MAXILLOFACIAL PROSTHETICS TEMPOROMANDIBULAR JOINT SECTION
I. KENNETH ADISMAN
LOUIS J. BOUCHER
The etiulogy, diagnosis, dysfunctio&pain-syndrome. Lawrence
and treatment of TMJ Part I: Etioloy
New York, N. Y.
n order to treat temporomandibular joint (TMJ) dysfunction-pain syndrome it is necessary to understand etiology and to establish a systematic procedure for differential diagnosis. The question is, should we treat pain as a symptom or as a disease? When only the symptom of pain is treated, reoccurence is highly probable; whereas if the causes are eliminated, the prognosis of long-term relief is much more favorable. To accomplish this objective more knowledge is needed about the etiology of pain, as well as differential diagnosis, in order that specific treatment procedures for each patient may be designed. This series of articles will be divided into three categories: etiology, diagnosis, and treatment.
The etiology of pain in TMJ dysfunction-pain syndrome may be (1) neurologic, (2) vascular, temporomandibular joint, (4) muscular, and/or from conversion. Muscular pain may result from contracture (nerves), (2) ischemic entrapment, stress, (4) dysfunction, (5) trigger points, and biochemistry.
(3) (5) (1) (3) (6)
Neurologic pain Neurologic pain can be caused by cervico-occipital, trigeminal, or glossopharyngeal neuralgia. The incidence is higher in women, the affected age group is usually over 40 years, and the right side is affected two thirds of the time. Most often trigger zones which respond to light touch are present. For instance, the lower lip and gingivae are often trigger zones in trigeminal neuralgia; however, the teeth and tongue are seldom involved. It is pathognomanic that the pain comes on suddenly, with periods of remission, and is not associated with function. As the pain increases in intensity, the trigger zone becomes
Dental Department, Nassau County East Meadow, N. Y.
more definitive and is stimulated by light touch. In describing the pain, patients will never touch the face but will remain a discreet half inch away. They often report tha,t they will avoid washing the face or combing the hair on the affected side. Often glossopharyngeal neuralgia will refer pain to the auditory meatus. The patient will reveal that pressure within the auditory meatus decreases the pain. Neurologic pain can be caused by direct pressure on the nerve root from a spinal disk, neoplasm, or blood vessel. For instance, the superior cerebella artery curves around the root of the trigeminal nerve.’ Aging tends to elongate arteries, and in conjunction with athrosclerosis and increased blood pressure, direct pressure by the artery on the nerve can result. Jannetta’ has devised a procedure in which a spongy pad is placed between the trigeminal nerve and the artery, thus eliminating the pain. The same mechanism can take place with the glossopharyngeal nerve, where the anterior inferior cerebella artery is in close proximation with the nerve root.” In summary, trigeminal and glossopharyngeal neuralgia can be caused by direct pressure of’ the blood vessels on the nerve roots. Neuralgia pain. Fig. 1 illustrates a 78-year-old woman who developed typical trigeminal neuralgic pain. The trigger zones were the lower right lip and gingivae. The right TMJ radiograph (Fig. 2) and the left TMJ radiograph (Fig. 3) were essentially noncontributory. Reduction of blood pressure alone, which was stress-induced, has minimized symptoms. A neoplasm can also produce pain by exerting pressure on the nmerve; however, it may be accompanied by numbneTs. Whenever numbness occurs, the possibility of neoplasm should be looked into thoroughly.* Contracture pain. Muscle spasm can produce
1979 The C V Mosby
Fig. 2 Right TMJ
Fig. Left ;,,
