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Temporomandibular joint dysfunction—Symptoms and management
Temporomandibular joint and current research
Temporomandibular joint dysfunctionmSymptoms and management Nathan Allen Shore, D.D.S. New York, N. Y.
Head pain is one of the most common afflictions of mankind~ yet one that most frequently eludes diagnosis. Although, in common with all pain, it is a signal of "something wrong," it most often can be a biologic reprimand, rather than a threat. As Wolff has pointed out, " . . . with headache it [pain] often means 'wrong direction' or 'wrong pace.' . . . Thus, the vast majority of discomforts and pains of the head stem from readily reversible bodily changes. ''1 The headache specialist sees the patient after he has made the rounds of the medical specialists. Depending upon the area of the head pain, he may have seen an otolaryngologist for symptoms focusing on the ear, the sinuses, or deglutition, or the orthopedist because of a limitation of movement in the temporomandibular joint and the mandible. Perhaps a neurologist was consulted for vague, yet persistent head pain. Finally, in the absence of any special findings, he may have sought psychiatric help. In short, he is quite likely to have seen many specialists before his ailment is diagnosed. It is my opinion that the headache specialist should consider adding to his differential diagnostic procedure a test for dysfunction of temporomandibular joints. Temporomandibular joint dysfunction must be considered in the absence of definitive, pathologic conditions. Indeed, this new concept is being recognized with increasing frequency by physicians, and it is my firm belief that the recognition of temporomandibular joint dysfunction would explain many recurrent head pains. Physicians should be alerted to the prevalence of this condition, and to the need for competent medical-dental management. Temporomandibular joint arthrosis (dysfunction) is a noninfectious, trophic, degenerative affection of the joint tissues initiated by intrinsic trauma, and causing Read before the American Equilibration Society in Chicago, Ill. *Post Graduate Faculty Member, Temple University Dental College, University of Detroit Dental College; Guest Lecturer, University of Louisville Dental College; formerly Chief, Temporomandibular Joint Division, Hospital for Joint Diseases, New York, N. Y. 365
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a b n o r m a l changes in the function of the joint. A p p r o x i m a t e l y 90 p e r cent of the cases are due to a b n o r m a l dental occlusion." DIAGNOSIS T h e p r o b l e m of a differential diagnosis is the f u n d a m e n t a l one confronting physicians. I t is pertinent to emphasize the fact that the result of a pathologic occlusion is not merely i m p a i r m e n t of the functions of the masticatory system_ Dysfunction of the n e u r o m u s c u l a r system occurs, as well as p a i n symptoms in such seemingly unrelated areas as the neck, shoulders, and arms. W h e n careful examination reveals no overt disease state such as the arthritides, head or ear infections, migraine, or eye disorders, t e m p o r o m a n d i b u l a r joint arthrosis should be suspected. These symptoms will always be a p p a r e n t u p o n e x a m i n a t i o n : (1) Pain and tenderness in and around the joint. (2) Clicking and crepitation elicited by stethoscopic examination. (3) Spasm of the external pterygoid muscles. Palpation of the muscle (posterior to the last upper molar) on the affected side produces exquisite pain, which in turn radiates to the ear_ (4) When the mouth is opened, the jaw does not move in a normal, straight vertical line, but veers toward the affected side. (5) Hyper- or hypomobility of the mandible, accompanied by locking of the jaw_ T h e pain m a y encompass a wide range of intensity from a dull to an extreme ache; and it m a y be triggered by eating, yawning, speaking, singing, or shouting. Often there is eye a n d / o r ear pain. As Wolff:' said: " T h e ear is unique in that there is no structure in the body of c o m p a r a b l e size that is supplied by sensory nerves from so m a n y neural segments . . . . Hence, high intensity pain m a y be felt in the vicinity of the ear associated with . . . disorders of the t e m p o r o m a n d i b u l a r joint . . . . " Because of the condition of neuromuscular dysfunction created by a state of pathologic occlusion, a vicious cycle of p a i n - m u s c l e s p a s m - p a i n develops through the m e c h a n i s m of referred pain. A schematic representation of this m a y be seen in Fig. 1, in which the direct neural relationship between pathologic occlusion as the noxious stimulus, and resultant feedback cycles of muscle spasm, trigger areas, and referred p a i n - - a l l distant from the p r i m a r y s t i m u l u s - - m a y be observed. Thus, temp o r o m a n d i b u l a r joint dysfunction can often be held responsible for countless pain areas in the head, which, in turn, m a y radiate into the neck and shoulder regions. W i t h i n the initial area of muscle spasm (i.e., the pterygoid a n d the masseter muscles) lie w h a t T r a v e l P a n d others ~' 6 have called the "trigger" areas. Travell defines trigger areas as points of exquisite tenderness within the muscle in spasm, from which impulses b o m b a r d the central nervous system and give rise to referred pain (cycle 1 of Fig. l ) . T h e initial noxious focus maintains a p e r p e t u a l feedback cycle, a n d the referred p a i n it incited m a y be felt long after the original stimulus from the malocclusion has passed. Those areas of referred pain not associated with muscle spasm are illustrated by Fig. 2. I t will be noted that the trigger a r e a ( X ) is located directly in front of the ear. I t must be emphasized that these symptoms will usually occur on the affected side only, a n d it has been m y experience that a careful and thorough examination can discover 10 to 50 symptoms in a single patient.
