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Etiology of the pain-dysfunction syndrome
Etiology of the pain-dysfunction syndrom e
Daniel M. Laskin,
DDS, MS, Chicago
According to the psychophysiologic theory, masti catory muscle spasm is the primary factor responsi ble for the symptoms of the pain-dysfunction syn drome. The most common cause is thought to be muscle fatigue produced by chronic oral habits thatare often an involuntary tension-relieving mech anism. Organic changes such as occlusal dishar monies, degenerative arthritis, and contracture, which may result, tend to make the condition selfperpetuating. Five types of experimental evidence are given in support of this theory.
There are two aspects to the successful manage ment of any disease process: one is the establish ment of an accurate diagnosis; the other is an un derstanding of its etiology so that a rational treat ment plan can be formulated. Unfortunately, in the management of many problems involving the temporomandibular joint, we have not been high ly successful in either of these areas. Much of the difficulty began in the 1930’s when Costen1 took a conglomeration of symptoms— some unrelated clinically, some unrelated anatom ically— and developed what was to become known as Costen’s syndrome. It took a period of almost 20 years until the many inaccuracies of this theory finally were clarified.2-5 However, just as the corpse of Costen’s syndrome was being laid to rest, the spirit of the “TMJ syndrome” arose. Al though this description of the problem was some what more accurate, since it eliminated such unre lated symptoms as impaired hearing, tinnitus, diz ziness, and burning seasations in the throat and tongue, it still meant that almost all patients with pain of undetermined origin related to the preauricular region, the side of the face, or the tem poral area were thrown into the same diagnostic wastebasket. The undesirable thing about such situations is that they lead to a one disease-one treatment philosophy in conditions of diverse etiology, merely because the symptoms happen to be quite similar.6 It is this lack of diagnostic dis crimination that probably accounts for many of the failures in the management of patients with TMJ disorders. 147
In 1955 Schwartz7 reported that he was able to delineate from the mass of patients with supposed “TMJ syndrome” a more definitive group of indi viduals whose problem was characterized by pain ful, limited mandibular movement due, in his opinion, to spasm in the masticatory musculature. He applied the term “temporomandibular joint pain-dysfunction syndrome” to this condition. The studies of Schwartz had a profound influence on the thinking of many individuals interested in TMJ problems and produced the first major shift away from the narrow mechanical concept of an occlusal etiology to the broader implication of the entire masticatory apparatus, as well as to the psychological characteristics of the patient.8 It is the purpose of this paper to discuss current theories of the etiology of the pain-dysfunction syn drome. The viewpoint to be presented was de veloped as a result of experimental studies and clinical observations on the patient population seen at the Temporomandibular Joint Research Center of the University of Illinois over the past six years. While differing to some degree from that of Schwartz and his coworkers,8 the two hypoth eses are far from being mutually exclusive.
Diagnosis of the pain-dysfunction syndrome Because there is still some variation of opinion about what constitutes the pain-dysfunction syn drome, it is necessary to begin this discussion with a brief consideration of what we consider the es sential signs and symptoms that place a patient in this category. The most common finding is pain of unilateral origin.6 This pain usually is described by the patient as a dull ache felt in the ear or preauricular area, that may radiate to the angle of the mandible, the temporal area, or the lateral cervical region. The pain can be relatively con stant, but more often is reported as worse on aris ing in the morning, or else as relatively mild in the morning but gradually worsening as the day progresses. It frequently also is exacerbated at mealtime. The next most common finding is muscle ten derness.6 Although not usually reported by the patient, this symptom can be determined easily by the examiner. The most frequent areas of ten derness are over the neck of the mandible and in the region distal and superior to the maxillary tuberosity. The mandibular angle and the tem 148 ■ JADA, Vol. 79, July 1969
poral crest are other common sites. These sites of tenderness are presumed to represent areas of spasm in the masticatory muscles. The third most common symptom is a clicking or popping noise in the TMJ. Patients having this symptom alone, however, are not included in the category of the pain-dysfunction syndrome. They also must have accompanying symptoms such as pain or tenderness or both. Limitation of jaw function is the fourth cardinal symptom of the pain-dysfunction syndrome. It may be characterized either by inability to open as wide as usual, or by deviation of the mandible on opening. Patients with limitation of opening will rarely have clicking, although their past history frequently will reveal that this had been present sometime in the course of their condition.6 Besides having one or more of the four cardinal symptoms, of pain, tenderness, clicking, and limi tation, the patient considered to have the paindysfunction syndrome must also have these nega tive characteristics: ■ Absence of clinical, radiographic, or bio chemical evidence of organic changes in the TMJ. ■ Lack of tenderness in the TMJ when this area is palpated via the external auditory meatus. The significance of these negative character istics in establishing the final diagnosis lies in their indication that the primary site of the problem is in the masticatory musculature rather than in the structures of the joint. This distinction forms the essential basis for understanding the etiology of the pain-dysfunction syndrome. Although it is our belief that this syndrome gen erally begins as a functional problem, ultimately, as we will see, it can lead to organic changes so that these negative diagnostic criteria may no long er be applicable. In the latter stage there occasion ally is difficulty in determining clinically whether the patient actually belongs in the category of the pain-dysfunction syndrome or if the pathologic con dition is primary. The past history may be helpful in making this distinction.
Previous theories of etiology Discrepancies in occlusion, or maxillo-mandibular relationships, or both, formed the basis for most of the early theories of the etiology of the “TMJ syndrome.” While originally it was suggested that mandibular overclosure was the prime initiating factor,1>9>10 more refined theories related to occlu-
sal disharmony were subsequently developed.11-13 Such “tooth theories” essentially proposed that when the teeth are brought together during chew ing or swallowing the discrepancies in occlusion produce a displacement of the mandible, usually in a posterior direction, with resultant compression of the highly vascular, densely innervated, loose retrocondylar connective tissue. It was reasoned that continued compression of this tissue would then cause not only pain but impairment of the blood supply to the joint structures, thus leading to degenerative changes. The difficulties with this explanation for the etiology of the pain-dysfunction syndrome were multiple. First and foremost it failed to explain satisfactorily how occlusal interferences could de velop in a functioning dentition unless they were iatrogenically induced. Second, it did not explain why most of the symptoms, particularly in the early phases of the condition, were related mainly to the masticatory musculature rather than to the joint itself. Third, the peculiar age, sex, racial, and social distribution of the patients suffering from this condition was not explained8-14 nor was the ability of other factors, such as clenching or grind ing, to act as etiologic agents. Finally, it did not account for the high degree of clinical success claimed in the treatment of such patients by what often appeared to be diametrically opposed forms of therapy.8-15-18 The inadequate explanation provided by the “tooth theories” apparently disturbed many in vestigators and ultimately led to what might be called the “tooth-muscle theories.”19-20 These theories, while somewhat less mechanical in prin ciple, still had as their etiologic basis a discrepancy in occlusion. However, rather than proposing that the altered occlusion directly produced mandibu lar displacement, they hypothesized that the occlu sal interferences caused an altered proprioceptive feedback, leading to incoordination and spasm of some of the muscles of mastication. Although these theories were superior to the “tooth theories” in that they did implicate the neuromusculature and helped to explain more of the symptoms, they still failed to answer the other criticisms that had been leveled against the earlier theories. It was not until the studies of Schwartz and his co-workers in the late 1950’s8 that there began to be a gradual shift in emphasis from consideration of the influence of occlusion to the recognition that functional disturbances in the masticatory mus culature could play a primary role in the etiology of “TMJ” dysfunction. While the hypothesis we
have developed at the Temporomandibular Joint Research Center tends to support Schwartz’s view point concerning the role of stress and its influence on muscle tension,8 it differs considerably in its interpretation of the contribution of occlusal ab normalities.
