Dysfunctional Disturbance of the TMJ and Masticatory Muscles (Etiology, Pathology, and Diagnosis)
by Dinh X. Bui, D.D.S., M.S.

Dysfunctional Disturbance of the TMJ and Masticatory Muscles (Etiology, Pathology, and Diagnosis)
The masticatory system consist of the skeletal component, the muscle of mastication, the neural component, and the teeth. The skeletal component consists of the jaw and the temporomandibular joint (TMJ). The physiology of the masticatory muscles and the neuromuscular activities associated with mastication consists of cyclical movements produced by the elevation and depression of the mandible as food is sheared and formed into a bolus in preparation for swallowing. Controlled movement of the mandible is used in biting, chewing, and swallowing of food and fluids, and in the production of speech sounds. Concurrent with the jaw movements are integrated movements of the tongue and other muscles controlling the perioral areas, pharynx and larynx. The TMJ acts as the fulcrum of which the movement of mandible rotated and translate in the horizontal, vertical, and sagittal plane. Together with the masticatory muscle, the TMJ coordinated the skeletal component of the masticatory system. Any functional disturbance occurs to the TMJ will have an effect on the muscle of mastication and vice versa, any disturbance occur to the muscle of mastication will have an effect on the TMJ. Thus, functional disturbances of TMJ and masticatory muscle must be located and diagnosed as early as possible. The etiology and pathology must be identified prior to select an appropriate therapy in treating the patient.
Numerous studies have been attempted to record the muscle activity during masticatory cycle using electromyographic recorder. Researcher have also identified the pattern of chewing cycle, i.e., the envelope movement of mandible during mastication. In this cycle, closing muscles are usually inactive during jaw opening, whereas the jaw-opening muscles are very active. Activity in jaw-closing muscles begins to be apparent at the beginning of the jaw closing. Activity of the jaw-closing muscles increases slowly as the teeth begin to interdigitate or as soon as food is encountered between the teeth. The closing muscles on the side where food is being crushed (so-called working side) are more active than the contralateral jaw-closing muscles. Any kind of disturbance in masticatory muscle will result in splinting, translated into clicking and poping of TMJ, and ultimately, pain will occur.
The temporomandibular joints, as described by Harry Sicher, is a bilateral articulation, right and left joints, though anatomically separted, forming functionally one articulation. There is only one position of the mandible in the dead that imitates the position of the mandible in the living, that is, the position of full occlusion. This centric occlusion is established by intercuspation of the maxillary and mandibular teeth. When the teeth in is CO, there is no bony contact exists at the mandibular articulation of the skull. There is always a space between mandibular condyles and the cranial base at the articular tubercles. Normal physiologic CR position of the jaws may be defined as the stable, comfortable, functional craniomandibular relationship in which the condyles are in their most superior position in intimate contact with the thinnest central bearing area of their respective discs against the distal surface of the articular eminences at any vertical rotational postion of the mandible. CR is a comfortable physiologic work position during mastication and swallowing, provided there are no deflective interferences from the teeth. It is not a rest postion; therefore when the mandible is in CR, considerable electromyographic activity may be observed. When CO = CR, CR is used during mastication and swallowing about 5000 times a day. This position has been found clinically to be the best location for the maximum intercuspation of teeth. Clinically, CR may be defined as the completely retruded position of the mandible with the condyles in their most superior anterior postion at any vertical rotational position of the mandible. As the jaw open, the condyle brace themselves against the postglenoid process as the mandible travels upward and backward. Studies have shown that physiological bone remodelling observed in the condyle has no orientation that could be related to the changed occlusion. However, occlusal forces brought about rebuilding of the bone in the neck of the condyle. Longitudinal studies have shown that changes associated with orthodontic treatment of class II malocclusion are related mainly to altered growth patterns of the alveolar processes rather than to joint changes. It appears that the changes in temporomandibular joint morphology may be the result of pathological rather than physiological processes. Furthermore, there has been striking evidence of periodontal trauma from occlusion and subsequent movement of teeth in all studies of occlusal disharmony and TMJ morphology. The clinical significance of these research findings to the practice of dentistry should be the adaptation of the occlusion to be in harmony with the TMJ rather than hoping for the TMJ to adapt to the occlusion.