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Fig. 1
A schematic representatmn of the neural relationship between muscle spasms in the temporomandibular joint region and the resultant feedback cycles of referred pain and secondary muscle spasm, all distant from the primary noxious stimulus. (A) the pathologically enlarged joint gap, (B) the compressed joint gap, (C) the interfering tooth contact, (D,) the point of reference showing eccentric displacement of mandible (toward the left).
An occasional locking of the jaw occur. Although this is at first easily reducible, it eventually becomes less so, and m a y ultimately result in the restriction of the jaw opening. This is then followed by recurrent subluxation of the joint opposite the painful, restricted one. Recognition of the type of pain (dull, paroxysmal, or lancinating) and which specific type of mandibular m o v e m e n t producing it is particularly important. Figs. 3, 4, and 5 clarify what occurs during the cycle of mandibular closure in a normal and in a pathologic case, and illustrate the basic cause of temporom a n d i b u l a r joint dysfunction and its associated symptomatology. Fig. 3 represents a profile view of a normal centric relation and centric occlusion, with the correct
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Fig. 2 A schematic illustration of areas of referred pain and muscle spasm radiating from the temporomandibular joints; a composite of approximately 1500 cases. Note that the area of noxious stimulus, X, is located directly in front of the ear (after Travell).
Fig. 3 A correct intercuspation of the teeth, in harmony with the neuromuscular closure path of the mandible and the temporomandibular joints. The mandible has described the arc of closure, ]K. The center of the condyle, X, is the pivotal point, Note that the joint gap, F., is evenly spaced in the glenoid fossa, B. This even spacing of the joint gap can be verified by comparison with F in the roentgenogram of the normal temporomandibular joint (Fig. 6, b).
intercuspation of the teeth. Normal masticatory function involves the synchronous working together of the temporomandibular joints, the muscles, and the teeth. U n d e r such circumstances, the jaw closes on a hinge whose pivotal point, represented in Fig. 3 by (X), describes an arc (l-K), which, in turn, allows the teeth to mesh correctly. If for any reason (such as loss of teeth) malocclusion exists, the mandible
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F
B
Fig. 4 The first stage of pathologic closure involving an occlusal contact of an upper and a lower tooth. The pathologic interfering occlusal contact at E has prevented the mandible from completing the closure. The mandible has described the arc ]E'; the condyle has rotated on X, so the closure has not reached K.
Fig. 5 Completion of a pathologic closure involving an occlusal contact of an upper and a lower tooth. The pathologic interfering occlusal surface at E has brought about a deflection of the mandible and malpositioning of both condyles. As the mandible described the arc of closure, [E', it struck the interfering contact at E, causing the mandible to shift forward and complete the arc E'H instead of continuing on to K. The center of the condyle, X, has shifted inferiorly and anteriorly from the point of intersection of a, b, c, and d. Note that the joint gap, F, is narrow anteriorly and wider superiorly and posteriorly. Compare with F of Fig. 3. This uneven spacing of the joint gap can be verified by comparison with F in the roentgenogram of the pathologic temporomandibular joint (Fig. 7, a).
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begins to function abnormally. This initial stage of pathologic closure involving an improper occlusal contact is illustrated by Fig. 4. T h e interfering occlusal contact at (E) has prevented the mandible from completing closure on the arc (]E'), while the condyle has rotated on (X). The completed closure of the mandible, with attendant deflection of the condyles is shown in Fig. 5. As the mandible described the arc of closure (/E') it struck an interfering contact (E), which caused it to shift forward and complete the arc (E'H). Thus, the center of condyle (X) has shifted both inferiorly and anteriorly from the intersection point of lines a-c and b-d in Fig. 5. Malposition of the condyles within both temporomandibular joints has occurred, and the equilibrium of the controlling muscles and ligaments is upset, as well as the highly synchronous movement of the two parts of the external pterygoid muscle, and all of the capsular ligaments. Thus, the patient must learn to accommodate himself to a pathologic neuromuscular positioning of the mandible, which in turn creates an incorrect habit pattern, and initiates the muscle-spasm cycle. Seldom do all symptoms occur simultaneously. Many are presented in various combinations, while individual ones may come and go. Hence, when the examining dentist or physician is confronted by any in combination, and has been alerted to the possibility of temporomandibular joint dysfunction, he can confirm his diagnosis by roentgenograms. It is most helpful to compare the patient's roentgenograms with a similar view of a normal joint, as illustrated by Fig. 6. A roentgenogram of an oblique-lateral transcranial projection of normal left and right joints (Fig. 6) when compared to a similar view of an abnormal joint (Fig, 7) clearly indicates a temporomandibular joint arthrosis in the latter. In closed position (a and b) of Fig. 6, it will be noted that the right and left joint gaps at F are equidistant. Compare this to the dissimilar joint gaps at F in Fig. 7 (a and b). In (a) the left joint gap (F) in the closed position is wide posteriorly at (X), and almost obliterated superiorly at (Y) and anteriorly at (Z). In (b), the right joint gap (F') is seen to be narrow anteriorly at (Z') and wider superiorly at (Y') and posteriorly at (X')_ It will be seen that in Fig. 7 [open positions (d)] the condyle center line OK has passed beyond the eminence center line JM, causing a state of hypermobility. (A state of hypomobility exists when the condyle center lines NH and OK do not quite approach GL and JM.) In the normal open position, however [(c,) and (d) of Fig. 6], the condyle centers (NH) and (OK) should appear beneath lines (GL) and (JM), the centers of articular eminences. PSYCHOGENIC FACTOR
The strong psychogenic factor that has been noted in many patients with temporomandibular joint dysfunction cannot be overlooked, and makes it necessary for the physician to determine what proportion of the symptomatology is due to neurotic components. This is often both baffling and challenging. For example, 95 per cent of the patients are short, blond women between the ages of 35 and 45 with a hypertensive disposition. T h e preponderance of women suffering from this condition is partially explained by Lubosch/ who has pointed out that men have a larger articular eminence which tends to restrict the condyle into a normal position. Close medical-dental coordination is essential in the therapeutic approach to
Temporomandibular joint dys[unction
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Fig. 6 Temporomandibular joint roentgenogram (oblique-lateral transcranial projection) of normal right and left temporomandibular joints in the closed (a, b) and open (c, d) positions. In the closed position; A, the external auditory meatus, B, glenoid fossa, C, articular eminence, D, condyle, E, posterior wall of the articular eminence, F, joint gap. Note that the right and left joint gaps are equidistant (in temporomandibular joint arthrosis, these joint gaps are dissimilar). In the open position (c), the center of the left condyle, line NH, is directly under the center of the eminence, line GL; in (d) the center of the right condyle, line OK, is direct!y under the center of the right eminence, line ]M.
