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Clinical report on the etiology and diagnosis of TMJ dysfunction-pain syndrome
MAXILLOFACIAL PROSTHETICS TEMPOROMANDIBULAR JOINT SECTION
. DENTAL
IMPLANTS
EDITORS
I. KENNETH
LOUIS J. BOUCHER
ADISMAN
Clinical report on the etiology and diagnosis of TMJ dysfunction-pain syndrome Lawrence A. Weinberg, Nassau County
Medical
D. D. S., M. S. ,* and Lynn A. Lager, D. D. S. * *
Center,
East Meadow,
N. Y.
1 his article presents a clinical report on the etiology and diagnosis of temporomandibular joint (TMJ) dysfunction-pain syndrome in 138 patients (90 from the clinic and 48 from private practice). Since craniomandibular disorders are multicausal,’ the literature is often conflicting, with one group accentuating stress’-” while others emphasize various aspects of occlusion”-” and/or condylar displacement within the fossae.‘“-‘” Recently, anterior displacement of the disk has also been shown with the aid of arthrography, to be another cause of TMJ symptoms in some patients.“. lx To further complicate the issue, the term myofascial pain-dysfunction (MPD) was introduced in 1969.“’ The new terminology did not acknowledge the role of the TMJ, except in arthritis, or the bilateral aspect of craniomandibular disorders. As a result, confusion in etiology and treatment concepts has threatened the credibility of the whole field of craniomandibular disorders, despite the fact that Age&erg and Carlsson’s” epidemiologic study reported that 12% of the population have pain on opening and up to 24% have pain in the face and head. The objectives of this article are (1) to explain why the “definitive scientific study” on the cause and syndrome cannot be effect of TMJ dysfunction-pain produced and (2) to report on the clinical findings of 138 patients which will help clarify etiology and diagnosis.
SCIENTIFIC
METHOD
The scientific method of investigation consists of five parts: (1) hypothesis, (2) isolation of variables, *Director, **Associate
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TMJ Service, Dental Department. Director, TMJ Service, Dental Department
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(3) experimental data, (4) statistical analysis, and (5) conclusions. If we could follow the scientific method in the investigation of TMJ dysfunction-pain syndrome, a simple cause-and-effect relationship might be demonstrated that would eliminate controversy and confusion and provide an aImost 100% cure. However, the problem in human research is that we cannot isolate the variables as we can in a test tube situation. Therefore, a clinical correlation does not necessarily prove causality; it shows a trend. For instance, in a recent medical study it was shown that there was a correlation between those patients that drank five or more cups of coffee a day and a two-fold increase in the incidence of heart attacks (Fig. 1). This correlation does not prove causality because those patients who drink a lot of coffee often have sugar with the coffee and smoke. Caffeine may play an indirect role in causing the heart attack by stimulating the central nervous system and adding to the person’s anxiety. It is possible that the anxiaus type of person has a greater tendency for heart attacks and that the increased consumption of coffee is an incidental behavioral manifestation of the person’s anxiety.
Isolation of variables Unless the variables am isolated, variable A can be correlated with variable B without the experimentor being aware that other variables C, B, and E are also at work producing the elect of variable B (Fig. 2). The conclusion can be drawn that a correlation between two factors, in a human, does not prove causality but merely reports on a trend.
Research on TMJ The scientific method cannot be applied to research of TMJ dysfunction-pain syndrome (eranio-
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TM] DYSFUNCTION-PAIN
SYNDROME
ISOLATION 15
CUPS OF
COFFEE1
CORRjlATED 2X TEND, FOR HEART ATTACKS CIGARETTES SUGAR CAFFEINE ANXIETY Fig.
1.
Correlation
METHOD
Empiricism is the practice of relying on observations and experiment, especially in the natural sciences. Correlations indicate a trend, not a cause and effect (Fig. 3). These trends, such as occlusion, stress, palliative, and/or definitive treatment, are applied clinically. The documented results, in a sufficient sampling, permit a constant feedback mechanism which facilitates an on-going reevaluation of the original trend. This continual process of reevaluation is necessary to support the original trend, but does not prove it. Under the circumstances, it is the best available; however, it leads to controversy and confusion if the reporting of a trend is thought to be a proof, as if it were validated by the scientific method.
Disadvantages of empiricism There are several disadvantages with the empirical method as applied to TMJ dysfunction-pain syndrome. A differential diagnosis must be made before one of the trends (occlusion, stress, etc.) can be applied clinically (Fig. 4). This can produce errors in
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VARIABLE
C
VARIABLE
D’
VARIABLE
E,’
/
Fig. 2. Isolation of variables.
IEMPIR~cAL METHODI
does not prove causality.
mandibular disorders) because the human variables cannot be isolated. In addition, the multicausality of its etiology prevents individual study. Multicausality has been established by the clinical response to palliative therapy’.’ as well as occlusal adjustment.“.‘” The onset of craniomandibular pain can be triggered by sudden occlusal changes as well as acute stress situations. Most often, a combination of etiologic events produce the symptoms; however the etiologic profile will vary from patient to patient in that one patient might have a very strong stress factor while in the next, occlusion is the predominant cause.’ EMPIRICAL
OF VARIABLES
B
DOCUMENTED RESULTS Fig. 3. Empirical method; correlation nof cause and effect.
indicates a trend,
the experimentor’s diagnosis which would unknowingly negate the results. Thus, the documented results would be a false-negative due to the diagnostic error. Another problem is in the clinical application where there is a built-in variant in operator skill. This can also produce a false-negative response. During the reevaluation process, experimentor bias can unconsciously prejudice the results in either direction, depending on the preconceived opinion of the clinician. It is obvious that this procedure deviates from the scientific method which isolates one variable at a time. This stresses the need for continual documentation and reevaluation of those trends that have been reported. The process is long and repetitive but essential to progress.
AGE GROUP Patients were grouped into three age categories: 16 to 20 years of age (17%), 21 to 40 years of age (57%), and 41 to 71 years of age (26%).
Proportion
of women to men
The 90 clinic patients had a ratio of 8 women for every 1 man, possibly due to the limited hours the
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Fig. 4. Disadvantages of empiricism; differential re&aluation of the Trend being tested.
diagnosis and experimentor
bias affects the
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-132
OVER 4 YEARS
%o[ I “/o1
INJURY--m DENTAL TR,+%j
v.4 ( 138 patients)
II 0 o/al
( 138 patients) Fig. 5. Dispersion of patients relative to symptom duration. clinic is open. However, in the private practice group of 48 patients, the ratio was 2.7:1. The latter is closer to the findings of Helkimo, et al” who reported that the incidence of women was only slightly greater than men and not as exaggerated as was previously reported.“. ‘Ii It is well known that women tend to seek medical intervention for symptoms more readily than men, which may account for the disproportion between the sexes.‘;’ Most dental practices contain more women than men; therefore, it is felt that the incidence of TMJ dysfunction-pain is not necessarily sex-related.
ONSET OF PAIN The patients seeking treatment had been suffering from craniomandibular pain for varying time intervals (Fig. 5). The dispersion indicates that most patients had long histories of chronic pain. Fifty four percent had been unsuccessfully treated with drugs;
Fig. 6. Trigger symptoms.
mechanisms
of TMJ dysfunction-pain
15% had occlusal adjustments; 21% had prostheses; and 3% had been given injections. Many had several treatment modalities.
Trigger mechanism A trigger factor initiates an over-response to an irritant by previously sensitized tissue but is not usually the primary “cause.“’ For instance, an injury can trigger an over-response due to a previously existing subclinical TMJ dysfunction. In that case, the tissue response to the injury, as well as the cause of the chronic subclinical TMJ dysfunction, should be treated.
Discussion Patients that sustained a joint injury (21%) usually had a long period of recuperation (6 months to over a year), regardless of the type of treatment. Twentyfour percent of the patients experienced discomfort 6 to 8 weeks after the insertion of an extensive restoration or after prosthetic dentistry. This confirms one
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TEMPORAl
TMJ [?%%I
pm
AUD, MEATUS(18%f MASSETE R I?!?=%1
NECK 133%-1 MED. PTERY, g?zq STERNO%- M,
07
(138 patients)
SHOULOER
Fig. 7. Incidence of subjective pain symptoms on the basis of location. Fig. 8. Incidence of unilateral and bilateral subjective pain symptoms.
trend observed, that occlusion plays a definite role in TMJ dysfunction-pain syndrome. Similarly, 26% of the patients reported the onset of symptoms after an acute stressful period. It would seem justified to conclude that sudden occlusal change as well as acute stress can act as triggers for craniomandibular pain. Thirty-six percent of the patients had no trigger factors, while 51% had identified a recent stress or occlusal change that initiated the acute response (Fig. 6). Two or more trigger factors were present in 13% of the patients. Summary In 51% of the patients, acute craniomandibular pain was initiated by sudden occlusal change and/or acute emotional stress. It should be remembered that a trigger factor is not the main etiologic agent but apparently serves as an initiating mechanism. This conclusion is supported by the fact that in most patients the original acute stress was terminated, but the TMJ dysfunction-pain remained in full force.
PAIN LOCATION The distribution of subjective pain location is shown in Fig. 7. The pain symptoms are wide spread throughout the head and neck, and indicate that only rarely is one limited area involved. It is also significant that the incidence of subjective pain in
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I
01AG~os~sj
1DIFFERENTIAL
I
PAI N
WORSE WITH ANY FUNCTION WORSE DURING MEALS WORSE AFTER
MEALS
WORSE AFTER
TALKING
HISTORY OF TRISMUS---------(5 PAIN ON OPENING
7% r39 % _
PATTERN
145 %
(A.M.,
0 F OCCURANCE Afternoon,
P.M.)
