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] :
See also Temporomandibular Disorders.
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.
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.
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.
See the list below:
Symptoms of temporomandibular joint syndrome consist of the following:
Characteristic findings on physical examination include the following:
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:
Imaging studies generally are not indicated in the emergency department, unless a fracture is suspected. Considerations are as follows:
For more information, see Imaging of Meniscus Abnormalities in the Temporomandibular Joint.
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.
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] :
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.
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.
Clinical Context: 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.
Clinical Context: 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.
Clinical Context: 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.
Clinical Context: 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.
Clinical Context: Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Clinical Context: Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis.
Clinical Context: Decreases activity of cyclooxygenase, which, in turn, inhibits prostaglandin synthesis; effects decrease formation of inflammatory mediators.
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.
Clinical Context: 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.
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.
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:
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.
See the list below:
Complications may include the following:
See the list below:
Patient education measures may include the following: