eMedicine Specialties > Emergency Medicine > Rheumatology
Temporomandibular Joint Syndrome
Updated: Feb 18, 2010
Introduction
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.
Uyanik et al identifies 3 distinct causes of pain at the TMJ, which collectively fall under the broader term of TMJ syndrome.[1 ]
- 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
Pathophysiology
The pathophysiology of temporomandibular joint syndrome is not entirely understood. It is believed that the etiology of TMJ dysfunction syndrome 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 has demonstrated TMJ displacement in 84% of patients with symptomatic TMJ versus 33% of asymptomatic subjects.[2 ]
The TMJs can also be affected by conditions such as rheumatoid arthritis, 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.
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.[3 ]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.
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.[4 ]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
No apparent association with race exists.
Sex
Female-to-male ratio is roughly 4:1.
Age
- Greatest incidence of temporomandibular joint (TMJ) syndrome is in adults aged 20-40 years.
- TMJ syndrome is found infrequently in the pediatric population.
Clinical
History
- Symptoms of temporomandibular joint syndrome
- 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
- 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
Differential Diagnoses
| Dental, Infections | Myopathies |
| Dislocations, Mandible | Otitis Media |
| Fractures, Mandible | Sinusitis |
| Gout and Pseudogout | Temporal Arteritis |
| Headache, Cluster | Tick-Borne Diseases, Lyme |
| Headache, Migraine | Trigeminal Neuralgia |
| Headache, Tension |
Other Problems to Be Considered
Parotid gland disorders
Lesions of the oropharyngeal cavity
Tick-borne diseases
Lyme disease
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.
- 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 and rheumatoid factor if rheumatoid arthritis is suspected
Imaging Studies
- Imaging studies generally are not indicated in the ED, unless a fracture is suspected.
- 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.[5 ]
- 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.
Other Tests
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.[6 ]
- Diagnostic anesthesia block: Use a 25- to 30-gauge needle, 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. Conservative management should be attempted before invasive therapies, such as orthodontics or surgery, are recommended.[7 ]
- 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
NSAIDs and benzodiazepines are the mainstays of treatment for TMJ syndrome within the ED. Patients eventually may require tricyclics, opioids, muscle relaxants, or steroid (intraarticular) therapy for protracted pain syndromes.
Nonsteroidal anti-inflammatory drugs (NSAIDs)
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.
Dosing
Adult
200-400 mg PO q4-6h prn; not to exceed 3.2 g/d
Pediatric
<6 months: Not established
6 months to 12 years: 10-70 mg/kg/d PO divided tid/qid; start at lower end of dosing range and titrate upward; not to exceed 2.4 g/d
>12 years: Administer as in adults
Interactions
Probenecid may increase concentrations and possibly toxicity of NSAIDs; ibuprofen may decrease effect of loop diuretics when coadministered; PT may increase when ibuprofen is coadministered with anticoagulants; monitor PT and bleeding closely; ibuprofen and other NSAIDs may increase serum lithium levels and risk of methotrexate toxicity
Contraindications
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding; because of potential cross-sensitivity to other NSAIDs, do not administer to patients with documented hypersensitivity to aspirin, iodides, or other NSAIDs
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; caution in congestive heart failure, hypertension, and decreased hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy; severe GI tract ulceration and bleeding can occur; monitor patients closely when administering prolonged treatments; NSAIDs can inhibit platelet aggregation, but at a lower degree than that observed with aspirin; low WBC counts can occur but usually return to normal as therapy continues; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia is present
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.
Dosing
Adult
250-500 mg PO bid; not to exceed 1.25 g/d; may increase to 1.5 g/d for limited periods
Pediatric
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Interactions
Probenecid and lithium may increase concentrations and possibly toxicity of NSAIDs; effect of loop diuretics may decrease with coadministration; PT may increase with coadministration of anticoagulants; monitor PT and bleeding; coadministration with phenytoin may increase serum phenytoin levels, resulting in an increase in pharmacologic and toxic effects of phenytoin
Contraindications
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; caution in congestive heart failure, hypertension, and decreased hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy; severe GI tract ulceration and bleeding can occur; monitor patients closely when administering prolonged treatments; NSAIDs can inhibit platelet aggregation, but at a lower degree than that observed with aspirin; low WBC counts can occur but usually return to normal as therapy continues; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia is present
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.