Fig. 9. Differential pain diagnosis; incidence of symptoms are related to function and pattern of occurrence. the TMJ itself was 76%, twice that of any other region (Fig. 7). Furthermore, the incidence of bilateral subjective pain was 49%, and unilateral pain was 42% (Fig. 8). The unusually high incidence of subjective pain in the TMJ region itself (76%) does not necessarily rule out MPD, because some of those symptoms could be referred. However, the incidence of bilateral pain in 49% of the patients automatically eliminates them from MPD, according to its definition originally described by Laskin.” The evaluation
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LACER
I30 “/ol HEAD NECK -139 %I SHOULDER---+%-] BACK ---+I 4’101
CLENCHING ----@@ii
Fig. 10. Incidence of life-style
AND
factors (clenching,
bruxism,
stress) and associated pain
areas.
!
(DENTAL ~~srofw~
ORTHODONTICS e i DENTAL SURGERY+=1 i RESTORATIONS~-[ml COMP. DENTURES-+x] PART, DENTURES Fig. 11. Dental TMJ symptoms.
history
directly
\q related to etiology
of TMJ pain will require clinical palpation occlusal and radiographic examination.
DIFFERENTIAL
of
and
DIAGNOSIS
A differential diagnosis is aided by a thorough qualitative pain profile which will help separate TMJ dysfunction-pain from neurologic and/or other causes. This process has been previously described;‘” therefore, only the symptoms related to function will be given here because it is pathognomonic of TMJ dysfunction-pain syndrome. Fig. 9 illustrates the incidence of functional symptoms: 67% of the patient sampling had an increase in pain with some type of function, such as when chewing (59%), after meals (33%), or after talking (26%). This means that more than two thirds of our sampling can be screened as probable TMJ dysfunction-pain patients on the basis of the pain history, even before the clinical and radiologic examination. The higher incidence of pain during meals, rather than afterward, might be caused by intrajoint involvement. Pain during chewing (59%), trismus (57%), and pain on opening (39%) complete the “triad” of symptoms that are pathognomonic for TMJ dysfunction-pain syndrome. Another helpful diagnostic sign is the pattern ofpain occurrence. For instance, if the pain seems
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to occur in the morning, afternoon, or evening, it would tend to eliminate neurologic pain which usually happens suddenly, at random. The percentages of occurrence indicate that not all three dysfunction symptoms occur in every patient. However, when a patient exhibits all, or several, of the pathognomonic dysfunction symptoms (pain during chewing, trismus, pain on opening) as well as evidence of a pattern of occurrence, the prognosis for successful treatment is very good. The differential diagnosis is confirmed by clinical and radiologic supporting evidence. The latter two procedures also help establish treatment modalities.
EAR SYMPTOMS Forty-eight percent of the patients show evidence of some type of ear symptom (ringing, stuffiness, or dizziness). Although the mechanism has never been adequately explained, clinical experience has indicated that ear symptoms have been associated with posterior condylar displacement (as originally described by Costen)“’ and that anterior condylar repositioning,‘” rather than vertical opening, has been successful in eliminating or controlling symptoms. Stuffiness has been treated the most suceessfully in this manner; dizziness has been treated with more modest success; and attempts to treat ringing have produced poor results (including vertical dimension changes). It has been thought that posterior condylar displacement causes “soft tissue” impingement (rather than direct condylar impingement) on the anterior tympanic artery which arises from the internal maxillary artery and passes through the petrotympanic fissure (posterior wall of the temporomandibular fossa) to the interior of the tympanum. It anastomoses with the other tympanic arteries forming the posterior tympanic artery. It has not been established that “soft tissue” impingement on the blood supply and drainage of the middle ear,
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Fig. It. Incidence of pain from muscle and joint palpation. unilateral and bilateral pain. through the petrotympanic fissure, would be sufficient to cause symptoms because of the vascular supply through other routes such as the stylomastoid, the superficial petrosal, inferior tympanic, and the carotico-tympanic arteries and veins. However, anterior condylar repositioning with a removable prosthesis has been shown to eliminate or reproduce the symptoms by insertion or removal of the prosthesis.‘”
Joint noises On clinical examination joint “noises” were present in 68% of the patients. This finding was similar to that of a previous report in 1972.” Clicking was evidenced 55% of the time. Popping occurred in 23% of the patients. (Popping is considered a disk derangement, or a disarrangement of the disk and condylar assembly where there is no firm attachment of the disk to the medial and lateral poles of the condyle.) Crepitus was present in 18% of the patients, and many patients exhibited more than one sign of joint noise. Crepitus can be produced by (1) dry synovial cavities, (2) the perforation of a disk, and (3) localized osteoarthritis which roughens the bony surfaces. The arthritides that produce surface bony changes have also been associated with crepitus.
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Fig. 13. (Inset) Incidence of
LIFE STYLE FACTORS It has long been thought that many patients exhibit a TMJ dysfunction-pain profile’ that includes clenching and bruxism,‘7 stress,‘-’ and increased susceptibility to generalized muscle pain.” The data in Fig. 10 do not support this concept. It is noteworthy that the incidence of clenching was almost one and one-half times that of significant stress, as expressed by the patient. In a previous article, it was shown that stress is not a causeand-effect factor in TMJ dysfunction-pain syndrome. Rather, stress worked through the behavioral mechanism of clenching. ” This is not idle semantic debate; it vitally affects the treatment approach. Clenching can produce TM J symptoms in four ways, either separately or in combination, by: (1) muscle fatigue3’ which has been experimentally produced by Christensen;“’ (2) increased stimulation of the neuromuscular feed-back mechanism by the proprioceptors in the periodontal membrane, TMJ capsule,“’ and stretch receptors in the muscles (painspasm-pain cycle); (3) condylar displacement’, ‘L ” anteriorly,‘-*. I’ superiorly,“, ” and posteriorly;‘3. ” and (4) intrajoint inflammation (capsulitis) which can be caused by chronic condylar displacement (anteriorly OY posteriorly) and in turn produces irritation of the posterior auricular nerve branches in
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(OPENING1 16 mm. 20 - 26mm.qm
LATERAL
1 2%)
DEVIATION+?%]
ESALANCING CONTACT i-1 Fig. 14. Incidence of limitation of opening, lateral deviation, and balancing contact.
Fig. 15. Incidence of centric relation, deflective contact, and balancing contact.
the capsular ligament (posterior, medial, and lateral) causing pain and irritation of the branches of the masseteric and posterior deep temporal nerves (anterior portion of capsule) which can produce trismus3’. 33 The splinting action of muscles was first described by Hiltor?” in 1879.
Associated pain areas Approximately one third of the patients had subjective pain in the neck and shoulders which would tend to support the view of Krau?’ that muscles tend to go into spasm in groups and “chains” rather than individually. However, only 14% of the patients had back pain which does not seem to support the concept that TMJ dysfunctionpain patients have a greater susceptibility to generalized muscle spasm and pain.‘* (This was recorded on a subjective basis and not measured myographitally.) The significance of these findings is that there is valid reasonfor the patient to complain of pains in the head, in the neck and shoulders, and in widely dispersed areas (as well as bilaterally). This, when combined with the emotional stress from long-
AND
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standing chronic pain, often causes the patient to be erroneously labeled as “psychosomatic,” hypochondriacal, or passive-aggressive.
DENTAL
HISTORY
Thirty-three percent of the patients had a history of orthodontic treatment (Fig. 11). Dental surgery was a trigger factor in 9% of these patients. It was thought to be associated with exaggerated opening, muscle fatigue, or joint injury. Extensive dental restorations were trigger factors in 10% of the patients. Here the mechanism was thought to be a sudden change in occlusion, upsetting the neuromuscular mechanism and/or condylar displacement. Complete and removable partial dentures seem to function in a similar manner. The acute symptoms were usually initiated earlier with surgery, while occlusal changes were associated with a delayed onset of symptoms after approximately 6 to 8 weeks. In most patients, the iatrogenic trigger factors were superimposed on previously existing subclinical TMJ dysfunction or a predilection for craniomandibular disorders due to asymptomatic condylar displacement. In a previous report, 36% of an asymptomatic control group had posterior condylar displacement.‘6
MUSCLE PALPATION The incidence of palpable pain and its dtstribution is illustrated in Fig. 12. Palpation of the lateral and medial pterygoid muscles (posterior and superior to the buccal aspect of the tuberosity of the maxillae) showed the highest incidence of occurrence (64%). However, the insertion of the temporal muscle on the coronoid process (53%) and the masseter muscle (52%) were also frequently involved. The wide distribution of tenderness supports the views of KrauS:‘” that muscles tend to go into spasm in chains and groups. We should expect TMJ dysfunctionpain patients to elicit extensive pain patterns as an expression of the ‘syndrome” rather than a psychosomatic personality.
Joint pain and bilateral incidence Two of the criteria for MPD (as MPD is defined by Laskin”) are that the symptoms be unilateral and not include pain in the TMJ itself. Fifty-eight percent of the patients exhibited bilateral symptoms on palpation. Of those patients who had unilateral pain (31%), 9% of the patients had pain in the TMJ itself (Fig. 13). Combining the two groups of “non-MPLY’
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patients produces an incidence of 67% of the sampling (11% were non-TMJ patients). In other words, only 22% of the sampling fulfilled the criteria of MPD.
Nonpalpable pain group Eleven percent of the sampling had no palpable pain. After a complete examination, these patients’ pains were diagnosed as odontogenic, neurologic, atypical TMJ dysfunctional-pain, multiple-etiologic, and pain of unknown origin.
