- Email: [email protected]
An aid to diagnosis of temporomandibular joint disorders
AN AID TO DIAGNOSIS TEMPOROMANDIBULAR
OF JOINT
DISORDERS
W. 0. RAMSEY, D.D.S.” Baltimore
College of Dental Surgery,
Maryland,
Baltimore,
D,ental School, University
of
Md.
vv
ALL FAMILIAR with the cardinal signs and symptoms of temporomandibular joint disorders : pain, limitation of movement, clicking or crepitus, and deviation of the mandibular midline, often accompanied by occlusal dysharmony. We are equally familiar with the uncertain prognosis attending treatment of these disorders. An area of confusion confronts us: it is the diagnosis of the problem. In no area of dentistry is it more necessary to be a close observer of patient behavior and function than in the diagnosis of temporomandibular joint problems, and in no area is it more necessary to establish a diagnosis which relates symptoms to etiology, if we are to prevent recurrence. Sarnatl classifies the origins of joint dysfunction as inflammatory, congenital, neoplastic, and traumatic-an academically accurate classification. Fortunately, most problems of the mandibular articulation are traumatic in nature and this discussion will be limited to this phase of the problem. However, we must always consider the possibility of inflammatory, congenital, and neoplastic processes producing pathosis within the joint structures; and we must be aware of the high incidence of what might be termed pseudotemporomandibular problems, problems which often produce signs and symptoms mimicking those of joint disorders. Such factors include dental and aural infections, postoperative trismus, trismus resulting from faulty or nonsterile injections, interference with the coronoid process by erupting maxillary third molars, edema of the infratemporal fossa, pathosis of major salivary glands, mandibular fractures, neoplasms occurring outside of the articular structures, partial ankylosis of the mandibular condyles, pain referred front the cervical musculature,3 and the bizarre results of hysteria, Clinical experience indicates that the majority of temporomandibular joint disorders follow a well-defined sequence : repeated or prolonged strained positioning of the mandible, muscle hyperactivity leading to muscle spasm or trismus, compression or tension of joint structures, and ultimately, degenerative changes in joint tissues. Diagnosis of temporomandibular joint disorders may be simplified if we consider the muscles of mastication as postural muscles directing mandibular placeE ARE
Presented before the American Academy of Crown and Bridge Prosthodontics *Professor, Department of Complete Denture Prosthodontics. 152
in Chicago.
“Nzx:‘I4
TEMPOROMANDIBULAR
JOINT
DISORDERS
153
ment in a highly coordinated, proprioceptively controlled, reflex manner. Any mandibular position which jeopardizes the precise coordination and synergistic action of this muscular system imposes trauma upon one or more of its components. If a strained mandibular position is maintained for prolonged periods of time, or is forcefully repeated over a period of time, the muscles responsible for maintaining the abnormal posture or those whose normal contractile pattern is forcefully and repeatedly interrupted may become hyperactive and develop localized areas of spasm which may progress to fibrosis and contracture. The initial signs and symptoms of temporomandibular joint dysfunction can be attributed to such pathologic conditions of these muscles. Superimposed upon these signs and symptoms may be the secondary signs and symptoms of intracapsular damage (osteoarthritis) produced by chronic tension or compression of joint structures by spastic muscles. Strained mandibular positioning and the accompanying hyperactivity of the muscles of mastication may be initiated at three commonly recognized levels of mandibular closure : (1) the open mouth, subocclusal or infraocclusal level, (2) the normal occlusal level or occlusal position, and (3) the overclosed or supraocclusal level.4 Let us examine the common clinical situations predisposing to muscle spasm at these various levels, relate these situations to the muscles involved, and point out the sequence of pathosis which may result. DISORDERS
ARISING
AT
INFRAOCCLUSAL
LEVELS
We include in this category the chronic subluxations or problems of condylar hypermobility. This type of disorder is most frequently the result of gross trauma with distention and tearing of the capsular and temporomandibular ligaments. Frequently, however, such an injury serves as a precursor to those disorders which evidence painful limitation of mandibular movement. Extensive anterior hypermobility of one or both condyles requires a greater than normal degree of contraction of the external pterygoid muscles. Such activity, if consistently repeated, constitutes hyperactivity of these muscles. When muscle fibers and bundles, which normally alternate periods of work with periods of rest, are either continually stimulated or over-contracted, muscle spasm ensues. The external pterygoid muscle presents a dual insertion, the superior fibers inserting into the articular disc by way of the capsular ligament, the inferior fibers inserting into the neck of the condyle. The dual action of this muscle consists of protraction of the mandible and stabilization of the condyle and disc against the articular eminence in open mouth positions. As Sicherj points out, although the articular disc is pulled forward by muscle action, it has no retractive muscle and must depend upon ligamentous attachments to the poles of the condyle to maintain its cap-like relationship to the condyle during translation from protrusive to centric relationship. If the external pterygoid muscle develops spasm or trismus, the condyle-disc relationship is jeopardized. As the elevator muscles of the mandible (the masseter, the temporal, and the internal pterygoitl) retune the mandible to occlusal position under consicleral~le force, the disc may 11ehrltt
154
RAMSEY
J. Pros. lhl. Jan:Feb., 19h.i
in a protruded position by the spastic superior head of the external pterygoid muscle. At the same time, the inferior head of the external pterygoid muscle yields to the overpowering force of the elevators and the condyle is displaced distally as the disc is held in an anterior position. Stretching and tearing of the disccondyle attachment occurs and, as a result, these two structures may fail to translate simultaneously. A popping or clicking sound is then produced during mandibular movement whenever we have a separation or readaptation of condyle to disc. If complete separation of the condyle and disc occurs, there is usually a pause during the opening or closing stroke of the mandible as the patient readapts the disc to the condyle by shifting the mandible to one side before he can continue its path of movement. If the disc-condyle relationship is disrupted while the condyle is firmly engaged against the articular eminence, the thickened, enervated posterior border of the disc is impinged between the condyle and articular eminence. Pain results from this impingement as well as from any accompanying muscle spasm. Normally, we do not find complete separation of the disc from the condyle. Clicking of the joint still occurs as a result of partial disc detachment, and pain is a reflection of impingement of the posterior border of the disc. We may find the same sequence of events occurring in the absence of capsular looseness and condylar hypermobility. Habitual, eccentric positioning of the mandible below the occlusal position often occurs in patients presenting a Class II malocclusion. These patients may develop a compensatory protrusion for esthetic effect, thus subjecting the protractors (the external pterygoid) to periods of sustained contraction and spasm. Partial detachment of the articular disc may occur. Impingement of the periphery of the disc occurs, and is intensified by spasm induced in the elevator muscles due to their continued contraction in maintaining the horizontal protrusive Dosition of the mandible. A similar sequence may result from postural habits such as smoking, pencil chewing, chin-in-hand study or reading positions, or sleeping habits. JVe may find an entirely different traumatic mechanism developed at infraocclusal levels in those patients presenting a Class II jaw relationship in which molars and bicuspids have attained a normal degree of eruption, but in which the incisors have over-erupted. In the presence of a deep vertical overlap with a small horizontal overlap and normal 2 to 3 mm. interocclusal distance, these patients may encounter incisal interference during speech. In an effort to prevent incisal contacts, these patients may actively retrude the mandible while speaking. This sustained effort produces spasm in the muscles controlling mandibular retrusion, notably in the deep portion of the masseter, secondarily in the posterior fibers of the temporal, and occasionally in the digastric muscles. Treatment of disorders of the temporomandibular articulation which originate at infraocclusal levels consists essentially of relief of muscle spasm, correction of the habit or incisor over-eruption which produced and perpetuated the problem, and supportive therapy (such as intracapsular injection of hytlrocortisone) for the injured articular structures. ‘L’oluntary limitation (not splinting) of the extent nf mandibular movenWnt is a necessary adjunct to sliccessfnl treatment.
