Articles

Temporal Mandibular Joint Disorder (TMJ)

Introduction

Temporomandibular joint syndrome is characterized by pain and tenderness in the jaw muscles, sound and/or pain over the temporomandibular joint (TMJ), with limitation of mandibular movement. (1) The disorder has received much attention in the lay press in recent years as a cause of chronic headache and facial pain. Although severe cases may require dental or oral surgical intervention, most TMJ dysfunction is psychophysiologic in origin, the consequence of chronic bruxism (nocturnal jaw clenching and teeth grinding). This tension-relieving oral habit develops in response to situational and intrapsychic stresses and can lead to masticatory muscle fatigue and spasm. (2)

In its 1996 consensus statement, the National Institutes of Health Consensus Development conference defined temporomandibular disorders as follows: "Temporomandibular disorders (TMD) refer to a collection of medical and dental conditions affecting the temporomandibular joint (TMJ) and/or the muscles of mastication, as well as contiguous tissue components. Although specific etiologies such as degenerative arthritis and trauma underlie some TMD, as a group these conditions have no common etiology or biological explanation and comprise a heterogeneous group of health problems whose signs and symptoms are overlapping, but not necessarily identical." (3) In clinical practice the term TMD has been assigned to a very wide range of symptoms, varying from noticeable but clinically insignificant signs to seriously debilitating pain or dysfunction. For this reason, the term TMD is not universally endorsed, and generally accepted, scientifically based guidelines for diagnosis and management are still unavailable.

In most instances, the problem remains extracapsular, with no actual derangement of the temporomandibular joint. However, if there has been severe and prolonged bruxism, there may be intracapsular joint derangement. This may lead to degenerative disease of the joint. Intracapsular TMJ disease may be differentiated from extracapsular by the presence of markedly limited jaw movement, jaw deviation when opening the mouth, and presence of crepitus and clicking on jaw movement. There is, however, significant overlap of symptoms, and jaw clicking may even be noted in normal patients. Confirmation of internal joint derangement requires a MRI of the temporomandibular joint. This method provides the best visualization of the soft tissues and bony structures, but should be reserved for patients in whom conservative measures have failed and internal derangement is suspected.

Other etiologies include degenerative arthritis and trauma, ankylosis, growth disorders, recurrent dislocation, neoplasia, condyle fracture, and systemic illness.

Statistic

National Institutes of Health, 1999.

    More than 10 million Americans have symptoms associated with TMD.

National Institute of Dental and Craniofacial Research, 1999.

    The disorders appear to affect about twice as many women as men.

Signs and Symptoms

[span class=alert]The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.[/span]

Symptoms of TMJ dysfunction include chronic, dull, aching unilateral discomfort about the jaw, behind the eyes and ears, and even down the neck into the shoulders. Jaw pain, clicking sounds and difficulty opening the mouth widely, especially in the morning are characteristic. Other characteristics include locking of the jaw, masticatory muscle tenderness, clicking, mandibular hypomotility and joint deviation upon opening. Chewing often exacerbates symptoms. Also, molar prominences may be flattened due to teeth grinding.

General

    Facial and/or TMJ pain Locking or catching jaw TMJ noises-clicking, grinding, popping Headache Earache Neck pain

Treatment Options

Conventional

Evidence suggests that TMJ dysfunction is frequently self-limiting. Treatment plans must be evidence-based and patient centered. The patient’s perception of pain, and impact on the quality of life are important issues to be considered. In the absence of overt pathology, the patient and practitioner should work together to devise a plan of patient self-management with education and understanding of the role of personal factors. Patients with underlying systemic joint diseases, or muscle conditions associated with systemic disease, obviously require treatment for the underlying problem.

Because TMJ dysfunction is largely psychophysiologic in nature, psychotherapy should be an important part of treatment. Most persons improve without formal psychiatric care, however, should receive counseling concerning areas of stress and tension. Education aimed at eliminating certain behaviors perceived to be harmful, such as clenching and grinding of teeth, is frequently beneficial. Other helpful symptomatic measures include dietary advice, local physiotherapy, analgesics, minor tranquilizers, and sometimes antidepressants.

Dietary advice includes cutting food into small pieces and using a diet that minimizes hard, repetitive chewing. Physiotherapy includes the use of local heat and massage to the muscles of mastication. This helps relieve the pain and muscle spasms.

The use of analgesics such as aspirin and low dose non-steroidal anti-inflammatory drugs are also helpful in the relief of pain. Patients with more refractory pain may respond to a trial of sedating tricyclic anti-depressants. Patients with severe grinding may need a custom-made splint or bite guard for nighttime use. Occasionally, short-term use of minor tranquilizers at bedtime may help reduce muscle spasms and complement analgesic therapy. Long-term therapy should be avoided due to risks of dependence.

A regimen that incorporates all these measures into a comprehensive treatment program has a success rate of over 75%. Patients who are refractory may need to be considered for regrinding or surgical intervention, as they may have suffered joint damage.

Nutritional Supplementation

This category contains no therapies clinically applicable to this disease state.

