Background
The joint
The human skull comprises a pair of temporomandibular joints (TMJs), pivotal connections between the cranium and the lower jaw (mandible) that orchestrate the intricate choreography of mouth opening and closing. A complex gliding joint, the TMJ is the outcome of the harmonious interplay between the mandible's condyle and the temporal bone's squamous portion. Wrapped in fibrous connective tissue, it finds protection within a fibrous capsule spanning from the superior periphery of the temporal joint to the inferior extent of the mandible's neck.
Marking its articular landscape, the temporal bone showcases an anteriorly arched convex articular eminence and a posteriorly concave articular fossa. Meanwhile, the mandible's articulation presents itself through the condyle's uppermost facet. Intervening these mandibular and temporal surfaces is the articular disk—an anatomical partition that bifurcates the joint cavity into the superior and inferior compartments, each hosting distinct movements. The superior compartment accommodates the seamless gliding maneuvers like retrusion and protrusion, while the inferior compartment guides the pivotal hinge actions of elevation and depression.
Fortified by a network of ligaments bridging the mandible to the sphenoid and temporal bones, and bolstered by the muscles governing mastication, the TMJ assumes a critical role. This joint, however, resides within a delicate milieu, ensconced by vital structures that warrant meticulous care to prevent compromise during medical interventions.
Notably, the articular disk, or meniscus, emerges as a biconcave fibrocartilaginous structure integral to the TMJ's harmonious operation. Comprising a substantial anterior band, a delicate intermediate zone, and another substantial posterior band, the meniscus serves as a supple conduit for the mandibular condyle's gliding movement. In the closed mouth posture, the thick posterior band keeps the condyle clear of the temporal bone's articular fossa. Upon mouth opening, the thin intermediate zone emerges, fostering a separation between the condyle and the temporal bone's articular eminence.
The intricate symphony of TMJ movement finds its composers in the muscles of mastication—namely, the masseter, medial and lateral pterygoids, and temporalis. Emerging from the first pharyngeal arch and animated by the mandibular nerve, a branch of the trigeminal nerve, these muscles harmonize to facilitate food mastication, orchestrating mouth closure and lateral tooth motions. However, the TMJ's health can be compromised by parafunctional actions such as clenching and grinding.
The act of mouth opening primarily hinges on gravity, while controlled resistance is administered by the infrahyoid muscles and the platysma. Together, these elements intricately modulate the dynamic tableau of TMJ function.
The syndrome
Temporomandibular disorder(s) (TMD), or temporomandibular joint syndrome, represent an array of pathologies affecting the TMJ and its surrounding structures. These disorders are linked in that they all can cause pain and limit the function of the TMJ. TMD is the most common cause of facial pain after toothache. In the past, many physicians called this condition TMJ disease or TMJ syndrome, but this nomenclature was replaced due to the growing body of scientific research regarding these disorders.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:
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Muscle-related TMD (myogenous TMD), sometimes called TMD secondary to myofascial pain and dysfunction
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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. In addition, due to the anatomy of the mandible, dysfunction of one joint can impact the contralateral joint, and bilateral symptoms are common.
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 most common is displacement disorder, which has two subtypes: anterior displacement with reduction and anterior displacement without reduction.
The Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) also exist. [1] 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, and consideration of these factors necessitates a multidisciplinary approach in difficult cases.
Pathophysiology
In myogenous temporomandibular disorder, the most common cause of the symptomatology (ie, pain, tenderness, and spasm of the mastication muscles) is muscular hyperactivity and dysfunction due to either parafunctional activities, or malocclusion of variable degree and duration. Psychological factors may also play a role. Studies have also linked regulatory pain pathways and local spread of pain signals within the cells of the spinal trigeminal nucleus to the severity, chronicity, and location of pain.
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. It must be emphasized, however, that the presence of pops and clicks denoting anterior displacement with reduction does not necessarily denote pathology and studies of healthy populations have found these signs in a large percentage of individuals who did not later develop symptoms of TMD.
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, and the distance between the incisors is usually less than 25mm. The jaw will usually deviate to the side of pathology. 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. [2]
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.
Epidemiology
Frequency
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-, sex-, and age-related demographics
In a 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. [3]
Temporomandibular disorder primarily affects women with a male-to-female ratio of 1:4.
Highest incidence is among young adults, especially women aged 20–40 years.
Prognosis
Most cases of temporomandibular disorder (TMD) respond to simple treatment and the prognosis is good. Symptoms usually remit with simple care. In cases of secondary involvement of temporomandibular joint (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. Myofascial pain and dysfunction 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 degenerative joint disease 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, avoiding chewing gum and pens, 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, see eMedicineHealth's patient education article Temporomandibular Joint (TMJ) Syndrome.