\~dullle Numl,er
11 1
DISORDliKS
TEMPOROJIANDIBULAR
ARISING
AT
OCCLUSAL
JOINT
DISORDERS
1.55
LEVELS
The fact that virtually all disorders of the temporomandibular joint evidence some occlusal dysharmony has resulted in an overemphasis of occlusal relations as a diagnostic aid and occlusal equilibration as a means of treatment. It must be remembered that during normal closure of the mandible, the musculature directs the teeth toward the intended occlusal position of centric relation, while tooth inclines dictate the actual jaw relation at the occlusal position. Jaw relations at the occlusal position and at centric relation (at the occlusal level) should be synonymous and harmonious. Two factors may disrupt this harmony: (1) a deflective occlusal contact which shifts the mandible into an eccentric relation after initial tooth contact (a tooth-dictated malposition), and (2) a spastic muscle which deflects the mandible during opening and closing movements below the level of tooth contact (a muscle-dictated malposition) . In the first instance, the musculature may adapt by reflexly changing its direction of action to avoid the prematurity (interceptive occlusal contact) or its contraction may be forcefully interrupted by the deflective contact during the power stroke of closure. Either situation is conducive of muscle spasm. In the second instance, a spastic muscle may guide the mandible into an eccentric occlusal position. Normal intercuspation of teeth is disrupted, simulating the appearance of premature and deflective contacts. Moreover, tooth movement may occur over a period of time permitting an intercuspation of cusps in the acquired position dictated by the muscles. Diagnosis and treatment planning must take into account the fact that the occlusal relationship of the teeth may be either a CUUS~of muscle spasm or the resz& of muscle spasm. We must, therefore, first direct our attention to providing relief of all muscle spasm so that the mandible can be returned to a normal centric relation at the point of initial tooth contact. Secondly, we must recognize and correct the etiologic factors producing and perpetuating the spasm. At this point, occlusal equilibration may be required to restore harmony of the occlusal position with centric relation. Three spasm-producing entities may be identified at the occlusal level: (1) deflective occlusal contacts, (2) bruxism and tooth clenching, and (3) the Class II jaw relation evidencing under-eruption of the molar and bicuspid teeth. DEFLECTIVE
OCCLUSAL
CONTACTS
Interruption to the forceful closure of the jaws by a deflective occlusal contact results in an eccentric positioning of the mandible. The muscle so interrupted may respond by recruiting additional muscle fibers and bundles in an effort to overcome the resistance, or it may adapt by reflexly altering its contractile pattern in an effort to avoid the interference. 6,7 In the first instance, repetition of traumatic contact produces a recruitment of muscle fibers and summation resulting in spasm of the masseter and internal pterygoid muscles. In the second instance, the avoidance pattern repeatedly calls upon specific portions of the muscle which soon develop fatigue and spasm. The elevator muscles are those primarily concerned in this sequence, with the deep, retractive elements of the masseter and the temporal muscles most frequently being involved in reflex avoidance patterns.
156
RAMSEY
.r. I’ros. Den. .l;111.-I’d,., 19hl
Deflective contacts producing a symmetrical anterior displacement of the mandible seem to be reasonably well tolerated without producing symptoms of joint disorder. Such displacement permits the patient to masticate in an acquired protrusive relationship, but with a diminished muscular effort. When the deflective occlusal contact, which frequently is found on the balancing cusps, produces a posterolateral mandibular displacement on one side with a rotation or anteromedial displacement of the condyle on the opposite side, the reaction is pronounced. The posteriorly or laterally displaced condyle becomes the focus of severe discomfort. Four potentials exist for pathosis. (1) The areas of hyperactivity produce summation and spasm in the elevator muscles. (2) Posterior displacement of the condyle subjects the external pterygoid muscle to a slight stretch; the stretch reflex is excited and the muscle attempts to contract in opposition to the closing force of the elevators. Such repeatedly opposed contraction results in spasm of thg external pterygoid muscle producing (3) an anterior displacement of the articular disc. Because the mandible is under the forceful closing pressure of the elevators, such anterior disc displacement produces painfully destructive force upon the thickened, enervated posterior portion of the disc. (4) An ‘exaggerated bodily lateral or posterior shift (Bennett movement) of the mandible stretches or tears the temporomandibular ligament. BRUXISM
AND
CLENCHING
During habitual tooth clenching, sustained contraction of the elevator muscles of the mandible results in a gradual involvement of large bundles of these muscles in spasm. When the sustained contraction of the elevators is combined with the repeated alternate contraction of right and left external pterygoid muscles, bruxism results. Muscular hyperactivity induced by bruxism produces an exaggerated picture of the sequence resulting from compensatory protrusion at subocclusal levels: spasm of the elevators and protractors, anterior disc displacement, and disc impingement. Prolonged bruxism results in the further complication of occlusal wear rapidly exceeding physiologic tooth eruption, mandibular overclosure, and a superior displacement of the condyles. This latter factor accentuates the degree of disc displacement and impingement. Successful resolution of these problems depends upon correction of the emotional and physical problems producing this form of aggressive oral behavior, relief of muscle spasm, and restoration of an adequate vertical facial dimension. An acceptable interocclusal distance must be provided. CLASS