The psychophysiologic theory— A new concept of etiology It is our belief that masticatory muscle spasm is the primary factor responsible for the signs and symptoms of the pain-dysfunction syndrome (illus tration). Since pathologic involvement of the joint structures occurs only in the late stages, if at all, the terms “myofascial pain-dysfunction (MPD) syndrome” or “masticatory myalgesia syndrome” are actually more descriptive of the condition than the name temporomandibular joint pain-dysfunc tion syndrome originally proposed by Schwartz.7 Spasm can be initiated in one of three ways: muscular overextension, muscular overcontraction or muscle fatigue. Such acute incidents as external trauma or excessively wide opening, while also capable of initiating muscle spasm, are usually self-limiting episodes of short duration and need not be considered in this discussion. Examples of some of the factors that can produce overexten sion of the various masticatory muscles are dental restorations or fixed and removable prostheses that
TENSION
»
ORAL HABIT
------ "D ental I r r ita tio n "
MUSCULAR FATIGUE
M u sc u la r --------^ I MYOSPASM 1-^--------- M u sc u la r O v e rc o n tra c tio n O v e re x ten sio n | M i u s r a a ----
1
Etiology of the myofascial pain-dysfunction syndrome. A l though there are three means of entry into the syndrome, the darker arrows indicate the m ost com m on pathway. Th e explanation of this m echanism is termed the Psychophysi ologic Theory.
Laskin: ETIOLOGY OF PAIN-DYSFUNCTION SYNDROME ■ 149
encroach on the intermaxillary space. Overcon traction, on the other hand, can be caused by over closure resulting from such things as bilateral loss of posterior teeth or by the “settling” of partial dentures replacing them. Similarly, it can occur in patients wearing complete dentures after ex cessive alveolar resorption. Although adverse mechanical factors leading either to muscle overextension or overcontraction may cause some instances of MPD syndrome, we believe the most common cause to be muscle fa tigue produced by chronic oral habits such as clenching or grinding of the teeth (illustration). These habits can be initiated by an annoying “den tal irritation” like an improperly occluding resto ration or an overhanging margin. Generally, how ever, we believe that they are an involuntary ten sion-relieving mechanism. Since this explanation for most cases of MPD syndrome implicates emo tional rather than mechanical factors as prime eti ologic agents, it has been termed the “psychophysiologic theory.” The development of spasm in one or more of the masticatory muscles, regardless of whether it is caused by fatigue, overcontraction, or overex tension, not only leads to pain and limitation, but also may produce a slight change in jaw position so that the teeth do not occlude properly, if this abnormal jaw relationship persists for several days or longer, the teeth then may gradually shift to accommodate to the new position. This is one of the reasons why some patients suddenly exhibit occlusal disharmonies when the spasm is relieved and the rebalanced musculature returns the jaws to their original relationship. In addition to producing possible alterations in occlusion, persistent myospasm also can cause two other organic changes, namely: degenerative ar thritis and contracture (illustration). Degenerative changes in the TMJ can arise from continued jaw function with the condyle in an abnormal position. Contracture is a degenerative change in muscle that accompanies long-term spasm. Thus, the MPD syndrome, although originating as a func tional problem in most instances, ultimately can lead to organic disease. The condition then be comes self-perpetuating because all of these or ganic changes result in an altered chewing pattern with attendant reinforcement of the original spasm and pain. This proposed scheme for explaining the patho genesis of the MPD syndrome (illustration) has a number of advantages over the previous “tooth” and “tooth-muscle” theories. Not only does it 150 ■ JADA, Vol. 79, July 1969
adequately explain the origin of the various signs and symptoms, but it also shows how occlusal dis harmonies can arise in a functioning dentition as a result rather than as a cause of the problem. This is a concept diametrically opposed to that sug gested by previous investigators. Furthermore, since there are three paths of entry into the syn drome (illustration), the suggested scheme also ex plains how diverse etiologic factors can produce like symptoms. On a similar basis it offers a logi cal explanation of how different forms of therapy may be successful in what symptomatically ap pears to be the same condition. Although this scheme offers a more inclusive explanation of the pathogenesis of the MPD syn drome than any of those previously suggested, such presumptive evidence alone does not make it correct. The psychophysiologic theory has there fore served as the basis for direct experimental test ing at the Temporomandibular Joint Research Center during the past six years. Although the pub lished findings of others also could be used to sup port the theory, this discussion will be limited to those studies performed at the Center, since most of these have not been published yet in extensive form.
Experimental evidence for the psychophysiologic theory The experimental evidence for the psychophysi ologic theory can be divided into five main cate gories: epidemiologic, radiologic, psychologic, biochemical, and physiologic. ■ Epidemiologic studies: Analysis of the exam ination data on a series of 277 consecutive patients treated at the Temporomandibular Joint Research Center revealed that over 80% had tenderness in one or more of the masticatory muscles.6 This analysis not only supports the theory of muscle spasm as a key factor, but also indicates that pa tients with MPD syndrome comprise the greatest percentage of those having “TMJ” problems. The history data on another series of patients showed that about 80% presently have or previous ly had other psychophysiologic diseases such as ulcer, migraine headache, or dermatitis.21 Seventyseven percent also reported having chronic oral habits such as clenching or grinding of the teeth, gum chewing, or biting on hard objects.