ICONDYLAR
POSITION]
CONCENTRIC -------[I I %I POSTERIOR DISPLACEMENT-j=] ANTERIOR DISPLACEMENT-+mJ REDUCED JOI NT SPACE ---j--?$%j [PATHOLOGY] PATHOLOGIC REMODELING --m OSTEOARTHRITIC CHANGES---j%\
OPENING Although 57% of the patients had a history of trismus at some time during their symptom period, this usually occurred in the early stages. Most of the chronic TMJ dysfunction-pain patients (74%) could open their mouths between 27 and 53 mm, indicating that the incidence of trismus was not as high as is commonly suspected (Fig. 14). Only 16% of the patients were limited in opening to less than 26 mm (Fig. 14). Seventeen percent of the patients exhibited lateral deviation on opening. Finally, there was a 36% incidence of nonworking (balancing) side interferences. We feel that the relatively low incidence of trismus, lateral jaw deviation, and nonworking (balancing) side interferences are all interrelated. This study tends to confirm the general view that when nonworking (balancing) side interferences are present they tend to exacerbate TMJ dysfunction-pain symptoms.“”
OCCLUSION The incidence of centric relation coinciding with centric occlusion was 31% (Fig. 15). This is much higher than the classically accepted 10% in symptom-free patients.36. 37
RADIOGRAPHIC FINDINGS All TMJ radiographs are made with the teeth closed in the maximum contact of centric occlusion (habitual centric occlusion). Diagnosis is made and treatment planned by observing the occlusion and evaluating it in relation to the condylar displacement as seen in the TMJ radiographs. However, condylar position in the fossae is also recorded and studied separately because it gives insight as to the physiologic state of the condylar suspension mechanism under muscle loading and frequent nonrest positioning during swallowing and/or clenching. Posterior condylar displacement had a higher inci-
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Fig. 16. Incidence of condylar position (with teeth in centric occlusion), and radiographic pathology.
dence (53%) than any other condylar position in this sampling (Fig. 16). Twenty-seven of the patients had anterior displacement, which was slightly higher than the sampling previously reported.‘” The current study supports the conclusion that no more than approximately one third of TMJ dysfunction-pain patients should have the classical occlusal adjustment (of deflective contacts) in the most retruded mandibular position of centric relation. Paradoxically, clinical experience has indicated that when the condyles are not displaced (the 11% concentrically located in the fossae) there seems to be a higher incidence of stress as a major cause of the symptoms (Fig. 16). It is thought that the neuromuscular imbalance and/or intracapsular inflammation associated with condylar displacement is not active; therefore, the source of discomfort is probably due to muscle spasm caused by stress-induced clenching and/or bruxism. These patients are usually more resistant to early successful treatment, but adjunctive psychologic counseling has been found to be helpful. Reduced joint space (9%) is a generalized description which should be differentiated from superior condylar displacement.“. I1 The latter is a specific pathologic entity that must meet certain clinical and radiographic diagnostic criteria: (1) reduced joint space radiographically when compared to the other side (usually not posteriorly displaced), (2) pain on the affected side, (3) clinical trial of inferior condylar repositioning, and (4) radiographic evidence of inferior condylar repositioning.” Patients requiring inferior condylar repositioning are less than 3%. Howev-
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.._-.
,..,..,-,.
CENTRIC RELATION DIA-
1
FUNCTIONAL CR 0 DYSFUNCTIONAL C.R7------2°/~~ ATYPICAL TM J NON-TMJ Fig. 17. Centric relation diagnosis.
I
IDESCRIPTIVE
D~AGNo~I~J
LOST VERT. DI MENSION.-m NEUROLOG I C OSTEOARTHRITIC PSYCHOLOGIC INCREASED VERT. DIMEN.DEVIATE SWALLOWE RpFig. 18. Descriptive logic factors.
I m [9%;1 a
diagnosis with miscellaneous
etio-
er, they do not respond well to other forms of treatment because the source of pain is pressure on the peripheral borders of the disk.
Clenching Fifty-four percent of the acute TMJ dysfunctionpain patients reported an awareness of clenching (Fig. lo), and a separate study of condylar position was recorded on those patients. It was found that the incidence of posterior condylar displacement in clenchers was the same as the other whole TMJ dysfunction-pain group itself. It has been clinically demonstrated that continual clenching can interfere with physiologic eruption or actually cause depression of the teeth in the sockets. The result is a loss of vertical dimension. However, there doesn’t seem to be an association of clenching with a higher incidence of posterior condylar displacement. Thus, this report sheds no light on the possible cause or causes of posterior condylar displacement.
Radiologic
pathology
Four percent of the TMJ radiographs examined showed evidence of pathologic remodeling (Fig. 16). Osteoarthritic lesions were observed in 9% of the patients. The incidence was higher (18%) in private practice where the TMJ radiographic technique can be more controlled and greater clarity and contrast are routine. It can be suggested that many osteoar-
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thritic lesions are overlooked on lateral transcranial TMJ radiographs because we “are not supposed to see them.” The erosions and radiolucent areas are not identified because of poor radiographs and/or a lack of confidence in the TMJ radiograph itself. This has come to light with serial TMJ radiographs over a period of years, so that a comparison can be made before the lesion becomes obvious.‘” Repeated radiographs produce the same pathologic radiolucency which eliminates “artifacts.” The outline of the fossa and condyle should be clean and obviously radioopaque, while broken outlines and marked changes in the degree of radioopacity as well as radiolucent mottled areas are evidences of osteoarthritic lesions. as they would be in any other bone.
DIAGNOSIS I
AND
OF CENTRIC
RELATION
The concept of functional or dysfunctional centric relation differentiates a healthy (or optimal) suspension mechanism of the condyle within the fossa from one that does not have the disk, ligaments, and muscles in physiologic balance. The clinical occlusal findings are related to the condylar positions in the TMJ radiographs to evaluate the suspension mechanism (centric relation).’ “-“‘. “‘. .I’ The optimum condylar position in the fossae (physiologic balance) has been established by comparing the clinical signs of function and dysfunction with the TMJ radiographs.‘“. ” This is the third such report, totaling 316 patients in all.‘“. ”
Functional
centric relation
The centric relation is functional in two clinical situations: (1) when there is no deflective contact in centric relation and the condyles are symmetrically placed in the middle of each fossa and (2) when a centric relation deflective contact is present and the “hit and slide” to the acquired centric occlusion can be correlated with the condylar displacement observed in the TMJ radiographs.“, ‘li A functional centric relation means that the suspension mechanism of the condyles in the fossae is essentially correct, and the classical (most retruded) mandibular position of centric relation is used for therapy.
Dysfunctional
centric relation
The centric relation can also be dysfunctional with or without a centric relation deflective contact.‘” When there is harmony between centric relation and centric occlusion and the condyles are not symmetritally placed in the middle of the fossae, the centric relation is classified as dysfunctional.” The condyies
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a~ orally displaced posteriorly and/or superiorly on one or both sides. Often a centric relation deflective contact and the “hit and slide” to the acquired centric occlusion cannot be correlated with the condylar displacement as observed on the TMJ radiographs. I’ In both cases, the centric relation is classified as dysfunctional, requiring different diagnostic and treatment methods.‘“-’ ‘. “j
At&xl
Some patients exhibit conflicting subjective and objective findings which prevents definitive diagnosis. An atypical TMJ patient does not have clear cut symptoms of any disorder, which requires special diagnostic procedures and clinical trials.“” Others have both TMJ and neurologic symptoms in clear cut fashion, which permits a differential diagnosis of both conditions superimposed on one another.
Sunimazy Only 25% of the patients had a functional centric relation requiring classical treatment based on the (most retruded) mandibular position of centric relation (Fig. 17):. ‘. ” Most patients (62%) were diagnosed as having a dysfunctional centric relation requiring anterior or inferior condylar repositioning techniques.‘“. 11.1?.I~ In other words, most TMJ dysfunction-pain patients had defective condylar suspension mechanisms which would involve the joints themselves, as well as muscles, in the dysfunction-pain. This is a departure from the belief that TtiJ pain is mostly muscular in origin.‘-“. “’ The treatment procedures are designed to correct both muscle andjoint dysfunction and will be evaluated in a subsequent clinical report. Some patients (6%) simply did not fit into any diagnostic category and were classified as “atypical.” Clinical trial procedures are helpful in screening these medical, dental, and psychosomatic patients.‘” True vertical dimension loss was found in only 1% of the patients (Fig. 18); yet, the most common prosthesis used in the treatment of TMJ dysfunctionpain increases the vertical dimension, as originally suggested in 1947 by Goodfriend”” and Block.“’ Various prostheses were reviewed in a previous and it was concluded that interferences in article,” the interocclusal space can aggravate the stretch reflex of muscles and actually increase muscle spasm. Paradoxically, clinical reaction to these prostheses can initially give a false-positive response because they interrupt the pain-spasm-pain cycle. Often, the pain returns worse than ever, and the patient is
OF PROSTHETIC
WITH
C.R = co.
(3174
Fig. 19. Incidence of condylar position with centric relation position identical to centric occlusion.
TM] cases
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uncomfortable either with or without the prosthesis. These patients usually alternate the use of the prosthesis, trying to find some relief, and eventually run from doctor to doctor. Neurologic patients can usually be differentiated with an accurate history and clinical examination procedures (the incidence in this sampling was 1%). Dilantin,* (100 mg, three times daily, for ‘2 to 3 weeks) is useful in differential diagnosis because it usually helps decrease neurologic pain but has no significant effect on TMJ pain. Osteoarthritic lesions were observed in 9% of the patients, although the incidence was higher in private practice. It is suggested that more attention should be paid to evaluating TMJ radiographs for early signs of osteoarthritic activity and to subsequent TMJ radiographs for a comparison of the effect of condylar displacement on pathologic joint remodeling.” One percent of the patients had primary psychiatric problems with TMJ symptoms in a secondary role. One complete denture patient had TMJ dysfunction-pain as a result of an exaggerated increase in the vertical dimension of occlusion which obliterated the interocclusal and speaking space. The dentures were remounted with a centric relation record, and the artificial teeth were adjusted to reestablish a more optimal (reduced) vertical dimension. The symptoms were reduced immediately. Deviate swallowing, and the resultant malocclusion, were evident in 3% of the patients. In this sampling of 138 TMj dysfunction-pain patients, the incidence of centric relation identical to centric occlusion was 31% or three times that found in normal patients (lo%).““. “’ The condylar position in the fossae was reported on only those patients who had a centric relation identical to centric occlusion (Fig. 19). The majority (60%) had posterior condylar displacement; 25% had anterior condylar displace*Dilantin,
Parke Davis and Co., Detroit, MI.