Fig. 1. The teeth and occlusion of a ‘%-year-old woman with trigeminal neuralgia. Figs. 2 and 3. The right and left (respectively) TMJ radiographs do not indicate in;olvement in the etiology. contracture pain, which is caused by pressure on nerves distributed within the muscle itself.’ The upper cervical nerves pass through the trapezius muscle and are distributed to the back of the ear, the inferior border of the mandible, and into the occipital and temporal muscles.’ The great auricular nerve innervates the angle of the mandible. Muscle contraction around these nerve fibers can simulate TMJ dysfunction-pain syndrome.’ Condylar displacement. Condylar displacement can produce pressure pain. It was originally thought, as described by Costen,’ that posterior condylar displacement could cause pain by direct pressure on the auriculotemporal nerve. Figs. 4 and 5 illustrate a patient who has bilateral posterior condylar displacement with pain on both sides. This degree of condylar retrusion is not unusual. Sicher’ has pointed out that although direct condylar pressure on the auricular temporal nerve itself is not likely, the pain can come from sensitive soft tissue posterior to the condyle. Thilander’ demonstrated that branches of the auriculotemporal nerve supply the posterior portion of the capsule as well as most of the medial and lateral walls (Fig. 6) A branch of the posterior deep temporal nerve innervates part of the anterior portion of the capsule and a small part of the lateral aspect. A branch of the masseteric nerve THE JOURNAL
innervates the remaining anterior portion of the capsule and a small amount of the medial aspect. Zimmerman” pointed out that the sensory nerve endings of the auriculotemporal nerve, in the posterior aspect of the capsule, can produce pain due to posterior condylar displacement rather than direct pressure on the nerve root itself. Superior condylar displacement. Superior condylar displacement can cause pain due to impingement of nerve fibers located in the periphery of the disk. In Fig. 7 note the reduced joint space on the right TMJ radiograph, which was the side with symptoms, whereas the joint space is considerably wider on the opposite asymptomatic side (Fig. 8). Summary: Neurologic pain can be caused by pressure on a nerve root from a neoplasm, a displaced spinal disk, or a blood vessel. Peripherally, pressure on nerve fibers can be caused by muscle contracture and condylar displacement. Vascular
Vascular pain must be distinquished from muscle contraction headache and TMJ dysfunction-pain syndrome. The two major types of vascular pain are migraine and temporal arteritis. An accurate history can establish a differential diagnosis. It is generally accepted that migraine is associated with constric655
Fig. 4 light TMJ Posterior condylar diq Aacement
Fig. 7 R.ight TMJ Reduced joint space
Figs. 4 and 5. Note the bilateral
in both the right and left
Fig. 6. Sensory branches of the auriculotemporal nerve supply the posterior, lateral, and medial portions of the capsule. Branches of the posterior deep temporal and masseteric nerves innervate the lateral and medial aspect (respectively) of the anterior portion of the capsule. Figs. 7 and 8. The joint space is reduced on the right symptomatic side (Fig. 7) when compared to the opposite asymptomatic left side (Fig. 8).
tion of the cranial and cerebral vessels in the preheadache phase followed by vasodilation in the headache phase.; It is treated with ergotomine, which is specific for migraine, but will however, usually make other types of (muscle-contraction) headaches worse due to its vasoconstriction properties. The symptoms of migraine headache are usually unilateral and rarely remain more than 24 hours, and a familial history is often present. The second type of vascular head pain is temporal
arteritis, which is inflammatory in nature. The patient usually has loss of appetite and weight, leukocytosis, fever, and tenderness of the scalp along the temporal vessels.’ The location of pain is usually more inferior in the temporal region than in migraine. There is giant cell formation, and if untreated the patient can have irreversible blindness. With an)- visual disturbances temporal arteritis must be ruled out immediately, and the usual treatment is the administration of steroids.’ An accurate history
OF TMJ DYSFUNCTION-PAIN
R!ight TMJ Slight posterior disl Jlacement
Left Path ologic remc ldeling
Fig. 9. Rapid mandibular alveolar bone loss was caused by natural teeth occluding with the mandibular denture. Fig. 10. The right TMJ radiograph reveals slight posterior displacement (reduced posterior joint space. Fig. Il. Posterior condylar displacement over a long period of time caused pathologic joint remodeling @rows). will differentiate vascular tion-pain syndrome.
