Temporomandibular Joint Syndrome 

Updated: Jan 02, 2018
Author: Vivian Tsai, MD, MPH, FACEP; Chief Editor: Herbert S Diamond, MD 

Overview

Background

The temporal mandibular joint (TMJ) is the synovial joint that connects the jaw to the skull. These two joints are located just in front of each ear. Each joint is composed of the condyle of the mandible, an articulating disk, and the articular tubercle of the temporal bone. The movements allowed are side to side, up and down, as well as protrusion and retrusion. This complicated joint, along with its attached muscles, allows movements needed for speaking, chewing, and making facial expressions.

Pain and functional disturbances related to the TMJ are common.[1] Uyanik et al identifies the following three distinct causes of pain at the TMJ, which collectively fall under the broader term of TMJ syndrome[2] :

  • Myofascial pain dysfunction (MPD) syndrome, pain at the TMJ due to various causes of increased muscle tension and spasm. It is believed that MPD syndrome is a physical manifestation of psychological stress. No primary disorder of the joint itself is present. Pain is secondary to events such as nocturnal jaw clenching and teeth grinding. Treatment is focused on behavioral modification as opposed to joint repair.

  • Internal derangement (ID), where the problem lies within the joint itself, most commonly with the position of the articulating disc

  • Degenerative joint disease, where arthritic changes result in degeneration of the articulating surfaces

See also Temporomandibular Disorders.

Pathophysiology

The pathophysiology of TMJ syndrome is not entirely understood. It is believed that the etiology is likely multifactorial and arises from both local insults and systemic disorders. Local problems frequently arise from articular disc displacement and hereditary conditions affecting the structures of the joint itself, such as hypoplastic mandibular condyles. A study by Tallents et al found TMJ displacement in 84% of patients with symptomatic TMJ versus 33% of asymptomatic subjects.[3]

The TMJs can also be affected by conditions such as rheumatoid arthritis, juvenile idiopathic arthritis,[4] osteoarthritis, and diseases of the articular disks. In addition, hypermobile TMJs, nocturnal jaw clenching, nocturnal bruxism, jaw clenching due to psychosocial stresses, and local trauma also play a significant role.

A study of 299 females aged 18-60 years suggests that compared with nonsmokers, female smokers younger than 30 years had a higher risk of temporomandibular disorder than older adults.[5]

As described by Hegde, a strong understanding of how the trigeminal nerve innervates the TMJ and surrounding structures explains the pain and referred pain patterns of TMJ disorders.[6] Irritation of the mandibular branch (V3) of the trigeminal nerve results in pain locally at the TMJ and also to other areas of V3 sensory innervation, which include the ipsilateral skin, teeth, side of the head, and scalp.

Epidemiology

Frequency

United States

Currently, an estimated 10 million people have TMJ disorders, and roughly 25% of the population have symptoms at some point in their lives.

Mortality/Morbidity

The morbidity of the disorder is related to significant pain on movement of the jaw. While some patients' symptoms may resolve within weeks, others may have chronic symptoms that persist even with extensive therapy.

One study by Rammelsberg et al followed 235 patients over 5 years.[7] In this study, roughly one third of patients had completely resolved pain, one third had continuous pain over the 5 years, and one third had recurrent episodes with periods of remission.

Race-, Sex-, and Age-related Demographics

See the list below:

  • No apparent association with race exists.
  • Female-to-male ratio is roughly 4:1.
  • Highest incidence of TMJ syndrome is in adults aged 20-40 years
  • TMJ syndrome is found infrequently in the pediatric population
 

Presentation

History

Symptoms of temporomandibular joint syndrome consist of the following:

  • Chronic pain in the muscles of mastication described as a dull ache, typically unilateral

  • Pain may radiate to the ear and jaw and is worsened with chewing

  • Locking of the jaw when attempting to open the mouth

  • Ear clicking or popping, usually when displacement of the articular disk is present

  • Headache and/or neck ache: In some cases, patients may complain of headache without localized pain in the temporomandibular joint

  • A bite that feels uncomfortable or different from usual

  • Neck, shoulder, and back pain

  • Bruxism, teeth clenching

  • Increasing pain over the course of the day

  • History of jaw and/or facial trauma

Physical

Characteristic findings on physical examination include the following:

