AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Background

The joint

The normal human skull has 2 temporomandibular joints (TMJs), one on the right and one on the left. They connect the skull to the lower jaw bone (the mandible) so as to allow the mouth to open and close. The TMJ is a gliding joint, formed by the condyle of the mandible and the squamous portion of the temporal bone. The articular surface of the temporal bone consists of a convex articular eminence anteriorly and a concave articular fossa posteriorly. The articular surface of the mandible consists of the top of the condyle. Articular surfaces of the mandible and temporal bone are separated by an articular disk, which divides the joint cavity into 2 small spaces.

The articular disk, also known as the meniscus, is a biconcave, fibrocartilaginous structure, which provides the gliding surface for the mandibular condyle, resulting in smooth joint movement. The meniscus has 3 parts—a thick anterior band, a thin intermediate zone, and a thick posterior band. With the mouth closed, the condyle is separated from the articular fossa of the temporal bone by the thick posterior band. When the mouth is open, the condyle is separated from the articular eminence of the temporal bone by the thin intermediate zone.

The syndrome

Temporomandibular disorder(s) (TMD) or temporomandibular joint (TMJ) syndrome is the most common cause of facial pain after toothache. In the past, many physicians called this condition TMJ disease or TMJ syndrome. Even earlier, it was called Costen syndrome after Dr. James Costen who elucidated many aspects of the syndrome in 1934, with a predominant emphasis on dental malocclusion. Today, a much more comprehensive view of this condition exists, and the term temporomandibular disorder (TMD) is the preferred term according to the American Academy of Orofacial Pain (AAOP) and most other groups who sponsor studies into its origins and treatment. Interestingly, the National Institute of Dental and Craniofacial Research (NIDCR) puts TMJ and TMD together and refers to them as temporomandibular joint disorder (TMJD) on its Web site. The authors preferentially use the term temporomandibular disorder (TMD) in this article.

No unequivocal definition of the disease exists. However, despite discrepancies concerning the terminology and definitions, a reasonably congruent outlook has emerged among those who study and treat this problem.

Two widely used classification schemes exist. The AAOP classification divides TMD broadly into 2 syndromes: (1) muscle-related TMD (myogenous TMD), sometimes this is called TMD secondary to myofacial pain and dysfunction (MPD), and (2) joint-related (arthrogenous) TMD, that is TMD secondary to true articular disease. The 2 types can be present at the same time, making diagnosis and treatment more challenging.

Myogenous TMD is more common. In its pure form, it lacks apparent destructive changes of the TMJ on radiograph and can be caused by multiple etiologies such as bruxism and daytime jaw clenching in a stressed and anxious person.

Arthrogenous TMD can be further specified as disk displacement disorder, chronic recurrent dislocations, degenerative joint disorders (DJDs), systemic arthritic conditions, ankylosis, infections, and neoplasia.

The Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) also exist. The RDC/TMD criteria comprise a highly structured method (ie, algorithms) of obtaining a diagnosis along two separate axes. The Axis I score provides what is considered the clinical diagnosis, and the Axis II score provides an assessment of mandibular function, psychological status, and level of TMD-related psychosocial disability. This discussion emphasizes the terminology and viewpoint of the AAOP approach. However, the authors are mindful of the important features of the RDC/TMD system. As is the case for most diseases and syndromes, the effect on the patient's life is a major feature of the problem and the psychological and psychosocial aspects are of great importance.

Pathophysiology

In myogenous TMD, the cause of the symptomatology (ie, pain, tenderness, and spasm of the mastication muscles) is muscular hyperactivity and dysfunction due to malocclusion of variable degree and duration. Psychological factors may also play a role.

In TMD of articular origin, disk displacement is the most common cause. Abnormal anterior displacement and interposition of the posterior band between the condyle and the eminence cause pain, pops, and crepitus. If the anteriorly displaced posterior band spontaneously returns to the normal position before the completion of jaw opening, it is called anterior displacement with reduction.

The sudden reduction of the posterior band causes the characteristic pop or click. If the posterior band remains anteriorly displaced at all times during jaw opening, it is called anterior displacement without reduction; full jaw opening may not be possible. Inability to attain a jaw opening of more than 10 mm is known as closed lock. In TMD of articular origin, the spasm of the mastication muscle is secondary in nature.