Temporomatidibular joint pain Pain can originate from the TMJ itself. Symptoms can be caused by traumatic injury, microtrauma, infection, inflammation, and condylar displacement. A common cause of injury is whiplash, or hyperextension, and intubation during general anesthesia. Edema usually results, with microhemmorage in the joint spaces. The synovial fluid contains enzymes which lyse small fibrin clots. Heat or ultrasound has been found to be beneficial. It is possible to tear the lateral and/or medial aspect of the attachment of the disk to the condyle. The disk itself may become displaced and be particularly difficult to diagnose if it is displaced medially.$ In this event, surgery may be indicated; Occasionally the trauma can initiate osteoarthritis. Microtratima. Another cause of joint pain is microtrauma associated with posterior condylar displacement or loss of posterior teeth. The patient illustrated in Fig, 9 had a rapid loss of vertical
dimension due to alvelor ridge absorption. The right normal TMJ radiograph (Fig. 10) revealed almost condylar position, but on the left side the condyle was retruded (arrows, Fig. 11). Over a period of time the microtrauma caused pathologic joint remodeling. The patient was unaware of the destructive process. Infection. It is rare to have infection in the TMJ. However, a gonorrhea infection can affect any of the joints in the body. If this history is revealed, it may be necessary to culture the joint to establish a differential diagnosis. A wider joint space will often be revealed on the radiograph. Osteoarthritis. Another source of joint pain is inflammatory in nature and includes osteoarthritis, which is most often unilateral. Fig. 12 (arrows) shows the right TMJ radiograph with marked destruction of the condyle and a flattening of the eminentia. Usually osteoarthritis produces a widening of the joint space (Fig. 12) while on the opposite (ieft) side the TMJ radiograph is normal (Fig. 13). This condition was associated with the loss of posterior tooth support and mild symptoms. In another
Fig. 12 light Th4J Osteoarthritis
Left Non nal
Fig. 14 Rlight TMJ Osteoarthritic mottling
Fig. Left Ante trior displ :acemel
Fig. 16 RLight TMJ Del;;enerative arthritis
Fig. 12. Widening of the joint space was caused by osteoarth,.ritis of the condyle and eminentia (arrows). Fig. 13. The left TMJ radiograph is essentially normal. Fig. 14. Early osteoarthritic signs are demonstrated by mottling on the periphery of the condyle (arrows). Fig. 15. The left TMJ is essentially normal for bone pathology, but the condyle is anteriorly displaced as demonstrated by the narrow anterior joint space (A1.S). Fig. 16. Degenerative arthritis usually results in narrowing of the joint space, flattening of the eminentia, and “lipping” of the anterior portion of the condyle (c1rrows). Fig. 17. On the left side, note the mottling itself (urrows). patient, early symptoms can be clearly observed in the right TMJ radiograph (arrows, Fig. 14). Note the mottled effect of the bone of the condyle (arrows, Fig. 14). However, marked deformity has not yet taken place. The opposite (left) TMJ radiograph is essentially n&contributory (Fig. 15). Extensive pathologic destruction includes a flat-
on the superior
tening of the eminentia and the condyie producing “lipping” on the anterior portion of the condyle (arrow, Fig. 16). On the opposite (left) side the condyle shows early bony changes on the superior portion and a mottling effect on the condyle itself (arrows, Fig. 17). This patient demonstrates that osteoarthritis i.s not a&ys limited to one side. In the
OF TMJ DYSFUNCTION-PAIN
Fig. 18 Right TMJ (Before) Acute osteoarthritis
Fig. 19 Left TMJ (Before) Normal
(4 months) .
Fig. 21 Right TMJ (12 months) Arrested osteoarthriti!
Fig. 22 Left TMJ (12 months) Normal
Fig. 18. (urrom). Fig. 19. Fig. 20. well as a
on the superior
of the condyle
The left TMJ radiograph is essentially negative. In 4 months, acute osteoarthritis produced a severe widening of the TMJ space as complete change in the artchitecture of the condyle (arrows). Compare this with Fig.
Fig. 21. Within a year the eminentia was flattened (arrorus) and the destructive breakdown of the condyle had arrested (arrows). Fig. 22. On the left side no change was observed in 1 year. last two patients (Figs. 14 to 17) microtrauma and systemic causes rather than condylar displacement were involved. The disease process in acute osteoarthritis can be very rapid. The right TMJ radiograph of a patient with mild discomfort of the right side and trismus revealed good condylar position within the fossae. However, initial bone breakdown was observed on the superior portion of the condyle (UYYOWS, Fig. 18).