Dosing
Adult
200-300 mg/d PO divided bid/qid
Pediatric
Not established
Interactions
Probenecid and lithium may increase concentrations and possibly toxicity of NSAIDs; effect of loop diuretics may decrease with coadministration; coadministration with anticoagulants may prolong PT; monitor PT and bleeding; nephrotoxicity of both cyclosporine and flurbiprofen may be increased; coadministration with phenytoin may increase serum phenytoin levels, resulting in increase in pharmacologic and toxic effects of phenytoin
Contraindications
Documented hypersensitivity; epithelial herpes simplex keratitis
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; caution in congestive heart failure, hypertension, and decreased hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy; severe GI tract ulceration and bleeding can occur; monitor patients closely when administering prolonged treatments; NSAIDs can inhibit platelet aggregation, but at a lower degree than that observed with aspirin; low WBC counts can occur but usually return to normal as therapy continues; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia is present
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.
Dosing
Adult
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
Pediatric
<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults
Interactions
Probenecid and lithium may increase concentrations and possibly toxicity of NSAIDs; effect of loop diuretics may decrease with coadministration; PT may increase when ketoprofen is coadministered with anticoagulants; monitor for bleeding; coadministration with phenytoin may increase serum phenytoin levels, resulting in increase in pharmacologic and toxic effects of phenytoin
Contraindications
Documented hypersensitivity; GI disease; cardiovascular disease; renal or hepatic impairment; patients receiving anticoagulants
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; caution in congestive heart failure, hypertension, and decreased hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy; severe GI tract ulceration and bleeding can occur; monitor patients closely when administering prolonged treatments; NSAIDs can inhibit platelet aggregation, but at a lower degree than that observed with aspirin; low WBC counts can occur but usually return to normal as therapy continues; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia is present
Mefenamic acid (Ponstel)
Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Dosing
Adult
500 mg PO initially followed by 250 mg q4h prn
Pediatric
<12 years: Not established
>12 years: Administer as in adults
Interactions
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and possibly toxicity of NSAIDs; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Contraindications
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
May have adverse effects in fetus; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
Indomethacin (Indocin, Indochron E-R)
Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis.
Dosing
Adult
25-50 mg PO bid/tid
75 mg SR PO bid; not to exceed 200 mg/d
Pediatric
1-2 mg/kg/d divided PO bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d
Interactions
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and possibly toxicity of NSAIDs; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Contraindications
Documented hypersensitivity; GI bleeding or renal insufficiency
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia)
Piroxicam (Feldene)
Decreases activity of cyclooxygenase, which, in turn, inhibits prostaglandin synthesis; effects decrease formation of inflammatory mediators.
Dosing
Adult
10-20 mg/d PO qd
Pediatric
0.2-0.3 mg/kg/d PO qd; not to exceed 15 mg/d
Interactions
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and possibly toxicity of NSAIDs; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Contraindications
Documented hypersensitivity; active GI bleeding
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia)
Benzodiazepines
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.
Dosing
Adult
2-10 mg PO bid/qid
Pediatric
0.05-0.3 mg/kg/dose PO over 2-3 min q15-30min; not to exceed 10 mg; repeat in 2-4 h prn
Interactions
Toxicity of benzodiazepines in CNS is increased when used concurrently with alcohols, phenothiazines, barbiturates, and MAOIs; cisapride significantly can increase diazepam levels
Contraindications
Documented hypersensitivity; narrow-angle glaucoma; first trimester of pregnancy
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in patients receiving other CNS depressants; caution in patients diagnosed with low albumin levels or hepatic failure since diazepam toxicity may increase
Follow-up
Further Outpatient Care
- Outpatient therapies should begin conservative and become more invasive when other options have been exhausted. Along with NSAIDs and muscle relaxants, initial treatment should also include behavior and diet modification.
- 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.
- If failure of these more conservative treatments occurs, operative repair may be considered. Operative repair can range from arthroscopic procedures that can wash out the joint and allow for small repairs to open procedures. Open procedures can utilize jaw implants and synthetic articular disks. Surgery, however, is far from a cure. Friction et al demonstrated in a long-term study in which patients with synthetic implants did not have improved outcome over patients with nonimplant surgical repair or patients with nonsurgical rehabilitation.[8 ]This was determined by looking at subjective and objective measures of symptom severity and functional deficits.
Inpatient & Outpatient Medications
- 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. Clinical efficacy of this drug for TMJ syndrome has not been studied.
Complications
- Alterations in dentition
- Chronic facial pain
- Malocclusion
Prognosis
- 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 symptomatology tend to have a prolonged course of illness.
Patient Education
- Control pain as needed.
- 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.
- Provide behavior modification and counseling.