t e m p o r o m a n d i b u l a r joint dysfunction. While the dentist assumes the responsibility for m a n a g i n g the pathologic occlusion of the teeth, the physician must evaluate the psychogenic a n d nutritional status of the patient, and treat him accordingly?' ~' O n c e the diagnosis has been established by the physician, and the patient is referred to a dentist who can deal with this syndrome, d r a m a t i c results ensue. Once p a i n remission has occurred and m a n d i b u l a r m o v e m e n t is restored, the existing pathologic occlusion can be treated, a n d its recurrence prevented?", 11
CASE HISTORY A 38-year-old woman developed a dull, aching pain in the right cheek region. A third molar tooth had been extracted several months earlier. The patient described the pain as beginning gradually, and it was first noticed as a dull sensation which kept increasing in intensity
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:Right TMJ
Left TMJ
(a)
(c)
(b)
40 mrn
(d)
Fi 9. 7 Roentgenograms (oblique-lateral transcranial projection) of abnormal left and right temporomandibular joints in the closed (a, b) and open (c, d) positions. In the closed position (a), note that the left joint gap, F, is wide posteriorly at X, and almost obliterated superiorly at Y, and anteriorly at Z. In (b), the right joint gap, F', is narrow anteriorly at Z', and wider superiorly at Y', and posteriorly at X'. Compare these dissimilar joint gaps with F in Fig. 6, a and b. In the open position (c), the center of the left condyle, line NH, is directly under the center of the eminence, line GL. In (d), the center of the right condyle, line OK, is anterior to the center of the eminence, line ]M. A state of hypermobility exists in (d), because line OK is 10 mm_ anterior to line ]M.
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Fig. 8 Roentgenograms (oblique-lateral transcranial projection) of abnormal left and right temporomandibular joints in the closed (a, b) and open (c, d) positions. At X and F in (a) the joint gap is almost obliterated, and is very wide at Y and Z. In (b) the joint gap at X is obliterated, and is quite wide at Y and Z. This is evidence of condylar displacement in an inferior and posterior position. Note that the line NH does not rest under line GL, and line OK does not rest under ]M, thus indicating a state of hypomobility.
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until t h e temple throbbed. She likened it to a n i n t e r m i t t e n t headache_ T h o u g h slightly less severe at night, f r e q u e n t m e d i c a t i o n was necessary, a n d the h i g h e s t pain intensity was d u r i n g late a f t e r n o o n a n d evening_ O f t e n she was u n a b l e to control the pain, despite medication. S u d d e n w e a t h e r c h a n g e s h a d a n adverse effect on her. T e m p o r a r y relief was sometimes afforded by exerting pressure over t h e cheek bone or by c l e n c h i n g the inside of the m o u t h b e t w e e n the teeth, a n d h o l d i n g it in t h a t position for several m i n u t e s . A s s u m i n g the p a i n to be caused by a sinus difficulty, the p a t i e n t m a n a g e d to control it by daily" use of aspirin, h a v i n g been confirmed in h e r diagnosis by her family physician. However. the pain increased in intensity a n d s u b s e q u e n t m e d i c a t i o n failed to relieve it. A routine dental e x a m i n a t i o n disclosed an u n h e a l e d cleft n e a r the second m o l a r on the u p p e r right side, with a part of the bone a n d tooth root exposed. T h e area was curetted, after w h i c h an e x a m i n a t i o n was m a d e to d e t e r m i n e w h e t h e r or n o t bone f r a g m e n t a t i o n was c a u f i n g a n infection. T h e e x a m i n i n g physician stated that t h o u g h infection m i g h t be the cause, the possibility of sinus i n v o l v e m e n t m u s t be ruled out. Consequently, roentgenograrns of the sinus were m a d e , b u t no a b n o r m a l i t y was found. Nevertheless, the pain persisted. A series of v i t a m i n - B c o m p l e x injections was tried to no avail. T h e possibility of tic d o u l o u r e u x a n d arthritis was eliminated. Cortisone injections failed to relieve the pain, w h i c h was a p p a r e n t l y localized in the second division of t h e trigeminal nerve_ A neurologic e x a m i n a t i o n d,_'sclosed nothing, a n d skull r o e n t g e n o g r a m s as well as n e u r o s