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merit; and 15% had displacement in the middle of the fossae. These findings are practically the same as the entire patient sampling. In other words, without referral to the TMJ radiographs, 60% of those patients who had identical centric relation and centric OCC~Usions would ordinarily be diagnosed as “normal,” by the classical definition; they would in fact be dysfunctional. Thus, research utilizing only the classical clinical dejnition of malocclusion (centric relation deflective slide to centric occlusion) would have a 60% false-negative immediately built into the data. The correlation between the occlusion and the TMJ radiographs, not clinical observations of the occlusion alone, establishes whether the condylar suspension mechanism (centric relation) is functional or dysfuncti0nal.H. 11.16.?J. .ISThese data suggest that the definition of “malocclusion” be modified to include its relation to the temporomandibular joints and that the occlusal relationship alone has no real significance.
SUMMARY
AND CONCLUSIONS
The clinical examination and diagnostic records of 138 clinic and private TMJ dysfunction-pain patients have been summarized. The scientific method cannot be applied to TMJ patients because of the impossibility of isolating variables and due to the multicausality of the syndrome. Therefore, empirical methods must be used which report on trends that show correlations, but do hot actually prove causality. These trends should be tested and retested to reevaluate the concepts being tried. Even so, empirical methods are subject to errors in differential diagnosis, operator technique, and experimentor bias. This report indicated that a trigger mechanism (such as injury, occlusal change, or stress) was present 51% of the time and that there were two or more of these in 13% of the patients. Subjective pain symptoms were distributed in widely dispersed regions of the head, neck, and shoulders bilaterally (49%) as well as unilaterally (42%). Differential diagnosis of TMJ dysfunction-pain syndrome can be facilitated by the pain history. The pathognomonic symptoms are pain with (any) function (67%), history of trismus (57%), pain on opening (39%), and a pattern of occurrence (45%). Usually there are ear symptoms (48%) and joint noises (68%) which accompany TMJ dysfunction. Many patients were aware of clenching (54%) and reported the onset of symptoms related to dental surgery (9%) and restorations (10%).
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Palpation of the patients indicated that 58% had bilateral pain; of the 31% that had unilateral symptoms, 9% had pain in the TMJ itself. This means that 67% of the sampling did nvl have MPD as described by Laskin.“’ Only 22% could be defined as MPD patients; the balance (11%) were classified as atypical, neurologic, combined, or having pain of unknown origin. Occlusal examination revealed that 31% had centric relation position identical to centric occlusion. However, correlation with the TMJ radiographs revealed that most (60%) of these patients had posterior condylar displacement. ‘This leads to the conclusion that the definition of “malocclusion” cannot be based on intraoral examination alone but should be correlated with TMJ radiographs. The patient sampling revealed that posterior condylar displacement had the highest incidence (53%:/c),with anterior displacement 27%, concentric placement 1570, and reduced joint spaces 9%. Posterior condylal displacement has been established as a major factor in TMJ dysfunction-pain syndrome in this report and previous reports as well.” Iii As a correlary. 52% of the condylar suspension mechanisms of the TMJ patients revealed a diagnosis of dysfunctional centric relation; whereas, only 34% had a functional centric relation where the disk, condyle, and muscles were in physiologic (optimum) balance. The diagnostic criteria for functional and dysfunctional centric relation were discussed. Treatment procedures and their evaluation will be given in a subsequent report. REFERENCES 1.
Weinberg, L. A.: Temporomandibular dysfunctional A patient-oriented approach. .J PROSTHET Dmw
profile: 32:312.
1974. 2.
3. 4.
5. 6.
7.
8. 9.
Luptom, D.: Psychological aspects of temporomandibular joint dysfunction. J Am Denr Assoc 79:131, 1969. Moulton, R.: Psychiatric considerarion in maxiilofacial pain. J Am Dent Assoc 51:408, 1955. Evaskus, D., and Laskin, D.: A biochemical measureof stress in patients with myofascial pain-dysfunction syndrome J Dent Res 51:1464, 1972. Lefer, L.: A psychoanalytic view of a dental phenomenon. Contemp Psychoanal 2:135, 1966. Shore, N. A.: Occlusal Equilibration and Temporomandibuiar Joint Dysfunction. Philadelphia, 1959, J.B. Lippincorr co. Lindbloom, G.: Disorders of the temporomandibular joint: Causal factors and the value of temporomandibular radiographs in their diagnosis and therapy. .4cta Odontol Stand 11:61, 1953. Weinberg, L. A.: Temporomandibular joint function and its effect on centric relation. J PROSTHET DENT 30:176, 1973. Gelb, H.: An orthopedic approach to occlusal imbalance and T’MJ dysfunction. Dent Clin North Am 23:181, 1979.
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10. Gerber, V.: Kiefergelenk und zahnolljusion. Dtsch Zahnaerztl 2 26:119, 1971. 11. Weinberg, L. A.: Superior condylar displacement: Its diagnosis and treatment. J PROSTHETDENT 34:59, 1975. 12. Weinberg, L. A.: Anterior condylar displacement: Its diagnosis and treatment. J PROSTHETDENT 34:195, 1975. 13. Weinberg, L. A.: Posterior bilateral condylar displacement: Its diagnosis and treatment. J PROSTHET DENT 36:426, 1976. 14. Weinberg, L. A.: Posterior unilateral condylar displacement: Its diagnosis and treatment. J PROSTHET DENT 37:559,
27. 28. 29. 30.
31.
1977.
dys15. Weinberg, L. A.: Correlation of temporomandibular function with radiographic findings. J PROSTHET DENT 28:519, 1972. 16. Weinberg, L. A.: Role of condylar position in TMJ dysfunction-pain syndrome. J PROSTHET DENT 41:636, 1979. 17. Wilkes, C.: Structural and functional alterations of the temporomandibular joint. Northwest Dent 57:287, 1978. 18. Farrar, W., and McCarty, W.: Inferior joint space arthrography and characteristics of the condylar paths in internal derangements of the TMJ. J PROSTHETDENT 41:548, 1979. 19. Laskin, D.: Etiology of the pain-dysfunction syndrome. J Am Dent Assoc 79:147, 1969. 20. Agerberg, G., and Carlsson, G.: Functional disorders of the masticatory system. I: Distribution of symptoms according to age and sex as judged from investigation by questionnaire. Acta Odontol Stand 30:597, 1972. 21. Helkimo, M., Carlsson, B., Hedegiird, B., Helkimo, E., and L&n, T.: Function and dysfunction of the masticatory system in Lapps in Northern Finland. Svensk Tandlak T 65:95, 1972. 22. Lammie, G.: Dental Orthopaedics. Oxford, 1966, Alden Press. 23. Schwartz, L., and Cobin, H.: Symptoms associated with the temporomandibular joint. Oral Surg 10:339, 1957. 24. Bakal, D.: Headache: A biopsychological perspective. Psychol Bull 82:369, 1975. 25. Weinberg, L. A.: The etiology, diagnosis, and treatment of TMJ dysfunction-pain syndrome. J PROSTHET DENT 42:654, 1979; 43:58, and 43:186, 1980. 26. Costen, J. B.: Syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomandibular joint. Ann Otolaryngol 43:1, 1934.
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32.
33.
34. 35. 36.
37. 38.
39 40.
41
Ramfjord, S., and Ash, M.: Occlusion. Philadelphia, 1966, W. B. Saunders. Moller, E.: Elektromyografi. In Norkisk Klinisk Odontologi. Copenhagen, 1968, Forlaget for Faglitteratur. Weinberg, L. A.: An evaluation of stress in TMJ dysfunction-pain syndrome. J PROSTHETDENT 38:192, 1977. DiSalvo, N. A.: Neuromuscular mechanisms involved in mandibular movement and posture. Am J Orthod 47:330, 1961. Christensen, L. V.: Facial pain and internal pressure of masseter muscle in experimental bruxism in man. Arch Oral Biol 16:1021, 1971. Thilander, B.: Innervation of the temporomandibular joint capsule in man. Tran Roy Schools Stockholm Umea, No. 7, l-69, 1961. Ransjo, K., and Thilander, B.: Perception of mandibular position in cases of temporomandibular joint disorders. Odontol Foren Tidsskr 71:134, 1963. Hilton, J.: In Jacobson, W. H. A., editor: Rest and Pain, ed 2. New York, 1879, William Wood and Co., p 96. Kraus, H.: Principles and Practice of Therapeutic Exercises. Springfield, Ill., 1949, Charles C Thomas Publishing Co. Posselt, U.: Temporomandibular joint syndrome and occlusion: Research committee report-American Equilibration Society Compendium, 7:51, 1963-64. Beyron, H.: Optimal occlusion. Dent Clin North Am 13:537, 1969. Weinberg, L. A.: Temporomandibular joint function and its effect on concepts of occlusion. J PROSTHETDENT 35:553, 1976. Goodfriend, D. J.: Deafness, tinnitus, vertigo, and neuralgia. Arch Otolaryng 46:1, 1947. Block, L. S.: Diagnosis and treatment of disturbances of the temporomandibular joint, especially in relation to vertical dimension. J Am Dent Assoc 34:253, 1947. Weinberg, L. A.: Treatment prosthesis in TMJ dysfunctionpain syndrome. J PROSTHET DENT 39:654, 1978.