Herbal Supplementation


Kava

Kava has been used for centuries by South Pacific natives. The root is used in the preparation of a recreational beverage known by a variety of local names (kava, yaqona, awa) and occupies a prominent position in the social, ceremonial, and daily life of Pacific island peoples as coffee or tea does in the Western cultures. In European phytomedicine, kava has long been used as a safe, effective treatment for mild anxiety states, nervous tension, muscular tension, and mild insomnia. (4) , (5) Studies have reported that kava preparations compare favorably to benzodiazepines in controlling symptoms of anxiety and minor depression, while increasing vigilance, sociability, memory, and reaction time. (6) , (7) Reports are conflicting as to whether kava’s anti-anxiety actions are GABA mediated. (8) , (9) Kavalactones appear to act on the limbic system, in particular the amygdala complex – the primitive part of the brain that is the center of the emotional being and basic survival functions. (10) It is thought that kava may promote relaxation, sleep, and rest by altering the way in which the limbic system modulates emotional processes. Tolerance does not seem to develop with kava use. (11) , (12)


St. John's Wort

St. John’s wort has gained a great deal of attention for its use in minor depression. Its popularity has stemmed from its extensive use by physicians in Europe as an agent of choice in the treatment of mild to moderate depression. There are a variety of studies which are claimed to support the use of St. John’s wort in treating depression. (13) , (14) , (15) Studies with St. John’s wort have centered around the use of a 0.3 percent hypericin content standardized extract at a dose of 300mg, three times a day. It is viewed as safe and effective in Europe and its monograph is part of the Commission E Monographs for herbal medicines in Europe. St. John’s wort has several possible effects on body chemistry, including (1)the inhibition of cortisol secretion and the blocking of catabolic hormones, such as interleukin 6 (IL-6), (16) (2) the inhibition of the breakdown of several central nervous system neurotransmitters, including serotonin. It may have mild MAO-inhibiting activity. This has not been clearly defined and cannot explain all the activity of St. John’s wort. Researchers do not consider this to be its major mechanism of action, (17) , (18) , (19) (3) amplification and improvement in the signal produced by serotonin once it binds to its receptor sites in the brain. (20) , (21) (4) contains the chemical melatonin (approximately 4.39 mcg/gm), which may also contribute to the antidepressant effects of the plant. (22)

Although the constituent hypericin was originally thought to have the antidepressant effects seen when using St. John’s wort, recent research has reported that the constituents pseudo-hypericin and hyperforin may enhance serotonin, catecholamines, and glutamine levels in the brain. (23)

Recent literature has reported cytochrome P-450 enzyme-inducing activity of St. John’s wort in human studies. Interactions between St. John’s wort and anticoagulants, indinavir, cyclosporin, digoxin, ethinyloestradiol/desogestrel, and theophylline have occurred. (24) The mechanism of action was believed to be liver enzyme induction and subsequent alterations of drug levels by the herb. Also, several reports have suggested that concurrent use of St. John’s wort and SSRIs may result in "serotonin syndrome", including sweating, tremor, confusion, flushing, and agitation. (25) , (26) Use St. John’s wort with caution if individuals are on these medications.

Clinical Notes

Methylsulfonylmethane (MSM): There are no scientific studies that report the use of MSM in individuals with TMJ. However, in a book titled The Miracle of MSM: The Natural Solution for Pain, author Stanley Jacob, M.D. provides the case history of a 56 year old woman who developed severe TMJ. Chiropractic adjustments and acupuncture were not effective. She learned about MSM and began taking it regularly and the pain gradually diminished. After 6 months of use, the pain was reduced by 75% and eventually, she became virtually pain free. However, the lady stated that if she forgets to take MSM for a day or two, she could feel the discomfort start to return. Apparently the physical condition is still there, but MSM reduces the pain so that she can lead a normal, enjoyable life. (27)

D-Phenylalanine (DPA): There are no scientific studies that report the use of D-phenylalanine in individuals with TMJ. However, is an amino acid that inhibits carboxypeptidase A, an enzyme that regulates the degradation of enkephalins, which are the body’s endogenous morphine-like analgesic-producing compounds. Preventing the enzymatic degradation of enkephalins means that more of the body’s endogenous pain-relieving compounds will be active for longer periods of time.

Although there no studies have been conducted on the use of this compound in patients with TMJ, studies have been published reporting that D-phenylalanine is effective in the alleviation of some forms of chronic pain. Therefore, there is a logical rational for a trial of DPA in patients with chronic pain from TMJ.

