Written by Keith Yount, DDS Thursday, 31 October 2002 19:00
The patient who presents with a toothache or tooth pain that has no obvious dental etiology poses a diagnostic dilemma for the clinician. Prior to initiating dental treatments (such as endodontic treatment, occlusal equilibration, or restorative dentistry), the clinician should consider the differential diagnosis. Initiating tooth-centered treatment that does not address the source of the patient’s pain can be frustrating for both the clinician and the patient, and even have legal ramifications. The proper management of an atypical toothache or tooth pain begins with the knowledge of the full range of conditions that can manifest as this type of discomfort. The physical examination and detailed history of the entire stomatognathic system become critical to an accurate diagnosis.1
In the majority of cases of toothache, the tooth is the source of the pain. In a small percentage of cases, however, the site of the pain is not the specific source. The literature suggests that 6% of the population suffers from persistent periodontal pain,2 and 3% to 5% of patients have persistent pain after endodontic treatment.3,4 The purpose of this article is to explore the differential diagnosis of patient complaints of pain that feels like a toothache, but is not related to the teeth. If all appropriate diagnostic tests focusing on the tooth in question are negative (including referral to an endodontist), this information will enhance the clinician’s ability to provide the appropriate care for patients who experience such pain.
In a limited number of cases, pain is referred from a source other than a tooth to the region of a tooth. An analogy of a commonly referred pain in which the site and source are different is when a myocardial infarction presents as indigestion.
The differential list for atypical toothache is a list of disorders that should be considered when the diagnosis of tooth-related pain, ie, pulpal hyperemia or cracked tooth, is not clear. This list should be considered when tooth-directed diagnostic tests are negative, additional treatment is not indicated, and there is a clear sense that pain relief will not result from treatment of the tooth.
|Table. Disorders to Consider When Diagnosing Atypical Toothache5-7|
•Muscles of mastication (masseter, temporalis, medial pterygoid, etc)
•Cervical muscles (sternocleidomastoid [SCM], trapezius, splenius capitis, etc)
(2) Periodontal ligament
(3) Temporomandibular joint
Diagnosis of these disorders is not difficult if a logical diagnostic scheme is followed. The list of disorders in their frequency of occurrence is shown in the Table.5-7
The most common cause of atypical tooth pain is referral of pain from muscles of mastication. Muscle pain tends to be deep pain, which is not location-specific. The two most common pain referral patterns from muscles of mastication are the masseter muscle referring to mandibular posterior teeth, and the temporalis muscle referring to maxillary posterior teeth.8 A common cervical muscle referral pattern is when the sternocleidomastoid (SCM) refers pain to the ipsilateral periorbital area. The trigeminal nerve travels primarily to the trigeminal ganglion, but some of the neurons synapse with the superior-cervical ganglion, which can elicit a response from cranial nerves Nos. 7, 9, and 10. Atypical pains in the head region referred from the SCM can be mistaken for vascular headaches or atypical facial neuralgias.9 Furthermore, nociceptive input from virtually the entire head and neck converge on the trigeminal spinal nucleus, which can also lead to unusual pain referral patterns.10,11 Nociception from deep structures (muscle, vasculature, and joint) is generally non-topographic in nature and often difficult for a patient to localize.12 Regardless of the exact mechanism, referred tooth pain does occur.8 Thus, many patients with pain of muscular origin are misdiagnosed with other conditions.13
It has been reported that between 75% and 85% of the patients with atypical toothache also have pain and dysfunction in the cervical region.14 The connection is the stabilization kinetic chain (muscles are used to keep joints in place at rest, resist gravity, and stabilize a joint when a structure is moved in a certain direction or held in a certain position). An example is when the abdominal muscles are contracted, the back muscles contract to keep the person upright. The muscles in the shoulders and upper chest must contract to stabilize the torso, and the muscles of the neck contract to stabilize the shoulder. Considering normal daily activity, the muscles of mastication (masseter, medial pterygoid, lateral pterygoid, and temporalis) are among the most frequently used of all muscles, and contraction of the neck muscles plays a role in stabilizing the jaw. Trauma, hyperextension, hyperflexion injuries, and prolonged opening of the mouth have been related to discomfort reported by more than 50% of all patients with temporomandibular dysfunction.15
Injury to Periodontal Ligament
Injury to the periodontal ligament (PDL) is the second most likely cause of tooth pain.16 Tooth innervation and vascular supply can be pulpal or periodontal, and insult, infection, or injury can be signaled from either source. Heavy occlusal forces can create the symptoms of pulpitis.17 If there is no reason for pulpal pain, the next thing to consider is the PDL that surrounds the tooth, generally protecting it from excessive chewing forces. During the day, the fast reactive two-neuron protective loop keeps a patient from injuring the tooth, PDL, and bone complex when biting.18 At night the protective reflex mechanisms are reduced, and a major force such as clenching or grinding teeth can cause injury to the PDL. These forces can also contribute to alveolar bone loss,19,20 and cause hot and cold sensitivity, cervical erosion,21 masseter muscle enlargement, bony exostosis, and tooth fractures.22 Parafunctional causes of injury to the PDL include the following:
•grinding—lateral movement of the teeth
•clenching—static holding of the teeth in maximum intercuspation
•tooth bracing—locking of upper and lower teeth together in any position outside of centric relation, especially a forward or forward lateral position.