■ Radiologic studies: Many of the earlier theo ries proposed in connection with TMJ disorders depended heavily on radiographic evidence for substantiation. A high incidence of pathologic change or alteration in the spacial relations of the joint components has been reported by numer ous investigators,11'22-25 and entire philosophies of treatment, not the least of which is surgical, have been predicated on these alleged findings. At our Center, however, less than 5 % of all patients have shown radiographic evidence of pathologic change in the structures of the TMJ. This differ ence seems to be related to the use of the more accurate procedure of corrected laminagraphy,26 in which reproducible, true lateral profiles of the condyles are obtained. On the other hand, routine radiographs of the TMJs, cephalometric headplates,27 and even standard laminagraphic tech nics induce artifacts which can easily be misin terpreted as evidence of pathology. Moreover, many clinicians fail to take into consideration the normal variations in condylar morphology that have been clearly documented by Yale and others.28 The lack of significant radiographic evi dence of pathologic condition in patients with MPD syndrome supports the contention that the joint itself is not actually the primary site of in volvement in this disorder. ■ Psychologic studies: Since the psychophysio logic theory is based on the premise that persistent tension-relieving oral habits are the primary cause of most cases of MPD syndrome, the uniformity in the psychological makeup of such patients is important evidence in support of this theory. Lupton21 has shown that about 75% of an unselect ed sample of women patients from the Temporo mandibular Joint Research Center whom he sub jected to psychological testing fell within two “dominant” personality categories. They were characterized best as “hypernormal” individuals who tended to describe themselves, or were seen by others, as responsible, generous, and mana gerial. They differed significantly from other den tal patients, medical patients afflicted with rheu matoid arthritis, a control group of normal indi viduals, and a group of psychotic and neurotic patients. Lupton has suggested that the attempt of these patients to maintain the facade of hyper normality leads to generalized somatic tension; this tension accounts for their frequent addiction to tension-relieving oral habits and past histories of psychosomatic illnesses. Another study which tends to emphasize the
etiologic role of psychologic factors is one which showed that a program of dental therapy plus concomitant psychological counseling or educa tional instruction provided better therapeutic re sults than dental therapy alone.29 Moreover, Lup ton also has demonstrated in a preliminary series of 35 patients that only psychological counseling can be equally as effective as dental treatment in alleviating symptoms.30 These findings, as well as those which have indicated a relatively significant response of patients to both placebo splints31 and placebo drugs,32 not only strongly support the psy chophysiologic theory but also tend to negate the role of noniatrogenic occlusal disharmonies as a primary etiologic factor in the MPD syndrome. ■ Biochemical studies: There is biochemical as well as psychological evidence to indicate that persons with the MPD syndrome are under great er than normal stress. Since increased levels of urinary 17-OH steroids and catecholamines have been linked to the stress phenomenon, the con centration of these substances was compared in normal individuals and a group of patients with the MPD syndrome. An overnight urine sample was analyzed since ordinarily this should be a period of minimal physical and emotional activ ity. Results of the experiment showed both the average steroid and catecholamine levels to be significantly higher in the patients than in the con trol group.33 ■ Physiologic studies: Since the psychophysio logic theory is based on muscle fatigue as an im portant factor in the production of myospasm, it raises the question of whether the masticatory muscles of patients with MPD syndrome can be come fatigued more readily than those of normal individuals. This possibility was examined by a muscle endurance test that measured the length of time one could bite with maximum force on a strain gauge from which a 500 gm weight was sus pended.34 It was found that while the mean hold ing time for the patient and control groups did not vary significantly, the normal individuals general ly exhibited greater biting force during the test period. Thus, when the force-time factor was con sidered as an indicator of fatigability, the masti catory muscles of patients with MPD syndrome proved to be more susceptible. Of equal interest, however, was the finding of pain and limitation in both the patients and the controls in the posttest period. In the patients, al though they may have been asymptomatic before Laskin: ETIOLOGY OF PAIN-DYSFUNCTION SYNDROME ■ 151
the test, the recrudescence of symptoms often last ed for several days. The pain was described as being in the preauricular area, at the angle of the mandible, or occasionally in the temporal or frontal regions— the same sites ordinarily involved in the syndrome. Such symptoms might be expected in the patients, but it was significant that they also developed in the control group, although they did not last as long. Here, in essence, the MPD syn drome was being produced in normal individuals, not by affecting occlusal relationships but rather by fatiguing the masticatory musculature. Another experiment which supports the concept that chronic muscle fatigue can lead to masticatory myospasm involves the production of bruxism in adult monkeys.35 With use of an electric stimulator which permitted controlled, periodic unilateral depolarization of the masseter, medial pterygoid, and temporal muscles, clenching and grinding of the teeth was induced for 20 minutes/hour, day and night, for six weeks. Electromyographic re cordings at the termination of the experimental period invariably showed an increase in both the frequency and amplitude of spike potentials, a situation indicative of muscle spasm. Here again, muscle fatigue rather than occlusal disharmony was responsible for producing a situation akin to the MPD syndrome.
Implications of the psychophysiologic theory Although there are still some gaps in our total un derstanding of the etiology of the MPD syndrome, when the findings from the various epidemiologic, radiologic, psychologic, biochemical, and physio logic studies done at the Temporomandibular Joint Research Center are integrated, they form a solid basis for the validity of the psychophysiologic theory. This position is strengthened further when one includes many of the related studies in these fields done by other investigators. To complete the picture, however, it is now necessary to extend our understanding of this theory into the areas of diagnosis and treatment. Although it is not the purpose of this paper to discuss the specific treatment of the MPD syn drome, there are certain general conclusions re garding therapy which can be deduced from the psychophysiologic theory. First, because the initi ating factors for the syndrome are generally emo tional rather than physical, treatment must be 152 ■ JADA, Vol. 79, July 1969
directed toward this aspect of the problem as well as toward the management of the physical symp toms and the organic sequelae. Disregard for this principle probably is responsible for most of the failures encountered. Second, in the functional stage of the syndrome, when primarily the masti catory muscles are involved, there are obviously no indications for such drastic forms of therapy as joint surgery, intra-articular drug injections, or extensive forms of occlusal equilibration or re construction. It is even questionable whether these procedures generally are indicated in the later stages because the muscles of mastication are still the major site of involvement. Third, it must be realized that correction of the underlying conflicts leading to the production of tension-relieving oral habits may not always be possible, even when the patient receives psychotherapy. It is not mere ra tionalization, therefore, to assume that a small number of patients will never be completely cured. However, one should not use this as a license to relegate any difficult case into the incurable cate gory before all logical forms of treatment have been tried. On the other hand, excessively radical thera peutic measures should not be attempted in des peration, because these may only induce iatrogenic problems that will further complicate the situation. Finally, it is clear that the MPD syndrome, along with the many conditions that directly in volve the TMJ, form a complex group of problems of diverse etiology and pathology frequently re quiring diagnostic and therapeutic skills beyond the capabilities of any single individual. Not only as a matter of expediency, but also to provide the most effective patient care, there is an obvious need for a team approach to the management of these conditions.