One example of D-phenylalanine’s ability to relieve chronic pain comes from a study with terminally ill cancer patients. The patients included 3 males and 6 females, between 49 and 78 years of age who were all experiencing severe incident pains related to complications of their disease. These patients were administered DPA, 250 mg three times a day in a cyclical pattern of 15 days on followed by a 10 day days pause. 7 of the 9 patients had successful alleviation of pain and never had to ask for additional analgesics until they died. Four patients achieved a very calm, peaceful state during the same time with a mean survival time of about 100 days and no side effects were reported. The authors concluded that D-phenylalanine is an enkephalinase inhibitor that can be used to help prevent acute or incident pain in malignant diseases. (28)

References

  1. Fields SA. Temporomandibular joint syndrome. In: Dambro MR ed. Griffith’s 5-Minute Clinical Consult. Philadelphia: Lippincott, Williams, & Wilkins; 1999:1046-47.
  2. Goroll AH, May LA, Muley AG. Management of Temporomandibular Joint Dysfunction, Primary Care Medicine, Office Evaluation and Management of the Adult Patient, 3rd ed. Philadelphia: JB Lippincott; 1995:1020-1.
  3. National Institutes of Health Consensus Development Conference Consensus Statement, Volume 0. 1996.
  4. View Abstract: Volz HP, et al. Kava-kava Extract WS 1490 Versus Placebo in Anxiety Disorders--A Randomized Placebo-controlled 25-week Outpatient Trial. Pharmacopsychiatry. Jan1997;30(1):1-5.
  5. View Abstract: Singh YN. Kava: An Overview. J Ethnopharmacol. Aug1992;37(1):13-45.
  6. View Abstract: Munte TF, et al. Effects of Oxazepam and an Extract of Kava Roots (Piper methysticum) on Event-related Potentials in a Word Recognition Task. Neuropsychobiology. 1993;27(1):46-53.
  7. Drug Therapy of Panic Disorders. Kava-specific Extract WS 1490 Compared to Benzodiazepines. Nervenarzt. Jan1994;65(1Supp):1-4.
  8. View Abstract: Jussofie A, et al. Kavapyrone Enriched Extract from Piper methysticum as Modulator of the GABA Binding Site in Different Regions of Rat Brain. Psychopharmacology. Berl. Dec1994;116(4):469-74.
  9. View Abstract: Davies LP, et al. Kava Pyrones and Resin: Studies on GABAA, GABAB and Benzodiazepine Binding Sites in Rodent Brain. Pharmacol Toxicol. Aug1992;71(2):120-26.
  10. View Abstract: Holm E, et al. The Action Profile of D,L-kavain. Cerebral Cites and Sleep-wakefulness-Rhythm in Animals. Arzneimittelforschung. Jul1991;41(7):673-83.
  11. View Abstract: Duffield PH, et al. Development of Tolerance to Kava in Mice. Clinical and Experimental Pharmacology & Physiology. 1991;18(8):571-78.
  12. View Abstract: Singh YN. Kava: An Overview. J Ethnopharmacol. Aug1992;37(1):13-45.
  13. View Abstract: Volz HP. Controlled Clinical Trials of Hypericum Extracts in Depressed Patients--An Overview. Pharmacopsychiatry. 1997;30(Suppl 2):72-76.
  14. View Abstract: Muller WE, et al. Effects of Hypericum Extract (LI 160) in Biochemical Models of Antidepressant Activity. Pharmacopsychiatry. 1997;30(Supp 2):102-07.
  15. View Abstract: Linde K, et al. St. John's Wort for Depression--An Overview and Meta-analysis of Randomised Clinical Trials. BMJ. 1996;313m:253-58.
  16. View Abstract: Nordfors M, Hatvig P.Hypericum Perforatum in the Treatment of Mild Depression. Lakrtidningen. 1997;94:2365-67.
  17. Bloomfield H, et al. Can Depression Be Successfully Treated with a Safe, Inexpensive, Medically Proven Herb Available Without a Prescription? Hypericum and Depression. California: Prelude Press; 1996:110-12.
  18. Suzuki O, et al. Inhibition of Monoamine Oxidase by Hypericin. Planta Medica. 1984;50:272-74.
  19. View Abstract: Bladt S, et al. Inhibition of MAO by Fractions and Constituents of Hypericum Extract. J Geriatric Psychiatry and Neurology. 1994;7:S57-S59.
  20. Murray M. Natural Alternatives to Prozac. New York: William Morrow and Company, Inc; 1996:137.
  21. View Abstract: Muller WEG, et al. Effects of Hypericum Extract on the Expression of Serotonin Receptors. J Geriatric Psychiatry and Neurology. 1994;7:S63-S64.
  22. Murch SJ, et al. Melatonin in Feverfew and Other Medicinal Plants. Lancet. Nov1997;350(9091):1598-9.
  23. View Abstract: Kaehler ST, et al. Hyperforin Enhances the Extracellular Concentrations of Catecholamines, Serotonin and Glutamate in the Rat Locus Coeruleus. Neurosci Lett. Mar1999;262(3): 199-202.
  24. Ernst E. Second Thoughts About Safety of St John's wort. Lancet. Dec1999;354(9195):2014-6.
  25. Gordon JB. SSRIs and St.John's Wort: Possible Toxicity? Am Fam Physician. Mar1998;57(5):950,953.
  26. View Abstract: Lantz MS, et al. St. John’s wort and Antidepressant Drug Ineractions in the Elderly. J Geriatr Psychiatr Neurol. 1999;12:7-10.
  27. Jacob SW, Lawrence RM, Zucker M. The Miracle of MSM: The Natural Solution for Pain. New York NY: GP Putnam’s Sons; 1999:145-148.
  28. View Abstract: Donzelle G, et al. Curing trial of complicated oncologic pain by D-phenylalanine. Anesth Analg. Paris. 1981;38(11-12):655-8.