Each of these nonfunctional activities of the masticatory apparatus can damage or injure bone, muscles, joints, or teeth. The discomfort associated with injury to the PDL can feel like pulpal pain.17 Injury to the PDL may be associated with tooth mobility,23 which may lead to further confusion. If endodontic treatment is provided in situations where the pain is related to the PDL, no relief will be reported. When a general dentist or an endodontist rules out the teeth as the cause for pain, occlusal trauma should be considered.2 A diagnostic anesthetic injection is not usually helpful because it will block both the pulpal and PDL innervation. The occlusal trauma may be reduced by simple adjustment of a tooth, but in moderate cases occlusal appliance therapy and medication are necessary. In more complicated cases, referral to an orofacial pain specialist is required. Note that in some cases of PDL-related pain, endodontic therapy may be performed in the course of care. However, if the pain is not relieved, no further dental treatment should be initiated until the cause of the pain is properly identified.
The temporomandibular joint (TMJ) can directly or indirectly refer pain to the dentition. The concept of the three-legged stool presented by Pankey and Dawson,24 where instability in one leg leads to instability in the whole system, is a helpful analogy.24,25 If the sum of all the muscular forces lies in the triangle of support formed by the two condyles and bitepoint, then the force system is said to be stable. If the bitepoint is more posterior, the resultant force will create stress on the working side condyle and muscles.25 The most common problem with the TMJ is internal derangement (disc displacement), and this can lead to indirect referral of pain to the teeth. Of 200 patients diagnosed as having internal derangement of the joint, 67% had disc displacement with reduction (recapturing the central non-innervated thin area of disc by the condyle head as you open), 22% had disc displacement without reduction, and 10% had osteoarthritis.26 Pathology of the joint induces muscle splinting (a protective mechanism by the muscle to restrict joint activity), which when added to bruxism, chewing, and increased muscle tone related to stress, can induce referred pain. According to Hilton’s Law (Dorland’s medical dictionary), the nerve that innervates muscles of a given joint also supplies the joint,27 allowing the muscles surrounding an injured joint to protect the joint. This increase in loading force to an already unstable joint, or increase in muscle activity to that joint, can lead to referred pain.