On the opposite (left) side, the TMJ radiograph is essentially negative (Fig. 19). Progressive pathologic changes occurred on the right side. The original right TMJ radiograph is shown in Fig. 18. Four months later the architecture of the condyle had changed, with a widening of the joint space (arrows, Fig. 20). The eminentia has not yet been altered in its configuration. After 8 to 12 months the eminentia usually flattens and the destructive process seems to
Fig. 24 Right TM3 (Before) .ent
Fig. 26 Right TMJ (6-year follow-up)
Fig. 28 Right TMJ (B-year follow-up)
Figs. 23 through
29. For legends see facing page.
OF TMJ DYSFUNCTION-PAIN
terminate.g However, in this patient it took 12 months (Fig. 21). On the left side there was no essential change in architecture (Fig. 22). Acute or chronic osteoarthritis can take place with or without condylar retrusion. It is most often unilateral, and the patient may not have severe symptoms. In acute osteoarthritis, muscle pain and trismus can simulate a myofascial pain-dysfunction syndrome, while radiographic findings will reveal a rapid destructive process of the condyle and eminentia. In the event symptoms persist up to 2 years, surgical intervention may be necessary. Tollerg described 130 osteoarthritic patients as having pain on movement which usually disappeared in 8 months. The pain was not constant. Radiographs revealed fuzzy margins on the condyle (Pig. 20) followed by the articular eminence (Fig. 21) and radiolucent spots (Fig. 14) or spur formation on the condyle (Fig. 16). However, complete flattening of the condyle and the articular eminence usually takes a year (Fig. 21) .9 Crepitus occurs early with a limitation of movement due to the splinting of the muscles. The disease process is most often unilateral and affects the center of the joints working its way peripherally. Tollerg also found that 30% of the osteoarthritic patients had poor occlusion, although the incidence was six times greater in women than men. In other joints the incidence ratio between women and men is only 2: 1. Pathologic joint remodeling. Blackwood”‘. I1 maintains that the disk degenerates first, followed by bony changes in the condyle and eminen tia. In 19 18, Prentis” and Summa’.’ suggested a relationship between loss of teeth, thinning of the disk, and subsequent bony changes of the articulating surfaces of the condyle and fossae. This has been confirmed recently with Agerberg and associates’la study on age changes of the disk. Moffet and associates*” has
emphasized the similarities and dissimilarities between remodeling due to functional requirements of the TMJ and pathologic osteoarthritic change. He stated that perforations of the disk are often associated with progressive remodeling of that portion of the condyle adjacent to the perforation. Breakdown of the disk appears to be a stimulus for subsequent remodeling activity on the condyle and temporal bone at the sight of the perforation.” Rheumatoid arthritis. Rheumatoid arthritis must be differentiated from osteoarthritis. In rheumatoid arthritis the synovial cells are converted to panus cells that secrete an enzyme which erodes the articular surface. This is associated with acute inflammation of the marrow spaces. Typically the condyle is affected first and the fossae later on, as in osteoarthritis. However, the pathologic process erodes from the periphery toward the center, corresponding to the location of the synovial cells._ Osteoarthritis is the reverse, it begins in the center and works its way peripherally. Rheumatoid arthritis is usually a bilateral disease, and other joints of the body, such as the hip, knee, and elbow, are affected first. Posterior condylar displacement. Posterior condylar displacement associated with the loss of vertical dimension has previously been shown to cause pathologic osteoarthritic remodeling (Figs. 9 to 11). However, a reduction in the vertical dimension is not always involved. For instance, a patient had a full complement of teeth (Fig. 23) with the right condyle almost in the middle of the fossa (Fig. 24) and the left condyle displaced posteriorly (PJS, Fig. 25). Six years later the right TMJ radiograph revealed very little change (Fig. 26). On the left side, 6 years after the original examination, the beginning of osteoarthritic change on the anterior portion of the condyle can be seen with very minor subjective symptoms (arrows, Fig. 27). Eight years after the first examination the
Fig. 25. The patient has a full complement of teeth. Centric relation and centric occlusion are harmonious. Fig. 24. The right condyle is almost in the middle of the fossa with very slight retrusion VW. Fig. 25. The left condyle is displaced posteriorly as seen by the reduced posterior joint space uw. Fig. 26. A 6-year follow-up TMJ radiograph of the right side revealed little change. Fig. 27. Six-year follow-up TMJ radiograph on the left side reveals osteoarthritic change on the anterior-superior surface of the condyle (arrows). Fig. 28. Eight-year follow-up TMJ radiograph of the right side reveals no change. Fig. 29. Eight-year follow-up TMJ radiograph of the left side reveals more extensive osteoarthritic degeneration of the condyle (arroros).
