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18 Articles in Volume 11, Issue #9
Pain and Sleep: A Delicate Balance
Management of Insomnia: Considerations For Patients With Chronic Pain
PPM Editorial Board Outlines Management Strategies for Chronic Pain Patients With Insomnia
Attention Deficit Hyperactivity Disorder And Patients With Pain
Dry Needling Offers Relief From Chronic Low Back Pain
Etiology of Chronic Pain and Mental Illness: How To Assess Both
Temporomandibular Disorder: Examining the Cause And Treatments
Highlights From PAINWeek 2011
Is Your Patient Using Heroin?
Medications For Low Back Pain
Nonpharmacologic Treatments for Patients With Sleep Disorders and Pain
Man With Constant, Daily Headache Pain, Photophobia, Phonophobia, and Nausea
Successful Nonoperative Treatment of Persistently Painful Knees Following Total Knee Arthroplasty—A Case Series
Insomnia in Chronic Pain Patients
What Is Going Wrong With Research? Finding the Right Answer
Testing Positive for Marijuana in Urine
Hydrocodone, Carisoprodol, and Alprazolam—A Most Lethal Combination
Pro-inflammatory Diet

Temporomandibular Disorder: Examining the Cause And Treatments

Although there is no cure, the goal of TMD management is to decrease joint pain, muscle pain, and associated inflammation.

The muscles, nerves, and structures of the mouth and jaw play a significant role in daily life—eating, drinking, speaking, and so forth. Thus, when a patient experiences pain in this area, it can be especially debilitating.1

One of the most common causes of such pain and discomfort is temporomandibular disorder (TMD). It has been estimated that 25% of the general population has TMD—a group of pathologies that affect the masticatory muscles (myogenous) and/or the temporomandibular joint (TMJ) (arthrogenous).2 Disability related to this disorder also has been found to have a major influence on socioeconomic factors and is associated with decreased employment.3

This review examines the pathophysiology of TMD as well as the available treatment options, including pharmacotherapy, physical therapy, and osteopathic manipulative medicine (OMM).

Pathophysiology of TMD
The function of the temporomandibular area is deeply dependent on a balanced coordination of joint and myofascial components. There also are nociceptors present, which are very sensitive to any tip in this delicate balance that can cause the symptoms of TMD. These include deep and diffuse pain associated with jaw motion, headache, neck pain, earache, TMJ clicking, and limited jaw opening.4

Although the pathophysiology of TMD is still not well understood, the factors that lead to TMD pain are being elucidated.5 The primary cause of TMD pain often is related to joint degeneration, disk displacement, or inflammatory destruction due to a variety of conditions, including osteoarthritis and rheumatoid arthritis.6 The primary afferent nociceptors of the orofacial region are Aδ or C fibers.7 These nociceptors can be further subdivided into mechano-nociceptors (sensitive to mechanical stimuli), thermo-nociceptors (sensitive to heat or cold), and chemo-nociceptors (sensitive to chemicals).8 Noxious chemical and mechanical stimuli generally excite the TMJ, which suggests that the area is richly innervated by chemo- and mechano-nociceptors.9 These mechano-nociceptors fire with supranormal protrusion, lateral movement, and rotation of the jaw.10 This leads to the conclusion that TMD pain occurs because of excessive mechanical stress on the joint and related ligaments. Interestingly, individuals with significant anterior disk displacement still can have no evidence of pain.11

Biochemical influences play a large role in the transmission and modulation of TMD pain. In the periphery, there is a correlation between the expression of substance P and calcitonin gene-related peptide and patients with TMD pain.12 However, it is unclear whether this is a cause or an effect. The release of these pain-associated neuropeptides may be caused by the excessive stresses and in turn become the cause of the pain. Alternatively, these compounds, as potent vasodilators, may be a compensatory response to the relative hypoxia caused by the pain.13

