Predisposing causes for temporomandibular joint dysfunction

Predisposing causes for temporomandibular joint dysfunction

Temporomandibular joint dyslunction Predisposing causes for temporomandibular joint dysfunction A. V. Newton, M.D.S.* University o/Liverpool, School...

246KB Sizes 0 Downloads 77 Views

Temporomandibular joint dyslunction

Predisposing causes for temporomandibular joint dysfunction A. V. Newton, M.D.S.*

University o/Liverpool, School o[ Dental Surgery, Liverpool, England

D e s p i t e the substantial body of opinion that the principal predisposing factor in temporomandibular joint dysfunction is emotional disorder, ~-3 much attention is still focused on the dentition. 4 Ramjford and Ash 5 considered that hypertonicity of the elevator muscles could be due either to influences of the central nervous system or to local disharmony between the functional parts of the masticatory system. Many of the measures taken to relieve joint symptoms are directed toward peripheral factors, such as the elimination of interfering contacts between teeth by occlusal splints or grinding procedures, and the relief of muscle spasm. The effectiveness of these procedures is mainly responsible for the dentition remaining a significant etiolo~c factor in temporomandibular joint dysfunction. In assessing the value of physical treatment, it is difficult to eliminate the effect of the dentist on a patient. Firm reassurance that the symptoms are nothing to worry about and that they can be relieved by wearing a simple appliance may have more profound results than the direct effect of the appliance itself. In addition, some of the procedures advocated for the relief of joint symptoms, if carried out wisely, may, in an otherwise normal patient, precipitate undesirable joint conditions? Thomson 6 has shown no significant correlation between occlusal irregularity and the incidence of joint symptoms by statistical comparison of a large group of patients and a control group of similar size. The occlusal splint is usually only a temporary device. The number of patients who require permanent alteration of their dentitions is extremely small. Further, the reflex protective mechanisms of the muscles controlling the mandible appear to be very efficient. Schaerer, Stallard, and Zander" have shown that the elevator muscles cease active contraction for short periods when teeth encounter experimentally inserted interfering contacts. T h e e:dstence of such a well-developed mechanism which is capable of dealing with the introduction of new variables into the dentition makes it difficult to see how occlusal irregularities *Lecturer in Prosthetic Dentistry.

647

648

Newton

J_ Pros. Dent.

December, 1969

could trigger muscle spasm in a patient with joint pain but no recent alteration to the dentition. In view of the learning capacity of the central nervous system, it would seem that mandibular control would be well integrated with the overall arrangement of the dental arches, except perhaps in situations of gross abnormalities. Therefore, the question is raised as to whether the success of purely physical treatment, of what Schwartz 1 termed the "Pain-dysfunction Syndrome," is due to the indirect effect of association with a sympathetic dentist, or whether there is a direct, physical benefit. As long as medical treatment is provided by human beings, as 013posed to computers, presumably there will be a psychologic component accompanying even the most routine therapeutic procedures. In any situation, this component is difficult to evaluate. Recent work 9-1~ on experimental animals suggests a reasonably clear physiologic basis to at least partly account for the observed benefit which usually follows the implementation of physical treatment. THE G A M M A SYSTEM