II JAW
RELATION
WITH
MOLAR
UNDER-ERUPTION
Patients possessing a Class II jaw relation with under-erupted molars may present the same final picture of pathosis as described for bruxism with excessive occlusal wear. Only the mechanism developing this pathosis differs. These patients usually present a large interocclusal distance, and firm closure into centric occlusion calls for overcontraction of the elevator muscles which, if persistent, constitutes hyperactivity. At the same time, the condyles are placed deep into the
Volume Number
14 1
TEMPOROMANDIBULAR
JOINT
DISORDERS
1.57
glenoid fossae, producing a stretching of the external pterygoid muscles with attempted, but opposed, contraction of these muscles. Spasm of the elevators and protractors ensues. Many patients compensate for this developmental defect and avoid temporomandibular joint injury by effective use of the tongue against the palate as a masticating mechanism and by regulating the degree of jaw closure during swallowing by inserting the tongue between the incisors. Such compensation, however, produces an expanded maxillary arch, separation of the incisors, and condensation of the mandibular arch. Treatment of the Class II jaw relation with molar under-eruption usually permits reduction of the interocclusal distance by splints or occlusal onlays. The use of onlays or splints under other circumstances (except in cases of excessive physiologic wear unaccompanied by physiologic eruption) invariably results in a depression of the posterior teeth. In some instances, this type of Class II jaw relation and its associated temporotnandibular joint problem may be treated by the use of a palatal guide plane opposing the mandibular incisors. It is hoped that the rate of eruption of the posterior teeth will exceed the rate of intrusion of the tnandibular incisors. DISORDERS
ARISING
AT
SUPRAOCCLUSAL
LEVELS
Repeated positioning of the mandible at overclosed levels appears to present the same basic mechanisms as the overclosure of severe bruxism and probletns of molar under-eruption, i.e., posterior or superior displacement of the condyles. Most cases of overclosure encountered in clinical practice are represented by totally or posteriorly edentulous mouths. However, these patients rarely present temporotnandibular joint dysfunction unless such disturbances originated prior to the loss of posterior teeth. The totally edentulous patient and the patient wearing complete dentures with an excessive interocclusal distance compensate for overclosure by protrusion of the mandible, greatly decreased muscular force during mastication, and effective use of the tongue during mastication and swallowing. The patient retaining six lower incisors in function against a natural or artificial maxillary dentition is likewise protected from temporomandibular joint disorders by virtue of the reduced force employed in incisal mastication. The condyles, in this instance, perform their normal bracing action against the articular eminences. (Deflective occlusal contacts are rarely productive of joint injury in complete denture wearers. Denture displacement occurs rather than condyle displacement.) The patient who is unilaterally edentulous is the most susceptible to traumatic overclosure. The unilateral loss of posterior teeth permits the elevator muscles on the side of the intact dentition to function at their normal length while the elevators on the edentulous side may overcontract and develop trismus. Such spasm results in the condyle on the edentulous side being drawn into firm apposition with the articular disc and articular eminence in a superior and anterior direction. Compression of the disc results. If the remaining natural teeth occlude in such a manner as to produce a posterior, superior displacement of the condyle on the edentulous side, the sequalae of disc displacement follow.
158
RAMSEY
J. Pros. Jax-Feb.,
Den. 1964
SUMMARY
Commonly encountered disorders of the temporomandibular joint have been considered as postural problems resulting from chronic or forceful eccentric positioning of the mandible. Muscular hyperactivity produced by such eccentric positioning results in muscle spasm with attendant compression or tension of articular and periarticular structures. The level of mandibular closure at which eccentric positioning originates is suggested as a supplementary aid to routine diagnostic procedures. Such an approach facilitates the removal of cause as well as symptoms of temporomandibular joint disorders. REFERENCES
1. Sarnat, B. G., Editor: The Temporomandibular Joint, Springfield, Ill., 1951, Charles C Thomas, Publisher. 2. Vaughan, H. C.: External Facial Symptoms Resulting From Indirect Trauma In and About the Infratemporal Fossa, J. PROS. DEN. 12:486-492,1962. 3. Travell, J.: Temporomandibular Joint Pain Referred From Muscles of the Head and Neck, J. PROS. DEN. 10:745-763,196O. 4. Ramsey, W. 0.: Disorders of the Mandibular Articulation, J. Maryland D.A. 2:9-14, 1959. 5. Sicher, H.: Oral Anatomy, St. Louis, 1949, The C. V. Mosby Company,.p. 477. 6. Perry, H. T., Jr.: Muscular Changes Associated With Temporomandtbular Joint Dysfunction, J.A.D.A. 54:644-653, 1957. 7. Sarnat, B. G., Editor: The Temporomandibular Joint, Springfield, Ill., 1951, Charles C Thomas, Publisher, p. 80. 618 W.
