cases of MPD, and the response to botulinum toxin is not predictable. Intraarticular procedures, including arthrocentesis, arthroscopy, and arthroplasty, have no place in the management of isolated MPD.

The current patient was encouraged to manage her life stressors more effectively by taking stress management classes and using biofeedback to reduce muscle tension. She was instructed to avoid hard-to-chew foods and to apply moist heat (using a warm, moist towel) to the affected muscles as often as necessary for symptomatic relief. A short course of ibuprofen 800 mg three times a day was prescribed (a muscle relaxant can be added to this regimen). A hard, flat-plane maxillary occlusal splint was constructed, and the patient wore this at all times, except while eating or brushing her teeth. The splint was adjusted weekly to ensure good contacts in centric relation and no interferences during lateral excursions. Splint adjustments became less frequent as the occlusion stabilized, and by 2 months the patient was wearing the splint only at night and was able to open to 44 mm, with complete resolution of her pain.

Complications

With conservative (nonsurgical) approaches to the treatment of MPD, complications are relatively uncommon and are mostly related to the failure of available treatments to alleviate pain, the side effects of medications, or difficulties with occlusal splint therapy.

NSAIDs are often helpful and carry no risk of physiologic dependence, although gastrointestinal irritation and/or bleeding, platelet dysfunction, and decreased renal function are potential complications. The use of some muscle relaxants and anxiolytics can be associated with dependence and abuse, which are compounded by the frequently chronic and recurrent nature of MPD.

Occlusal splint therapy is not without complications (especially when the splint is inappropriately designed). Several different types of splints are used by prescribing clinicians, and unfortunately, there are no clear evidence-based guidelines for splint therapy. Different splints include maxillary, mandibular, flat-plane, anterior repositioning, and pivotal splints. Flat-plane occlusal splints, whether maxillary or mandibular, are the most popular and technically the least demanding. Although complications related to conservative splint therapy are uncommon, an incorrectly adjusted splint can result in exacerbation of the preexisting TMJ dysfunction, tooth movement, and/or the development of new symptoms. Anterior repositioning splints are occasionally useful in patients with Class II malocclusions and function by holding the mandible in a forward position; this unloads the richly innervated retrodiscal tissue within the TMJ and helps to reestablish a more normal disk-condyle relationship. These splints are likely to be associated with permanent occlusal changes, and considerable clinician experience is required in their use. Pivotal splints are rarely used and are thought to function by decreasing masticatory muscle forces (via periodontally mediated biofeedback).

After splint therapy, changes in the occlusion are not uncommon. Before splint therapy, most patients have a centric occlusion–centric relation discrepancy. A flat-plane occlusal splint may eliminate this discrepancy over time, resulting in a less than ideal occlusion when the splint is removed or discontinued. This may necessitate continued splint therapy, occlusal adjustment, orthodontics, or orthognathic surgery.

Discussion

Myofascial pain disorder of the masticatory muscle system is the most common of all temporomandibular joint disorders. The main muscles of mastication are the temporalis, masseter, lateral pterygoid, and medial pterygoid muscles. They all function harmoniously during speech and deglutination. As with any group of muscles, they are susceptible to inflammation, which may in turn cause pain. This is commonly due to excessive activity of these muscles, but the exact pathophysiology has not been clearly defined. The causes of muscle hyperactivity are many and may include malocclusion, parafunctional habits, TMJ internal derangement, cervical pain, and psychological stressors. Management of the acute symptoms of MPD is generally similar, regardless of the etiology, but long-term treatment and success need to address any known precipitating or etiologic factors. As is often the case, no definitive factors can be identified; consequently, a generic approach using several modalities must be adopted.

CC

A 24-year-old female college student presents with several months of a painless “pop” in front of her right ear while eating. (Temporomandibular joint dysfunction [TMD] is a heterogenous group of disorders, including temporomandibular joint [TMJ] internal derangement, and is more commonly diagnosed in females.)

HPI

The patient first noted a “popping” sound in her right temporomandibular joint soon after she had her annual visit to her dentist 4 months earlier. The sound is noticeable when she is chewing, yawning, and brushing her teeth. The click is not associated with pain. She denies any history of trauma (which may precipitate internal derangement), and she had never had any symptoms of temporomandibular joint dysfunction (e.g., popping, clicking, pain, open lock, closed lock, or limited range of motion) before her annual dental visit.

