CASE REPORT

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History of illness. A 62-year-old woman visited me at the Faculty Practice Clinic at the University of Texas Health Science Center at San Antonio for a TMD evaluation. She complained of constant pain at a level of 9 of a possible 10 (intensity being rated on a scale of 0 to 10, on which 0 = no pain and 10 = the worst pain imaginable) bilaterally in the preauricular and masseter muscle areas. She indicated that the pain was a throbbing, dull ache, greater on the right than on the left. The pain increased when a cold stimulus came into contact with teeth in the mandibular right premolar region. Her pain increased when she lay down, and it awakened her several times each night. When the patient awoke, she was able to open her mouth to only a limited degree, but this gradually improved throughout the day.

This pain complaint had begun 20 years earlier after a motor vehicle accident. At that time, the patient was treated with daytime and nighttime stabilization appliances, which provided her minimal benefit. Six months before the evaluation described here, the patient’s general dentist had evaluated her and ruled out any dental disease.

Clinical examination. The patient’s mandibular range of motion was as follows: 22-millimeter opening (including a 2-mm vertical overlap), 5 mm right lateral, 5 mm left lateral and 2 mm protrusive. Palpation of the patient’s masticatory and cervical muscles and her temporomandibular joints (TMJs) revealed that all of her masticatory structures were extremely tender, with the masseter muscles being the most tender. I detected a left TMJ click digitally when the patient opened her mouth. Because the patient related that her TMD symptoms worsened when cold liquids came into contact with teeth in the mandibular right premolar region, worsened when she lay down and awakened her several times during the night, pulpalgia needed to be assessed as a possible causative or contributing factor.

The findings of the visual oral examination were within normal limits. All other teeth were mildly tender to percussion, but tooth no. 28 (the mandibular right first premolar) was extremely tender to percussion. I obtained and evaluated a panoramic radiograph, bitewing radiographs of the patient’s right posterior teeth and a periapical radiograph of tooth no. 28. All radiographic results were within normal limits, and the peri-apical radiograph of tooth no. 28 did not show evidence of apical pathosis.

I applied a cold stimulus to tooth no. 28, and this significantly increased her complaint of bilateral preauricular and masseter muscle area pain; the increased pain lingered for 45 seconds. Ligamentary injection of tooth no. 28 using 0.2 milliliter of 2 percent lidocaine with 1:100,000 epinephrine eliminated her bilateral preauricular and masseter muscle area pain. The patient also related that her masticatory muscles no longer felt tight bilaterally. Her mandibular opening range of motion improved to 44 mm (including a 2-mm vertical overlap), 8 mm right lateral, 8 mm left lateral and 7 mm protrusive. Palpation of the patient’s masticatory muscles and TMJs revealed moderate tenderness. Tooth no. 28 had a disto-occlusal restoration of moderate depth and no evidence of caries.

Clinical impression. I determined that the patient’s primary pain diagnosis was pulpalgia in tooth no. 28. It was not possible to determine whether the pulpalgia was reversible or irreversible. Therefore, I took a conservative approach, treating it first as a reversible pulpalgia and then following the patient’s symptom response.

Treatment. I adjusted tooth no. 28’s occlusion so that it was light in maximum intercuspation and so that the tooth no longer occluded in excursive movements.

I provided the patient with written and oral TMD self-management instructions and prescribed closure muscle-stretching exercises (obtained from Wright⁴). The goal of these was to help speed the recovery of the masticatory musculature. I prescribed 800 milligrams of ibuprofen to be taken as needed, as often as three times a day.

I advised the patient that this therapy might eliminate her TMD-like pain and made an appointment for her to return in two weeks to gauge the results of the therapy. I also advised her that if the pain was not eliminated, tooth no. 28 likely would need root canal therapy and a crown or, alternatively, would need to be extracted.

Two weeks later, the patient related that during the first day or two after her appointment, her constant bilateral 9-level pain had been reduced to a constant 6-level pain and was localized to tooth no. 28, but no additional improvement occurred during the remainder of the two weeks. The patient now could tell that the source of her pain was tooth no. 28; the pain radiated into her right masseter area and was no longer bilateral. The pain now was a dull ache with occasional throbbing, it continued to awaken her at night and she continued to experience limited ability to open her mouth on awakening.

I referred the patient to the endodontic clinic at the University of Texas Health Science Center at San Antonio, where an endodontics resident confirmed that she had irreversible pulpalgia and performed root canal therapy. One week later, the patient told me that all of her symptoms were gone and that she no longer awoke with limited jaw opening.

	DISCUSSION

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The dental literature contains many reports of patients who have complained of tooth pain to the dentist; in three of these reports, the dentist could not detect a dental origin for the pain but was able to reproduce the pain by palpating a masticatory muscle, and the pain subsequently was resolved by means of TMD therapy.^12–14 These are examples of pain referred to a tooth or teeth from the masticatory muscles. The case report presented here involves a similar referred pain pattern, but the patient perceived the pain to be in the masticatory muscles when it was actually of dental origin.

The two primary mechanisms for referred pain are central convergence and central sensitization. More nerves carry information into the central nervous system (CNS) than there are neurons to transfer the information to the higher centers; this results in the need for the information carried by multiple nerves to be consolidated to fewer neurons carrying this information to the higher centers. The higher centers receive the information in such a way that two or more regions may be perceived as its source^9,15 (Figure).