LOMBARD ST. 1, MD. BALTIMORE
OF JOINT
DISORDERS
W. 0. RAMSEY, D.D.S.” Baltimore
College of Dental Surgery,
Maryland,
Baltimore,
D,ental School, University
of
Md.
vv
ALL FAMILIAR with the cardinal signs and symptoms of temporomandibular joint disorders : pain, limitation of movement, clicking or crepitus, and deviation of the mandibular midline, often accompanied by occlusal dysharmony. We are equally familiar with the uncertain prognosis attending treatment of these disorders. An area of confusion confronts us: it is the diagnosis of the problem. In no area of dentistry is it more necessary to be a close observer of patient behavior and function than in the diagnosis of temporomandibular joint problems, and in no area is it more necessary to establish a diagnosis which relates symptoms to etiology, if we are to prevent recurrence. Sarnatl classifies the origins of joint dysfunction as inflammatory, congenital, neoplastic, and traumatic-an academically accurate classification. Fortunately, most problems of the mandibular articulation are traumatic in nature and this discussion will be limited to this phase of the problem. However, we must always consider the possibility of inflammatory, congenital, and neoplastic processes producing pathosis within the joint structures; and we must be aware of the high incidence of what might be termed pseudotemporomandibular problems, problems which often produce signs and symptoms mimicking those of joint disorders. Such factors include dental and aural infections, postoperative trismus, trismus resulting from faulty or nonsterile injections, interference with the coronoid process by erupting maxillary third molars, edema of the infratemporal fossa, pathosis of major salivary glands, mandibular fractures, neoplasms occurring outside of the articular structures, partial ankylosis of the mandibular condyles, pain referred front the cervical musculature,3 and the bizarre results of hysteria, Clinical experience indicates that the majority of temporomandibular joint disorders follow a well-defined sequence : repeated or prolonged strained positioning of the mandible, muscle hyperactivity leading to muscle spasm or trismus, compression or tension of joint structures, and ultimately, degenerative changes in joint tissues. Diagnosis of temporomandibular joint disorders may be simplified if we consider the muscles of mastication as postural muscles directing mandibular placeE ARE
Presented before the American Academy of Crown and Bridge Prosthodontics *Professor, Department of Complete Denture Prosthodontics. 152
in Chicago.
“Nzx:‘I4
TEMPOROMANDIBULAR
JOINT
DISORDERS
153
ment in a highly coordinated, proprioceptively controlled, reflex manner. Any mandibular position which jeopardizes the precise coordination and synergistic action of this muscular system imposes trauma upon one or more of its components. If a strained mandibular position is maintained for prolonged periods of time, or is forcefully repeated over a period of time, the muscles responsible for maintaining the abnormal posture or those whose normal contractile pattern is forcefully and repeatedly interrupted may become hyperactive and develop localized areas of spasm which may progress to fibrosis and contracture. The initial signs and symptoms of temporomandibular joint dysfunction can be attributed to such pathologic conditions of these muscles. Superimposed upon these signs and symptoms may be the secondary signs and symptoms of intracapsular damage (osteoarthritis) produced by chronic tension or compression of joint structures by spastic muscles. Strained mandibular positioning and the accompanying hyperactivity of the muscles of mastication may be initiated at three commonly recognized levels of mandibular closure : (1) the open mouth, subocclusal or infraocclusal level, (2) the normal occlusal level or occlusal position, and (3) the overclosed or supraocclusal level.4 Let us examine the common clinical situations predisposing to muscle spasm at these various levels, relate these situations to the muscles involved, and point out the sequence of pathosis which may result. DISORDERS
ARISING
AT
INFRAOCCLUSAL
LEVELS
