Inflammation

Primary inflammatory conditions of the TMJ include capsulitis, synovitis, and the polyarthritides. Polyarthritides are uncommon and are associated primarily with rheumatologic disease. Inflammatory conditions, such as synovitis or capsulitis, frequently occur secondary to trauma, irritation, or infection, and they often accompany other TMDs .

Several proinflammatory cytokines have been detected in painful TMDs, which suggests that they may play a role in pain . Capsulitis, an inflammation of the capsule that is related to sprain of capsular ligaments, is clinically difficult, if not impossible, to differentiate from synovitis. The pain that is related to capsulitis increases during all translatory movements and joint distraction, but not usually during clenching, however . Both conditions may be accompanied by a fluctuating swelling (due to effusion) that decreases the ability to occlude on the ipsilateral posterior teeth. Pain that is associated with inflammation is localized to the TMJ capsule and the intracapsular tissues. Typically, the pain is dull achy, but it may be throbbing. It is described frequently as sharp with jaw movements. The pain is continuous, but worsens with jaw function.

Disk derangement disorders

Articular disk displacement is the most common TMJ arthropathy; it is characterized by several stages of clinical dysfunction that involve the disk–condyle relation. The usual direction for displacement is anterior or anteromedial , although other directions have been described. Pain or mandibular movement symptoms are not specific for disk derangement disorders , and disk position may not be related to any presenting symptom .

The causes of disk displacement are not agreed upon; however, it is postulated that in most cases, stretched or torn ligaments that bind the disk to the condyle permit the disk to become displaced An increased horizontal angle of the mandibular condyle has been associated with more advanced TMJ internal derangement Lubrication impairment also has been suggested as a possible etiologic factor of disk displacement . Disk displacement is subdivided into disk displacement with reduction or disk displacement without reduction.

Disk displacement with reduction

Disk displacement with reduction is described when a temporarily misaligned disk reduces or improves its structural relation with the condyle when mandibular translation occurs during opening. This produces a joint noise (sound) that is described as clicking or popping. Disk displacement with reduction usually is characterized by “reciprocal clicking,” a reciprocal noise that is heard during the opening movement and again before the teeth occlude during the closing movement. Because disk displacement with reduction is so common, it may represent a physiologic accommodation without clinical significance . Clicking in reducing disk displacement is not pathologic, because more than one third of an asymptomatic sample can have moderate to severe derangement, and as many as one quarter of clicking joints show normal or only slightly displaced disk positions. Disk displacement may or may not be a painful condition. If the condition is painful, inflammation of the retrodiskal tissue, the synovial tissues, the capsule or the ligaments, or pressure and traction on the disk attachments are more likely the causes of the pain . TMJ disk displacement with reduction may persist for several years up to decades without progression or complication . de Leeuw and colleagues reported that if clicking in patients who have disk displacement with reduction does not respond to treatment and is still present after 2 to 4 years, it is likely to persist for several decades. Disk displacement with reduction may progress to disk displacement without reduction. This condition is characterized by the sudden cessation of clicking and the sudden onset of restricted mouth opening, and frequently is accompanied by pain.

Disk displacement without reduction

Disk displacement without reduction is a permanently displaced disk that does not improve its relation with the condyle on translation. When acute, it is characterized by sudden and marked limited mouth opening because of a jamming or fixation of the disk secondary to disk adhesion, deformation, or dystrophy. Often, pain is present and is related especially to the patient’s attempt to open the mouth. The acute stage is manifested clinically as a straight-line deflection to the affected side on opening, a marked limited laterotrusion to the contralateral side, and a lack of joint noise in the affected joint. As the condition becomes chronic, the pain is reduced markedly from the acute stage to the point of becoming nonpainful in many cases; the opening range may approach normal dimensions over time . If chronic, there usually is a history of joint noise or limitation of mandibular opening ; the condition may progress to reveal radiographically visible osteoarthritic changes. Generally, disk displacement is treated with reassurance and education, rest, instructions to avoid loading, control of contributing factors, and mobility exercises within the pain-free range. In the presence of pain, mild analgesics or anti-inflammatory medications are the drugs of choice. Additional management may consist of splint therapy, physical therapy, arthrocentesis, or arthroscopy to restore range of motion. In an acute disk displacement without reduction, one may try to reduce the disk manually and temporarily maintain the disk–condyle relationship with an anterior repositioning splint. This splint holds the lower jaw forward of its resting position, thereby translating it with the objective of keeping the disk in a favorable position. Outcome is poor. When the disk cannot be reduced, a stabilization appliance can be part of the treatment for painful disk displacement with or without reduction. The high degree of spontaneous reduction of symptoms has to be taken into account before recommending any kind of treatment. Surgical treatments, such as arthroscopy and open joint surgeries, may be considered, but only after reasonable nonsurgical efforts have failed and the patient’s quality of life is affected significantly .