u r g e r y a n d psychiatry were suggested. T h e skull r o e n t g e n o g r a m s showed no abnormalities. T h e p a t i e n t was t h e n a d m i t t e d to a hospital for specialized tests, w h e r e she r e m a i n e d for two weeks. D u r i n g this time she s u b m i t t e d to an e l e c t r o e n c e p h a l o g r a m , a l u m b a r p u n c t u r e , blood tests, a n d o t h e r routine tests a n d X-rays. All of the results were negative, except for a blood c o u n t w h i c h revealed severe a n e m i a , but no blood abnormality. D a r v o n a n d aspirin were a d m i n i s t e r e d a p p r o x i m a t e l y every four hours. A l t h o u g h the pain persisted, the i m p r o v e m e n t of h e r blood condition enabled h e r to w i t h s t a n d it better with the help of Empirin, codeine, a n d aspirin. Because of the p a t i e n t ' s tooth c l e n c h i n g a n d grinding, she was given a n i g h t g u a r d as well as a series of m e d i c a t i o n s for nerve conditions. T h e p a i n r e m a i n e d as intense as ever_ T h e p a t i e n t was referred for t e m p o r o m a n d i b u l a r joint examination. T h e p a t i e n t was t h e n e x a m i n e d for t e m p o r o m a n d i b u l a r joint dysfimction, a n d h e r condition diagnosed as such. T h e r o e n t g e n o g r a m s in Fig. 8, a a n d b d e m o n s t r a t e the wide superior joint gaps at Y a n d Y', a n d the almost obliteration of the posterior joint gaps at X a n d X'. Note the proximity of the condyles to A a n d A', the external auditory meati. C o m p a r e Fig. 8, a a n d b to the n o r m a l Fig. 6, a a n d b, a n d note the d i s p l a c e m e n t of the condyles inferiorly. I n the open position of Fig. 8, c a n d d, note t h a t the lines OK a n d NH do not reach the lines GL a n d ]M. T h i s indicates a state of hypomobility. T h e patient received 12 injections of xylocaine into the spastic external pterygoid muscles at 12 weekly intervals. M e p r o b a m a t e (400 rag. twice daily) was prescribed. A Shore M a n d i b u l a r Auto-repositioning A p p l i a n c e ( m a d e by the a u t h o r ) z , J'~ was fabricated to reorient the m a n d i b l e into the correct cycle of occlusion. At the end of six weeks, all p a i n s y m p t o m s h a d disappeared, a n d the occlusion was t h e n equilibrated. Correct i n t e r c u s p a t i o n of the teeth in h a r m o n y with the n e u r o m u s c u l a r closure of the m a n d i b l e was developed. T h e patient was checked at weekly intervals for the next six weeks, after w h i c h she was p u t on a r e g u l a r recall in order to observe h e r progress, a n d to p r e v e n t any recurrence of the condition. T h e p a t i e n t has been free of p a i n for the past five years.
References 1. Wolff, H.: H e a d a c h e a n d O t h e r H e a d Pain, N e w York, 1950, O x f o r d U n i v e r s i t y Press, p. 466. 2. Shore, N_ A.: Occlusal Equilibration a n d T e m p o r o m a n d i b u l a r Joint D y s f u n c t i o n , Philadelphia, 1959, J. B. L i p p i n c o t t C o m p a n y , p. 132. 3. Wolff, H.: H e a d a c h e a n d O t h e r H e a d Pain, N e w York, 1950, O x f o r d U n i v e r s i t y Press, p. 555.
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4. Travell, J_, and Rinzler, S. H'_ Scientific Exhibit: The Myofascial Genesis of Pain, Postgrad. Med_ 11: 425, 1952. 5. Lewis, T.: Pain. New York, 1942, The Macmillan Company, p. 80_ 6. Kellgren, J. H.: O n distribution of pain arising from deep somatic structures with charts of segmental pain areas, Clin. Sc. 4: 35, 1939. 7. Lubosch, W : Anat_ Anz., 1906; Morphol. Jahrb. 35, 1906. 8. Neter, F.: Nervous System, Summit, N. J., 1953, Ciba Pharmaceutical Products, Inc., vol. 1, p. 49. 9. Gozum, E.: The role of trauma in the pathogenesis of temporomandibular joint arthrosis_ Ann. Otol. 69: 348, 1960. 10. Schiresou, S., and Robinson, M.: The nonsurgical temporomandibular joint syndrome. Arch. Otol. 73: 681, 1961. 11_ Costen, J. B.: Syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomandibular joint. Ann. Otol. Rhin. Laryng. 43: 1, 1934. 12. Shore, N. A.: Occlusal Equilibration and Temporomandibular Joint Dysfunction, Philadelphia, 1959, J. B. Lippincott Company, p. 169. 13. Shore, N. A_: Mandibular Auto-Repositioning Appliance, J. A. D. A. In press. 654 MADISON AVE. NEW YORK, N. Y. 10021
Temporomandibular joint dysfunctionmSymptoms and management Nathan Allen Shore, D.D.S. New York, N. Y.