PMHX/PDHX/Medications/Allergies/SH/FH

The patient's past medical and dental histories are noncontributory. She is in her final year of college.

Examination

General. The patient is a well-developed and well-nourished woman in no apparent distress.

Maxillofacial. The right external auditory meatus is patent, without evidence of erythema or exudate. The tympanic membrane is normal. There is no TMJ capsular tenderness. An opening click (caused by the condyle translating and recapturing a normal position beneath the disk) and a reciprocal click (a second click that occurs during closure of the mandible with anterior displacement of the disk) are evident within the right TMJ to both lateral capsular and endaural palpation. Auscultation over the TMJ reveals a harsh opening click and a softer closing click. No crepitation is present (crepitus would be suggestive of disk perforation with degeneration of the condyle and glenoid fossa). The left TMJ clinical examination is within normal limits. There is no evidence of masticatory muscle tenderness (masseter and temporalis muscles). The patient has an initial interincisal opening of 22 mm with a right-sided deviation (due to restricted right condylar translation), followed by a right TMJ click and correction of the deviation (as the anteriorly displaced right disk is recaptured). The maximum interincisal opening is 44 mm. The Mahan test is bilaterally negative (biting on a tongue depressor on one side, eliciting pain in the contralateral TMJ, is a positive test result that suggests intracapsular pathology). The patient is noted to have a Class II division II malocclusion (may be associated with an increased incidence of TMD). The remainder of her clinical examination is unremarkable.

Imaging

The panoramic radiograph is the initial screening study of choice for assessment of TMDs, especially when pain is present (to assess pain of odontogenic origin). It provides a general overview of the bony morphology of the mandible and condyle. Magnetic resonance imaging (MRI), in open and closed mouth positions, is considered the standard when evaluating for TMJ internal derangement. It provides the most information regarding the soft tissue structures and disk position. A TMJ arthrogram (fluoroscopy with dye injected into the superior joint space) is an invasive procedure that shows the disk in dynamic function and is the only study that can readily identify disk perforations. Arthrograms can also be used to evaluate disk position, but the study is technique sensitive and is not readily available in most institutions. Computed tomography (CT) scans are indicated when bony or fibrous ankylosis of the TMJ or other bony pathology is suspected.

In the current patient, no osseous or dental abnormalities were seen on the panoramic radiograph. Sagittal and coronal MRI scans showed an anteromedially displaced (most frequent location of a dislocated disk) right TMJ disk in the closed mouth position ( Figure 10-1, A ), which reduced to a normal anatomic relationship in the open mouth position ( Figure 10-1, B ). The disk demonstrated a normal morphology (anatomy is best seen with T1-weighted images). No joint effusion was seen (inflammation and effusions are best evaluated with T2-weighted images).

Labs

No routine laboratory tests are indicated for the work-up of anterior disk displacement (ADD) of the TMJ. Clinical suspicion of systemic arthropathy (e.g., rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, and gout) would dictate further laboratory testing.

Assessment

Internal derangement of the right TMJ; a nonpainful anterior disk displacement (ADD) with reduction of the right TMJ.

Patients with ADD with or without reduction may present with or without pain originating from the joint itself or from the muscles of mastication (i.e., myofascial pain dysfunction [MPD]). ADD without reduction presents with different clinical findings, including no opening or closing click, and potentially with restricted condylar translation on the affected side (reduced lateral excursion to the contralateral side). The MRI scan would demonstrate anterior displacement of the disk with no evidence of disk recapture during opening. It is not uncommon for MPD to accompany a painful internal derangement of the TMJ. It is important to distinguish between internal derangement and MPD, because their treatment is very different. MPD may also present as the sole source of pain, which warrants proper diagnosis to avoid unnecessary and inappropriate surgical management (see the section Myofascial Pain Dysfunction earlier in this chapter).

The Wilkes classification system for internal derangement of the TMJ characterizes progression of the disease as having five stages, based on the clinical, radiographic, anatomic, and pathologic features ( Table 10-1 ).