Reprint requeststo: DR. LAWRENCE A. WEINBERG
57 W.57TH ST. NEW YORK, N. Y. 10019
653
. DENTAL
IMPLANTS
EDITORS
I. KENNETH
LOUIS J. BOUCHER
ADISMAN
Clinical report on the etiology and diagnosis of TMJ dysfunction-pain syndrome Lawrence A. Weinberg, Nassau County
Medical
D. D. S., M. S. ,* and Lynn A. Lager, D. D. S. * *
Center,
East Meadow,
N. Y.
1 his article presents a clinical report on the etiology and diagnosis of temporomandibular joint (TMJ) dysfunction-pain syndrome in 138 patients (90 from the clinic and 48 from private practice). Since craniomandibular disorders are multicausal,’ the literature is often conflicting, with one group accentuating stress’-” while others emphasize various aspects of occlusion”-” and/or condylar displacement within the fossae.‘“-‘” Recently, anterior displacement of the disk has also been shown with the aid of arthrography, to be another cause of TMJ symptoms in some patients.“. lx To further complicate the issue, the term myofascial pain-dysfunction (MPD) was introduced in 1969.“’ The new terminology did not acknowledge the role of the TMJ, except in arthritis, or the bilateral aspect of craniomandibular disorders. As a result, confusion in etiology and treatment concepts has threatened the credibility of the whole field of craniomandibular disorders, despite the fact that Age&erg and Carlsson’s” epidemiologic study reported that 12% of the population have pain on opening and up to 24% have pain in the face and head. The objectives of this article are (1) to explain why the “definitive scientific study” on the cause and syndrome cannot be effect of TMJ dysfunction-pain produced and (2) to report on the clinical findings of 138 patients which will help clarify etiology and diagnosis.
SCIENTIFIC
METHOD
The scientific method of investigation consists of five parts: (1) hypothesis, (2) isolation of variables, *Director, **Associate
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TMJ Service, Dental Department. Director, TMJ Service, Dental Department
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(3) experimental data, (4) statistical analysis, and (5) conclusions. If we could follow the scientific method in the investigation of TMJ dysfunction-pain syndrome, a simple cause-and-effect relationship might be demonstrated that would eliminate controversy and confusion and provide an aImost 100% cure. However, the problem in human research is that we cannot isolate the variables as we can in a test tube situation. Therefore, a clinical correlation does not necessarily prove causality; it shows a trend. For instance, in a recent medical study it was shown that there was a correlation between those patients that drank five or more cups of coffee a day and a two-fold increase in the incidence of heart attacks (Fig. 1). This correlation does not prove causality because those patients who drink a lot of coffee often have sugar with the coffee and smoke. Caffeine may play an indirect role in causing the heart attack by stimulating the central nervous system and adding to the person’s anxiety. It is possible that the anxiaus type of person has a greater tendency for heart attacks and that the increased consumption of coffee is an incidental behavioral manifestation of the person’s anxiety.
Isolation of variables Unless the variables am isolated, variable A can be correlated with variable B without the experimentor being aware that other variables C, B, and E are also at work producing the elect of variable B (Fig. 2). The conclusion can be drawn that a correlation between two factors, in a human, does not prove causality but merely reports on a trend.
Research on TMJ The scientific method cannot be applied to research of TMJ dysfunction-pain syndrome (eranio-
OOZ-3913/80/120542
+ 12$01.20/0Q1980
‘Ihe ‘2. V. Mosbv Co
TM] DYSFUNCTION-PAIN
SYNDROME
ISOLATION 15
CUPS OF
COFFEE1
CORRjlATED 2X TEND, FOR HEART ATTACKS CIGARETTES SUGAR CAFFEINE ANXIETY Fig.
1.
Correlation
METHOD
Empiricism is the practice of relying on observations and experiment, especially in the natural sciences. Correlations indicate a trend, not a cause and effect (Fig. 3). These trends, such as occlusion, stress, palliative, and/or definitive treatment, are applied clinically. The documented results, in a sufficient sampling, permit a constant feedback mechanism which facilitates an on-going reevaluation of the original trend. This continual process of reevaluation is necessary to support the original trend, but does not prove it. Under the circumstances, it is the best available; however, it leads to controversy and confusion if the reporting of a trend is thought to be a proof, as if it were validated by the scientific method.
Disadvantages of empiricism There are several disadvantages with the empirical method as applied to TMJ dysfunction-pain syndrome. A differential diagnosis must be made before one of the trends (occlusion, stress, etc.) can be applied clinically (Fig. 4). This can produce errors in
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VARIABLE
C
VARIABLE
D’
VARIABLE
E,’
/
Fig. 2. Isolation of variables.
IEMPIR~cAL METHODI
does not prove causality.
mandibular disorders) because the human variables cannot be isolated. In addition, the multicausality of its etiology prevents individual study. Multicausality has been established by the clinical response to palliative therapy’.’ as well as occlusal adjustment.“.‘” The onset of craniomandibular pain can be triggered by sudden occlusal changes as well as acute stress situations. Most often, a combination of etiologic events produce the symptoms; however the etiologic profile will vary from patient to patient in that one patient might have a very strong stress factor while in the next, occlusion is the predominant cause.’ EMPIRICAL
OF VARIABLES
B
DOCUMENTED RESULTS Fig. 3. Empirical method; correlation nof cause and effect.
indicates a trend,
the experimentor’s diagnosis which would unknowingly negate the results. Thus, the documented results would be a false-negative due to the diagnostic error. Another problem is in the clinical application where there is a built-in variant in operator skill. This can also produce a false-negative response. During the reevaluation process, experimentor bias can unconsciously prejudice the results in either direction, depending on the preconceived opinion of the clinician. It is obvious that this procedure deviates from the scientific method which isolates one variable at a time. This stresses the need for continual documentation and reevaluation of those trends that have been reported. The process is long and repetitive but essential to progress.
AGE GROUP Patients were grouped into three age categories: 16 to 20 years of age (17%), 21 to 40 years of age (57%), and 41 to 71 years of age (26%).
Proportion
of women to men
The 90 clinic patients had a ratio of 8 women for every 1 man, possibly due to the limited hours the
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DISADVANTAGES OF EMj’@BCISM
Fig. 4. Disadvantages of empiricism; differential re&aluation of the Trend being tested.
diagnosis and experimentor
bias affects the
[0~sf3 0F fwj 3 WKS,- I YEAR-[37 Ii- - 2 YEARS
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-132
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INJURY--m DENTAL TR,+%j
v.4 ( 138 patients)
II 0 o/al
( 138 patients) Fig. 5. Dispersion of patients relative to symptom duration. clinic is open. However, in the private practice group of 48 patients, the ratio was 2.7:1. The latter is closer to the findings of Helkimo, et al” who reported that the incidence of women was only slightly greater than men and not as exaggerated as was previously reported.“. ‘Ii It is well known that women tend to seek medical intervention for symptoms more readily than men, which may account for the disproportion between the sexes.‘;’ Most dental practices contain more women than men; therefore, it is felt that the incidence of TMJ dysfunction-pain is not necessarily sex-related.
ONSET OF PAIN The patients seeking treatment had been suffering from craniomandibular pain for varying time intervals (Fig. 5). The dispersion indicates that most patients had long histories of chronic pain. Fifty four percent had been unsuccessfully treated with drugs;
Fig. 6. Trigger symptoms.
mechanisms
of TMJ dysfunction-pain
15% had occlusal adjustments; 21% had prostheses; and 3% had been given injections. Many had several treatment modalities.
Trigger mechanism A trigger factor initiates an over-response to an irritant by previously sensitized tissue but is not usually the primary “cause.“’ For instance, an injury can trigger an over-response due to a previously existing subclinical TMJ dysfunction. In that case, the tissue response to the injury, as well as the cause of the chronic subclinical TMJ dysfunction, should be treated.
Discussion Patients that sustained a joint injury (21%) usually had a long period of recuperation (6 months to over a year), regardless of the type of treatment. Twentyfour percent of the patients experienced discomfort 6 to 8 weeks after the insertion of an extensive restoration or after prosthetic dentistry. This confirms one
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TEMPORAl
TMJ [?%%I
pm
AUD, MEATUS(18%f MASSETE R I?!?=%1
NECK 133%-1 MED. PTERY, g?zq STERNO%- M,
07
(138 patients)
SHOULOER
Fig. 7. Incidence of subjective pain symptoms on the basis of location. Fig. 8. Incidence of unilateral and bilateral subjective pain symptoms.
trend observed, that occlusion plays a definite role in TMJ dysfunction-pain syndrome. Similarly, 26% of the patients reported the onset of symptoms after an acute stressful period. It would seem justified to conclude that sudden occlusal change as well as acute stress can act as triggers for craniomandibular pain. Thirty-six percent of the patients had no trigger factors, while 51% had identified a recent stress or occlusal change that initiated the acute response (Fig. 6). Two or more trigger factors were present in 13% of the patients. Summary In 51% of the patients, acute craniomandibular pain was initiated by sudden occlusal change and/or acute emotional stress. It should be remembered that a trigger factor is not the main etiologic agent but apparently serves as an initiating mechanism. This conclusion is supported by the fact that in most patients the original acute stress was terminated, but the TMJ dysfunction-pain remained in full force.
PAIN LOCATION The distribution of subjective pain location is shown in Fig. 7. The pain symptoms are wide spread throughout the head and neck, and indicate that only rarely is one limited area involved. It is also significant that the incidence of subjective pain in
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I
01AG~os~sj
1DIFFERENTIAL
I
PAI N
WORSE WITH ANY FUNCTION WORSE DURING MEALS WORSE AFTER
MEALS
WORSE AFTER
TALKING
HISTORY OF TRISMUS---------(5 PAIN ON OPENING
7% r39 % _
PATTERN
145 %
(A.M.,
0 F OCCURANCE Afternoon,
P.M.)