An occlusal splint increases the occlusal face height when it eliminates interfering contacts. In a patient suffering from spasm of the mandibular elevator muscles, the insertion of a splint will apply a slight, relatively permanent stretch to these muscles. According to Ritchie-Russell, s the best way to treat muscle spasm in any part of the body is to apply frequent, gentle and passive stretching to the tight muscles. Stretching a muscle usually induces a reflex contraction. However, stretch can be inhibitory to centrally initiated contraction. This effect was first noticed by Hunt 9 who found that on deafferentation of the gastrocnemius muscle of the cat, the rate of firing of the gamma motoneurons increased. Eldred, Granit, and Merton 1° reported similar findings, and proposed that voluntary movement initiated in the central nervous system is relayed through the gamma system before becoming finally effective as muscular contraction. The two immediate relays before the impulses reach the alpha motoneuron are the muscle spindle and the gamma motoneuron. At the spindle, the hnpulses from the central nervous system are integrated with impulses generated by the spindle itself which reflect the state of the muscle. The afferent fibers of the spindle transmit the combined response to the alpha motoneurons. If these latter fibers are cut, the muscle fails to contract but the gamma motoneurons continue to fire at an increased rate. I° Thus, the spindle afferents are excitatory to the alpha motoneurons but also have an inhibitory effect upon the gamma motoneurons. The inhibitory effect is much more prominent at high tension, but at this stage, the inhibition is augmented by the discharge of impulses from Golgi tendon organs. The output from the primary spindle ending can reflect almost completely the state of the muscle in the absence of voluntary control or it may be a combined signal resulting f r o m central and peripheral input. Although the relative proportions of these two signals have not been determined in great detail, two points stand out: ( 1 ) t h e autogenetic inhibition of the gamma drive, and (2)" the ability of the gamma drive to dominate the spindle output when necessary. Eldred, Granit and Melton 1° considered the gamma afferents to eonsititute a

Volume 22 Number 6

Temporomandibular joint dysfunction, 649

highly active and potent system capable of switching the spindle up and down the extremes of its range. This view of the spindle strongly suggests that muscle spasm not obviously initiated by some peripheral lesion is more likely to be due to disturbances in g a m m a drive than to the local state of the muscle itself. SUPRASPINAL CONTROL A variety of excitatory and inhibitory foci which are capable of influencing the firing of g a m m a motoneurons have been found in the central nervous system ~:,f experimental animals. These loci are believed to be part of the reticular system which, although phylogenetically an old system, retains correlative activity ~ t w e e n sensory and motor ,signals. n Domino ~2 and DelP a considered the maintainance c~f vigilance as a prime feature of the reticular system and that its control over mo~,~ primitive reflexes is closely related to this concept of vigilance. In a sleeping ~r resting animal, a painful stimulus produces a withdrawal movement. However, ia the waking animal, this reflex, while still present, is no longer dominant. Reticular inhibition of the polysynaptic flexion reflex releases the antigravity muscles from inhibition, and thus creates the necessary conditions for more general activity such as the maintenance of posture and the act of walking. Finally, in the waking state, diversified and adaptive motor behavior becomes possible in response to sensory input as the reticular system facilitates corticomotor discharges. Dell 1~ has investigated the effect of the reticular system on the various jaw :reflexes in experimental animals. Weak reticular stimulation suppresses the activity of the digastric muscle and releases the masseter nmscle from reciprocal inhibition. In addition, intense stimulation directly facilitates the contraction of the masseter muscle. However, if this level of stimulation is prolonged, the reticular ci~,charge is gradually regulated. T h e suggestion was raised previously that spasm of elevator muscles was most likely due to increased g a m m a firing? ° This suggestion was supported only on cor~siderations of spindle physiology. However, the work of DelW on the reticular system and jaw reflexes supports this contention in more detail. The over-all effect of the reticular system on these reflexes facilitates contraction of the masseter muscle and inhibits the contraction of the digastric muscle. The latter, as the nociceptive flex(~r reflex, ~ is probably most important for avoiding peripheral damage. Therefor,:', intense reticular stimulation will not only tend to initiate strong contraction in the mandibular elevator muscles but, at the same time, will render the nociceptixe inflow from oral structures less effective than it would otherwise be. This reduction in the efficiency of protective reflexes by way of a central mechanism may accom;t for the uncertainty that exists about the role of the dentition in the etiology of the temporomandibular joint dysfunction. EMOTION AND MUSCLE TENSION Emotional exteriorization is effected by parts of the cerebral cortex which have rich connections with the hypothalamus and reticular system. The function of the reticular system is to modify motoneuron activity? '~ The significance of clenching the jaws as an expression of rage has not escaped attention with regard to the etiology of temporomandibular joint dysfunction. 2 Therefore, the basis is established ~7or