In discussing the disturbance involves the TMJ and the muscle of mastication, we must examine the bruxism, the myofacial pain syndrome (MPD), and the temporomandibular joint disorder (TMD).
Bruxism is the most common disturbance of masticatory muscle. As Karolyi have stated, " all person may at one time or another grind their teeth". Etiology and nature of bruxism have been explored in numerous studies. Researcher have found that the major common denominator of all bruxing patient is stress. Thus stress is the only proven factor as to tip the neuromuscular balance and resulting in pathological phenomena. Every body has some type of occlusal interference and learn to compensate them with various tolerance level. However, as the stress increase, this tolerance level may be altered by psychic stress affecting the tonus activity in the jaw muscles. It has also been shown that bruxism can be reduced by biofeedback or by relief of stress, thus demonstrating the strong central nervous system input in this condition. The significance of bruxism in the cause of periodontal disease depends on whether bruxism results in trauma from occlusion. Since trauma from occlusion does not cause periodontal disease but exacerbate this condition, bruxism plays the similar role. Progressing of advanced periodontal breakdown due to bruxism thus may necessitate splinting of the teeth. Bruxism ultimately may lead to occurence of dysfunctional muscle and temporomandibular joint pain. Discomfort from the muscle, the teeth, the joints in association with bruxism often increased the spychic tension and irritability, and further increases muscle tonus and bruxism.
Myofacial pain-dysfunction syndrome is a psychophysiologic disease that primarily involves the muscles of mastication. The condition is characterized by dull, aching, radiating pain that may become acute during use of the jaw, and mandibular dysfunction that generally involves a limitation of opening. Generally the condition involves only one side of the face and, upon examination, tenderness can usually be elicited in one or more of the muscles of mastication or their tendinous attachments. Although MPD syndrome starts as a functional disorder, it can ultimately lead to organic changes in the temporomandibular joint (TMJ) and the masticatory muscles, and even cause possible alterations in the dentition. MPD syndrome is believed to be a stress-related disorder. It is hypothesized that centrally induced increases in muscle tension, frequently combined with the presence of parafunctional habits such as clenching or grinding of the teeth, result in muscle fatigue and spasm that produce the pain and dysfunction. Similar symptoms, however, occasionally can also result from muscular overextension, muscle overcontraction, or trauma. Two major groups of conditions must be considered in the differential diagnosis of MPD syndrome: the nonarticular problems that can mimic MPD syndrome, and the various pathologic disorders of the TMJ that may sometimes also produce similar signs and symptoms. Nonarticular problems include conditions that produce pain resembling that of MPD syndrome and those that produce mainly limitation of jaw opening. Management of MPD syndrome is founded on certain basic principles that include the establishment of an accurate diagnosis, gradual escalation of therapy, and avoidance of irreversible forms of treatment. Several different treatments have been recommended for MPD syndrome, ranging from structural alterations to psychotherapy. These treatment modality will be discussed in later seminars.
Patient with MPD must realize that this is a psychophysiologic disease of which the psychologic stress can cause physical disorders. Patient therefore must identify his or her stress in life and converted these stress or adapt to it with a healthier attitude. they must understand how stress can result in centrally generated increases in muscle activity and parafunctional habits such as clenching and grinding of the teeth, and how this leads to muscle fatigue, spasm, pain, and dysfunction. It may not be possible to provide a permanent cure for the problem. The patient can learn to manage it in a satisfactory manner by controlling stress and by using the recommended forms of simple therapy at the first sign of recurrent symptoms.
Temporomandibular disorders (TMD) should be viewed as a group of related disorders in the masticatory system and not as a single syndrome. The most common symptoms associated with TMD are limited mandibular movement, joint sounds, pain in the temporomandibular joint (TMJ) area, facial pain, ear pain, temporal headaches, and neck aches. Symptoms usually have a direct relationship to mandibular movement and function. An increase in pain is often noted with palpation of the joint or the masticatory muscles.