These investigations were supported by USPHS Research Grant DE-01849 from the N ational In s titu te of Dental Re search, National In s titu te s of Health, Bethesda, Md. Doctor Laskin is professor and associate head o f the de p artm ent of oral and m axillofacial surgery and d ire cto r of the Tem porom andibular Jo in t Research Center, U niversity of I llin o is at the M edical Center, Chicago, 60612. S ta ff mem bers of th e research team include Doctors Seym our Yale, Charles Greene, M artin Lerman, Daniel Lupton, and Howard Sutcher.
1. Costen, J.B. Syndrome of ear and sinus sym ptom s de pendent upon disturbed fu n ctio n of tem porom andibular jo in t. Ann Otol Rhin & Laryngol 43:1 March 1934. 2. Schier, M.B.A. Facts and fa lla cie s on tem porom andib-
ular a rtic u la tio n and jaw relationships as pertains to deaf ness. Dental Items 62:507 June 1940. 3. Shapiro, H.H., and Truex, R.C. Tem porom andibular jo in t and th e auditory fu n ctio n . JADA 30:1147 Aug 1943. 4. Sicher, H. Tem porom andibular a rtic u la tio n in man d ib u la r overclosure. JADA 36:131 Feb 1948. 5. Zim m erm an, A.A. An evaluation o f Costen's syndrome from an anatom ic p o in t of view. In Sarnat, B.G. (ed.) The tem porom andibular jo in t. S p ringfield, III, Charles C Thomas, 1951, p 82-110. 6. Greene, C.S., and others. The TMJ pain-dysfunction syndrome: heterogeneity of the p a tie nt population. JADA (in press). 7. Schwartz, L. Pain associated w ith th e tem porom andib ular jo in t. JADA 51:394 Oct 1955. 8. Schwartz, L. Disorders o f the tem porom andibular jo in t. Philadelphia, W. B. Saunders Co., 1959. 9. G oodfriend, D.J. Sym ptom atology and trea tm e nt of ab n orm alities of the m andibular a rtic u la tio n . Dent Cosmos 75:844 1933. 10. H arris, H.L. E ffe ct o f loss o f v e rtic a l dim ension on anatom ic structu re s of the head and neck. JADA 25:175 Feb 1938. 11. Thompson, J.R. Tem porom andibular disorders: diag nosis and dental treatm ent. In Sarnat, B.G. (ed.) The te m porom andibular jo in t. S prin g fie ld , III, C harles C Thomas, 1951, p 122-144. 12. Hankey, G.T. Tem porom andibular arthrosis. Analysis of 150 cases. B rit Dent J 97:249 Nov 1954. 13. Granger, E.R. Occlusion in tem porom andibular jo in t pain. JADA 56:659 May 1958. 14. Franks, A.S.T. Social character of tem porom andibular jo in t dysfunction. Dent Pract (B ristol) 15:94 Nov 1964. 15. Sears, V.H. Occlusal pivots. J Prosth Dent 6:332 May 1956. 16. Jankelson, B. Technique fo r o b ta in in g optim um fu n c tional relatio n sh ip fo r the natural d e n titio n . D ent Clin N Am er March 1960 p 131-141. 17. Mann, A.W., and Pankey, L.D. Concepts o f occlu sion: the P.M. philosophy of occlusal re h a b ilita tio n . Dent C lin N Am er Nov 1963 p 621-636. 18. Boman, K. Tem porom andibular jo in t arthrosis and its trea tm e nt by e xtirp a tio n o f disk; c lin ic a l study. Acta C hirS cand (suppl 118) 95:1 1947. 19. Sicher, H. S tru ctu ra l and fu n c tio n a l basis fo r dis
orders of the tem porom andibular a rticu la tio n . J Oral Surg 13:275 Oct 1955. 20. Ram fjord, S., and Ash, M., Jr. O cclusion. Philadel phia, W. B. Saunders Co., 1966. 21. Lupton, D.E. A pre lim in a ry investigation of the per so nality of fem ale tem porom andibular jo in t dysfunction patients. Psychother Psychosom 14:199 1966. 22. Lindblom , G. Disorders of th e tem porom andibular jo in t. Acta O dont Scand 11:61 July 1953. 23. R icketts, R.M. Roentgenography of the tem porom an d ib u la r jo in t. In Sarnat, B.G. (ed.) The tem porom andibular jo in t, 2nd ed. S pringfield, III, Charles C Thomas, 1964 p 102-132. 24. Bell, W.E. Oral and facial pain and the tem porom an d ib u la r jo in t; synopsis. Dallas, Weldon E. Bell, 1967. 25. Henny, F.A., and M e rrill, R.G. Roentgenographic changes in 39 patients subjected to m a n d ib u la rco n d ylo to m y. IADR Abstracts, 360, 1966. 26. Rosenberg, H.M. Laminagraphy: m ethods and ap p lica tio n in oral diagnosis. JADA 74:88 Jan 1967. 27. Sutcher, H.D. E ffe ct o f the intra-m eatal cephalom etric headholder on occlusion. IADR Abstracts, 5, 1967. 28. Vale, S.H.; A llison, B.D.; and Hauptfuehrer, J.D. An epidem iological assessment of m an d ib u la r condyle m orphology. Oral Surg 21:169 Feb 1966. 29. Lupton, D.E. A com parative analysis of th e e ffe ctive ness o f counseling, in stru ctio n and dental treatm ent. PhD D issertation, U niversity of Chicago, 1967. 30. Lupton, D.E. Psychological aspects of tem porom an d ib u la r jo in t dysfunction. JADA th is issue p 131. 31. Sutcher, H., and others. Comparison o f responses to pharm acological and physical placebo therapy in TMJ dys fu n c tio n patients. IADR Abstracts, 243, 1969. 32. Greene, C.S., and Laskin, D.M. Evaluation of mepro bamate therapy in TMJ d ysfunction patients. IADR Ab stracts, 242, 1969. 33. Evaskus, D.S., and Laskin, D.M. A biom echem ical measure of stress in patients w ith m yofascial pain-dysfunctio n syndrome. IADR Abstracts, 610, 1968. 34. D irenfeld, V.N. Muscle endurance in pa tie nts w ith tem porom andibular jo in t d ysfunction. MS Thesis, Univer sity o f Illin o is a t Medical Center, 1967. 35. Banasik, P.M., and Laskin, D.M. Experim ental in d u c tio n o f bruxism by e le ctrica l stim u la tio n o f m ajor muscles of m astication. IADR Abstracts, 409, 1969.