Head pain is one of the most common afflictions of mankind~ yet one that most frequently eludes diagnosis. Although, in common with all pain, it is a signal of "something wrong," it most often can be a biologic reprimand, rather than a threat. As Wolff has pointed out, " . . . with headache it [pain] often means 'wrong direction' or 'wrong pace.' . . . Thus, the vast majority of discomforts and pains of the head stem from readily reversible bodily changes. ''1 The headache specialist sees the patient after he has made the rounds of the medical specialists. Depending upon the area of the head pain, he may have seen an otolaryngologist for symptoms focusing on the ear, the sinuses, or deglutition, or the orthopedist because of a limitation of movement in the temporomandibular joint and the mandible. Perhaps a neurologist was consulted for vague, yet persistent head pain. Finally, in the absence of any special findings, he may have sought psychiatric help. In short, he is quite likely to have seen many specialists before his ailment is diagnosed. It is my opinion that the headache specialist should consider adding to his differential diagnostic procedure a test for dysfunction of temporomandibular joints. Temporomandibular joint dysfunction must be considered in the absence of definitive, pathologic conditions. Indeed, this new concept is being recognized with increasing frequency by physicians, and it is my firm belief that the recognition of temporomandibular joint dysfunction would explain many recurrent head pains. Physicians should be alerted to the prevalence of this condition, and to the need for competent medical-dental management. Temporomandibular joint arthrosis (dysfunction) is a noninfectious, trophic, degenerative affection of the joint tissues initiated by intrinsic trauma, and causing Read before the American Equilibration Society in Chicago, Ill. *Post Graduate Faculty Member, Temple University Dental College, University of Detroit Dental College; Guest Lecturer, University of Louisville Dental College; formerly Chief, Temporomandibular Joint Division, Hospital for Joint Diseases, New York, N. Y. 365
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a b n o r m a l changes in the function of the joint. A p p r o x i m a t e l y 90 p e r cent of the cases are due to a b n o r m a l dental occlusion." DIAGNOSIS T h e p r o b l e m of a differential diagnosis is the f u n d a m e n t a l one confronting physicians. I t is pertinent to emphasize the fact that the result of a pathologic occlusion is not merely i m p a i r m e n t of the functions of the masticatory system_ Dysfunction of the n e u r o m u s c u l a r system occurs, as well as p a i n symptoms in such seemingly unrelated areas as the neck, shoulders, and arms. W h e n careful examination reveals no overt disease state such as the arthritides, head or ear infections, migraine, or eye disorders, t e m p o r o m a n d i b u l a r joint arthrosis should be suspected. These symptoms will always be a p p a r e n t u p o n e x a m i n a t i o n : (1) Pain and tenderness in and around the joint. (2) Clicking and crepitation elicited by stethoscopic examination. (3) Spasm of the external pterygoid muscles. Palpation of the muscle (posterior to the last upper molar) on the affected side produces exquisite pain, which in turn radiates to the ear_ (4) When the mouth is opened, the jaw does not move in a normal, straight vertical line, but veers toward the affected side. (5) Hyper- or hypomobility of the mandible, accompanied by locking of the jaw_ T h e pain m a y encompass a wide range of intensity from a dull to an extreme ache; and it m a y be triggered by eating, yawning, speaking, singing, or shouting. Often there is eye a n d / o r ear pain. As Wolff:' said: " T h e ear is unique in that there is no structure in the body of c o m p a r a b l e size that is supplied by sensory nerves from so m a n y neural segments . . . . Hence, high intensity pain m a y be felt in the vicinity of the ear associated with . . . disorders of the t e m p o r o m a n d i b u l a r joint . . . . " Because of the condition of neuromuscular dysfunction created by a state of pathologic occlusion, a vicious cycle of p a i n - m u s c l e s p a s m - p a i n develops through the m e c h a n i s m of referred pain. A schematic representation of this m a y be seen in Fig. 1, in which the direct neural relationship between pathologic occlusion as the noxious stimulus, and resultant feedback cycles of muscle spasm, trigger areas, and referred p a i n - - a l l distant from the p r i m a r y s t i m u l u s - - m a y be observed. Thus, temp o r o m a n d i b u l a r joint dysfunction can often be held responsible for countless pain areas in the head, which, in turn, m a y radiate into the neck and shoulder regions. W i t h i n the initial area of muscle spasm (i.e., the pterygoid a n d the masseter muscles) lie w h a t T r a v e l P a n d others ~' 6 have called the "trigger" areas. Travell defines trigger areas as points of exquisite tenderness within the muscle in spasm, from which impulses b o m b a r d the central nervous system and give rise to referred pain (cycle 1 of Fig. l ) . T h e initial noxious focus maintains a p e r p e t u a l feedback cycle, a n d the referred p a i n it incited m a y be felt long after the original stimulus from the malocclusion has passed. Those areas of referred pain not associated with muscle spasm are illustrated by Fig. 2. I t will be noted that the trigger a r e a ( X ) is located directly in front of the ear. I t must be emphasized that these symptoms will usually occur on the affected side only, a n d it has been m y experience that a careful and thorough examination can discover 10 to 50 symptoms in a single patient.