right TMJ radiograph reveals no change (Fig. 28). On the left side however, more extensive osteoarthritic degeneration of the condyle is seen (arrows, Fig. 29). Summary. It can be concluded that osteoarthritic change can take place with or without a change in the vertical dimension of occlusion, and the patient may not be aware of the joint pathology. Unless preoperative TMJ radiographs are available before subjective symptoms, the joint changes that have already taken place may not be evident. It is suggested that joint pathology may go undetected because of poor radiographic techniques and secondary muscle spasm which masks the primary joint inflammation. Osteoarthritis can be initiated by perforations of the disk, posterior condylar displacement, and microtrauma (without condylar displacement) in association with systemic involvement. Differential diagnosis can be made on the basis of the history and the fact that osteoarthritis is usually unilateral, whereas rheumatoid arthritis is often bilateral and other joints of the body are affected first. Muscle
There are many causes of pain associated with muscle spasm. Franks”‘ described the high incidence of bruxism in TMJ dysfunction-pain syndrome. Christensen” showed that experimental clenching could produce TMJ dysfunction pain. Kraus” maintained that sudden stretching of the musculature can result in spasm and pain. However, DeSalvo“’ pointed out that muscle fatigue, in itself, could produce pain. Posterior condylar displacement, as a source of pain, has been controversial since Costen’ first described it in 1934. Sicher’ has indicated that direct nerve impingement is hardly likely and that pain symptoms can come from sensitive soft tissue posterior to the condyle. As discussed previously, branches of the auriculotemporal nerve are located in the posterior portion of the capsule.‘, ‘? Any inflammatory process located within the joint can cause trismus due to spasm of the masseter and temporal muscles, precipitated by irritation of the branches of the masseteric and posterior deep temporal nerves in the anterior portion of the capsular ligament.z” There is mounting evidence that longstanding microtrauma due to condylar displacement can lead to inflammation within the joint that will then cause muscle spasm and a splinting action of the muscles moving that joint.” .” It is well known,
as described by Hilton”’ and TravelI,” that there is a splinting effect by the muscles of an injured joint and that the nerves that innervate the joint also innervate the muscles that move that joint, as well as the skin. Weinberg”]. ?’ has demonstrated a 90% incidence of TMJ dysfunction-pain syndrome with condylar asymmetry in the fossae. This has been corroborated by Bassette and associates”’ in subsequent myographic studies. Posterior condylar displacement. The concept is presented that posterior condylar displacement need not necessarily cause direct nerve impingement to produce pain. The microtrauma of posterior condylar displacement can cause an intrajoint inflammatory response which in turn causes muscle spasm and pain. Muscle contracture. Muscle contracture can have a direct effect on nerves and blood sessels. Nerve fibers located within a muscle in contraction will have direct pressure exerted on them, precipitating more pain. Si:milarly, entrapped blood vessels can have a decreased blood flow (ischemic entrapment) which will impede the removal of waste products and will add to the inflammatory response, producing pain. Stress. Another factor contributing to muscle spasm is stress.. Copland,‘” Kydd,‘” Franks,“’ Berry,“’ and Newton“ have demonstrated increased muscle activity associated with stress. There is also a specific exaggerated response in the masseter and temporal muscles to anger and frustration which Perry and associates’” and Yemm”’ have demonstrated. Butler and Stallard I1 reported more frequent and prolonged tooth contact during stress in normal subjects. Dysfunction pain. Kydd”) has shown an increase in temporal and masseter muscle activity during stress w-ith TMJ patients. Muscle hyperactivity in TMJ patients was also shown by Jarabak.;’ Perry,’ and Griffin and Munro. ” Berry:’ reported that TMJ patients have 10 times the incidenct: of back pain and migraine compared to a controlled group. The evidence suggests that Th4J patients have a higher degree of muscle response to stress compared to the general population. Schwartz and t.:obin. ,i Ricketts, “I Berry. r: Laskin, ” and others have maintained that it is the muscle spasm that produces pain rather than the joint itself. Trigger points. Travell,‘! Lewis, ” and Kellgren”’ describe trigger points as referred pain originating from sites of severe tenderness within rhe muscle
OF TMJ DYSFUNCTION-PAIN
spasm, from which many impulses bombard the central nervous system to produce referred pain. However, Kraus’” maintains that the trigger point is a breakdown of muscle tissue which serves as a constant irritation to stimulate the muscle back into spasm. Muscle function. Muscles work in group function with a graded antagonistic reaction to permit smooth coordinated movement. Simple opening and closing of the mandible requires coordinated movement of muscle groups all the way to the clavicle. The neck muscles maintain cranial posture as a fixed based from which the mandible opens and closes. Once one muscle goes into spasm as part of a group, eventually the whole group goes into spasm. It is extremely rare to find only one muscle in spasm. Eventually, when a group of muscles are in spasm the postural position usually changes, altering function and causing spasm on the opposite side. Once muscles are in spasm there is the tendency to form the so-called “pain-spasm-pain cycle,” which perpetuates itself. If diagnosed early, interruption of the pain, such as with anesthetics, can stop the cycle. Biochemistry. The final mechanism of pain production in a muscle spasm is biochemical in nature. Any process that interferes with the supply of oxygen and nutrients to the muscle, as well as the removal of waste products, will precipitate spasm and pain as nature’s protective mechanism to stop function and further injury. This can take place by decreased blood flow caused by the autonomic nervous system, ischemic entrapment, localized inflammation in the muscle tissue, or nutritional factors that interfere with cellular metabolism and intercellular fluid transport.