Laskin: ETIOLOGY OF PAIN-DYSFUNCTION SYNDROME ■ 153
Daniel M. Laskin,
DDS, MS, Chicago
According to the psychophysiologic theory, masti catory muscle spasm is the primary factor responsi ble for the symptoms of the pain-dysfunction syn drome. The most common cause is thought to be muscle fatigue produced by chronic oral habits thatare often an involuntary tension-relieving mech anism. Organic changes such as occlusal dishar monies, degenerative arthritis, and contracture, which may result, tend to make the condition selfperpetuating. Five types of experimental evidence are given in support of this theory.
There are two aspects to the successful manage ment of any disease process: one is the establish ment of an accurate diagnosis; the other is an un derstanding of its etiology so that a rational treat ment plan can be formulated. Unfortunately, in the management of many problems involving the temporomandibular joint, we have not been high ly successful in either of these areas. Much of the difficulty began in the 1930’s when Costen1 took a conglomeration of symptoms— some unrelated clinically, some unrelated anatom ically— and developed what was to become known as Costen’s syndrome. It took a period of almost 20 years until the many inaccuracies of this theory finally were clarified.2-5 However, just as the corpse of Costen’s syndrome was being laid to rest, the spirit of the “TMJ syndrome” arose. Al though this description of the problem was some what more accurate, since it eliminated such unre lated symptoms as impaired hearing, tinnitus, diz ziness, and burning seasations in the throat and tongue, it still meant that almost all patients with pain of undetermined origin related to the preauricular region, the side of the face, or the tem poral area were thrown into the same diagnostic wastebasket. The undesirable thing about such situations is that they lead to a one disease-one treatment philosophy in conditions of diverse etiology, merely because the symptoms happen to be quite similar.6 It is this lack of diagnostic dis crimination that probably accounts for many of the failures in the management of patients with TMJ disorders. 147
In 1955 Schwartz7 reported that he was able to delineate from the mass of patients with supposed “TMJ syndrome” a more definitive group of indi viduals whose problem was characterized by pain ful, limited mandibular movement due, in his opinion, to spasm in the masticatory musculature. He applied the term “temporomandibular joint pain-dysfunction syndrome” to this condition. The studies of Schwartz had a profound influence on the thinking of many individuals interested in TMJ problems and produced the first major shift away from the narrow mechanical concept of an occlusal etiology to the broader implication of the entire masticatory apparatus, as well as to the psychological characteristics of the patient.8 It is the purpose of this paper to discuss current theories of the etiology of the pain-dysfunction syn drome. The viewpoint to be presented was de veloped as a result of experimental studies and clinical observations on the patient population seen at the Temporomandibular Joint Research Center of the University of Illinois over the past six years. While differing to some degree from that of Schwartz and his coworkers,8 the two hypoth eses are far from being mutually exclusive.
Diagnosis of the pain-dysfunction syndrome Because there is still some variation of opinion about what constitutes the pain-dysfunction syn drome, it is necessary to begin this discussion with a brief consideration of what we consider the es sential signs and symptoms that place a patient in this category. The most common finding is pain of unilateral origin.6 This pain usually is described by the patient as a dull ache felt in the ear or preauricular area, that may radiate to the angle of the mandible, the temporal area, or the lateral cervical region. The pain can be relatively con stant, but more often is reported as worse on aris ing in the morning, or else as relatively mild in the morning but gradually worsening as the day progresses. It frequently also is exacerbated at mealtime. The next most common finding is muscle ten derness.6 Although not usually reported by the patient, this symptom can be determined easily by the examiner. The most frequent areas of ten derness are over the neck of the mandible and in the region distal and superior to the maxillary tuberosity. The mandibular angle and the tem 148 ■ JADA, Vol. 79, July 1969
poral crest are other common sites. These sites of tenderness are presumed to represent areas of spasm in the masticatory muscles. The third most common symptom is a clicking or popping noise in the TMJ. Patients having this symptom alone, however, are not included in the category of the pain-dysfunction syndrome. They also must have accompanying symptoms such as pain or tenderness or both. Limitation of jaw function is the fourth cardinal symptom of the pain-dysfunction syndrome. It may be characterized either by inability to open as wide as usual, or by deviation of the mandible on opening. Patients with limitation of opening will rarely have clicking, although their past history frequently will reveal that this had been present sometime in the course of their condition.6 Besides having one or more of the four cardinal symptoms, of pain, tenderness, clicking, and limi tation, the patient considered to have the paindysfunction syndrome must also have these nega tive characteristics: ■ Absence of clinical, radiographic, or bio chemical evidence of organic changes in the TMJ. ■ Lack of tenderness in the TMJ when this area is palpated via the external auditory meatus. The significance of these negative character istics in establishing the final diagnosis lies in their indication that the primary site of the problem is in the masticatory musculature rather than in the structures of the joint. This distinction forms the essential basis for understanding the etiology of the pain-dysfunction syndrome. Although it is our belief that this syndrome gen erally begins as a functional problem, ultimately, as we will see, it can lead to organic changes so that these negative diagnostic criteria may no long er be applicable. In the latter stage there occasion ally is difficulty in determining clinically whether the patient actually belongs in the category of the pain-dysfunction syndrome or if the pathologic con dition is primary. The past history may be helpful in making this distinction.