Fig. 9. Differential pain diagnosis; incidence of symptoms are related to function and pattern of occurrence. the TMJ itself was 76%, twice that of any other region (Fig. 7). Furthermore, the incidence of bilateral subjective pain was 49%, and unilateral pain was 42% (Fig. 8). The unusually high incidence of subjective pain in the TMJ region itself (76%) does not necessarily rule out MPD, because some of those symptoms could be referred. However, the incidence of bilateral pain in 49% of the patients automatically eliminates them from MPD, according to its definition originally described by Laskin.” The evaluation
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LACER
I30 “/ol HEAD NECK -139 %I SHOULDER---+%-] BACK ---+I 4’101
CLENCHING ----@@ii
Fig. 10. Incidence of life-style
AND
factors (clenching,
bruxism,
stress) and associated pain
areas.
!
(DENTAL ~~srofw~
ORTHODONTICS e i DENTAL SURGERY+=1 i RESTORATIONS~-[ml COMP. DENTURES-+x] PART, DENTURES Fig. 11. Dental TMJ symptoms.
history
directly
\q related to etiology
of TMJ pain will require clinical palpation occlusal and radiographic examination.
DIFFERENTIAL
of
and
DIAGNOSIS
A differential diagnosis is aided by a thorough qualitative pain profile which will help separate TMJ dysfunction-pain from neurologic and/or other causes. This process has been previously described;‘” therefore, only the symptoms related to function will be given here because it is pathognomonic of TMJ dysfunction-pain syndrome. Fig. 9 illustrates the incidence of functional symptoms: 67% of the patient sampling had an increase in pain with some type of function, such as when chewing (59%), after meals (33%), or after talking (26%). This means that more than two thirds of our sampling can be screened as probable TMJ dysfunction-pain patients on the basis of the pain history, even before the clinical and radiologic examination. The higher incidence of pain during meals, rather than afterward, might be caused by intrajoint involvement. Pain during chewing (59%), trismus (57%), and pain on opening (39%) complete the “triad” of symptoms that are pathognomonic for TMJ dysfunction-pain syndrome. Another helpful diagnostic sign is the pattern ofpain occurrence. For instance, if the pain seems
646
to occur in the morning, afternoon, or evening, it would tend to eliminate neurologic pain which usually happens suddenly, at random. The percentages of occurrence indicate that not all three dysfunction symptoms occur in every patient. However, when a patient exhibits all, or several, of the pathognomonic dysfunction symptoms (pain during chewing, trismus, pain on opening) as well as evidence of a pattern of occurrence, the prognosis for successful treatment is very good. The differential diagnosis is confirmed by clinical and radiologic supporting evidence. The latter two procedures also help establish treatment modalities.
EAR SYMPTOMS Forty-eight percent of the patients show evidence of some type of ear symptom (ringing, stuffiness, or dizziness). Although the mechanism has never been adequately explained, clinical experience has indicated that ear symptoms have been associated with posterior condylar displacement (as originally described by Costen)“’ and that anterior condylar repositioning,‘” rather than vertical opening, has been successful in eliminating or controlling symptoms. Stuffiness has been treated the most suceessfully in this manner; dizziness has been treated with more modest success; and attempts to treat ringing have produced poor results (including vertical dimension changes). It has been thought that posterior condylar displacement causes “soft tissue” impingement (rather than direct condylar impingement) on the anterior tympanic artery which arises from the internal maxillary artery and passes through the petrotympanic fissure (posterior wall of the temporomandibular fossa) to the interior of the tympanum. It anastomoses with the other tympanic arteries forming the posterior tympanic artery. It has not been established that “soft tissue” impingement on the blood supply and drainage of the middle ear,
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Fig. It. Incidence of pain from muscle and joint palpation. unilateral and bilateral pain. through the petrotympanic fissure, would be sufficient to cause symptoms because of the vascular supply through other routes such as the stylomastoid, the superficial petrosal, inferior tympanic, and the carotico-tympanic arteries and veins. However, anterior condylar repositioning with a removable prosthesis has been shown to eliminate or reproduce the symptoms by insertion or removal of the prosthesis.‘”
Joint noises On clinical examination joint “noises” were present in 68% of the patients. This finding was similar to that of a previous report in 1972.” Clicking was evidenced 55% of the time. Popping occurred in 23% of the patients. (Popping is considered a disk derangement, or a disarrangement of the disk and condylar assembly where there is no firm attachment of the disk to the medial and lateral poles of the condyle.) Crepitus was present in 18% of the patients, and many patients exhibited more than one sign of joint noise. Crepitus can be produced by (1) dry synovial cavities, (2) the perforation of a disk, and (3) localized osteoarthritis which roughens the bony surfaces. The arthritides that produce surface bony changes have also been associated with crepitus.
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Fig. 13. (Inset) Incidence of
LIFE STYLE FACTORS It has long been thought that many patients exhibit a TMJ dysfunction-pain profile’ that includes clenching and bruxism,‘7 stress,‘-’ and increased susceptibility to generalized muscle pain.” The data in Fig. 10 do not support this concept. It is noteworthy that the incidence of clenching was almost one and one-half times that of significant stress, as expressed by the patient. In a previous article, it was shown that stress is not a causeand-effect factor in TMJ dysfunction-pain syndrome. Rather, stress worked through the behavioral mechanism of clenching. ” This is not idle semantic debate; it vitally affects the treatment approach. Clenching can produce TM J symptoms in four ways, either separately or in combination, by: (1) muscle fatigue3’ which has been experimentally produced by Christensen;“’ (2) increased stimulation of the neuromuscular feed-back mechanism by the proprioceptors in the periodontal membrane, TMJ capsule,“’ and stretch receptors in the muscles (painspasm-pain cycle); (3) condylar displacement’, ‘L ” anteriorly,‘-*. I’ superiorly,“, ” and posteriorly;‘3. ” and (4) intrajoint inflammation (capsulitis) which can be caused by chronic condylar displacement (anteriorly OY posteriorly) and in turn produces irritation of the posterior auricular nerve branches in
WEINBERG
(OPENING1 16 mm. 20 - 26mm.qm
LATERAL
1 2%)
DEVIATION+?%]
ESALANCING CONTACT i-1 Fig. 14. Incidence of limitation of opening, lateral deviation, and balancing contact.
Fig. 15. Incidence of centric relation, deflective contact, and balancing contact.
the capsular ligament (posterior, medial, and lateral) causing pain and irritation of the branches of the masseteric and posterior deep temporal nerves (anterior portion of capsule) which can produce trismus3’. 33 The splinting action of muscles was first described by Hiltor?” in 1879.
Associated pain areas Approximately one third of the patients had subjective pain in the neck and shoulders which would tend to support the view of Krau?’ that muscles tend to go into spasm in groups and “chains” rather than individually. However, only 14% of the patients had back pain which does not seem to support the concept that TMJ dysfunctionpain patients have a greater susceptibility to generalized muscle spasm and pain.‘* (This was recorded on a subjective basis and not measured myographitally.) The significance of these findings is that there is valid reasonfor the patient to complain of pains in the head, in the neck and shoulders, and in widely dispersed areas (as well as bilaterally). This, when combined with the emotional stress from long-
AND
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standing chronic pain, often causes the patient to be erroneously labeled as “psychosomatic,” hypochondriacal, or passive-aggressive.
DENTAL
HISTORY
Thirty-three percent of the patients had a history of orthodontic treatment (Fig. 11). Dental surgery was a trigger factor in 9% of these patients. It was thought to be associated with exaggerated opening, muscle fatigue, or joint injury. Extensive dental restorations were trigger factors in 10% of the patients. Here the mechanism was thought to be a sudden change in occlusion, upsetting the neuromuscular mechanism and/or condylar displacement. Complete and removable partial dentures seem to function in a similar manner. The acute symptoms were usually initiated earlier with surgery, while occlusal changes were associated with a delayed onset of symptoms after approximately 6 to 8 weeks. In most patients, the iatrogenic trigger factors were superimposed on previously existing subclinical TMJ dysfunction or a predilection for craniomandibular disorders due to asymptomatic condylar displacement. In a previous report, 36% of an asymptomatic control group had posterior condylar displacement.‘6
MUSCLE PALPATION The incidence of palpable pain and its dtstribution is illustrated in Fig. 12. Palpation of the lateral and medial pterygoid muscles (posterior and superior to the buccal aspect of the tuberosity of the maxillae) showed the highest incidence of occurrence (64%). However, the insertion of the temporal muscle on the coronoid process (53%) and the masseter muscle (52%) were also frequently involved. The wide distribution of tenderness supports the views of KrauS:‘” that muscles tend to go into spasm in chains and groups. We should expect TMJ dysfunctionpain patients to elicit extensive pain patterns as an expression of the ‘syndrome” rather than a psychosomatic personality.
Joint pain and bilateral incidence Two of the criteria for MPD (as MPD is defined by Laskin”) are that the symptoms be unilateral and not include pain in the TMJ itself. Fifty-eight percent of the patients exhibited bilateral symptoms on palpation. Of those patients who had unilateral pain (31%), 9% of the patients had pain in the TMJ itself (Fig. 13). Combining the two groups of “non-MPLY’
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patients produces an incidence of 67% of the sampling (11% were non-TMJ patients). In other words, only 22% of the sampling fulfilled the criteria of MPD.
Nonpalpable pain group Eleven percent of the sampling had no palpable pain. After a complete examination, these patients’ pains were diagnosed as odontogenic, neurologic, atypical TMJ dysfunctional-pain, multiple-etiologic, and pain of unknown origin.