We include in this category the chronic subluxations or problems of condylar hypermobility. This type of disorder is most frequently the result of gross trauma with distention and tearing of the capsular and temporomandibular ligaments. Frequently, however, such an injury serves as a precursor to those disorders which evidence painful limitation of mandibular movement. Extensive anterior hypermobility of one or both condyles requires a greater than normal degree of contraction of the external pterygoid muscles. Such activity, if consistently repeated, constitutes hyperactivity of these muscles. When muscle fibers and bundles, which normally alternate periods of work with periods of rest, are either continually stimulated or over-contracted, muscle spasm ensues. The external pterygoid muscle presents a dual insertion, the superior fibers inserting into the articular disc by way of the capsular ligament, the inferior fibers inserting into the neck of the condyle. The dual action of this muscle consists of protraction of the mandible and stabilization of the condyle and disc against the articular eminence in open mouth positions. As Sicherj points out, although the articular disc is pulled forward by muscle action, it has no retractive muscle and must depend upon ligamentous attachments to the poles of the condyle to maintain its cap-like relationship to the condyle during translation from protrusive to centric relationship. If the external pterygoid muscle develops spasm or trismus, the condyle-disc relationship is jeopardized. As the elevator muscles of the mandible (the masseter, the temporal, and the internal pterygoitl) retune the mandible to occlusal position under consicleral~le force, the disc may 11ehrltt
154
RAMSEY
J. Pros. lhl. Jan:Feb., 19h.i
in a protruded position by the spastic superior head of the external pterygoid muscle. At the same time, the inferior head of the external pterygoid muscle yields to the overpowering force of the elevators and the condyle is displaced distally as the disc is held in an anterior position. Stretching and tearing of the disccondyle attachment occurs and, as a result, these two structures may fail to translate simultaneously. A popping or clicking sound is then produced during mandibular movement whenever we have a separation or readaptation of condyle to disc. If complete separation of the condyle and disc occurs, there is usually a pause during the opening or closing stroke of the mandible as the patient readapts the disc to the condyle by shifting the mandible to one side before he can continue its path of movement. If the disc-condyle relationship is disrupted while the condyle is firmly engaged against the articular eminence, the thickened, enervated posterior border of the disc is impinged between the condyle and articular eminence. Pain results from this impingement as well as from any accompanying muscle spasm. Normally, we do not find complete separation of the disc from the condyle. Clicking of the joint still occurs as a result of partial disc detachment, and pain is a reflection of impingement of the posterior border of the disc. We may find the same sequence of events occurring in the absence of capsular looseness and condylar hypermobility. Habitual, eccentric positioning of the mandible below the occlusal position often occurs in patients presenting a Class II malocclusion. These patients may develop a compensatory protrusion for esthetic effect, thus subjecting the protractors (the external pterygoid) to periods of sustained contraction and spasm. Partial detachment of the articular disc may occur. Impingement of the periphery of the disc occurs, and is intensified by spasm induced in the elevator muscles due to their continued contraction in maintaining the horizontal protrusive Dosition of the mandible. A similar sequence may result from postural habits such as smoking, pencil chewing, chin-in-hand study or reading positions, or sleeping habits. JVe may find an entirely different traumatic mechanism developed at infraocclusal levels in those patients presenting a Class II jaw relationship in which molars and bicuspids have attained a normal degree of eruption, but in which the incisors have over-erupted. In the presence of a deep vertical overlap with a small horizontal overlap and normal 2 to 3 mm. interocclusal distance, these patients may encounter incisal interference during speech. In an effort to prevent incisal contacts, these patients may actively retrude the mandible while speaking. This sustained effort produces spasm in the muscles controlling mandibular retrusion, notably in the deep portion of the masseter, secondarily in the posterior fibers of the temporal, and occasionally in the digastric muscles. Treatment of disorders of the temporomandibular articulation which originate at infraocclusal levels consists essentially of relief of muscle spasm, correction of the habit or incisor over-eruption which produced and perpetuated the problem, and supportive therapy (such as intracapsular injection of hytlrocortisone) for the injured articular structures. ‘L’oluntary limitation (not splinting) of the extent nf mandibular movenWnt is a necessary adjunct to sliccessfnl treatment.