In addition to these peripheral mechanisms, there also are biochemical influences within the central nervous system. In the brainstem, the primary afferent neurons terminate at the trigeminal spinal tract nucleus. This nucleus consists of three subnuclei: subnucleus oralis, subnucleus interpolaris, and subnucleus caudalis. The subnucleus caudalis serves as the main brainstem relay for nociception and is so structurally similar to the spinal dorsal horn, an important structure in spinal nociception, that it is often referred to as the trigeminal dorsal horn.14

The subnucleus caudalis contains receptors for many neuropeptides, including γ-aminobutyric acid (GABA), neurokinin-1, N-methyl-D-aspartate (NMDA), opioids, and glutamate. Injection of glutamate, in particular into rat TMJ, has been shown to cause sensitization of nociceptors in both the TMJ and the subnucleus caudalis as well as increase the receptive field of noxious stimuli.15 Furthermore, injection of glutamate in these rat models activates the mastication muscles of the jaw, thereby causing a protective jaw-clenching reflex that limits the size of the opening.16 If this protective reflex is excessive, it may cause more pain, which will further increase masticatory muscle tone, causing a vicious cycle of increased muscle tone and pain.17

There are aspects of TMD pain that are not easily explained through its direct pathophysiology. TMD pain has been associated with many psychological factors.18 Interestingly, TMD also seems to be associated with irritable bowel syndrome, another pain syndrome with a very different anatomic location. These associations suggest that chronic pain conditions such as TMD are related via a central mechanism, regardless of the site of pain.19 Recent studies also have suggested that there are genetic risk factors associated with TMD symptomatology, especially those related to estrogen.20 Estrogen status and chronic inflammation, through a common mitogen-activated protein kinase/extracellularly regulated kinase, enhance central nociception in TMD.21

Diagnosis of TMD
The diagnosis of TMD begins with a careful history and physical examination, which may include signs and symptoms such as jaw tenderness, muscle spasm, clicking, and misalignment or discomfort with opening of the mouth. These signs and symptoms are not specific for TMD; therefore, the clinician must rule out systemic mimickers such as infection, connective tissue disease, and temporal arteritis by ordering such laboratory tests as complete blood count, rheumatoid, antinuclear antibody, and erythrocyte sedimentation rates, respectively. Imaging studies including jaw x-ray, arthrography, magnetic resonance imaging (MRI), ultrasound, and computed tomography scan also may be useful both in excluding other causes of temporomandibular pain as well as diagnosing TMD. Unfortunately, because there are no specific symptoms, lab tests, or imaging studies, TMD is largely a clinical diagnosis of exclusion.

Management of TMD
The approach to TMD pain management is based on the severity and etiology of the disorder. In general, nonsurgical approaches are preferred—either pharmacotherapy or physical therapeutic manipulation. The goal of therapy is to decrease joint pain, muscle pain, and associated inflammation.10

Pharmocotherapy of TMD
Ninety percent of patients with TMD are prescribed medications.22 The most commonly used agents include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, muscle relaxants, anxiolytics, and tricyclic antidepressants.23 Because one of the major goals of therapy is to decrease pain and inflammation, it is reasonable to assume that NSAIDs play a major role in the treatment of TMD pain. Although many different NSAIDs have been used to treat TMD pain, two particular medications have proven effective in clinical studies. Diclofenac given at 50 mg orally three times a day has been shown to decrease TMD pain by 50%,24 and topical diclofenac was found to be just as effective.25 It seems that the unique effectiveness of diclofenac is not due solely to its action as an NSAID, but also to its inhibition of the NMDA receptor for glutamate found both in the nociceptors of the TMJ and in the subnucleus caudalis.26 Interestingly, although it is established that peripheral NMDA receptors play a role in TMD pain,16 injection of ketamine into the TMJ in patients with TMJ arthralgia was not shown to be clinically useful.27