650

Newton

J. Pros. Dent. December, 1969

a self-perpetuating or positive feedback cycle centered around the reticular system. A difficult life situation which generates severe frustration may have no outlet other than that of bodily expression. It is likely to manifest itself at first by an unnoticed increase in tone in the mandibular elevator muscles, coupled with a decrease in the sensitivity of protective reflexes. The fine balance of control is disturbed, and it is probably only at this stage that occlusal irregularities begin to play a sufficiently important part in the final triggering of muscle spasm. Ramjford 16 pointed out the striking similarities between his own electromyographic findings in relation to bruxism and those of Lundervold's 17 on the arm and neck muscles of typists under stress. While the posture adopted by typists may predispose them to muscle spasm, no one would attempt to relate the minute details of this disability to irregularities in their typewriter keyboards. It seems equally unlikely that the primary etiology should be attributed to irregularities of the dentition in spasm of the mandibular elevator muscles.

SUMMARY A hypothesis has been proposed which may help to account for the therapeutic effect of passive stretch on the symptoms of dysfunction of the temporomandibular joint. Also, although both local and general factors have been implicated as causative in this condition, recent work suggests that any contribution from the natural, unaltered dentition may be only secondary to central predisposing factors. References 1. Schwartz, L.: Disorders of the Temporomandibular Joint, Philadelphia, 1959, W. B. Saunders Company. 2. Moulton, R. E. : In Schwartz, L-0 Disorders of the Temporomandibular Joint, Philadelphia, 1959, W. B. Saunders Company, pp. 209-220. 3. Franks, A. S. T.: Masticatory Muscle Hyperactivity and Temporomandibular Jeint Dysfunction, J. PRos. DENT. 15: 1122-1131, 1965. 4. Goodfriend, D. J.: Nature and Scope of Dentistry's Care of the Temporomandibular Joints, J. PRos. DENT. 15: 737-758, 1965. 5. Ramjford, S. P., and Ash, M.: Occlusion, Philadelphia, 1966, W. B_ Sannders Company. 6. Thomson, H.: Mandibular Joint Pain, Brit. Dent. J. 107: 243-251, 1959. 7. Schaerer, P., Stallard, R. E., and Zander, H. A.: Occlusal Interferences and Mastication, An Electromyographic Study, J. PRos. DENT. 17: 438-449, 1967. 8- Ritchie-Russell, W.: In Symposium on Skeletal Muscle Spasm, Leicester, 1961, Franklyn Ward and Wheeler, Ltd. 9. Hunt, C. C.: The Reflex Activity of Mammalian Small-Nerve Fibers, J. Physiol. 115: 456-469, 1951. 10. Eldred, E., Gra.nit, R., and Merton, P. A.: Supraspinal Control of Muscle Spindles and its Significance, J. Physiol. 122: 4-98-523, 1953. 11. Granit, R., and Kaada, B. R.: Influence of Stimulation of C.N.S. Structures on the Muscle Spindles in Cats, Acta physiol, scandinav. 27: 130-160, 1952. 12. Domino, E. F.: Pharmacological Analysis of Some Reticular and Spinal Cord Systems, in Jasper et al., editors: Reticular Formation of the Brain, London, 1957, J. & A. Churchill, Ltd. 13. Dell, P.: Reticular Homeostasis and Critical Reactivity, in Moruzzi, G., Fessard, A., and Jasper, H. H., editors: Brain Mechanisms, Amsterdam, 1963, The Elsevier Publishing Company, pp. 82-114. 14. Langley, L. L., and Cheraskin, E.: The Physiological Foundation of Dental Practice, ed. 2, St. Louis, 1956, The C. V. Mosby Company.

Temporomandibular joint dysfunction

Volume22 Number 6

651

15. Keele, C. A., and Neil, E., editors: Samson Wright's Applied Physiology, London~ 196~, Oxford University Press. 16. Ramjford, S. P_: In Ramjford, S. P. and Ash, M., Occlusion, Philadelphia, 1966, W. 8. Saunders Company, p_ 102. 17. Lundervold, A. J. S.: Electromyographic Investigation of Position and Manner of Working in Typewriting, Acta physiol, scandinav_ 24: Suppl. 84, 1951. UNIVERSITY OF LIVERPOOL SCHOOL OF DENTAL SURGERY BOUNDARY PLA~E LIVERPOOL

7,

ENGLAND