\~dullle Numl,er
11 1
DISORDliKS
TEMPOROJIANDIBULAR
ARISING
AT
OCCLUSAL
JOINT
DISORDERS
1.55
LEVELS
The fact that virtually all disorders of the temporomandibular joint evidence some occlusal dysharmony has resulted in an overemphasis of occlusal relations as a diagnostic aid and occlusal equilibration as a means of treatment. It must be remembered that during normal closure of the mandible, the musculature directs the teeth toward the intended occlusal position of centric relation, while tooth inclines dictate the actual jaw relation at the occlusal position. Jaw relations at the occlusal position and at centric relation (at the occlusal level) should be synonymous and harmonious. Two factors may disrupt this harmony: (1) a deflective occlusal contact which shifts the mandible into an eccentric relation after initial tooth contact (a tooth-dictated malposition), and (2) a spastic muscle which deflects the mandible during opening and closing movements below the level of tooth contact (a muscle-dictated malposition) . In the first instance, the musculature may adapt by reflexly changing its direction of action to avoid the prematurity (interceptive occlusal contact) or its contraction may be forcefully interrupted by the deflective contact during the power stroke of closure. Either situation is conducive of muscle spasm. In the second instance, a spastic muscle may guide the mandible into an eccentric occlusal position. Normal intercuspation of teeth is disrupted, simulating the appearance of premature and deflective contacts. Moreover, tooth movement may occur over a period of time permitting an intercuspation of cusps in the acquired position dictated by the muscles. Diagnosis and treatment planning must take into account the fact that the occlusal relationship of the teeth may be either a CUUS~of muscle spasm or the resz& of muscle spasm. We must, therefore, first direct our attention to providing relief of all muscle spasm so that the mandible can be returned to a normal centric relation at the point of initial tooth contact. Secondly, we must recognize and correct the etiologic factors producing and perpetuating the spasm. At this point, occlusal equilibration may be required to restore harmony of the occlusal position with centric relation. Three spasm-producing entities may be identified at the occlusal level: (1) deflective occlusal contacts, (2) bruxism and tooth clenching, and (3) the Class II jaw relation evidencing under-eruption of the molar and bicuspid teeth. DEFLECTIVE
OCCLUSAL
CONTACTS
Interruption to the forceful closure of the jaws by a deflective occlusal contact results in an eccentric positioning of the mandible. The muscle so interrupted may respond by recruiting additional muscle fibers and bundles in an effort to overcome the resistance, or it may adapt by reflexly altering its contractile pattern in an effort to avoid the interference. 6,7 In the first instance, repetition of traumatic contact produces a recruitment of muscle fibers and summation resulting in spasm of the masseter and internal pterygoid muscles. In the second instance, the avoidance pattern repeatedly calls upon specific portions of the muscle which soon develop fatigue and spasm. The elevator muscles are those primarily concerned in this sequence, with the deep, retractive elements of the masseter and the temporal muscles most frequently being involved in reflex avoidance patterns.
156
RAMSEY
.r. I’ros. Den. .l;111.-I’d,., 19hl
Deflective contacts producing a symmetrical anterior displacement of the mandible seem to be reasonably well tolerated without producing symptoms of joint disorder. Such displacement permits the patient to masticate in an acquired protrusive relationship, but with a diminished muscular effort. When the deflective occlusal contact, which frequently is found on the balancing cusps, produces a posterolateral mandibular displacement on one side with a rotation or anteromedial displacement of the condyle on the opposite side, the reaction is pronounced. The posteriorly or laterally displaced condyle becomes the focus of severe discomfort. Four potentials exist for pathosis. (1) The areas of hyperactivity produce summation and spasm in the elevator muscles. (2) Posterior displacement of the condyle subjects the external pterygoid muscle to a slight stretch; the stretch reflex is excited and the muscle attempts to contract in opposition to the closing force of the elevators. Such repeatedly opposed contraction results in spasm of thg external pterygoid muscle producing (3) an anterior displacement of the articular disc. Because the mandible is under the forceful closing pressure of the elevators, such anterior disc displacement produces painfully destructive force upon the thickened, enervated posterior portion of the disc. (4) An ‘exaggerated bodily lateral or posterior shift (Bennett movement) of the mandible stretches or tears the temporomandibular ligament. BRUXISM
AND
CLENCHING
During habitual tooth clenching, sustained contraction of the elevator muscles of the mandible results in a gradual involvement of large bundles of these muscles in spasm. When the sustained contraction of the elevators is combined with the repeated alternate contraction of right and left external pterygoid muscles, bruxism results. Muscular hyperactivity induced by bruxism produces an exaggerated picture of the sequence resulting from compensatory protrusion at subocclusal levels: spasm of the elevators and protractors, anterior disc displacement, and disc impingement. Prolonged bruxism results in the further complication of occlusal wear rapidly exceeding physiologic tooth eruption, mandibular overclosure, and a superior displacement of the condyles. This latter factor accentuates the degree of disc displacement and impingement. Successful resolution of these problems depends upon correction of the emotional and physical problems producing this form of aggressive oral behavior, relief of muscle spasm, and restoration of an adequate vertical facial dimension. An acceptable interocclusal distance must be provided. CLASS