ICONDYLAR
POSITION]
CONCENTRIC -------[I I %I POSTERIOR DISPLACEMENT-j=] ANTERIOR DISPLACEMENT-+mJ REDUCED JOI NT SPACE ---j--?$%j [PATHOLOGY] PATHOLOGIC REMODELING --m OSTEOARTHRITIC CHANGES---j%\
OPENING Although 57% of the patients had a history of trismus at some time during their symptom period, this usually occurred in the early stages. Most of the chronic TMJ dysfunction-pain patients (74%) could open their mouths between 27 and 53 mm, indicating that the incidence of trismus was not as high as is commonly suspected (Fig. 14). Only 16% of the patients were limited in opening to less than 26 mm (Fig. 14). Seventeen percent of the patients exhibited lateral deviation on opening. Finally, there was a 36% incidence of nonworking (balancing) side interferences. We feel that the relatively low incidence of trismus, lateral jaw deviation, and nonworking (balancing) side interferences are all interrelated. This study tends to confirm the general view that when nonworking (balancing) side interferences are present they tend to exacerbate TMJ dysfunction-pain symptoms.“”
OCCLUSION The incidence of centric relation coinciding with centric occlusion was 31% (Fig. 15). This is much higher than the classically accepted 10% in symptom-free patients.36. 37
RADIOGRAPHIC FINDINGS All TMJ radiographs are made with the teeth closed in the maximum contact of centric occlusion (habitual centric occlusion). Diagnosis is made and treatment planned by observing the occlusion and evaluating it in relation to the condylar displacement as seen in the TMJ radiographs. However, condylar position in the fossae is also recorded and studied separately because it gives insight as to the physiologic state of the condylar suspension mechanism under muscle loading and frequent nonrest positioning during swallowing and/or clenching. Posterior condylar displacement had a higher inci-
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Fig. 16. Incidence of condylar position (with teeth in centric occlusion), and radiographic pathology.
dence (53%) than any other condylar position in this sampling (Fig. 16). Twenty-seven of the patients had anterior displacement, which was slightly higher than the sampling previously reported.‘” The current study supports the conclusion that no more than approximately one third of TMJ dysfunction-pain patients should have the classical occlusal adjustment (of deflective contacts) in the most retruded mandibular position of centric relation. Paradoxically, clinical experience has indicated that when the condyles are not displaced (the 11% concentrically located in the fossae) there seems to be a higher incidence of stress as a major cause of the symptoms (Fig. 16). It is thought that the neuromuscular imbalance and/or intracapsular inflammation associated with condylar displacement is not active; therefore, the source of discomfort is probably due to muscle spasm caused by stress-induced clenching and/or bruxism. These patients are usually more resistant to early successful treatment, but adjunctive psychologic counseling has been found to be helpful. Reduced joint space (9%) is a generalized description which should be differentiated from superior condylar displacement.“. I1 The latter is a specific pathologic entity that must meet certain clinical and radiographic diagnostic criteria: (1) reduced joint space radiographically when compared to the other side (usually not posteriorly displaced), (2) pain on the affected side, (3) clinical trial of inferior condylar repositioning, and (4) radiographic evidence of inferior condylar repositioning.” Patients requiring inferior condylar repositioning are less than 3%. Howev-
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.._-.
,..,..,-,.
CENTRIC RELATION DIA-
1
FUNCTIONAL CR 0 DYSFUNCTIONAL C.R7------2°/~~ ATYPICAL TM J NON-TMJ Fig. 17. Centric relation diagnosis.
I
IDESCRIPTIVE
D~AGNo~I~J
LOST VERT. DI MENSION.-m NEUROLOG I C OSTEOARTHRITIC PSYCHOLOGIC INCREASED VERT. DIMEN.DEVIATE SWALLOWE RpFig. 18. Descriptive logic factors.
I m [9%;1 a
diagnosis with miscellaneous
etio-
er, they do not respond well to other forms of treatment because the source of pain is pressure on the peripheral borders of the disk.
Clenching Fifty-four percent of the acute TMJ dysfunctionpain patients reported an awareness of clenching (Fig. lo), and a separate study of condylar position was recorded on those patients. It was found that the incidence of posterior condylar displacement in clenchers was the same as the other whole TMJ dysfunction-pain group itself. It has been clinically demonstrated that continual clenching can interfere with physiologic eruption or actually cause depression of the teeth in the sockets. The result is a loss of vertical dimension. However, there doesn’t seem to be an association of clenching with a higher incidence of posterior condylar displacement. Thus, this report sheds no light on the possible cause or causes of posterior condylar displacement.
Radiologic
pathology
Four percent of the TMJ radiographs examined showed evidence of pathologic remodeling (Fig. 16). Osteoarthritic lesions were observed in 9% of the patients. The incidence was higher (18%) in private practice where the TMJ radiographic technique can be more controlled and greater clarity and contrast are routine. It can be suggested that many osteoar-
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thritic lesions are overlooked on lateral transcranial TMJ radiographs because we “are not supposed to see them.” The erosions and radiolucent areas are not identified because of poor radiographs and/or a lack of confidence in the TMJ radiograph itself. This has come to light with serial TMJ radiographs over a period of years, so that a comparison can be made before the lesion becomes obvious.‘” Repeated radiographs produce the same pathologic radiolucency which eliminates “artifacts.” The outline of the fossa and condyle should be clean and obviously radioopaque, while broken outlines and marked changes in the degree of radioopacity as well as radiolucent mottled areas are evidences of osteoarthritic lesions. as they would be in any other bone.
DIAGNOSIS I
AND
OF CENTRIC
RELATION
The concept of functional or dysfunctional centric relation differentiates a healthy (or optimal) suspension mechanism of the condyle within the fossa from one that does not have the disk, ligaments, and muscles in physiologic balance. The clinical occlusal findings are related to the condylar positions in the TMJ radiographs to evaluate the suspension mechanism (centric relation).’ “-“‘. “‘. .I’ The optimum condylar position in the fossae (physiologic balance) has been established by comparing the clinical signs of function and dysfunction with the TMJ radiographs.‘“. ” This is the third such report, totaling 316 patients in all.‘“. ”
Functional
centric relation
The centric relation is functional in two clinical situations: (1) when there is no deflective contact in centric relation and the condyles are symmetrically placed in the middle of each fossa and (2) when a centric relation deflective contact is present and the “hit and slide” to the acquired centric occlusion can be correlated with the condylar displacement observed in the TMJ radiographs.“, ‘li A functional centric relation means that the suspension mechanism of the condyles in the fossae is essentially correct, and the classical (most retruded) mandibular position of centric relation is used for therapy.
Dysfunctional
centric relation
The centric relation can also be dysfunctional with or without a centric relation deflective contact.‘” When there is harmony between centric relation and centric occlusion and the condyles are not symmetritally placed in the middle of the fossae, the centric relation is classified as dysfunctional.” The condyies
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a~ orally displaced posteriorly and/or superiorly on one or both sides. Often a centric relation deflective contact and the “hit and slide” to the acquired centric occlusion cannot be correlated with the condylar displacement as observed on the TMJ radiographs. I’ In both cases, the centric relation is classified as dysfunctional, requiring different diagnostic and treatment methods.‘“-’ ‘. “j
At&xl
Some patients exhibit conflicting subjective and objective findings which prevents definitive diagnosis. An atypical TMJ patient does not have clear cut symptoms of any disorder, which requires special diagnostic procedures and clinical trials.“” Others have both TMJ and neurologic symptoms in clear cut fashion, which permits a differential diagnosis of both conditions superimposed on one another.
Sunimazy Only 25% of the patients had a functional centric relation requiring classical treatment based on the (most retruded) mandibular position of centric relation (Fig. 17):. ‘. ” Most patients (62%) were diagnosed as having a dysfunctional centric relation requiring anterior or inferior condylar repositioning techniques.‘“. 11.1?.I~ In other words, most TMJ dysfunction-pain patients had defective condylar suspension mechanisms which would involve the joints themselves, as well as muscles, in the dysfunction-pain. This is a departure from the belief that TtiJ pain is mostly muscular in origin.‘-“. “’ The treatment procedures are designed to correct both muscle andjoint dysfunction and will be evaluated in a subsequent clinical report. Some patients (6%) simply did not fit into any diagnostic category and were classified as “atypical.” Clinical trial procedures are helpful in screening these medical, dental, and psychosomatic patients.‘” True vertical dimension loss was found in only 1% of the patients (Fig. 18); yet, the most common prosthesis used in the treatment of TMJ dysfunctionpain increases the vertical dimension, as originally suggested in 1947 by Goodfriend”” and Block.“’ Various prostheses were reviewed in a previous and it was concluded that interferences in article,” the interocclusal space can aggravate the stretch reflex of muscles and actually increase muscle spasm. Paradoxically, clinical reaction to these prostheses can initially give a false-positive response because they interrupt the pain-spasm-pain cycle. Often, the pain returns worse than ever, and the patient is
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C.R = co.
(3174
Fig. 19. Incidence of condylar position with centric relation position identical to centric occlusion.
TM] cases
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uncomfortable either with or without the prosthesis. These patients usually alternate the use of the prosthesis, trying to find some relief, and eventually run from doctor to doctor. Neurologic patients can usually be differentiated with an accurate history and clinical examination procedures (the incidence in this sampling was 1%). Dilantin,* (100 mg, three times daily, for ‘2 to 3 weeks) is useful in differential diagnosis because it usually helps decrease neurologic pain but has no significant effect on TMJ pain. Osteoarthritic lesions were observed in 9% of the patients, although the incidence was higher in private practice. It is suggested that more attention should be paid to evaluating TMJ radiographs for early signs of osteoarthritic activity and to subsequent TMJ radiographs for a comparison of the effect of condylar displacement on pathologic joint remodeling.” One percent of the patients had primary psychiatric problems with TMJ symptoms in a secondary role. One complete denture patient had TMJ dysfunction-pain as a result of an exaggerated increase in the vertical dimension of occlusion which obliterated the interocclusal and speaking space. The dentures were remounted with a centric relation record, and the artificial teeth were adjusted to reestablish a more optimal (reduced) vertical dimension. The symptoms were reduced immediately. Deviate swallowing, and the resultant malocclusion, were evident in 3% of the patients. In this sampling of 138 TMj dysfunction-pain patients, the incidence of centric relation identical to centric occlusion was 31% or three times that found in normal patients (lo%).““. “’ The condylar position in the fossae was reported on only those patients who had a centric relation identical to centric occlusion (Fig. 19). The majority (60%) had posterior condylar displacement; 25% had anterior condylar displace*Dilantin,
Parke Davis and Co., Detroit, MI.