Temporomandibular joint dys[unction
Voh,~ ]8 Number 4
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CONVENIENCE RELATIONSHIP OF THE MANDIBLE TRIGGERAREA AREA OF NOXIOUS STIMULU$
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NOXIOUS CYCLE2
Fig. 1
A schematic representatmn of the neural relationship between muscle spasms in the temporomandibular joint region and the resultant feedback cycles of referred pain and secondary muscle spasm, all distant from the primary noxious stimulus. (A) the pathologically enlarged joint gap, (B) the compressed joint gap, (C) the interfering tooth contact, (D,) the point of reference showing eccentric displacement of mandible (toward the left).
An occasional locking of the jaw occur. Although this is at first easily reducible, it eventually becomes less so, and m a y ultimately result in the restriction of the jaw opening. This is then followed by recurrent subluxation of the joint opposite the painful, restricted one. Recognition of the type of pain (dull, paroxysmal, or lancinating) and which specific type of mandibular m o v e m e n t producing it is particularly important. Figs. 3, 4, and 5 clarify what occurs during the cycle of mandibular closure in a normal and in a pathologic case, and illustrate the basic cause of temporom a n d i b u l a r joint dysfunction and its associated symptomatology. Fig. 3 represents a profile view of a normal centric relation and centric occlusion, with the correct
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Fig. 2 A schematic illustration of areas of referred pain and muscle spasm radiating from the temporomandibular joints; a composite of approximately 1500 cases. Note that the area of noxious stimulus, X, is located directly in front of the ear (after Travell).
Fig. 3 A correct intercuspation of the teeth, in harmony with the neuromuscular closure path of the mandible and the temporomandibular joints. The mandible has described the arc of closure, ]K. The center of the condyle, X, is the pivotal point, Note that the joint gap, F., is evenly spaced in the glenoid fossa, B. This even spacing of the joint gap can be verified by comparison with F in the roentgenogram of the normal temporomandibular joint (Fig. 6, b).
intercuspation of the teeth. Normal masticatory function involves the synchronous working together of the temporomandibular joints, the muscles, and the teeth. U n d e r such circumstances, the jaw closes on a hinge whose pivotal point, represented in Fig. 3 by (X), describes an arc (l-K), which, in turn, allows the teeth to mesh correctly. If for any reason (such as loss of teeth) malocclusion exists, the mandible
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F
B
Fig. 4 The first stage of pathologic closure involving an occlusal contact of an upper and a lower tooth. The pathologic interfering occlusal contact at E has prevented the mandible from completing the closure. The mandible has described the arc ]E'; the condyle has rotated on X, so the closure has not reached K.
Fig. 5 Completion of a pathologic closure involving an occlusal contact of an upper and a lower tooth. The pathologic interfering occlusal surface at E has brought about a deflection of the mandible and malpositioning of both condyles. As the mandible described the arc of closure, [E', it struck the interfering contact at E, causing the mandible to shift forward and complete the arc E'H instead of continuing on to K. The center of the condyle, X, has shifted inferiorly and anteriorly from the point of intersection of a, b, c, and d. Note that the joint gap, F, is narrow anteriorly and wider superiorly and posteriorly. Compare with F of Fig. 3. This uneven spacing of the joint gap can be verified by comparison with F in the roentgenogram of the pathologic temporomandibular joint (Fig. 7, a).
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begins to function abnormally. This initial stage of pathologic closure involving an improper occlusal contact is illustrated by Fig. 4. T h e interfering occlusal contact at (E) has prevented the mandible from completing closure on the arc (]E'), while the condyle has rotated on (X). The completed closure of the mandible, with attendant deflection of the condyles is shown in Fig. 5. As the mandible described the arc of closure (/E') it struck an interfering contact (E), which caused it to shift forward and complete the arc (E'H). Thus, the center of condyle (X) has shifted both inferiorly and anteriorly from the intersection point of lines a-c and b-d in Fig. 5. Malposition of the condyles within both temporomandibular joints has occurred, and the equilibrium of the controlling muscles and ligaments is upset, as well as the highly synchronous movement of the two parts of the external pterygoid muscle, and all of the capsular ligaments. Thus, the patient must learn to accommodate himself to a pathologic neuromuscular positioning of the mandible, which in turn creates an incorrect habit pattern, and initiates the muscle-spasm cycle. Seldom do all symptoms occur simultaneously. Many are presented in various combinations, while individual ones may come and go. Hence, when the examining dentist or physician is confronted by any in combination, and has been alerted to the possibility of temporomandibular joint dysfunction, he can confirm his diagnosis by roentgenograms. It is most helpful to compare the patient's roentgenograms with a similar view of a normal joint, as illustrated by Fig. 6. A roentgenogram of an oblique-lateral transcranial projection of normal left and right joints (Fig. 6) when compared to a similar view of an abnormal joint (Fig, 7) clearly indicates a temporomandibular joint arthrosis in the latter. In closed position (a and b) of Fig. 6, it will be noted that the right and left joint gaps at F are equidistant. Compare this to the dissimilar joint gaps at F in Fig. 7 (a and b). In (a) the left joint gap (F) in the closed position is wide posteriorly at (X), and almost obliterated superiorly at (Y) and anteriorly at (Z). In (b), the right joint gap (F') is seen to be narrow anteriorly at (Z') and wider superiorly at (Y') and posteriorly at (X')_ It will be seen that in Fig. 7 [open positions (d)] the condyle center line OK has passed beyond the eminence center line JM, causing a state of hypermobility. (A state of hypomobility exists when the condyle center lines NH and OK do not quite approach GL and JM.) In the normal open position, however [(c,) and (d) of Fig. 6], the condyle centers (NH) and (OK) should appear beneath lines (GL) and (JM), the centers of articular eminences. PSYCHOGENIC FACTOR
The strong psychogenic factor that has been noted in many patients with temporomandibular joint dysfunction cannot be overlooked, and makes it necessary for the physician to determine what proportion of the symptomatology is due to neurotic components. This is often both baffling and challenging. For example, 95 per cent of the patients are short, blond women between the ages of 35 and 45 with a hypertensive disposition. T h e preponderance of women suffering from this condition is partially explained by Lubosch/ who has pointed out that men have a larger articular eminence which tends to restrict the condyle into a normal position. Close medical-dental coordination is essential in the therapeutic approach to
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Fig. 6 Temporomandibular joint roentgenogram (oblique-lateral transcranial projection) of normal right and left temporomandibular joints in the closed (a, b) and open (c, d) positions. In the closed position; A, the external auditory meatus, B, glenoid fossa, C, articular eminence, D, condyle, E, posterior wall of the articular eminence, F, joint gap. Note that the right and left joint gaps are equidistant (in temporomandibular joint arthrosis, these joint gaps are dissimilar). In the open position (c), the center of the left condyle, line NH, is directly under the center of the eminence, line GL; in (d) the center of the right condyle, line OK, is direct!y under the center of the right eminence, line ]M.