The other causes of arthrogenous TMD are diseases such as degenerative joint disease (DJD), rheumatoid arthritis (RA), ankylosis, dislocations, infections, and neoplasia, the pathophysiology of which are self-explanatory. One study found that, in patients with chronic inflammatory connective tissue disease, the pain on mandibular movement and tenderness on posterior palpation of TMJ was related to the level of tumor necrosis factor alpha in the synovial fluid.

In a separate study, interleukin 1 receptor antagonist (IL-1ra) and soluble IL-1 receptor II (sIL-1RII) in the synovial fluid and blood plasma of patients with TMJ involvement of polyarthritis appeared to influence the TMJ inflammation.

An important development may connect some of the psychosocial aspects of the disease to underlying neurobiology. This is the discovery that the likelihood of a patient being diagnosed with TMD is related to his or her genetic variants (haplotypes) of the gene coding for catecholamine-O-methyltransferase (COMT), a gene that relates, among other things, to some aspects of pain sensitivity.

Frequency

United States

TMD is a commonly seen condition in primary care and dentistry practice. According to some authorities, as many as 75% of the people in the United States population will at some time have some of the signs and symptoms of TMD; however, all of these individuals are not believed to have TMD. Between 5% and 10% of Americans may sufficiently fulfill the criteria to merit a diagnosis of TMD.

Race

In a recent study of young women aged 19-23 years, facial pain and jaw symptoms related to TMDS were noted more frequently in Caucasians than in African Americans. Such symptoms also had an earlier onset in Caucasians.

Sex

TMD primarily affects women, more so young women. The male-to-female ratio is 1:4.

Age

Highest incidence is among young adults, especially women aged 20-40 years.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

History

A comprehensive, chronological history and physical examination of the patient, including dental history and examination, is essential to diagnose the specific condition to decide further investigations, if any, and to provide specific treatment.

• Symptoms are as follows:
• • Pain: Pain usually is periauricular, associated with chewing, and may radiate to the head but is not like a headache. It may be unilateral or bilateral in MPD, and usually is unilateral in TMD of articular origin, except in RA. In MPD, the pain may be associated with history of bruxism, jaw clenching, stress, and anxiety; the pain may be more severe during periods of increased stress. The assessment of pain is based principally on subjective estimation by the examining practitioner.
  • Click, pop, and snap: These sounds usually are associated with pain in TMD. The click with pain in anterior disk displacement is due to sudden reduction of the posterior band to normal position. An isolated click is very common in the general population and is not a risk factor for development of TMD.
  • Limited jaw opening and locking episodes: The lock can be open or closed; open lock is inability to close the mouth and is seen when the mandibular condyle dislocates anteriorly in front of articular eminence; if not reduced immediately, it is very painful. Closed lock is an inability to open the mouth because of pain or disk displacement.
  • Headaches: The pain of TMD is not like a usual headache. The TMD may act as a trigger in patients prone to headaches, and when present in association with TMD, they tend to be severe in nature. Some patients may have a history of headaches resistant to treatment; the diagnosis and treatment of TMD trigger should not be overlooked in such patients as it is essential for treating these headaches.
  • Other symptoms associated with TMD are otalgia, neck pain and/or stiffness, shoulder pain, and dizziness. About one third of these patients have a history of psychiatric problems. History of facial trauma, systemic arthritic disease, and recurrent dislocation also should be elicited.

Physical

• Observation
• • Asymmetry, muscle hypertrophy, malocclusion of jaw, abnormal dental wear, and missing teeth.
  • Limited range of motion: Normal range of motion for vertical jaw opening, measured between the incisors, is 5 cm; protrusive and lateral mandibular movement is normally 1 cm.
• Palpation
• • The TMJ is best palpated laterally as a depression just below the zygomatic arch, 1-2 cm anterior to the tragus. The posterior aspect of the joint is palpated through the external auditory canal. The joint should be palpated in both open and closed positions, and also both laterally and posteriorly.
  • While palpating, the examiner should feel for muscle spasm, muscle or joint tenderness, and joint sound. The muscles palpated as a part of complete TMJ exam are masseter, temporalis, medial pterygoid, lateral pterygoid, and sternocleidomastoid. In isolated MPD, joint tenderness and joint click are usually absent.
• Auscultation: In most patients, the joint movements causing the sounds can be felt during palpation of the joint; in some cases, however, a less obvious sound can be auscultated.

Causes

• Myogenous TMD (MPD)
• • Etiology is multifactorial and includes malocclusion, jaw clenching, bruxism, personality disorders, increased pain sensitivity, and stress and anxiety; in most patients more than one factor is present.
  • Significance of psychological factors has been recognized during the past few years.
  • Many patients also tend to score high on obsessive-compulsive scale, have increased levels of disease conviction, and are less likely to deny the existence of problems in their life.
• Arthrogenous TMD
• • Of the causes of arthrogenous TMD, disk displacement is the most common.
  • Other diseases such as DJD, polyarthritides such as RA, ankylosis, dislocation, infection, neoplasia, and congenital anomalies may contribute to pain.
• Future directions
• Quite recently, The National Institute of Dental and Craniofacial Research (NIDCR) began a new 7-year clinical study, the Orofacial Pain: Prospective Evaluation and Risk Assessment, or OPPERA study, aimed at identifying risk factors for development of TMD. The study will enroll individuals who do not presently have TMD, and it will assess them by physical, psychological, and biochemical testing (including genetic screening) in order to determine the factors that lead to the development of TMD disease.
• One very exciting new finding is that the incidence of TMD appears to be related to the genetic variants of the gene that encodes the enzyme catecholamine-O-methyltransferase (COMT). Three major variants of this gene exist, and they seem to relate to pain sensitivity. A low, intermediate, and high pain sensitivity variant exist. Those who possess either one or two copies of the low pain sensitivity gene have a much lower chance of developing myogenous TMD. The genetics of this gene and its relationship to TMD will be carefully examined in the OPPERA study mentioned above.

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Other Problems to be Considered

Carotidynia
Dental infections
Jaw myotonia
Otic infections
Paratrigeminal syndrome
Styloid process syndrome

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Lab Studies

• Blood work is required if systemic illness is suspected to be the cause of TMD.
• • CBC is done if infection is suspected.
  • Rheumatoid factor (RF), ESR, antinuclear antibody (ANA), and other specific antibodies are checked if RA, temporal arteritis, or a connective tissue disorder is suspected.
  • Uric acid should be checked for gout. Pseudogout has also been reported in TMJ. Arthrocentesis is required to demonstrate specific crystals.

Imaging Studies

• Imaging of TMJ is an area of ongoing research these days. A variety of new imaging techniques are being used and perfected to study TMJ.
• • Conventional radiography is the most utilized imaging study. It is simple, evaluates bony structures, and in most cases is sufficient. It involves specific techniques and views such as modified Schuller views of each TMJ, both open mouth and closed mouth. Radiographic findings in TMJ depend on the etiology of TMD; in cases of RA and seronegative spondyloarthropathies, plain films show erosions, osteophytes, subchondral bony sclerosis, and condylar-glenoid fossa remodeling.
  • A study using the Acuson 128 XP ultrasound apparatus and an 7.5-MHz linear probe allows visualization of the morphological elements and the functions of the TMJ, articular disk, mandibular condyle, and lateral pterygoid muscle, enabling the physician to plan treatment.
  • Conventional tomograms are no longer indicated. CT scan should be used in place of conventional tomograms. CT scan can explore both bony structures and muscular soft tissues. It is relatively less expensive and can be done with contrast material instilled into the joint cavity.
  • MRI, though costly, should be used as the study of choice if (1) an articular or meniscal pathology is suspected and an endoscopic or surgical procedure is contemplated and (2) in a case of traumatic TMD.
    • In one study, MRI was capable of identifying the meniscus in all cases, together with its morphology, signal, location, and movements during opening and closing of the mouth.
    • Disk dislocations were always identified correctly, and simultaneous study of both TMJ allowed the joints and their motion to be compared and asymmetries detected. The authors observed a high degree of agreement between MRI, arthroscopic, and surgical findings and concluded that MRI should be the study of choice in the evaluation of TMJ disease.

Other Tests

• Quantitative analysis of occlusal strain and stress using photoplastic phenomenon of some polymers: Results of strain analysis can help harmonize static and kinematic occlusal patterns by detecting and eliminating prematurities and interferences. Stress analysis helps to understand the temporomandibular mechanical relationship.
• Cephalometric analysis by the Delaire method allows specific craniofacial morphotypic criteria to be defined.

Procedures

• Diagnostic arthroscopy is an invasive diagnostic approach. It should be used mainly in patients suffering from internal TMJ derangements resistant to conservative treatments. A good MRI study should be obtained before contemplating arthroscopy.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Medical Care

• Most TMDs are self-limiting and do not get worse. Simple treatment, involving self-care practices, rehabilitation aimed at eliminating muscle spasms, and restoring correct coordination, is all that is required. Nonsteroidal anti-inflammatory analgesics (NSAIDs) should be used on a short-term, regular basis and not on an as needed basis.
• On the other hand, treatment of chronic TMD can be difficult and the condition is best managed by a team approach; the team consists of a primary care physician, a dentist, a physiotherapist, a psychologist, a pharmacologist, and in small number of cases, a surgeon. The different modalities include patient education and self-care practices, medication, physical therapy, splints, psychological counseling, relaxation techniques, biofeedback, hypnotherapy, acupuncture, and arthrocentesis.
• Medications: Commonly used medications include NSAIDs, muscle relaxants, and tricyclic antidepressants. More recently, injections of botulinum toxin have been used, in some cases as an adjunct to arthrocentesis (see arthrocentesis below).
• • Ibuprofen and naproxen are commonly used NSAIDs. They work best when given on a regular rather than a prn basis and are not associated with addiction problems. NSAIDs should be prescribed on a regular basis for a period of 2-4 weeks and then gradually tapered. Narcotics are reserved for patients with severe acute pain and should not be used for more than 10-14 days.
  • The commonly used muscle relaxants are diazepam, methocarbamol, and cyclobenzaprine; the lowest effective dose should be used initially. Adverse effects include sedation, depression, and addiction.
  • Tricyclic antidepressants, in low doses, have been used effectively for a long time in chronic painful conditions. They act by inhibiting pain transmission and also may reduce nighttime bruxism. Amitriptyline and nortriptyline, in small doses, are the most common tricyclic antidepressants used for chronic painful conditions.
  • Botulinum toxin is used both as a single treatment (Schwartz and Freund, 2002) and in conjunction with arthrocentesis (Freund and Schwartz, 2003; see arthrocentesis below). No controlled studies exist of the use of this medication in TMD. As noted in the article by Schwartz and Freund, care must be taken to isolate the muscle properly and inject appropriate doses. The authors know of no large-scale double-blind controlled trials on this subject, but some open-label studies have looked promising. A promising controlled study on facial pain associated with masticatory hyperactivity (von Lindern, 2003) did show a significant benefit to botulinum toxin. However, the patients were not diagnosed with TMD per se, and it is not possible to tell which of them may have fulfilled criteria of (probably myogenous) TMD.
• Occlusal splints
• • These are known as nightguards, bruxism appliances, or orthotics. Various kinds of splints are available; most of them can be classified into 2 groups—anterior repositioning splints and autorepositional splints. Physiologic basis of the pain relief provided by splints is not well understood. Factors such as alteration of occlusal relationships, redistribution of occlusal forces of bite, and alteration of structural relationship and forces in the TMJ seem to play some role.
  • Autorepositional splints, also known as muscle splints, are used most frequently. Some sort of pain relief is seen in as many as 70-90% of patients using splints. In acute cases, the splint may be worn 24 hours a day for several months, later, as the condition permits, they may be worn at nighttime only.

Surgical Care

The treatment of chronic TMD is difficult, and at some time during the course of the disease surgical options are discussed with the patient. Some of the surgical options are described here.

• Arthrocentesis
• • Simple washing of the upper compartment of TMJ using arthrocentesis has been very effective in patients with a history of condylomeniscal incoordination; results have been comparable to those of arthroscopic surgery.
  • The benefit of this treatment brings into question the significance of disk position in the etiology of TMD.
  • A 22-gauge needle is inserted gently in the superior joint space and a small amount of saline is injected to distend the joint space, after which the fluid is withdrawn and evaluated. The joint then is redistended and a second needle is placed in the same joint space to lavage the joint; steroids and/or local anesthetics can be injected into the joint space at the conclusion of the procedure.
• Arthroscopic surgery
• • Indications include internal derangements, adhesions, fibrosis, and DJDs.
  • It appears to be as efficient as open surgery, causes less surgical morbidity, and has few severe complications as compared to open surgical procedure. One retrospective short-term study found it to be safe, minimally invasive, and an effective treatment method, with 80% of patients reporting reduced pain and increased range of motion; in acute TMJ lock, however, arthroscopy and arthroscopic lysis and lavage of the upper compartment of TMJ produce comparable success rates.
  • In one study, only 10.3% of 301 patients who underwent arthroscopic lysis and lavage had complications. More than 80% of complications were otological in nature; neurological complications were seen in 5 cases—of which 3 were fifth cranial nerve injury and 2 were seventh cranial nerve injury.
• Open surgery
• • Open surgery was the main surgical option in the 1970s and 1980s, and the most common procedure was disk repositioning and plication; in cases of severe disk damage, procedures such as disk repair and removal were done using artificial or autogenous material.
  • Myrhaug technique: Described in 1951, this procedure, by resecting the temporal condyle, creates a permanent and reducible chronic dislocation of the joint. One study found 70% good or excellent results in 60 patients. The main indications include (1) TMD not responding to all other treatments and (2) chronic subdislocations of one or both TMJ.
• Arthroplasty: This is the surgical procedure of choice for bony intracapsular ankylosis.

Consultations

• Physical therapy: Apart from patient education and pain control, the main goal of physical therapy is to stabilize the joint and restore its mobility, strength, endurance, and function. Common modalities used to accomplish these goals are the following:
• • Relaxation training using electromyographic (EMG) biofeedback: The patient first is educated about the contribution of stress and muscular hyperactivity to pain. An EMG monitor provides instant feedback to patients about the state of their muscle activity and allows the patient to easily correlate pain with hyperactivity of the muscles and decrease in pain with relaxation.
  • Friction massage: The hypothesis is that temporary ischemia and resultant hyperemia, produced by firm cutaneous pressure during massage, helps inactivate trigger points. Friction massage also may help disrupt small fibrous adhesions in the muscle formed as a result of surgery, injury, or prolonged restricted motion.
  • Ultrasonic treatment: ultrasonic waves produce tissue heating at a deeper level than moist heat; this increase in local tissue temperature leads to increase in blood flow and removal of metabolic byproducts responsible for pain and may help decrease adhesions by disrupting collagen cross-linkage. It also may help decrease intra-articular inflammation. To be effective, ultrasonic treatment should be done every other day, using about 1 watt/cm² for approximately 10 minutes over the affected muscles and joints.
  • Transcutaneous electronic nerve stimulation: Electronic stimulation of superficial nerve fiber overrides the pain input from mastication muscles and TMJ, causing release of endogenous endorphins. In some patients it provides longer duration of pain relief than the time during which the stimulation is actually applied.
• Cognitive-behavioral treatment: This consists of hypnosis, cognitive coping skills, and relaxation. Hypnotic susceptibility correlates with reductions in reported pain.
• Psychology: Chronic painful conditions worsen any preexisting anxiety or depression. In appropriate settings, psychological counseling may provide benefit.

MEDICATION

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Medications are helpful only for symptomatic relief and should be used only for short periods. NSAIDs, whenever used, should be administered on a short-term regular basis and not prn.

Drug Category: Nonsteroidal anti-inflammatory agents (NSAIDS)

These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

Drug Category: Muscle relaxant

These agents relieve muscle spasms.

Drug Category: Benzodiazepines

By binding to specific receptor sites, these agents appear to potentiate the effects of GABA and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters.

FOLLOW-UP

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Prognosis

• Most cases of TMD respond to simple treatment and the prognosis is good. Symptoms usually remit with simple care. In cases of secondary involvement of TMJ, the prognosis depends on the primary disease. A second opinion should be obtained in cases in which irreversible treatment is being considered.

Patient Education

• The pathology producing the pain and dysfunction should be discussed with the patient. Patients should be told about the possible prognosis of their problem. MPD tends to have a self-limiting course and needs simple treatment; even though these patients may have recurrences, the symptoms generally are controlled by simple treatment. A patient with TMD secondary to DJD should be made aware of the signs of further deterioration such as increasing pain, further limitation of movement, and increased joint sounds.
• Self-care includes simple measures such as soft diet with gradual progression to normal diet over 6-8 weeks, avoiding large bites and clenching of teeth, keeping jaw relaxed, yawning against pressure, massage of jaw and temple muscles, use of moist heat, avoiding cradling the phone between ear and shoulder, good sleep posture with adequate neck support, and passive or active range of motion 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.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

• Alstergren P, Benavente C, Kopp S. Interleukin-1beta, interleukin-1 receptor antagonist, and interleukin-1 soluble receptor II in temporomandibular joint synovial fluid from patients with chronic polyarthritides. J Oral Maxillofac Surg. Oct 2003;61(10):1171-8. [Medline].
• Arcan M, Zandman F. A method for in vivo quantitative occlusal strain and stress analysis. J Biomech. 1984;17(2):67-79. [Medline].
• Baggi L, Rubino IA, Zanna V. Personality disorders and regulative styles of patients with temporo-mandibular joint pain dysfunction syndrome. Percept Mot Skills. Feb 1995;80(1):267-73. [Medline].
• Barkin S, Weinberg S. Internal derangements of the temporomandibular joint: the role of arthroscopic surgery and arthrocentesis. J Can Dent Assoc. Apr 2000;66(4):199-203. [Medline].
• Bedrune B, Jammet P, Chossegros C. [Temporomandibular joint pain-dysfunction syndrome after whiplash injury. Medico-legal problems in common law]. Rev Stomatol Chir Maxillofac. 1992;93(6):408-13. [Medline].
• Blanchard P, Scheffer P, Lerondeau JC. [Craniofacial architecture and temporomandibular joint pain-dysfunction syndrome. The possibility of orthodontic treatment]. Rev Stomatol Chir Maxillofac. 1990;91 Suppl 1:105-7. [Medline].
• Borodic GE, Acquadro MA. The use of botulinum toxin for the treatment of chronic facial pain. J Pain. Feb 2002;3(1):21-7. [Medline].
• Cascone P, Spallaccia F, Rivaroli A. [Arthrocentesis of the temporomandibular joint. Long-term results]. Minerva Stomatol. Apr 1998;47(4):149-57. [Medline].
• Chossegros C, Cheynet F, Blanc JL. [Diagnostic temporo-mandibular arthroscopy. Principle lesions, apropos of 50 case reports]. Rev Stomatol Chir Maxillofac. 1991;92(3):141-8. [Medline].
• Costen JB. A syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomandibular joint. 1934. Ann Otol Rhinol Laryngol. Oct 1997;106(10 Pt 1):805-19. [Medline].
• Cros P, Freidel M, Borie J. [15 years of treatment of temporomandibular joint algo-dysfunctional syndromes]. Rev Stomatol Chir Maxillofac. 1989;90(6):409-14. [Medline].
• Diatchenko L, Slade GD, Nackley AG. Genetic basis for individual variations in pain perception and the development of a chronic pain condition. Hum Mol Genet. Jan 1 2005;14(1):135-43. [Medline].
• Esposito CJ, Panucci PJ, Farman AG. Associations in 425 patients having temporomandibular disorders. J Ky Med Assoc. May 2000;98(5):213-5. [Medline].
• Ey-Chmielewska H. [An attempt to use ultrasonic technique for confirming the diagnosis, planning and observation of long-term treatment results of painful temporo-mandibular joint dysfunction]. Ann Acad Med Stetin. 1998;44:223-36. [Medline].
• Fassauer H, Bethmann W, Begemeier I. [Diseases of the temporomandibular joint--a clinical statistical study]. Stomatol DDR. Jun 1977;27(6):359-67. [Medline].
• Ferrari R, Schrader H, Obelieniene D. Prevalence of temporomandibular disorders associated with whiplash injury in Lithuania. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. Jun 1999;87(6):653-7. [Medline].
• Freund BJ, Schwartz M. Intramuscular injection of botulinum toxin as an adjunct to arthrocentesis of the temporomandibular joint: preliminary observations. Br J Oral Maxillofac Surg. Oct 2003;41(5):351-2. [Medline].
• Gallucci M, Bozzao A, Splendiani A. [Magnetic resonance in condylo-meniscal incoordination pathology of the temporomandibular joint. Indications, diagnostic accuracy and optimization of study techniques]. Radiol Med (Torino). Apr 1991;81(4):404-11. [Medline].
• Goddard G. Controversies in TMD. J Calif Dent Assoc. Nov 1998;26(11):827-32. [Medline].
• Granat O, Pharaboz C, Gerber S. [The diagnostic importance of different imaging technics in temporomandibular joint dysfunction]. Actual Odontostomatol (Paris). Sep 1989;43(167):417-32. [Medline].
• Irving J, Wood GD, Hackett AF. Does temporomandibular disorder pain dysfunction syndrome affect dietary intake?. Dent Update. Nov 1999;26(9):405-7. [Medline].
• Losapio PL, Amaddeo P. [A case of true congenital temporo-mandibular ankylosis]. Minerva Stomatol. May 1989;38(5):505-8. [Medline].
• Modica R, Mongini F. [Limitations in the opening of the mouth of an arthrogenic nature]. Minerva Stomatol. Jul-Dec 1975;24(4):163-76. [Medline].
• Okeson JP, de Kanter RJ. Temporomandibular disorders in the medical practice. J Fam Pract. Oct 1996;43(4):347-56. [Medline].
• Plesh O, Crawford PB, Gansky SA. Chronic pain in a biracial population of young women. Pain. Oct 2002;99(3):515-23. [Medline].
• Schwartz M, Freund B. Treatment of temporomandibular disorders with botulinum toxin. Clin J Pain. Nov-Dec 2002;18(6 Suppl):S198-203. [Medline].
• Scutellari PN, Orzincolo C, Ceruti S. [The temporo-mandibular joint in pathologic conditions: rheumatoid arthritis and seronegative spondyloarthritis]. Radiol Med (Torino). Oct 1993;86(4):456-66. [Medline].
• Soudant J, Lamas G. [Surgical treatment of temporomandibular joint dysfunctions by Myrhaug's technic. Apropos 60 interventions]. Rev Stomatol Chir Maxillofac. 1987;88(3):208-12. [Medline].
• Speculand B, Goss AN, Hughes A. Temporo-mandibular joint dysfunction: pain and illness behaviour. Pain. Oct 1983;17(2):139-50. [Medline].
• Stam HJ, McGrath PA, Brooke RI. The effects of a cognitive-behavioral treatment program on temporo-mandibular pain and dysfunction syndrome. Psychosom Med. Nov-Dec 1984;46(6):534-45. [Medline].
• Tschopp K, Bachmann R. [Temporomandibular myoarthropathy syndrome--a frequent cause of facial pain]. Schweiz Rundsch Med Prax. Apr 7 1992;81(15):468-72. [Medline].
• Tsuyama M, Kondoh T, Seto K. Complications of temporomandibular joint arthroscopy: a retrospective analysis of 301 lysis and lavage procedures performed using the triangulation technique. J Oral Maxillofac Surg. May 2000;58(5):500-5; discussion 505-6. [Medline].
• Zajko J, Satko I, Hirjak D. [Treatment of dysfunction of the temporomandibular joint by an occlusion splint]. Prakt Zubn Lek. Jun 1990;38(5):151-4. [Medline].
• de Filippis C, Osti L, Osti R. [Algodystrophic syndrome of the temporo-mandibular joint: a clinical experience]. Acta Otorhinolaryngol Ital. Apr 1998;18(2):111-5. [Medline].
• von Lindern JJ, Niederhagen B, Berge S. Type A botulinum toxin in the treatment of chronic facial pain associated with masticatory hyperactivity. J Oral Maxillofac Surg. Jul 2003;61(7):774-8. [Medline].

Article Last Updated: Jun 30, 2006