Conversion It is rare to have hysterical conversion as a cause of myofascial pain. Most often stress will cause behavior modification and/or psychophysiologic responses which in turn can cause organic joint pathology or muscle dysfunction pain. A true conversion produces pain without joint pathology, muscle spasm, or neurologic disorders.
SUMMARY Craniomandibular pain has five major causes: neurologic, vascular, the temporomandibular joint itself, muscular, and hysterical conversion. When the pain source is purely in the muscles it has been termed MPD (myofascial pain dysfunction) by
Laskin.38 involved syndrome.
However, when it is called
the TMJ itself is also TMJ dysfunction-pain
I would like to express my appreciation to Dr. Hans Kraus, Dr. Parker Mahan, and Dr. Simon Markovich for their valuable contributions to this article from their own writings and lecture material. REFERENCES 1. Jannetta, P. J.: Microsurgical relief of nemovascular trigeminal nerve compression in tic doutoureauz. J Dent Res 53(Special issue):128, 1974. (Abst No. 294) 2. Markovich S.: Pain in the head: A neurological appraisal. From Gelb, H.: Clinical Management of Head, Neck, and TMJ Pain and Dysfunction. Philadelphia, 1977, W. B. Saunders Co., p 125. 3. Costen, J. B.: Syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomandibular joint. Ann Otolaryngol 43:1, 1934. 4. Sicher, H.: Structural and functional basis for disorders of the temporomandibular articulation. J Oral Surg 13:275, 1955. 5. Thilander, B.: Innervation of the temporomandibular joint capsule in man. Trans Roy Schools Stockh Umea 7:1, 1961. 6. Zimmerman, A. A.: An evaluation of Costen’s syndrome from an anatomic point of view. In Sarnat, B. G. (ed): The Temporomandibular Joint. Springfield, 1951, Charles C Thomas, Publisher, pp 82-110. 7. Dalessio, D. J.: Wolffs Headache and Other Head Pain. New York, 1972, Oxford University Press. 8. Farrar, W.: Differentiation of temporomandibular joint dysfunction to simplify treatment. J PROSTHET DENT 28:629, 1972. 9. Toller, P. A.: Osteoarthrosis of the mandibular condyle. Br Dent J 134:223, 1973. 10. Blackwood, H. J.: Arthritis of the mandibular joint. Br Dent J 115:317, 1963. 11. Blackwood, H. J.: Cellular remodeling in articular tissue. J Dent Res 45:480, 1966. 12. Prentis, H. J.: A preliminary report of the temporomandibula articulation in the human type. Dent Cosmos 60:512, 1918. 13. Summa, R.: The importance of the inter-articular fibrocartilage of the temporomandibular articulation. Dent Cosmos 60:512, 1918. 14. Agerberg, G., ,Carlsson, G. E., and Hasseler, 0.: Vascularization of the temporomandibular disk, a microangiographic study of human autopsy material. Sartyrk Odontol Tidskr 77~5, 1969. 15. Moffett,, B. C,, Johnson, L. C., McCabe, J. B., and Askew, H. C.: Articular remodeling in the adult human temporomandibular joint. Am J Anat 115:119, 1964. 16. Franks, A. S.: Masticator-y muscle hyperactivity and temporomandibular joint dysfunction. J PROSTHET DENT 15: 1122, 1965. . 17. Christensen, V,: Facial pain and internal pressure of masseter muscle in experimental bruxism in man. Arch Oral Biol 16:1021, 1971.