Neuropathic pain is not often encountered by general dentists, but may be seen by endodontists. Neuropathic pain must be included in the differential diagnosis, especially after the tooth, muscle, PDL, and joint have been evaluated and ruled out as a cause. The neuropathies are considered when no obvious local pathology is identified, there is a history of trauma or surgical intervention, and the patient is depressed. Neuropathies occur most commonly in the fifth or sixth decade of life, and the pain can be severe.28 A neuropathy may be central or peripheral. The location of the neuropathic pain needs to be determined by history of what triggers the pain, and if diagnostic anesthesia blocks the pain. If the pathology is a result of surgery or trauma, described as burning, and blocked at the foramen ovale (by providing a Gow-Gates injection, blocking the entire third division of trigeminal nerve), then a peripheral neuropathy is suspected. The peripheral neuropathies include postherpetic neuralgia, neuroma-related neuropathy, and trigeminal neuropathy. The central neuropathies include trigeminal neuralgia, glossopharyngeal neuralgia, postherpetic neuralgia, and tumors of the mid-cranial fossa.29
Postherpetic neuralgia is caused by a viral infection of one or more branches of the trigeminal nerve. In 10% of cases involving patients over 50 years of age, the nerve pain remains after resolution of the acute viral infection.30 The patient will report a vesicular lesion, moderate to severe pain, with a burning sensation. The pain can occur in any of the divisions of the trigeminal nerve; maxillary distribution (V1 or forehead) is the most common.30 The herpes virus selectively infects large diameter fibers, leaving the C fibers to dominate the gating mechanism of pain.31
The second type of neuropathic pain is nerve injury, leading to a neuroma. Nerve injury is associated with inflammation and release of nerve growth factor (NGF) from cells participating in the repair response, including mast cells.32 NGF stimulates growth of sympathetic nerve tissue.32 A neuroma, then, represents ineffective healing of a nerve, and is associated with excessive production of NGF and benign overgrowth of nerve tissue.33 Some neuromas develop ectopic nerve impulses as a result of release of the cytokine tumor necrosis factor from activated macrophages.25 Concurrently, the pain fibers in a neuroma develop adrenoceptors sensitive to stress-related neurotransmitters.31 A neuroma may result from the trauma of an anesthetic syringe needle injuring a nerve, or as a result of damage during surgery. Chronic neuropathic pain can result.34
The central neuropathies include trigeminal neuralgia, glossopharyngeal neuralgia, and tumors in the mid-cranial fossa. Trigeminal neuralgia is a neurological condition that may manifest as a toothache, but is not related to tooth pathology.35 If the burning pain is not blocked by anesthetic injection and is relieved by the drug Tegretol, a central neuropathic lesion is inferred.34 The central neuropathies are considered to be nerve dysfunction associated with a sensory impulse that crosses over to a pain impulse pathway, which in turn is caused by an artery abrading the myelin sheath of a nerve bundle or pressure from an expanding tumor.36 This is found in association with the trigeminal nerve (cranial nerve No. 5) or the glossopharyngeal nerve (cranial nerve No. 9).
The neurovascular pathologies are classified into two groups which have some similarities and certain differences. The first type is now referred to as atypical odontalgia. The patient describes the pain as throbbing, crawling, constant discomfort in the teeth, bone, or gingiva. The problem is thought to be a microconstriction of the blood vessels in a particular area, caused by autonomic dysfunction.2 Women 30 to 50 years of age, who suffer from depression and have a history of a recent surgical dental procedure seem to be predisposed to this condition.37 Although atypical odontalgia has symptoms very similar to pulpal pain, endodontic procedures will not relieve the pain. A clinical course of an antidepressant (Tofranil) will confirm the diagnosis.38
The second neurovascular pathology is called neuralgia-inducing cavitational osteonecrosis (NICO), and is thought to be related to trauma to bone with improper healing.39 The typical patient is female, 40 to 60 years of age, and describes the pain as throbbing or burning, which is not elicited by any specific activity. The diagnosis is usually confirmed by an unusual anesthetic response to lidocaine (variant anesthetic responses), such as blocking (partial anesthesia up to a certain point, then it stops), bridging (zone of complete anesthesia-zone of partial anesthesia-zone of complete anesthesia), or divergence (zone of anesthesia in another nerve distribution) instead of a complete nerve block of nerve.40 After the exact location of the bone cavity is determined, the area can be probed with an aspirating syringe to locate the thin area of cortical bone.39 A technetium 99 scan may reveal an area of active bone turnover.41 The technetium scan may not reveal the cavity if it is an older lesion without significant metabolic activity. These disorders are quite rare, and should be considered only when other causes of nondental toothache have been ruled out. Nevertheless, in an attempt to provide relief, patients suffering from atypical odontalgia and NICO may receive unnecessary and ineffective treatment. It is essential for the dentist and the physician treating facial pain to be aware of these conditions.38
Other disorders that can manifest as a toothache include sinus pathology and psychological problems. Only 4% of headaches or toothaches are related to sinus infections.42 Nevertheless, upper respiratory infections and allergies can manifest as tooth pain in the maxillary posterior regions. A clinical course of decongestants and/or antihistamines, or referral to an otolaryngologist, would confirm the diagnosis.