Successful management depends on an accurate determination of the structures that are responsible for symptoms. Most clinical problems emanate from the TMJs, masticatory muscles, and cervical structures (which are all part of the musculoskeletal system); however, other tissue systems may also be a source of pain. Therefore, dentists who manage patient with TMD must be aware of all the disorders that cause pain in the craniofacial area, specially with respect to chronic pain patients. These systems can be divided in extracranial, intracranial, musculoskeletal, vascular, neurologic, and psychogenic.

The diagnosis and treatment of TMD requires the clinician to use a full range of biological and clinical knowledge and experience. It is essential to remember that, although a variety of therapeutic modalities may prove to be effective, there can only be one accurate diagnosis. No definitive treatment should be initiated until the clinician has completed all of the exploratory procedures and has made a presumptive diagnosis. Nonetheless, it is often necessary to initiate some emergency therapy to assist the acutely distressed patient. Even if the emergency measures alleviate the acute symptoms, they do not remove the responsibility of the clinician to discover the etiology of the problem and seek its remedy. It must always be remembered that many TMD patients have psychologically contributing factors. It is often necessary that some type of counseling support (conducted by an appropriate mental health counselor) be administered simultaneously with the dentist's treatment. The chronicity of pain in many of these patients is extremely important. It means that clinician must be aware that many of the patient's complaints originate as part of the chronic pain pattern, and are not related to actual TMD pathology. These symptoms may continue to be manifested after all pathology in the stomatognathic system has been eliminated. Reversible treatments, when indicated, should be the initial treatment of choice. Irreversible procedures should be initiated for the most part after reversible procedures have not alleviated the patient's discomfort and further intervention is necessary for satisfactory treatment.

If the skeletal, traumatic, neurologic, neoplastic, internal derangements, and infectious causes of dentofacial pain are eliminated, there still remains 70% to 80% of patients presenting with TMD symptomatology. These are the patients with myospasm, trigger points, referred pain, occlusal disharmonies, parafunctional occlusal habits, and emotional stress patterns. The etiology of this TMD area is at present unresolved. However, several etiologic theories have evolved. Five major etiologic theories of myofacial pain disorder of the myospastic category have been categorized. These are the mechanical displacement theory, the muscle theory, the neuromuscular theory, the psychophysiologic theory, and the psychological theory.

Mechanical displacement theory is based on the observation that some TMD patients have an overclosure of the mandible. This may be caused by the loss or improper eruption of the posterior dentition. The overclosure of the mandible is thought to place undue pressure on the articulotemporal and chorda tympani nerves and the Eustachian tube. Adherents of this theory place great emphasis on the visualization of equal anterior and posterior joint spaces on roentgenographic examinations. The theory has been challenged on anatomic, radiological, and clinical grounds.

The basis of this theory is muscle hyperactivity. The hyperactivity serves as an initiator of myospasm, which then spreads to its primary and secondary referred pain sites. Although there is not a basis, at present, for the complete refutation of this theory, some believe this theory is narrow and restrictive. It does not take into account other variable causes of the TMD problem.

The neuromuscular theory is based on a functional disharmony between the occlusal interface and a physiologic joint muscle position. The incompatibility leads to parafunctional habits, such as grinding and clenching of the dentition (bruxism). The grinding and clenching may occur during daytime but is most often manifested during sleep. The bruxism habit leads to abnormal contractile states and, hence, myospastic activity. The theory covers many of the clinical TMD problems which are commonly seen and, indeed, may be the most popular theory. Its major weakness is that it does not explain, why many patients with abnormalities or variations from the norms in the occlusal interface do not have TMD problems.

The basis of Physiologic and Psychophysiologic Theories is that patients under stress have increased tension and activity in the masticatory and associated musculature. Some supporters of this school believe that the syndrome is purely psychogenic and should be treated from a psychological point of view. The psychophysiologic approach to TMD problems states that myospastic activity is the primary cause of TMD symptomatology. It is further believed that fatigue caused by tension related oral habits is the major cause of the abnormal myospastic activity. The theory does take into account the necessity for physiologic harmony between the components of the stomatognathic system as well as the obvious influence that psychological factors have in the TMD syndrome. At present there are too few data to unequivocally support this theory. However, it is believed that its multifactorial base is far more rational than the other existing theories of TMD dysfunction.

It can be stated that the myofacial aspect of this syndrome is multifactorial, and there can be little doubt that the emotional status of the patient is one of the most important of these factors. However, for any lasting improvement in the patient's symptoms, all of the components of the stomatognathic system must also be functioning within the physiologic parameters of the patient. TMD has both a physical and emotional aspect. Both must be accurately diagnosed and both must be accurately treated.