22. 23. 24.
25. 26. 27 28 29
Kraus, H.: Principles and Practice of Therapeutic Exercises. Springfield, 1949, Charles C Thomas, Publisher. DeSalvo, N. A.: Neuromuscular mechanisms involved in mandibular movement and posture. Am J Orthodont 47:330, 1961. Hilton, J.: Rest and Pain, ed 2. Jacobson, W. H. A. (ed), New York, 1879, William Wood and Co., p 96. Weinberg, L. .4.: Correlation of temporomandibular dysfunction with radiographic findings. J PROSTHET DENT 28:519. 1972. Weinberg. L. A. The role of condylar position in TMJ dysfunction pain syndrome. (Unpublished) Travell. J.: TMJ pain referred from muscles of the head and neck. .J PROSTHET DENT 10:745, 1960. Bassette, R.. Mohl, N.. and DiCosimo, C.: Comparison of results of electromyographic and radiographic examinations in patients with TMJ syndrome. J .4m Dent Assoc 89: 1358, 1974. Copland. J.: .4bnormal muscle tension and the mandibular joint. Dent Ret 74:331. 1954. Kydd, W. I,.: Psychosomatic aspects of temporomandibular joint dysfunction. J Am Dent Assoc 59:31, 1959. Berry, D. C.: Facial pain related to muscle dysfunction. Br J Oral Surg 4:222, 1967. Newton. A. V.: Predisposing caused for temporomandibular joint dysfunction. J PROSTHET DENT 22:647, 1969. Perry. H. T., Lammie, G. A., Main, .J., and Teuscher, G. W.: Occlusion in a stress situation. J Am Dent Assoc 60:626, 1960. _ Yemm. R.: A comparison of the electrical activity of masseter and temporal muscles of human subjects during experimental stress. Arch Oral Biol 16:269, 1971.
35. 36. 37. 38. 39. 40.
Butler,, J. H., and Stallard, R. E.: Physiologic stress and tooth contact J Periodontal Res 4: 152. 1969. Jarabak, J. R.: An electromyographic analysis of muscular and temporomandibular joint disturbances due to imbalances in occlusion. Angle Orthodont 25:170. 1956. Perry, H. T.: Muscular changes associated with temporomandibular joint dysfunction. J Am Dent Assoc 54:644. 1967. Griffin, C. J., and Munro, R. R.: Electromyography of the masseter and anterior temporalis muscles in patients with temporomandibular dysfunction. .4rch Oral Biol 16:X9, 1971. Schwartz, L. and Cobin, H. P.: Symptoms associated with the temporomandibular joint. Oral Surg 10:3X9, 1957. Ricketts, R. M.: Occlusion-The medim, of dentistry. J PROSTHET DENT 21:39, 1969. Berry. D. C.: Facial pain related to muscle dvsfunction. BrJ Oral Surg 4::!22, 1967. Laskin. D. M.: Etiology of the pain dysfunzvtion s)-ndrome. J Am Dent Assoc 79:147, 1969. Lewis, T.: Pain. New York, 1942, Macmillan Publishing Co.. Inc., p 80. Kellgren, J.: On distribution of pain ansing from deep somatic structures with charts of segmental pain area. Clin Sci 4:25, 1939.
57 W. 57~ NEW YORK.
The appearance of a code at the bottom of the first page of an original article in this jourxil indicates the copyright owner’s consent that copies of the article may be made for personal or internal use or for the personal or internal use of specific clients. This consent is given on the condition, however, that the copier pay the stated per copy fee through the Copyright Clearance Center, Inc., P.O. Box 765, Schenectady, N. Y. 123OL, 518-374-4430, for copying beyond that permitted by Sections 107 or 108 of the U. S. Copyright Law. This consent does not extend to other kinds of copying, such as copying for general distribution, for advertising or promotional purposes, for creating new collective works, or for rt:sale.