t e m p o r o m a n d i b u l a r joint dysfunction. While the dentist assumes the responsibility for m a n a g i n g the pathologic occlusion of the teeth, the physician must evaluate the psychogenic a n d nutritional status of the patient, and treat him accordingly?' ~' O n c e the diagnosis has been established by the physician, and the patient is referred to a dentist who can deal with this syndrome, d r a m a t i c results ensue. Once p a i n remission has occurred and m a n d i b u l a r m o v e m e n t is restored, the existing pathologic occlusion can be treated, a n d its recurrence prevented?", 11
CASE HISTORY A 38-year-old woman developed a dull, aching pain in the right cheek region. A third molar tooth had been extracted several months earlier. The patient described the pain as beginning gradually, and it was first noticed as a dull sensation which kept increasing in intensity
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:Right TMJ
Left TMJ
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(c)
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Fi 9. 7 Roentgenograms (oblique-lateral transcranial projection) of abnormal left and right temporomandibular joints in the closed (a, b) and open (c, d) positions. In the closed position (a), note that the left joint gap, F, is wide posteriorly at X, and almost obliterated superiorly at Y, and anteriorly at Z. In (b), the right joint gap, F', is narrow anteriorly at Z', and wider superiorly at Y', and posteriorly at X'. Compare these dissimilar joint gaps with F in Fig. 6, a and b. In the open position (c), the center of the left condyle, line NH, is directly under the center of the eminence, line GL. In (d), the center of the right condyle, line OK, is anterior to the center of the eminence, line ]M. A state of hypermobility exists in (d), because line OK is 10 mm_ anterior to line ]M.
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Fig. 8 Roentgenograms (oblique-lateral transcranial projection) of abnormal left and right temporomandibular joints in the closed (a, b) and open (c, d) positions. At X and F in (a) the joint gap is almost obliterated, and is very wide at Y and Z. In (b) the joint gap at X is obliterated, and is quite wide at Y and Z. This is evidence of condylar displacement in an inferior and posterior position. Note that the line NH does not rest under line GL, and line OK does not rest under ]M, thus indicating a state of hypomobility.
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until t h e temple throbbed. She likened it to a n i n t e r m i t t e n t headache_ T h o u g h slightly less severe at night, f r e q u e n t m e d i c a t i o n was necessary, a n d the h i g h e s t pain intensity was d u r i n g late a f t e r n o o n a n d evening_ O f t e n she was u n a b l e to control the pain, despite medication. S u d d e n w e a t h e r c h a n g e s h a d a n adverse effect on her. T e m p o r a r y relief was sometimes afforded by exerting pressure over t h e cheek bone or by c l e n c h i n g the inside of the m o u t h b e t w e e n the teeth, a n d h o l d i n g it in t h a t position for several m i n u t e s . A s s u m i n g the p a i n to be caused by a sinus difficulty, the p a t i e n t m a n a g e d to control it by daily" use of aspirin, h a v i n g been confirmed in h e r diagnosis by her family physician. However. the pain increased in intensity a n d s u b s e q u e n t m e d i c a t i o n failed to relieve it. A routine dental e x a m i n a t i o n disclosed an u n h e a l e d cleft n e a r the second m o l a r on the u p p e r right side, with a part of the bone a n d tooth root exposed. T h e area was curetted, after w h i c h an e x a m i n a t i o n was m a d e to d e t e r m i n e w h e t h e r or n o t bone f r a g m e n t a t i o n was c a u f i n g a n infection. T h e e x a m i n i n g physician stated that t h o u g h infection m i g h t be the cause, the possibility of sinus i n v o l v e m e n t m u s t be ruled out. Consequently, roentgenograrns of the sinus were m a d e , b u t no a b n o r m a l i t y was found. Nevertheless, the pain persisted. A series of v i t a m i n - B c o m p l e x injections was tried to no avail. T h e possibility of tic d o u l o u r e u x a n d arthritis was eliminated. Cortisone injections failed to relieve the pain, w h i c h was a p p a r e n t l y localized in the second division of t h e trigeminal nerve_ A neurologic e x a m i