Injections of other medications, however, have proven to be efficacious. Corticosteroids and hyaluronic acid are two such drugs that provide analgesia and anti-inflammatory relief for TMD pain. Injection of corticosteroids has been proven to be more efficacious in studies comparing it with saline in treating patients with rheumatoid arthritis with TMJ involvement.28 Corticosteroid injections also resulted in an improvement in pain scores in a 6-month trial without any signs of worsening of condylar dysfunction that may be a theoretical complication.29 Hyaluronic acid injection in the form of sodium hyaluronate is a much slower form of treatment that does not alter the progression of disease. It acts by lubricating the joint and diluting the inflammatory factors in the area, but its clinical efficacy in the treatment of TMD pain is still questionable.30

Physical Therapy
Because TMD is often viewed as pain associated with overuse, physical therapy has become a staple in the treatment of TMD pain. Although many different techniques are available, the goal of treatment is to find the most cost-effective treatment that is able to provide the greatest relief for the patient. This varies depending on the patient and the timing of TMD pain, but TMD self-management therapies, when used with compliant patients, usually prove to be the best therapeutic choice.31

Some patients with TMD experience pain at night and upon waking. This suggests that a nocturnal component is responsible for the pain. An occlusal orthotic is then the treatment of choice for such patients.

Such a splint device is made to cover the surface of the maxillary or mandibular teeth to protect the teeth, jaw muscles, and joints. Because wearing this device may interfere with speech, it is recommended that it be worn during sleep. It is generally effective in relieving nocturnal TMD pain or TMD pain upon waking.32

Additional physical therapy techniques are useful in treating daytime TMD pain. Relaxation and biofeedback techniques are often useful to help relax the masticatory muscles. Passive and active approaches, such as jaw-stretching exercises and jaw posture exercises, as well as indirect manual techniques also have proven to be beneficial to patients with TMD. Additionally, many patients with TMD have coexisting cervical dysfunctions, and manual treatment to the cervical region also has been found to be helpful in the treatment of TMD.33

OMM
OMM has been considered an alternative to many treatment-resistant forms of musculoskeletal disorders such as low back pain, neck pain, and headache.34 Because TMD can be viewed as similar to musculoskeletal disorders in other anatomic regions,28 it is reasonable to consider OMM as a treatment of TMJ.

Monaco et al evaluated the effectiveness of OMM on the mandibular kinetics of patients with TMD and showed that OMM may be a viable treatment modality for these patients. They divided 28 pediatric patients with TMD and limited mouth opening into a group who received OMM and a control group and monitored their progress with kinesiographic recording of mouth opening size and velocity. The patients who received OMM were shown to have an improvement in mouth opening that was moderately statistically significant (P<0.07) and an improvement in the mouth opening velocity that was statistically significant (P<0.03). Control group patients did not show any statistically significant improvement in mouth opening size or velocity.35

Cuccia et al were able to evaluate the effectiveness of OMM in the adult population. Fifty patients with TMD were evenly divided into two treatment groups: 25 patients were treated with OMM, and 25 were treated with conventional treatment. After the 6-month treatment period, both groups showed significant improvement in the pain, maximal mouth opening, and head mobility around the axis. The OMM group, however, was able to achieve the same level of improvement with much less pharmacotherapy compared with the conventional treatment group. This study again demonstrated that OMM has a potentially important role in the treatment of TMD.36

Conclusion
TMD is a prevalent disorder with socioeconomic implications; therefore, it is important to understand the pathophysiology and treatment options of this disease. It is best to examine this disorder through a multidisciplinary approach because there can be genetic, psychological, and social components to the development of TMD.

Similarly, the approach to the treatment of TMD also should be multidisciplinary. Although the use of pharmacotherapy is the most prevalent, physical therapy can be a very important treatment modality as well. Finally, although OMM is an exciting and promising adjunct that has been shown to be efficacious as well as to help lower the need for medication, more large-scale clinical studies should be conducted to elucidate its true value in the treatment of TMD.

Last updated on: December 15, 2011
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