View larger version (48K): [in this window] [in a new window]   Figure. Depiction of central convergence, in which there are fewer neurons following synapses to transmit information to the higher centers, and of central sensitization, in which a continuous barrage of painful input can sensitize additional receptors. Both may contribute to a painful tooth’s being perceived as a painful muscle in the higher centers.

Central sensitization occurs from a continuous barrage of painful input activating receptors that increase the sensitization of neurons, altering normal processing to the higher centers, expanding the receptive field area and causing nonpainful information to be relayed as painful.¹⁷ The figure illustrates two first-order neurons synapsing onto one second-order neuron, depicting how painful input from a tooth could sensitize the second-order neuron, the input of which may be perceived in the higher centers as coming from the muscle. In the case described here, initial therapy may have decreased the amount of painful input, decreasing the central sensitization and thereby enabling the patient to perceive that her pain originated in the affected tooth. Central convergence and central sensitization may occur in both the sensory trigeminal nucleus and the thalamus (Figure), but these mechanisms cannot fully explain all aspects of referred pain.⁹

The pain literature offers increasing findings that suggest that glial cells (astrocytes and microglia) play an important role in central sensitization.^18–20 Results of one study demonstrated that an inflammatory irritant placed on dental pulps could activate the glial cells and produce central sensitization. The application of an astroglial blocker or microglial inhibitor then was able to abolish the central sensitization induced by the inflammatory irritant.¹⁸

In the past, all pain research models focused on pain’s being processed by neurons, and all therapeutic developments were targeted toward the neurons. This focus may be the reason why there are no good pharmaceutical therapies for central sensitization and neuropathic pain.^18,19 New treatments targeting the glial cells recently have entered clinical trials to determine their safety and efficacy.²⁰

Results of animal studies also have indicated that when an irritating substance is placed on a tooth pulp, the masticatory muscle’s electromyographic activity significantly increases.^10,21 This finding may explain why the patient in this case report no longer felt the tightness in her masticatory muscles and had a greater range of motion after the ligamentary injection.

Referred pain in the trigeminal area generally does not cross the midline unless the source is near the midline.⁹ My clinical experience has led my colleagues and I^1,22 to speculate that this tendency is why pulpalgia involving one of the anterior teeth (canine or incisor) may cause bilateral referred pain, whereas posterior teeth refer pain to the ipsilateral side. To my knowledge, this is the only reported case in which a posterior tooth has caused bilateral referred pain.

The signs and symptoms experienced by the patient in this case report suggest that she probably had an underlying TMD. I believe her decreased mouth-opening on awakening to have been caused by nocturnal parafunctional habits. The mild tenderness to percussion of all her teeth is suggestive of a clenching habit. The moderate tenderness of her masticatory muscles and TMJs after the ligamentary injection of tooth no. 28, I believe, was caused by her TMD component or residual soreness.

When a practitioner suspects that pulpalgia may be causing or contributing to TMD-like symptoms, he or she should evaluate the suspected teeth by using traditional pulpalgia evaluation techniques, such as tooth percussion, thermal testing, palpation near the tooth’s apex, radiography and electric pulp testing.²³ Some offending teeth respond to thermal testing by being only hyperresponsive; others also reproduce the referred pain to the TMJ and/or other muscle regions.

Once the clinician identifies the offending tooth, he or she should perform a diagnostic anesthetic block to determine the effect that the tooth has on the pain complaint. A general protocol for providing diagnostic blocks is to identify the locations that could cause the pain and begin by blocking the most distant location from the CNS. If this block does not relieve the pain sensation, the practitioner may administer additional blocks closer to the CNS, thus providing larger areas of anesthetized tissue. For instance, if the clinician believes the cause of a patient’s pain is tooth no. 28, he or she should administer a ligamentary injection to provide as local an anesthetic effect as possible. If this does not relieve the pain, administration of an inferior alveolar block will help the dentist determine whether any of the teeth on the right side of the mandible are causing the pain. If the ligamentary injection does not eliminate the pain but the inferior alveolar block does, then the patient should be rescheduled for further evaluation after the anesthetic block wears off to determine through thermal and other tests which tooth on the mandible’s right side is responsible for the patient’s pain. The practitioner also must be cognizant that the inferior alveolar block anesthetizes other areas (for example, the body of the mandible and soft tissue) that also could be the source of the patient’s pain.

Even if endodontic tests suggest pulpalgia to be the source (the most likely etiology) of the pain, the practitioner should rule out other potential local causes.³ Once the practitioner identifies pulpalgia as a significant contributor to the patient’s pain, he or she should attempt to establish its cause and determine whether it is reversible or irreversible. An example of a reversible pulpalgia is a situation in which the patient has a heavy excursive contact and habitually tends to engage this excursive contact.²⁴ In this example, if the heavy excursive contact is eliminated or reduced, or if it is a nocturnal habit and the patient is provided a stabilization appliance to be worn at night, the reversible pulpalgia should resolve. As the pulpalgia resolves, the referred pain similarly should resolve. If it is determined that the pulpalgia is irreversible, endodontic therapy or extraction is needed to resolve the referred pain.

	CONCLUSION

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A pulpalgia may cause symptoms that mimic TMD or may contribute to TMD signs and symptoms. Patients with TMD-like symptoms due to pulpalgia tend to report that palpating the tender masticatory structures reproduces their pain, leading the practitioner to believe erroneously that the palpated structure is the source of the pain. When patients with TMD-like pain relate events such as a cold stimulus causing the perceived pain to increase, the practitioner should consider and evaluate carefully the possibility of pulpalgia.