Previous theories of etiology Discrepancies in occlusion, or maxillo-mandibular relationships, or both, formed the basis for most of the early theories of the etiology of the “TMJ syndrome.” While originally it was suggested that mandibular overclosure was the prime initiating factor,1>9>10 more refined theories related to occlu-
sal disharmony were subsequently developed.11-13 Such “tooth theories” essentially proposed that when the teeth are brought together during chew ing or swallowing the discrepancies in occlusion produce a displacement of the mandible, usually in a posterior direction, with resultant compression of the highly vascular, densely innervated, loose retrocondylar connective tissue. It was reasoned that continued compression of this tissue would then cause not only pain but impairment of the blood supply to the joint structures, thus leading to degenerative changes. The difficulties with this explanation for the etiology of the pain-dysfunction syndrome were multiple. First and foremost it failed to explain satisfactorily how occlusal interferences could de velop in a functioning dentition unless they were iatrogenically induced. Second, it did not explain why most of the symptoms, particularly in the early phases of the condition, were related mainly to the masticatory musculature rather than to the joint itself. Third, the peculiar age, sex, racial, and social distribution of the patients suffering from this condition was not explained8-14 nor was the ability of other factors, such as clenching or grind ing, to act as etiologic agents. Finally, it did not account for the high degree of clinical success claimed in the treatment of such patients by what often appeared to be diametrically opposed forms of therapy.8-15-18 The inadequate explanation provided by the “tooth theories” apparently disturbed many in vestigators and ultimately led to what might be called the “tooth-muscle theories.”19-20 These theories, while somewhat less mechanical in prin ciple, still had as their etiologic basis a discrepancy in occlusion. However, rather than proposing that the altered occlusion directly produced mandibu lar displacement, they hypothesized that the occlu sal interferences caused an altered proprioceptive feedback, leading to incoordination and spasm of some of the muscles of mastication. Although these theories were superior to the “tooth theories” in that they did implicate the neuromusculature and helped to explain more of the symptoms, they still failed to answer the other criticisms that had been leveled against the earlier theories. It was not until the studies of Schwartz and his co-workers in the late 1950’s8 that there began to be a gradual shift in emphasis from consideration of the influence of occlusion to the recognition that functional disturbances in the masticatory mus culature could play a primary role in the etiology of “TMJ” dysfunction. While the hypothesis we
have developed at the Temporomandibular Joint Research Center tends to support Schwartz’s view point concerning the role of stress and its influence on muscle tension,8 it differs considerably in its interpretation of the contribution of occlusal ab normalities.
The psychophysiologic theory— A new concept of etiology It is our belief that masticatory muscle spasm is the primary factor responsible for the signs and symptoms of the pain-dysfunction syndrome (illus tration). Since pathologic involvement of the joint structures occurs only in the late stages, if at all, the terms “myofascial pain-dysfunction (MPD) syndrome” or “masticatory myalgesia syndrome” are actually more descriptive of the condition than the name temporomandibular joint pain-dysfunc tion syndrome originally proposed by Schwartz.7 Spasm can be initiated in one of three ways: muscular overextension, muscular overcontraction or muscle fatigue. Such acute incidents as external trauma or excessively wide opening, while also capable of initiating muscle spasm, are usually self-limiting episodes of short duration and need not be considered in this discussion. Examples of some of the factors that can produce overexten sion of the various masticatory muscles are dental restorations or fixed and removable prostheses that
TENSION
»
ORAL HABIT
------ "D ental I r r ita tio n "
MUSCULAR FATIGUE
M u sc u la r --------^ I MYOSPASM 1-^--------- M u sc u la r O v e rc o n tra c tio n O v e re x ten sio n | M i u s r a a ----
1
Etiology of the myofascial pain-dysfunction syndrome. A l though there are three means of entry into the syndrome, the darker arrows indicate the m ost com m on pathway. Th e explanation of this m echanism is termed the Psychophysi ologic Theory.
Laskin: ETIOLOGY OF PAIN-DYSFUNCTION SYNDROME ■ 149
encroach on the intermaxillary space. Overcon traction, on the other hand, can be caused by over closure resulting from such things as bilateral loss of posterior teeth or by the “settling” of partial dentures replacing them. Similarly, it can occur in patients wearing complete dentures after ex cessive alveolar resorption. Although adverse mechanical factors leading either to muscle overextension or overcontraction may cause some instances of MPD syndrome, we believe the most common cause to be muscle fa tigue produced by chronic oral habits such as clenching or grinding of the teeth (illustration). These habits can be initiated by an annoying “den tal irritation” like an improperly occluding resto ration or an overhanging margin. Generally, how ever, we believe that they are an involuntary ten sion-relieving mechanism. Since this explanation for most cases of MPD syndrome implicates emo tional rather than mechanical factors as prime eti ologic agents, it has been termed the “psychophysiologic theory.” The development of spasm in one or more of the masticatory muscles, regardless of whether it is caused by fatigue, overcontraction, or overex tension, not only leads to pain and limitation, but also may produce a slight change in jaw position so that the teeth do not occlude properly, if this abnormal jaw relationship persists for several days or longer, the teeth then may gradually shift to accommodate to the new position. This is one of the reasons why some patients suddenly exhibit occlusal disharmonies when the spasm is relieved and the rebalanced musculature returns the jaws to their original relationship. In addition to producing possible alterations in occlusion, persistent myospasm also can cause two other organic changes, namely: degenerative ar thritis and contracture (illustration). Degenerative changes in the TMJ can arise from continued jaw function with the condyle in an abnormal position. Contracture is a degenerative change in muscle that accompanies long-term spasm. Thus, the MPD syndrome, although originating as a func tional problem in most instances, ultimately can lead to organic disease. The condition then be comes self-perpetuating because all of these or ganic changes result in an altered chewing pattern with attendant reinforcement of the original spasm and pain. This proposed scheme for explaining the patho genesis of the MPD syndrome (illustration) has a number of advantages over the previous “tooth” and “tooth-muscle” theories. Not only does it 150 ■ JADA, Vol. 79, July 1969
adequately explain the origin of the various signs and symptoms, but it also shows how occlusal dis harmonies can arise in a functioning dentition as a result rather than as a cause of the problem. This is a concept diametrically opposed to that sug gested by previous investigators. Furthermore, since there are three paths of entry into the syn drome (illustration), the suggested scheme also ex plains how diverse etiologic factors can produce like symptoms. On a similar basis it offers a logi cal explanation of how different forms of therapy may be successful in what symptomatically ap pears to be the same condition. Although this scheme offers a more inclusive explanation of the pathogenesis of the MPD syn drome than any of those previously suggested, such presumptive evidence alone does not make it correct. The psychophysiologic theory has there fore served as the basis for direct experimental test ing at the Temporomandibular Joint Research Center during the past six years. Although the pub lished findings of others also could be used to sup port the theory, this discussion will be limited to those studies performed at the Center, since most of these have not been published yet in extensive form.
Experimental evidence for the psychophysiologic theory The experimental evidence for the psychophysi ologic theory can be divided into five main cate gories: epidemiologic, radiologic, psychologic, biochemical, and physiologic. ■ Epidemiologic studies: Analysis of the exam ination data on a series of 277 consecutive patients treated at the Temporomandibular Joint Research Center revealed that over 80% had tenderness in one or more of the masticatory muscles.6 This analysis not only supports the theory of muscle spasm as a key factor, but also indicates that pa tients with MPD syndrome comprise the greatest percentage of those having “TMJ” problems. The history data on another series of patients showed that about 80% presently have or previous ly had other psychophysiologic diseases such as ulcer, migraine headache, or dermatitis.21 Seventyseven percent also reported having chronic oral habits such as clenching or grinding of the teeth, gum chewing, or biting on hard objects.