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merit; and 15% had displacement in the middle of the fossae. These findings are practically the same as the entire patient sampling. In other words, without referral to the TMJ radiographs, 60% of those patients who had identical centric relation and centric OCC~Usions would ordinarily be diagnosed as “normal,” by the classical definition; they would in fact be dysfunctional. Thus, research utilizing only the classical clinical dejnition of malocclusion (centric relation deflective slide to centric occlusion) would have a 60% false-negative immediately built into the data. The correlation between the occlusion and the TMJ radiographs, not clinical observations of the occlusion alone, establishes whether the condylar suspension mechanism (centric relation) is functional or dysfuncti0nal.H. 11.16.?J. .ISThese data suggest that the definition of “malocclusion” be modified to include its relation to the temporomandibular joints and that the occlusal relationship alone has no real significance.
SUMMARY
AND CONCLUSIONS
The clinical examination and diagnostic records of 138 clinic and private TMJ dysfunction-pain patients have been summarized. The scientific method cannot be applied to TMJ patients because of the impossibility of isolating variables and due to the multicausality of the syndrome. Therefore, empirical methods must be used which report on trends that show correlations, but do hot actually prove causality. These trends should be tested and retested to reevaluate the concepts being tried. Even so, empirical methods are subject to errors in differential diagnosis, operator technique, and experimentor bias. This report indicated that a trigger mechanism (such as injury, occlusal change, or stress) was present 51% of the time and that there were two or more of these in 13% of the patients. Subjective pain symptoms were distributed in widely dispersed regions of the head, neck, and shoulders bilaterally (49%) as well as unilaterally (42%). Differential diagnosis of TMJ dysfunction-pain syndrome can be facilitated by the pain history. The pathognomonic symptoms are pain with (any) function (67%), history of trismus (57%), pain on opening (39%), and a pattern of occurrence (45%). Usually there are ear symptoms (48%) and joint noises (68%) which accompany TMJ dysfunction. Many patients were aware of clenching (54%) and reported the onset of symptoms related to dental surgery (9%) and restorations (10%).
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Palpation of the patients indicated that 58% had bilateral pain; of the 31% that had unilateral symptoms, 9% had pain in the TMJ itself. This means that 67% of the sampling did nvl have MPD as described by Laskin.“’ Only 22% could be defined as MPD patients; the balance (11%) were classified as atypical, neurologic, combined, or having pain of unknown origin. Occlusal examination revealed that 31% had centric relation position identical to centric occlusion. However, correlation with the TMJ radiographs revealed that most (60%) of these patients had posterior condylar displacement. ‘This leads to the conclusion that the definition of “malocclusion” cannot be based on intraoral examination alone but should be correlated with TMJ radiographs. The patient sampling revealed that posterior condylar displacement had the highest incidence (53%:/c),with anterior displacement 27%, concentric placement 1570, and reduced joint spaces 9%. Posterior condylal displacement has been established as a major factor in TMJ dysfunction-pain syndrome in this report and previous reports as well.” Iii As a correlary. 52% of the condylar suspension mechanisms of the TMJ patients revealed a diagnosis of dysfunctional centric relation; whereas, only 34% had a functional centric relation where the disk, condyle, and muscles were in physiologic (optimum) balance. The diagnostic criteria for functional and dysfunctional centric relation were discussed. Treatment procedures and their evaluation will be given in a subsequent report. REFERENCES 1.
Weinberg, L. A.: Temporomandibular dysfunctional A patient-oriented approach. .J PROSTHET Dmw
profile: 32:312.
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Luptom, D.: Psychological aspects of temporomandibular joint dysfunction. J Am Denr Assoc 79:131, 1969. Moulton, R.: Psychiatric considerarion in maxiilofacial pain. J Am Dent Assoc 51:408, 1955. Evaskus, D., and Laskin, D.: A biochemical measureof stress in patients with myofascial pain-dysfunction syndrome J Dent Res 51:1464, 1972. Lefer, L.: A psychoanalytic view of a dental phenomenon. Contemp Psychoanal 2:135, 1966. Shore, N. A.: Occlusal Equilibration and Temporomandibuiar Joint Dysfunction. Philadelphia, 1959, J.B. Lippincorr co. Lindbloom, G.: Disorders of the temporomandibular joint: Causal factors and the value of temporomandibular radiographs in their diagnosis and therapy. .4cta Odontol Stand 11:61, 1953. Weinberg, L. A.: Temporomandibular joint function and its effect on centric relation. J PROSTHET DENT 30:176, 1973. Gelb, H.: An orthopedic approach to occlusal imbalance and T’MJ dysfunction. Dent Clin North Am 23:181, 1979.
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10. Gerber, V.: Kiefergelenk und zahnolljusion. Dtsch Zahnaerztl 2 26:119, 1971. 11. Weinberg, L. A.: Superior condylar displacement: Its diagnosis and treatment. J PROSTHETDENT 34:59, 1975. 12. Weinberg, L. A.: Anterior condylar displacement: Its diagnosis and treatment. J PROSTHETDENT 34:195, 1975. 13. Weinberg, L. A.: Posterior bilateral condylar displacement: Its diagnosis and treatment. J PROSTHET DENT 36:426, 1976. 14. Weinberg, L. A.: Posterior unilateral condylar displacement: Its diagnosis and treatment. J PROSTHET DENT 37:559,
27. 28. 29. 30.
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dys15. Weinberg, L. A.: Correlation of temporomandibular function with radiographic findings. J PROSTHET DENT 28:519, 1972. 16. Weinberg, L. A.: Role of condylar position in TMJ dysfunction-pain syndrome. J PROSTHET DENT 41:636, 1979. 17. Wilkes, C.: Structural and functional alterations of the temporomandibular joint. Northwest Dent 57:287, 1978. 18. Farrar, W., and McCarty, W.: Inferior joint space arthrography and characteristics of the condylar paths in internal derangements of the TMJ. J PROSTHETDENT 41:548, 1979. 19. Laskin, D.: Etiology of the pain-dysfunction syndrome. J Am Dent Assoc 79:147, 1969. 20. Agerberg, G., and Carlsson, G.: Functional disorders of the masticatory system. I: Distribution of symptoms according to age and sex as judged from investigation by questionnaire. Acta Odontol Stand 30:597, 1972. 21. Helkimo, M., Carlsson, B., Hedegiird, B., Helkimo, E., and L&n, T.: Function and dysfunction of the masticatory system in Lapps in Northern Finland. Svensk Tandlak T 65:95, 1972. 22. Lammie, G.: Dental Orthopaedics. Oxford, 1966, Alden Press. 23. Schwartz, L., and Cobin, H.: Symptoms associated with the temporomandibular joint. Oral Surg 10:339, 1957. 24. Bakal, D.: Headache: A biopsychological perspective. Psychol Bull 82:369, 1975. 25. Weinberg, L. A.: The etiology, diagnosis, and treatment of TMJ dysfunction-pain syndrome. J PROSTHET DENT 42:654, 1979; 43:58, and 43:186, 1980. 26. Costen, J. B.: Syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomandibular joint. Ann Otolaryngol 43:1, 1934.
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Ramfjord, S., and Ash, M.: Occlusion. Philadelphia, 1966, W. B. Saunders. Moller, E.: Elektromyografi. In Norkisk Klinisk Odontologi. Copenhagen, 1968, Forlaget for Faglitteratur. Weinberg, L. A.: An evaluation of stress in TMJ dysfunction-pain syndrome. J PROSTHETDENT 38:192, 1977. DiSalvo, N. A.: Neuromuscular mechanisms involved in mandibular movement and posture. Am J Orthod 47:330, 1961. Christensen, L. V.: Facial pain and internal pressure of masseter muscle in experimental bruxism in man. Arch Oral Biol 16:1021, 1971. Thilander, B.: Innervation of the temporomandibular joint capsule in man. Tran Roy Schools Stockholm Umea, No. 7, l-69, 1961. Ransjo, K., and Thilander, B.: Perception of mandibular position in cases of temporomandibular joint disorders. Odontol Foren Tidsskr 71:134, 1963. Hilton, J.: In Jacobson, W. H. A., editor: Rest and Pain, ed 2. New York, 1879, William Wood and Co., p 96. Kraus, H.: Principles and Practice of Therapeutic Exercises. Springfield, Ill., 1949, Charles C Thomas Publishing Co. Posselt, U.: Temporomandibular joint syndrome and occlusion: Research committee report-American Equilibration Society Compendium, 7:51, 1963-64. Beyron, H.: Optimal occlusion. Dent Clin North Am 13:537, 1969. Weinberg, L. A.: Temporomandibular joint function and its effect on concepts of occlusion. J PROSTHETDENT 35:553, 1976. Goodfriend, D. J.: Deafness, tinnitus, vertigo, and neuralgia. Arch Otolaryng 46:1, 1947. Block, L. S.: Diagnosis and treatment of disturbances of the temporomandibular joint, especially in relation to vertical dimension. J Am Dent Assoc 34:253, 1947. Weinberg, L. A.: Treatment prosthesis in TMJ dysfunctionpain syndrome. J PROSTHET DENT 39:654, 1978.
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