Myofascial pain

Myofascial pain is characterized as a regional muscle pain, described as dull or achy and associated with the presence of trigger points in muscles, tendons, or fascia . Myofascial pain is a common cause of persistent regional pain (eg, neck pain, shoulder pain, headaches, orofacial pain) . The major characteristics of myofascial pain include trigger points in muscles and local and referred pain. A trigger point is identified as a localized area of tenderness in a nodule or a palpable taut band of muscle, tendon, or ligament. The trigger points may be active or latent. Active trigger points are hypersensitive and display continuous pain in the zone of reference that can be altered with specific palpation. Latent trigger points display other characteristics of trigger points, such as increased muscle tension or muscle shortening, but do not produce spontaneous pain. Usually, the pain is dull and deep in quality, diffuse in nature, and present in subcutaneous tissues, including muscle and joints.

Myofascial therapy can be directed peripherally or centrally. The emphasis must be on management and controlling perpetuating factors, while enhancing central inhibition. Active relaxation exercises, spray and stretch, acupressure, ultrasound, deep massage, moist heat, electrical stimulation, transcutaneous electrical nerve stimulation, biofeedback, relaxation techniques, cognitive-behavioral techniques, occlusal stabilization appliances, myofascial release, pharmacotherapy (eg, nonsteroidal anti-inflammatory drugs, muscle relaxants, tricyclic antidepressants), needling, and infiltration of taut bands with local anesthetic alone or combined with botulinum toxin have been used .

Increased tenderness in pericranial muscles is the most prominent clinical finding in patients who have tension-type headache and migraine. The relationship between local tenderness (as seen in trigger points) and general tenderness (as seen in allodynia associated with migraine) must be differentiated. The first indication that there may be a correlation with the muscle tenderness and pain was shown in experiments by Kellgren . He injected an algesic substance (hypertonic saline) into the muscle, and asked the subjects to define the area in which they perceived pain. The subjects who received the hypertonic saline injections mapped out patterns of referral similar to those seen in tension-type headache. Further, he injected local anesthetic into similar areas after the pain was initiated and could abolish the pain. These tender points became known as myofascial trigger points. The question that may be asked is “Under what circumstances could referral take place in the patterns described?”.

Mense described a hypothesis for muscle pain referral to other deep somatic tissues remote from the original muscle stimulation site. He criticized the convergence-projection pain referral theory because there is little convergence evident at the dorsal horn from deep tissues. Mense’s hypothesis adds two new components to the convergence-projection theory. First, the convergent connections from deep tissues to dorsal horn neurons are opened only after nociceptive inputs from muscle are activated. The connections that are opened after muscle stimuli are called silent connections. Second, the referral to muscle, beyond the initially activated site, is due to central sensitization and spread to adjacent spinal segments. The initiating stimulus requires a peripheral inflammatory process (neurogenic inflammation). In the animal model that was described by Mense, the noxious stimulus was bradykinin injected into the muscle. In the work by Kellgren, a hypertonic saline solution was used to trigger the referred pain. This seems to mimic what is seen in the animal model. It is unclear what triggers the muscle referral in the clinical setting where there usually is no obvious inflammation-producing incident. Mense’s theory was used by Simons to discuss a neurophysiologic basis for trigger point pain. Simons hypothesized that when the tender area in the muscle is palpated, there is a neurotransmitter release in the dorsal horn (trigeminal nucleus) that results in previously silent nociceptive inputs becoming active. This, in turn, causes distant neurons to produce a retrograde referred pain. This model accounts for most of the clinical presentation and therapeutic options that are seen in myofascial pain, but it does not account for what initiates the peripheral tenderness that must be present to activate the silent connections. Perhaps a central nervous system–activated neurogenic inflammation, similar to migraine, stimulates nociceptors in muscle, rather than around the blood vessel. Calcitonin gene–related peptide, neurokinin A, and substance P have been used to demonstrate their contribution in myofascial pain . Fields described a means whereby the central nervous system may switch on nociception. He described the presence of “on” cells, which, when stimulated, may produce activation of trigeminal nucleus nociceptors.

In 1991, Olesen and Jensen were the first to suggest a relationship between myofascial pain and tension-type headache. They proposed a vascular-supraspinal-myogenic model for headache pain. This model hypothesizes that perceived pain (headache) intensity is modulated by the central nervous system. In tension-type headache, the inputs primarily are myofascial, whereas in migraine these inputs are vascular. This model helps to explain why the clinical presentation and treatment options often are similar for migraine and tension-type headache, and why there is only temporary relief with peripheral treatments (eg trigger point injections). The resultant hyperalgesia or trigger point sensitivity in myofascial pain may represent a peripheral sensitization to serum levels of serotonin. Ernberg and colleagues showed a significant correlation between serum serotonin levels and allodynia that is associated with muscular face pain. Based on this information, it is proposed that in patients who present with dull aching head pain and related muscle tenderness, the cause may be myofascial pain. In other words, myofascial pain and tension-type headache may be associated with the same or similar mechanisms. Bendtsen hypothesized that central neuroplastic changes may affect the regulation of peripheral mechanisms that lead to increased pericranial muscle activity or release of neurotransmitters in the muscle tissues. By these mechanisms, the central sensitization can be maintained even after the initial eliciting factors are gone. This may account for conversion of episodic headache into chronic tension-type headache.