In summary, essential signs and symptoms of the temporomandibular joint and muscle dysfunction are : pain related to jaw movement and palpation, the restriction of jaw movement, irregular movement pattern, aches in the head, neck, and ears, clicking which may or may not be related to dysfunction, prolonged EMG silent periods, and signs and symptom of bruxism. Often, patient with TMJ joint and muscle dysfunction may have episodes of remission and recurrent exacerbations. These may occur as the result of initial acute attack, or may have developed gradually over the long time. These symptom must be treated palliatively to relieve patient of pain, discomfort, and ultimately psychic stress which can exacerbate the condition. The practioner also must make a correct diagnosis as to eliminate other disturbance which may produce the similar sign or symptom such as Rheumatoid arthitis, infective arthritis, neuralgias, myalgias, Meniere disease, rhematism, and neoplasm. All these disorders leads to TMJ change and thus create a need for a functional or occlusal therapy.



1. Bates JF, Stafford GD and HarrisonA: Masticatory function: a review of the literature, I,The form of the masticatory cycle,Journal of Oral Rehabilitation 2:281- 301, 1975.

2. Mc Neill, C (ed): Craniomandibular Disorders: Guidelines for Evaluation, Diagnosis, and Management. Chicago, Quintessence Publishing, Inc. pp.13-33, 1990.

3. Buxbaum JD et al, The Physiology, Pathology, Pathophysiology, Diagnosis, and Treatment of the Stomatognathic System and Related Facial Pain, University of Maryland School of Dentistry, 2nd edition, 1990, p.173-174.

4. Butler JH, Folke LE, Brandt CL: A descriptive survey of signs and symptoms associated with the myofascial pain-dysfunction syndrome. J Am Dent Assoc 90:625, 1975.

5. Dohrmann R. Laskin DM: An evaluation of electromyographic biofeedback in the treatment of myofascial pain-dysfunction syndrome. J Am Dent Assoc 96:656, 1978.

6. Gessel AH: Electromyographic biofeedback and tricyclic antidepressants in myofascial pain-dysfunction syndrome: Psychological predicators of outcome. J Am Dent Assoc 91:1048, 1975.

7. Goodman P. Greene CS, Laskin DM: Rcsponsc of patients with myofascial pain-dysfunction syndrome to mock equilibration. J Am Dent Assoc 92:755, 1976.

8. Greene CS, Laskin DM: Meprobamate therapy for the myofascial pain-dysfunction (MPD) syndrome: A double-blind evaluation. J Am Dent Assoc 82:587, 1971.

9. Greene CS: Myofaseial pain-dysfunction syndrome: Nonsurgical treatment. In Sarnat BG, Laskin DM, editors: The Temporomandibular Joint, ed 3. Springfield, 111, 1979, Charles C Thomas, publ, pp 315-334.

10. Hannam AG. Internal organization in the human jaw muscles. Critical Reviews in Oral Biology & Medicine. 5(1):55-89,1994.

11. Kawamura Y, ed: Frontiers of oral physiology, vol 1, Physiology of mastication, Basel, 1974.

12. Kraus HT: Muscle tension and the temporomandibular joint. J PROSTHET DENT 13:950, 1963.

13. Laskin DM, Greene CS: Influence of the doctor-patient relationship on placebo therapy for patients with myofascial paindysfunction (MPD) syndrome. J Am Dent Assoc 85:892, 1972.

14. Laskin DM: Etiology of the pain-dysfunction syndrome. J Am Dent Assoc 79:147, 1969.

15. Thexton AJ. Mastication and swallowing: an overview. British Dental Journal. 173(6):197-206, 1992 Oct 10.

16. Wood WW. A review of masticatory muscle function. Journal of Prosthetic Dentistry. 57(2):222-32,1987Feb.

17. 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.

18. Yemm R: Temporomandibular dysfunction and masseter muscle response to experimental stress. Br Dent J 127:508, 1969.

19. Blackwood H. Pathology of the temporomandibular joint. J.A.D.A., 1969: 79: 118.

20. Costen, JB. Neuralgias and ear symptoms associated with disturbed function of the temporomandibular joint. JAMA 1936: 107: 252.

21. Perry, HT. The symptomology of temporomandibular joint disturbance. J. Prosth. dent. 1968: 19: 288.