■ Radiologic studies: Many of the earlier theo ries proposed in connection with TMJ disorders depended heavily on radiographic evidence for substantiation. A high incidence of pathologic change or alteration in the spacial relations of the joint components has been reported by numer ous investigators,11'22-25 and entire philosophies of treatment, not the least of which is surgical, have been predicated on these alleged findings. At our Center, however, less than 5 % of all patients have shown radiographic evidence of pathologic change in the structures of the TMJ. This differ ence seems to be related to the use of the more accurate procedure of corrected laminagraphy,26 in which reproducible, true lateral profiles of the condyles are obtained. On the other hand, routine radiographs of the TMJs, cephalometric headplates,27 and even standard laminagraphic tech nics induce artifacts which can easily be misin terpreted as evidence of pathology. Moreover, many clinicians fail to take into consideration the normal variations in condylar morphology that have been clearly documented by Yale and others.28 The lack of significant radiographic evi dence of pathologic condition in patients with MPD syndrome supports the contention that the joint itself is not actually the primary site of in volvement in this disorder. ■ Psychologic studies: Since the psychophysio logic theory is based on the premise that persistent tension-relieving oral habits are the primary cause of most cases of MPD syndrome, the uniformity in the psychological makeup of such patients is important evidence in support of this theory. Lupton21 has shown that about 75% of an unselect ed sample of women patients from the Temporo mandibular Joint Research Center whom he sub jected to psychological testing fell within two “dominant” personality categories. They were characterized best as “hypernormal” individuals who tended to describe themselves, or were seen by others, as responsible, generous, and mana gerial. They differed significantly from other den tal patients, medical patients afflicted with rheu matoid arthritis, a control group of normal indi viduals, and a group of psychotic and neurotic patients. Lupton has suggested that the attempt of these patients to maintain the facade of hyper normality leads to generalized somatic tension; this tension accounts for their frequent addiction to tension-relieving oral habits and past histories of psychosomatic illnesses. Another study which tends to emphasize the
etiologic role of psychologic factors is one which showed that a program of dental therapy plus concomitant psychological counseling or educa tional instruction provided better therapeutic re sults than dental therapy alone.29 Moreover, Lup ton also has demonstrated in a preliminary series of 35 patients that only psychological counseling can be equally as effective as dental treatment in alleviating symptoms.30 These findings, as well as those which have indicated a relatively significant response of patients to both placebo splints31 and placebo drugs,32 not only strongly support the psy chophysiologic theory but also tend to negate the role of noniatrogenic occlusal disharmonies as a primary etiologic factor in the MPD syndrome. ■ Biochemical studies: There is biochemical as well as psychological evidence to indicate that persons with the MPD syndrome are under great er than normal stress. Since increased levels of urinary 17-OH steroids and catecholamines have been linked to the stress phenomenon, the con centration of these substances was compared in normal individuals and a group of patients with the MPD syndrome. An overnight urine sample was analyzed since ordinarily this should be a period of minimal physical and emotional activ ity. Results of the experiment showed both the average steroid and catecholamine levels to be significantly higher in the patients than in the con trol group.33 ■ Physiologic studies: Since the psychophysio logic theory is based on muscle fatigue as an im portant factor in the production of myospasm, it raises the question of whether the masticatory muscles of patients with MPD syndrome can be come fatigued more readily than those of normal individuals. This possibility was examined by a muscle endurance test that measured the length of time one could bite with maximum force on a strain gauge from which a 500 gm weight was sus pended.34 It was found that while the mean hold ing time for the patient and control groups did not vary significantly, the normal individuals general ly exhibited greater biting force during the test period. Thus, when the force-time factor was con sidered as an indicator of fatigability, the masti catory muscles of patients with MPD syndrome proved to be more susceptible. Of equal interest, however, was the finding of pain and limitation in both the patients and the controls in the posttest period. In the patients, al though they may have been asymptomatic before Laskin: ETIOLOGY OF PAIN-DYSFUNCTION SYNDROME ■ 151
the test, the recrudescence of symptoms often last ed for several days. The pain was described as being in the preauricular area, at the angle of the mandible, or occasionally in the temporal or frontal regions— the same sites ordinarily involved in the syndrome. Such symptoms might be expected in the patients, but it was significant that they also developed in the control group, although they did not last as long. Here, in essence, the MPD syn drome was being produced in normal individuals, not by affecting occlusal relationships but rather by fatiguing the masticatory musculature. Another experiment which supports the concept that chronic muscle fatigue can lead to masticatory myospasm involves the production of bruxism in adult monkeys.35 With use of an electric stimulator which permitted controlled, periodic unilateral depolarization of the masseter, medial pterygoid, and temporal muscles, clenching and grinding of the teeth was induced for 20 minutes/hour, day and night, for six weeks. Electromyographic re cordings at the termination of the experimental period invariably showed an increase in both the frequency and amplitude of spike potentials, a situation indicative of muscle spasm. Here again, muscle fatigue rather than occlusal disharmony was responsible for producing a situation akin to the MPD syndrome.
Implications of the psychophysiologic theory Although there are still some gaps in our total un derstanding of the etiology of the MPD syndrome, when the findings from the various epidemiologic, radiologic, psychologic, biochemical, and physio logic studies done at the Temporomandibular Joint Research Center are integrated, they form a solid basis for the validity of the psychophysiologic theory. This position is strengthened further when one includes many of the related studies in these fields done by other investigators. To complete the picture, however, it is now necessary to extend our understanding of this theory into the areas of diagnosis and treatment. Although it is not the purpose of this paper to discuss the specific treatment of the MPD syn drome, there are certain general conclusions re garding therapy which can be deduced from the psychophysiologic theory. First, because the initi ating factors for the syndrome are generally emo tional rather than physical, treatment must be 152 ■ JADA, Vol. 79, July 1969
directed toward this aspect of the problem as well as toward the management of the physical symp toms and the organic sequelae. Disregard for this principle probably is responsible for most of the failures encountered. Second, in the functional stage of the syndrome, when primarily the masti catory muscles are involved, there are obviously no indications for such drastic forms of therapy as joint surgery, intra-articular drug injections, or extensive forms of occlusal equilibration or re construction. It is even questionable whether these procedures generally are indicated in the later stages because the muscles of mastication are still the major site of involvement. Third, it must be realized that correction of the underlying conflicts leading to the production of tension-relieving oral habits may not always be possible, even when the patient receives psychotherapy. It is not mere ra tionalization, therefore, to assume that a small number of patients will never be completely cured. However, one should not use this as a license to relegate any difficult case into the incurable cate gory before all logical forms of treatment have been tried. On the other hand, excessively radical thera peutic measures should not be attempted in des peration, because these may only induce iatrogenic problems that will further complicate the situation. Finally, it is clear that the MPD syndrome, along with the many conditions that directly in volve the TMJ, form a complex group of problems of diverse etiology and pathology frequently re quiring diagnostic and therapeutic skills beyond the capabilities of any single individual. Not only as a matter of expediency, but also to provide the most effective patient care, there is an obvious need for a team approach to the management of these conditions.