- Prescribe 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 excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center. Also, see eMedicine's patient education article Temporomandibular Joint (TMJ) Syndrome.
Miscellaneous
Medicolegal Pitfalls
- Failure to make appropriate diagnosis (ie, migraine or dental disease is an incorrect diagnosis), leading to delayed treatment of TMJ syndrome
- Failure to properly estimate patient's level of pain; ineffective pain management may lead to increased morbidity
References
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Tallents, RH, Katzberg, RW, Murphy W, Proskin, et al. Magnetic resonance imaging findings in asymptomatic volunteers and symptomatic patients with temporomandibular disorders. J Prosthet Dent. 1996;75:529. [Medline].
Hegde V. A review of the disorders of the temporomandibular joint. J Indian Prosthodont Soc. 2005;5:56-61.
Rammelsberg P, LeResche L, Dworkin S. Longitudinal outcome of temporomandibular disorders: a 5-year epidemiologic study of muscle disorders defined by research diagnostic criteria for temporomandibular disorders. J Orofac Pain. 2003;17(1):9-20. [Medline].
Ahn SJ, Kim TW, Lee DY. Evaluation of internal derangement of the temporomandibular joint by panoramic radiographs compared with magnetic resonance imaging. Am J Orthod Dentofacial Orthop. Apr 2006;129(4):479-85. [Medline].
American Academy of Family Physicians. Temporomandibular join (TMJ) pain. Am Fm Physician. Nov 2007;76(10):1483-4. [Medline].
[Guideline] American Society of Temporomandibular Joint Surgeons. Guidelines for diagnosis and management of disorders involving the temporomandibular joint and related musculoskeletal structures. Cranio. Jan 2003;21(1):68-76. [Medline].
Fricton JR, Look JO, Schiffman E, Swift J. Long-term study of temporomandibular joint surgery with alloplastic implants compared with nonimplant surgery and nonsurgical rehabilitation for painful temporomandibular joint disc displacement. J Oral Maxillofac Surg. Dec 2002;60(12):1400-11; discussion 1411-2. [Medline].
Dierks EJ. Temporomandibular disorders and facial pain syndromes. Otolaryngology. 1991;1:849-64.
Dionne RA. Pharmacologic treatments for temporomandibular disorders. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. Jan 1997;83(1):134-42. [Medline].
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Greenberg SA, Jacobs JS, Bessette RW. Temporomandibular joint dysfunction: evaluation and treatment. Clin Plast Surg. Oct 1989;16(4):707-24. [Medline].
Laskin DM. Etiology of the pain-dysfunction syndrome. J Am Dent Assoc. Jul 1969;79(1):147-53. [Medline].
Laskin DM. Temporomandibular joint disorders. Arch Otolaryngol Head Neck Surg. 1993;2:1443-50.
Mew JR. The aetiology of temporomandibular disorders: a philosophical overview. Eur J Orthod. Jun 1997;19(3):249-58. [Medline].
Moore KL, Dalley AF. Clinically Oriented Anatomy. 4th ed. 1999.
Okeson JP, de Kanter RJ. Temporomandibular disorders in the medical practice. J Fam Pract. Oct 1996;43(4):347-56. [Medline].
Pharaboz C, Carpentier P. [MR imaging of the temporomandibular joints]. J Radiol. May 2009;90(5 Pt 2):642-8. [Medline].
Weinerger BW. Introduction to the History of Dentistry. St. Louis: CV Mosby Co; 1948:390.
Keywords
temporomandibular joint dysfunction syndrome, TMJ syndrome, TMJ syndrome symptoms, TMJ syndrome causes, TMJ syndrome treatment, myofascial pain dysfunction syndrome, MPD syndrome, temporal mandibular joint, locked jaw, neck pain
Contributor Information and Disclosures
Author
Vivian Tsai, MD, MPH, Assistant Professor at Mount Sinai School of Medicine, Queens Hospital Center
Vivian Tsai, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Coauthor(s)
Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Steven M Heffer, MD, Consulting Staff, Department of Emergency Medicine, Greenwich Hospital
Steven M Heffer, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Medical Editor
Jerome FX Naradzay, MD, FACEP, Medical Director, Consulting Staff, Department of Emergency Medicine, Maria Parham Hospital; Medical Examiner, Vance County, North Carolina
Jerome FX Naradzay, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Managing Editor
Gino A Farina, MD, Associate Professor of Clinical Emergency Medicine, Program Director, Department of Emergency Medicine, Long Island Jewish Medical Center, Albert Einstein College of Medicine
Gino A Farina, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
CME Editor
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Chief Editor
Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment