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Temporomandibular Disorders

  • Author: Charles F Guardia, III, MD; Chief Editor: Robert A Egan, MD  more...
 
Updated: Jan 07, 2014
 

Background

The joint

The normal human skull possesses 2 temporomandibular joints (TMJs) that 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 syndrome, is the most common cause of facial pain after toothache. In the past, many physicians called this condition TMJ disease or TMJ syndrome. TMD was previously known under the eponymous title of Costen syndrome, after Dr. James Costen, who elucidated many aspects of the syndrome as it relates to 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). However, the term TMD is preferred and used in this article.

No unequivocal definition of the disease exists and 2 classification schemes are used. The AAOP classification divides TMD broadly into 2 syndromes:

  • Muscle-related TMD (myogenous TMD), sometimes called TMD secondary to myofascial pain and dysfunction
  • Joint-related (arthrogenous) TMD, or TMD secondary to true articular disease

Of note, these 2 types often coexist in one patient, 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.

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

The Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) also exist. The RDC/TMD criteria are composed of algorithms that aid in obtaining a diagnosis along 2 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.

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Pathophysiology

In myogenous temporomandibular disorder, 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, rheumatoid arthritis, 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 temporomandibular joints 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.[1]

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 genetic variations in the gene coding for catecholamine-O-methyltransferase (COMT), a gene that relates in to some aspects of pain sensitivity.

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Epidemiology

Frequency

United States

Temporomandibular disorder 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 TMD were noted more frequently in Caucasians than in African Americans. Such symptoms also had an earlier onset in Caucasians.

Sex

Temporomandibular disorder primarily affects women with a male-to-female ratio of 1:4.

Age

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

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Contributor Information and Disclosures
Author

Charles F Guardia, III, MD Instructor in Neurology, Department of Neurology, Dartmouth Hitchcock Medical Center, Geisel School of Medicine at Dartmouth

Charles F Guardia, III, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Radiological Society of North America, American Academy of Sleep Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, Phi Beta Kappa

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Robert A Egan, MD Director of Neuro-Ophthalmology and Stroke Service, St Helena Hospital

Robert A Egan, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, North American Neuro-Ophthalmology Society, Oregon Medical Association

Disclosure: Received honoraria from Biogen Idec for speaking and teaching; Received honoraria from Teva for speaking and teaching.

Additional Contributors

Michael J Schneck, MD, MBA Vice Chair and Professor, Departments of Neurology and Neurosurgery, Loyola University, Chicago Stritch School of Medicine; Associate Director, Stroke Program, Director, Neurology Intensive Care Program, Medical Director, Neurosciences ICU, Loyola University Medical Center

Michael J Schneck, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Society of Neuroimaging, Stroke Council of the American Heart Association, Neurocritical Care Society

Disclosure: Received honoraria from Boehringer-Ingelheim for speaking and teaching; Received honoraria from Sanofi/BMS for speaking and teaching; Received honoraria from Pfizer for speaking and teaching; Received honoraria from UCB Pharma for speaking and teaching; Received consulting fee from Talecris for other; Received grant/research funds from NMT Medical for independent contractor; Received grant/research funds from NIH for independent contractor; Received grant/research funds from Sanofi for independe.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Arun Chaudhary, MD; Jeffrey Appelbaum, DO; and Jennifer Ault, DO, DPT to the development and writing of this article.

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