  • Limitation of jaw opening (normal range is at least 40 mm as measured from lower to upper anterior teeth)

  • Palpable spasm of facial muscles (masseter and internal pterygoid muscles)

  • Unilateral facial swelling

  • Clicking or popping in the TMJ

  • Tenderness to palpation of the TMJ via the external auditory meatus (the tips of the fingers placed behind the tragi at each external acoustic meatus and pulled forward while the patient opens the jaw)

  • Crepitus over joint (in advanced disease)

  • Lateral deviation of mandible

 

DDx

 

Workup

Laboratory Studies

No laboratory studies are specifically indicated to rule in temporomandibular joint (TMJ) syndrome; however, appropriate laboratory samples may be drawn to help rule out other disorders, as follows:

  • Complete blood count (CBC), if infection is suspected
  • Calcium, phosphate, or alkaline phosphatase, for possible bone disease
  • Uric acid if gout is suspected
  • Serum creatine and creatine phosphokinase, indicators of muscle disease
  • Erythrocyte sedimentation rate if temporal arteritis is suspected
  • Rheumatoid factor if rheumatoid arthritis is suspected

Imaging Studies

Imaging studies generally are not indicated in the emergency department, unless a fracture is suspected. Considerations are as follows:

  • Panorex may show a fracture, evidence of osteoarthritis, or displacement of the articular disk; Ahn et al demonstrated that Panorex films can also be effective in evaluating patients with internal derangement of the TMJ[8]

  • Plain radiographs may demonstrate resting and hinge movement of the TMJ

  • CT scan may reveal greater detail of bones than radiographs alone

  • MRI is the test of choice when looking for disk displacement or pathology

For more information, see Imaging of Meniscus Abnormalities in the Temporomandibular Joint.

Diagnostic Nerve Block

The auriculotemporal branch of the trigeminal nerve provides the sensory innervation of the TMJ. A diagnostic nerve block of the auriculotemporal nerve can be helpful in differentiating whether the unilateral orofacial pain originates in the TMJ capsule.[9]

To perform a diagnostic anesthesia block, use a 25- to 30-gauge needle and inject 0.5 mL of short-acting anesthetic about 0.5 inches below the skin just inferior and lateral to the mandibular condyle. If the patient does not experience pain relief with the nerve block, consider other causes of the orofacial pain.

 

Treatment

Emergency Department Care

Signs and symptoms of temporomandibular joint (TMJ) disorders improve over time with or without treatment for most patients. As many as 50% of the patients have symptomatic improvement in 1 year and 85% in 3 years. The following conservative measures should be attempted before invasive therapies, such as orthodontics or surgery, are recommended[10] :

  • Analgesics - Nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Muscle relaxants - Benzodiazepines
  • Moist heat and massage of masticatory muscles

Consultations

Provide outpatient follow-up care with ear, nose, and throat (ENT) specialist or oral surgeon. However, if intractable pain is present, more urgent consultation is necessary.

 

Medication

Medication Summary

Nonsteroidal anti-inflammatory drugs (NSAIDs) and benzodiazepines are the mainstays of pharmacologic treatment for temporomandibular joint (TMJ) syndrome in the emergency deparment. Patients eventually may require tricyclics, opioids, muscle relaxants, or steroid (intra-articular) therapy for protracted pain syndromes.

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Class Summary

Most commonly used for relief of mild to moderate pain. Although effects of NSAIDs in treatment of pain tend to be patient specific, ibuprofen usually is the DOC for initial therapy. Other options include naproxen, flurbiprofen, mefenamic acid, ketoprofen, indomethacin, and piroxicam.

Ibuprofen (Motrin, Advil, Ibuprin, Nuprin)

Usually DOC for treatment of mild to moderate pain if no contraindications exist; inhibits inflammatory reactions and pain, probably by decreasing activity of enzyme cyclooxygenase, which results in inhibition of prostaglandin synthesis.

Naproxen (Aleve, Anaprox, Naprosyn)

Used for relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of enzyme cyclooxygenase, which results in decrease of prostaglandin synthesis.