II JAW
RELATION
WITH
MOLAR
UNDER-ERUPTION
Patients possessing a Class II jaw relation with under-erupted molars may present the same final picture of pathosis as described for bruxism with excessive occlusal wear. Only the mechanism developing this pathosis differs. These patients usually present a large interocclusal distance, and firm closure into centric occlusion calls for overcontraction of the elevator muscles which, if persistent, constitutes hyperactivity. At the same time, the condyles are placed deep into the
Volume Number
14 1
TEMPOROMANDIBULAR
JOINT
DISORDERS
1.57
glenoid fossae, producing a stretching of the external pterygoid muscles with attempted, but opposed, contraction of these muscles. Spasm of the elevators and protractors ensues. Many patients compensate for this developmental defect and avoid temporomandibular joint injury by effective use of the tongue against the palate as a masticating mechanism and by regulating the degree of jaw closure during swallowing by inserting the tongue between the incisors. Such compensation, however, produces an expanded maxillary arch, separation of the incisors, and condensation of the mandibular arch. Treatment of the Class II jaw relation with molar under-eruption usually permits reduction of the interocclusal distance by splints or occlusal onlays. The use of onlays or splints under other circumstances (except in cases of excessive physiologic wear unaccompanied by physiologic eruption) invariably results in a depression of the posterior teeth. In some instances, this type of Class II jaw relation and its associated temporotnandibular joint problem may be treated by the use of a palatal guide plane opposing the mandibular incisors. It is hoped that the rate of eruption of the posterior teeth will exceed the rate of intrusion of the tnandibular incisors. DISORDERS
ARISING
AT
SUPRAOCCLUSAL
LEVELS
Repeated positioning of the mandible at overclosed levels appears to present the same basic mechanisms as the overclosure of severe bruxism and probletns of molar under-eruption, i.e., posterior or superior displacement of the condyles. Most cases of overclosure encountered in clinical practice are represented by totally or posteriorly edentulous mouths. However, these patients rarely present temporotnandibular joint dysfunction unless such disturbances originated prior to the loss of posterior teeth. The totally edentulous patient and the patient wearing complete dentures with an excessive interocclusal distance compensate for overclosure by protrusion of the mandible, greatly decreased muscular force during mastication, and effective use of the tongue during mastication and swallowing. The patient retaining six lower incisors in function against a natural or artificial maxillary dentition is likewise protected from temporomandibular joint disorders by virtue of the reduced force employed in incisal mastication. The condyles, in this instance, perform their normal bracing action against the articular eminences. (Deflective occlusal contacts are rarely productive of joint injury in complete denture wearers. Denture displacement occurs rather than condyle displacement.) The patient who is unilaterally edentulous is the most susceptible to traumatic overclosure. The unilateral loss of posterior teeth permits the elevator muscles on the side of the intact dentition to function at their normal length while the elevators on the edentulous side may overcontract and develop trismus. Such spasm results in the condyle on the edentulous side being drawn into firm apposition with the articular disc and articular eminence in a superior and anterior direction. Compression of the disc results. If the remaining natural teeth occlude in such a manner as to produce a posterior, superior displacement of the condyle on the edentulous side, the sequalae of disc displacement follow.
158
RAMSEY
J. Pros. Jax-Feb.,
Den. 1964
SUMMARY
Commonly encountered disorders of the temporomandibular joint have been considered as postural problems resulting from chronic or forceful eccentric positioning of the mandible. Muscular hyperactivity produced by such eccentric positioning results in muscle spasm with attendant compression or tension of articular and periarticular structures. The level of mandibular closure at which eccentric positioning originates is suggested as a supplementary aid to routine diagnostic procedures. Such an approach facilitates the removal of cause as well as symptoms of temporomandibular joint disorders. REFERENCES
1. Sarnat, B. G., Editor: The Temporomandibular Joint, Springfield, Ill., 1951, Charles C Thomas, Publisher. 2. Vaughan, H. C.: External Facial Symptoms Resulting From Indirect Trauma In and About the Infratemporal Fossa, J. PROS. DEN. 12:486-492,1962. 3. Travell, J.: Temporomandibular Joint Pain Referred From Muscles of the Head and Neck, J. PROS. DEN. 10:745-763,196O. 4. Ramsey, W. 0.: Disorders of the Mandibular Articulation, J. Maryland D.A. 2:9-14, 1959. 5. Sicher, H.: Oral Anatomy, St. Louis, 1949, The C. V. Mosby Company,.p. 477. 6. Perry, H. T., Jr.: Muscular Changes Associated With Temporomandtbular Joint Dysfunction, J.A.D.A. 54:644-653, 1957. 7. Sarnat, B. G., Editor: The Temporomandibular Joint, Springfield, Ill., 1951, Charles C Thomas, Publisher, p. 80. 618 W.
LOMBARD ST. 1, MD. BALTIMORE