Toothaches associated with psychological disorders are sometimes difficult to diagnose because of difficulty in taking a complete and accurate history. These patients often present with impaired cognitive ability, inability to focus, and inability to reason. As a result, it is difficult to maintain continuity and clarity during the diagnostic phase of care. Because the history is an important part of the diagnostic process, if the reporting is compromised the dentist or the physician may begin treatment when there is no basis for such treatment. This is more likely to happen when a patient with a psychiatric problem presents with a poor dentition. This unnecessary treatment may even exacerbate the psychological condition. Patients with this condition seen in the dental office are most often suffering from severe depression.43
When a clinician suspects that the cause of a toothache may not be strictly dental in origin, referral to an appropriate specialist (orofacial pain specialist, neurologist, otolaryngologist) is often indicated. If endodontic therapy is the initial approach to treatment, but some doubt remains, the patient should be informed that diagnostic tests for endodontic disease are not always conclusive, and that this therapy may not eliminate the pain associated with the tooth. The fully informed patient should participate in the choice of treatment and be told about the reason for referral.
Reasons for not initiating endodontic therapy (and possibly for referral) include negative test results for pulpal pathology; the diagnostic anesthetic injection does not provide pain relief; and the masseter or temporalis muscle is tender to palpation. A careful diagnostic phase of care is essential. The differential diagnostic process helps the clinician decide to refer an informed patient for additional consultation. This is a valuable service, and helps avoid overtreatment.
Having a defined diagnostic plan for atypical toothache based on a differential list of causes is an essential first step in providing appropriate care for patients with these challenging problems. Using the differential diagnostic list described in this article, the clinician can conduct a variety of tests, provide treatment, or suggest referral. Such a process can help prevent or limit treatment that does not resolve the problem, and can better focus the clinician on the true cause of the patient’s pain. To be effective, treatment must be directed at the source of the pain, not the site of the pain.2
1. Mahan P. Facial Pain. 3rd ed. Philadephia, Pa: Fea & Febiger; 1991:4-143.
2. Brunsvold MA, Nair P, Oates TW, Jr. Chief complaints of patients seeding periodontal treatment. JADA. 1999;130:359-364.
3. Campbell RL, Parks KW, Dodds RN. Chronic facial pain associated with endondontic neuropathy. Oral Surg, Oral Med, Oral Path. 1990;69:287-290.
4. Marbach JJ, Hulbrock J, John C, Segal AG. Incidence of phantom tooth pain, an atypical facial neuralgia. Oral Surg. 1982;53:190-193.
5. Okeson J. Chronic pain. AAOP Convention. San Antonio, Texas, 2002.
6. Gremillion H. Epidemiology of chronic pain. Parker Mahan Study Cub, Parker E. Mahan Facial Pain Center at University of Florida, April 1997.
7. Yount K. Seven Reasons for Atypical Toothache. Academy of General Dentists of North Carolina Convention. Hilton Research Triangle. Raleigh, NC, June 2000.
8. Travel J, Simon D. Myofascial Pain and Dysfunction, Trigger Point Manual. Vol 1. Baltimore, Md: Williams & Wilkins; 1983.
9. Travel J. TMJ Pain from muscles of the head and neck. J Pros Dent. 1960;10:745-763.
10. Yu XM, Mense S. Somatotopical arrangement of rat spinal dorsal horn cells processing input from deep tissues. Neuroscience Lett. 1990;108:43-47.
11. Schaible HG, Schmidt RF, Willis WD. Enhancement of the responses of ascending tract cells in the cat spinal cord by acute inflammation of the knee joint. Exp Brain Res. 1987;66:479-499.
12. Sessle BJ, Hu JW, Amano N, Zhong G. Convergence of cutaneous, tooth pulp, visceral, neck, and muscle afferents onto nociceptive and non-nociceptive neurons in trigeminal subnucleus caudalis and its implications for referred pain. Pain. 1986;27:219-235.
13. Hubbard D, Jr. Clinical Overview and Pathogenesis. Practical Pain Management. Haworth Press; 1996:123-143.
14. Gremillion H. Multidisciplinary diagnosis and management of orofacial pain. Gen Dent. 2001;3:179-186.
15. Harkins SJ, Martiney JL. Extrinsic trauma: a significant factor in temporomandibular dysfunctions. J Pros Dent. 1985;54:271-272.