n a t i o n d,_'sclosed nothing, a n d skull r o e n t g e n o g r a m s as well as n e u r o s u r g e r y a n d psychiatry were suggested. T h e skull r o e n t g e n o g r a m s showed no abnormalities. T h e p a t i e n t was t h e n a d m i t t e d to a hospital for specialized tests, w h e r e she r e m a i n e d for two weeks. D u r i n g this time she s u b m i t t e d to an e l e c t r o e n c e p h a l o g r a m , a l u m b a r p u n c t u r e , blood tests, a n d o t h e r routine tests a n d X-rays. All of the results were negative, except for a blood c o u n t w h i c h revealed severe a n e m i a , but no blood abnormality. D a r v o n a n d aspirin were a d m i n i s t e r e d a p p r o x i m a t e l y every four hours. A l t h o u g h the pain persisted, the i m p r o v e m e n t of h e r blood condition enabled h e r to w i t h s t a n d it better with the help of Empirin, codeine, a n d aspirin. Because of the p a t i e n t ' s tooth c l e n c h i n g a n d grinding, she was given a n i g h t g u a r d as well as a series of m e d i c a t i o n s for nerve conditions. T h e p a i n r e m a i n e d as intense as ever_ T h e p a t i e n t was referred for t e m p o r o m a n d i b u l a r joint examination. T h e p a t i e n t was t h e n e x a m i n e d for t e m p o r o m a n d i b u l a r joint dysfimction, a n d h e r condition diagnosed as such. T h e r o e n t g e n o g r a m s in Fig. 8, a a n d b d e m o n s t r a t e the wide superior joint gaps at Y a n d Y', a n d the almost obliteration of the posterior joint gaps at X a n d X'. Note the proximity of the condyles to A a n d A', the external auditory meati. C o m p a r e Fig. 8, a a n d b to the n o r m a l Fig. 6, a a n d b, a n d note the d i s p l a c e m e n t of the condyles inferiorly. I n the open position of Fig. 8, c a n d d, note t h a t the lines OK a n d NH do not reach the lines GL a n d ]M. T h i s indicates a state of hypomobility. T h e patient received 12 injections of xylocaine into the spastic external pterygoid muscles at 12 weekly intervals. M e p r o b a m a t e (400 rag. twice daily) was prescribed. A Shore M a n d i b u l a r Auto-repositioning A p p l i a n c e ( m a d e by the a u t h o r ) z , J'~ was fabricated to reorient the m a n d i b l e into the correct cycle of occlusion. At the end of six weeks, all p a i n s y m p t o m s h a d disappeared, a n d the occlusion was t h e n equilibrated. Correct i n t e r c u s p a t i o n of the teeth in h a r m o n y with the n e u r o m u s c u l a r closure of the m a n d i b l e was developed. T h e patient was checked at weekly intervals for the next six weeks, after w h i c h she was p u t on a r e g u l a r recall in order to observe h e r progress, a n d to p r e v e n t any recurrence of the condition. T h e p a t i e n t has been free of p a i n for the past five years.
References 1. Wolff, H.: H e a d a c h e a n d O t h e r H e a d Pain, N e w York, 1950, O x f o r d U n i v e r s i t y Press, p. 466. 2. Shore, N_ A.: Occlusal Equilibration a n d T e m p o r o m a n d i b u l a r Joint D y s f u n c t i o n , Philadelphia, 1959, J. B. L i p p i n c o t t C o m p a n y , p. 132. 3. Wolff, H.: H e a d a c h e a n d O t h e r H e a d Pain, N e w York, 1950, O x f o r d U n i v e r s i t y Press, p. 555.
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4. Travell, J_, and Rinzler, S. H'_ Scientific Exhibit: The Myofascial Genesis of Pain, Postgrad. Med_ 11: 425, 1952. 5. Lewis, T.: Pain. New York, 1942, The Macmillan Company, p. 80_ 6. Kellgren, J. H.: O n distribution of pain arising from deep somatic structures with charts of segmental pain areas, Clin. Sc. 4: 35, 1939. 7. Lubosch, W : Anat_ Anz., 1906; Morphol. Jahrb. 35, 1906. 8. Neter, F.: Nervous System, Summit, N. J., 1953, Ciba Pharmaceutical Products, Inc., vol. 1, p. 49. 9. Gozum, E.: The role of trauma in the pathogenesis of temporomandibular joint arthrosis_ Ann. Otol. 69: 348, 1960. 10. Schiresou, S., and Robinson, M.: The nonsurgical temporomandibular joint syndrome. Arch. Otol. 73: 681, 1961. 11_ Costen, J. B.: Syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomandibular joint. Ann. Otol. Rhin. Laryng. 43: 1, 1934. 12. Shore, N. A.: Occlusal Equilibration and Temporomandibular Joint Dysfunction, Philadelphia, 1959, J. B. Lippincott Company, p. 169. 13. Shore, N. A_: Mandibular Auto-Repositioning Appliance, J. A. D. A. In press. 654 MADISON AVE. NEW YORK, N. Y. 10021