Flurbiprofen (Ansaid)

Analgesic, antipyretic, and anti-inflammatory effects; may inhibit cyclooxygenase enzyme, causing inhibition of prostaglandin biosynthesis that in turn may result in analgesic and anti-inflammatory activities.

Ketoprofen (Oruvail, Orudis, Actron)

Used for relief of mild to moderate pain and inflammation; administer small dosages initially to patients with small bodies, older persons, and those with renal or liver disease; doses >75 mg do not increase therapeutic effects; administer high doses with caution and closely observe patient for response.

Mefenamic acid (Ponstel)

Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Indomethacin (Indocin, Indochron E-R)

Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis.

Piroxicam (Feldene)

Decreases activity of cyclooxygenase, which, in turn, inhibits prostaglandin synthesis; effects decrease formation of inflammatory mediators.

Benzodiazepines

Class Summary

Used for muscle relaxant properties but relatively contraindicated in pediatric patients because of sedating properties; appear to potentiate effects of GABA and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters by binding to specific receptor sites.

Diazepam (Valium)

Depresses all levels of CNS, including limbic and reticular formation, possibly by increasing activity of GABA, a major inhibitory neurotransmitter.

Individualize dosage and increase cautiously to avoid adverse effects.

 

Follow-up

Further Outpatient Care

Outpatient therapies for temporomandicular joint (TMJ) syndrome should begin with conservative measures and become more invasive when other options have been exhausted. Initial treatment may include the following:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs) and muscle relaxants
  • Patients should eat a soft diet, and avoid habits such as excessive gum chewing. Warm and cold compresses should be used at night along with gentle massage of the TMJ area. Patients need to avoid jaw clenching and teeth grinding if possible.

  • If conservative therapies fail, or for severe acute exacerbations, intra-articular injection of local anesthetics or steroids may be used for TMJ syndrome. However, repeated intra-articular injections are not recommended.

  • Dental splints can be used to keep the jaw more properly aligned. They also help limit nocturnal bruxism and teeth grinding.

  • Some patients also find benefit from ultrasonic therapy. This provides deep heat to the area of tenderness and may alleviate some patients' symptoms. High-voltage electrogalvanic stimulation is sometimes used to reduce muscle spasms.

  • Low-intensity laser therapy has been investigated as a form of therapy, and it has been shown to reduce pain in TMJ syndrome.[11]

If failure of these more conservative treatments occurs, operative repair may be considered. Operative repair can range from arthroscopic procedures, which can wash out the joint and allow for small repairs,[12] to open procedures. Open procedures can utilize jaw implants, synthetic articular disks, or total TMJ replacement with custom-made alloplastic prostheses.[13] With TMJ ankylosis associated with juvenile idiopathic arthritis, reconstruction with a costochondral graft is the gold standard.[14]

However, in a long-term study by Fricton et al, synthetic implants did not lead to an improved outcome compared with nonimplant surgical repair or nonsurgical rehabilitation.[15] This was determined by looking at subjective and objective measures of symptom severity and functional deficits.

Inpatient & Outpatient Medications

See the list below:

  • NSAIDs are the first line of treatment for TMJ pain.
  • Prescribe benzodiazepines for significant muscle pain or spasm.
  • Cyclobenzaprine may be prescribed in patients unable to tolerate benzodiazepines. The clinical efficacy of this drug for TMJ syndrome has not been studied.

Complications

Complications may include the following:

  • Alterations in dentition
  • Chronic facial pain
  • Malocclusion

Prognosis

See the list below:

  • Prognosis of TMJ disorders is improved with early diagnosis.
  • TMJ disorders often progress to a chronic state.
  • Some cases may be self-limiting.
  • Patients with ear symptoms tend to have a prolonged course of illness.

Patient Education

Patient education measures may include the following:

  • Instruct patients to apply moist heat to affected area for no longer than 15 minutes per application.
  • Educate patients about bruxism and the need to avoid clenching and grinding teeth.
  • Suggest that stress can play a major role in illness; teach stress reduction strategies and provide behavior modification and counseling.
  • Prescribe a soft diet for patients with chewing pain, and advise them to chew more slowly and take smaller bites.
  • Instruct patient in jaw-opening exercises.
  • For patient education information, see Temporomandibular Joint (TMJ) Syndrome.
 

Questions & Answers