16. Burgett F. Trauma from occlusion. Dental Clinics NA. 1995;39:301-311.
17. Ikeda, Nakano, Brando, The effect of traumatic occlusal contact on tooth pain threshold. J Dent Res. 1991;70:330.
18. Melzack R, Wall P. Pain mechanisms. Pain Forum. 1996;5:3-11.
19. Waerhaug J. Pathogenesis of pocket formation in traumatic occlusion. J Perio. 1952;26:107-118.
20. Roberts WE. Bone physiology, metabolism, and biomechanics in orthodontic practice. Current Principles and Technique. St Louis, Mo: Mosby; 1994:193-234.
21. Garro, Stephenson, Good. Chronic illness of TMJ as experienced by support-group members. J Gen Intern Med. 1994;9:372.
22. Cannistraci AJ, Fredrich JA. A multidimensional approach to bruxism and TMD. NYS Dent J. 1987;53:31-34.
23. Hirt, Muhleeman. Diagnosis of bruxism by measurement of the tooth mobility. Dent Abst. 1956;1:356.
24. Dawson P. Evaluation, Diagnosis, and Treatment of Occlusal Problems. 2nd ed. St Louis, Mo: Mosby; 1989:275.
25. McNeil C. Science and Practice of Occlusion. Chicago, Ill: Quintessence Books; 1997:180.
26. Hoffman DC, Cubillos L. The effect of arthroscopic surgery on mandibular range of motion. J Cranio Prac. 1992;12:11-18.
27. Webster Medical Dictionary, 25th ed. Saunders.
28. Rosenkopf K. Current concepts concerning the etiology and treatment of trigeminal neuralgia. J Cranio Prac. 1989;7:312-318.
29. Hupp J. Facial neuropathology. Temporomandibular Disorders and Facial Pain. 697-712.
30. Currey TA, Dalsania MD. Tx for herpes zoster ophthalmicus: stellate ganglion block as a tx for acute pain and prevention of postherpetic neuralgia. Ann Ophthalmol. 1991;23:188-189.
31. Fields HL, Rowbotham M, Baron R. Postherpetic neuralgia: Irritable nociceptors and deafferrentation. Neurbiology of Disease. 1998;5:209-226.
32. Merrill RL. Neuropathic Pain. Seminars in Anesthesia. 1997.
33. Leon A, Buriani A, Toso R, et al. Mast cell synthesize, store, and release nerve growth factor. Proc Natl Acad Sci. 1994;91:3739-3743.
34. Dalessio D. Wolfe’s Headache. 6th ed. New York, NY: Oxford University Press; 1993:345.
35. Merrill RL, Graff-Radford SB. Trigeminal neuralgia. J Am Dent Assoc. 1962;123:63-68.
36. Puca A, Meglio M, Tamburrini GT, Vari R. Trigeminal Involvement in intracranial tumours. Acta Neurochir. 1993;125:47-51.
37. Schnurr R, Brooke R. Atypical odontalgia. Oral Surg, Oral Med, Oral Path. 1992;73:445-448.
38. Reik L. Atypical Odontalgia: Localized form of atypical facial pain. Headache. 1984;24:222-224.
39. Ratner EJ, Person P, Kleinman DJ. Jawbone cavities and trigeminal and atypical facial neuralgis. Oral Surg, Oral Med, Oral Path. 1979;48:3-20.
40. McMahon RE, Adams W, Spolnik KJ. Diagnostic anesthesia for referred trigeminal pain. Comp Cont Ed Dent. 1992;13:870-997.
41. Bullough PG, Dicarlo EF. Subchondral avascular necrosis. Annals Rheu Dis.1990;49:412-420.
42. Couch J. Sinus headache: a neurologist’s viewpoint. Seminars Neurology. 1988;8:298-302.
43. Vimpari SS, Knuutila ML, Sakki TK, Kivela SL. Depressive symptoms associated with symptoms of the temporomandibular joint pain and dysfunction syndrome. Psychom Med. 1995;57:439-444.
Dr. Yount is a diplomate of the American Board of Orofacial Pain and a fellow of the Academy of General Dentistry. He is a graduate of The Pankey Institute and Dawson Advanced Studies (Occlusion), and received a fellowship in cranio-facial pain from the University of Florida. He lectures on topics related to chronic pain and myofacial pain dysfunction, atypical toothache, and trigeminal neuropathies.
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