These investigations were supported by USPHS Research Grant DE-01849 from the N ational In s titu te of Dental Re search, National In s titu te s of Health, Bethesda, Md. Doctor Laskin is professor and associate head o f the de p artm ent of oral and m axillofacial surgery and d ire cto r of the Tem porom andibular Jo in t Research Center, U niversity of I llin o is at the M edical Center, Chicago, 60612. S ta ff mem bers of th e research team include Doctors Seym our Yale, Charles Greene, M artin Lerman, Daniel Lupton, and Howard Sutcher.
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ular a rtic u la tio n and jaw relationships as pertains to deaf ness. Dental Items 62:507 June 1940. 3. Shapiro, H.H., and Truex, R.C. Tem porom andibular jo in t and th e auditory fu n ctio n . JADA 30:1147 Aug 1943. 4. Sicher, H. Tem porom andibular a rtic u la tio n in man d ib u la r overclosure. JADA 36:131 Feb 1948. 5. Zim m erm an, A.A. An evaluation o f Costen's syndrome from an anatom ic p o in t of view. In Sarnat, B.G. (ed.) The tem porom andibular jo in t. S p ringfield, III, Charles C Thomas, 1951, p 82-110. 6. Greene, C.S., and others. The TMJ pain-dysfunction syndrome: heterogeneity of the p a tie nt population. JADA (in press). 7. Schwartz, L. Pain associated w ith th e tem porom andib ular jo in t. JADA 51:394 Oct 1955. 8. Schwartz, L. Disorders o f the tem porom andibular jo in t. Philadelphia, W. B. Saunders Co., 1959. 9. G oodfriend, D.J. Sym ptom atology and trea tm e nt of ab n orm alities of the m andibular a rtic u la tio n . Dent Cosmos 75:844 1933. 10. H arris, H.L. E ffe ct o f loss o f v e rtic a l dim ension on anatom ic structu re s of the head and neck. JADA 25:175 Feb 1938. 11. Thompson, J.R. Tem porom andibular disorders: diag nosis and dental treatm ent. In Sarnat, B.G. (ed.) The te m porom andibular jo in t. S prin g fie ld , III, C harles C Thomas, 1951, p 122-144. 12. Hankey, G.T. Tem porom andibular arthrosis. Analysis of 150 cases. B rit Dent J 97:249 Nov 1954. 13. Granger, E.R. Occlusion in tem porom andibular jo in t pain. JADA 56:659 May 1958. 14. Franks, A.S.T. Social character of tem porom andibular jo in t dysfunction. Dent Pract (B ristol) 15:94 Nov 1964. 15. Sears, V.H. Occlusal pivots. J Prosth Dent 6:332 May 1956. 16. Jankelson, B. Technique fo r o b ta in in g optim um fu n c tional relatio n sh ip fo r the natural d e n titio n . D ent Clin N Am er March 1960 p 131-141. 17. Mann, A.W., and Pankey, L.D. Concepts o f occlu sion: the P.M. philosophy of occlusal re h a b ilita tio n . Dent C lin N Am er Nov 1963 p 621-636. 18. Boman, K. Tem porom andibular jo in t arthrosis and its trea tm e nt by e xtirp a tio n o f disk; c lin ic a l study. Acta C hirS cand (suppl 118) 95:1 1947. 19. Sicher, H. S tru ctu ra l and fu n c tio n a l basis fo r dis
orders of the tem porom andibular a rticu la tio n . J Oral Surg 13:275 Oct 1955. 20. Ram fjord, S., and Ash, M., Jr. O cclusion. Philadel phia, W. B. Saunders Co., 1966. 21. Lupton, D.E. A pre lim in a ry investigation of the per so nality of fem ale tem porom andibular jo in t dysfunction patients. Psychother Psychosom 14:199 1966. 22. Lindblom , G. Disorders of th e tem porom andibular jo in t. Acta O dont Scand 11:61 July 1953. 23. R icketts, R.M. Roentgenography of the tem porom an d ib u la r jo in t. In Sarnat, B.G. (ed.) The tem porom andibular jo in t, 2nd ed. S pringfield, III, Charles C Thomas, 1964 p 102-132. 24. Bell, W.E. Oral and facial pain and the tem porom an d ib u la r jo in t; synopsis. Dallas, Weldon E. Bell, 1967. 25. Henny, F.A., and M e rrill, R.G. Roentgenographic changes in 39 patients subjected to m a n d ib u la rco n d ylo to m y. IADR Abstracts, 360, 1966. 26. Rosenberg, H.M. Laminagraphy: m ethods and ap p lica tio n in oral diagnosis. JADA 74:88 Jan 1967. 27. Sutcher, H.D. E ffe ct o f the intra-m eatal cephalom etric headholder on occlusion. IADR Abstracts, 5, 1967. 28. Vale, S.H.; A llison, B.D.; and Hauptfuehrer, J.D. An epidem iological assessment of m an d ib u la r condyle m orphology. Oral Surg 21:169 Feb 1966. 29. Lupton, D.E. A com parative analysis of th e e ffe ctive ness o f counseling, in stru ctio n and dental treatm ent. PhD D issertation, U niversity of Chicago, 1967. 30. Lupton, D.E. Psychological aspects of tem porom an d ib u la r jo in t dysfunction. JADA th is issue p 131. 31. Sutcher, H., and others. Comparison o f responses to pharm acological and physical placebo therapy in TMJ dys fu n c tio n patients. IADR Abstracts, 243, 1969. 32. Greene, C.S., and Laskin, D.M. Evaluation of mepro bamate therapy in TMJ d ysfunction patients. IADR Ab stracts, 242, 1969. 33. Evaskus, D.S., and Laskin, D.M. A biom echem ical measure of stress in patients w ith m yofascial pain-dysfunctio n syndrome. IADR Abstracts, 610, 1968. 34. D irenfeld, V.N. Muscle endurance in pa tie nts w ith tem porom andibular jo in t d ysfunction. MS Thesis, Univer sity o f Illin o is a t Medical Center, 1967. 35. Banasik, P.M., and Laskin, D.M. Experim ental in d u c tio n o f bruxism by e le ctrica l stim u la tio n o f m ajor muscles of m astication. IADR Abstracts, 409, 1969.
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