Ineffective or Harmful Bruxism Treatments

This section briefly describes widely used--but, for the most part ineffective--bruxism treatment modalities.  In each of the cases below, the picture which emerges from the literature is simple:   DON'T USE IT.

Psychotherapy

The belief that bruxism is traceable to stress and other emotional and psychological factors gives rise to a variety of psychotherapeutic approaches (Murray, 1998). For instance, calmness and self-confidence may be fostered by listening to progressive relaxation, visual imagery, or autosuggestion tapes just before going to sleep (Horowitz, 1989).   Evidence that this approach is effective: non-existent.

Wakeful EMG Feedback

Another psychological approach to stress reduction resorts to instrumentation. During bruxing, the relevant muscles are active, and this increased activity or tenseness can in turn be measured with an electromyograph (EMG: electro = electric; myo = muscle; graph = record). During treatment sessions at home or the laboratory, the patient sits or reclines comfortably. One or more pairs of recording electrodes are then attached to the surface of the skin, in close contact to appropriate muscles (e.g., masseter muscles). These electrodes transmit information about the level of muscle activity to a computer monitor. The patient is instructed to consciously lower that level below a threshold line (also visible on the screen). Gradually, by becoming alert to the presence of muscle tension, patients may develop techniques for reducing that tension, and hence, bruxism.

One problem with this approach is expense--of the machinery and expert guidance. Another problem is that muscles can be tense for a variety of reasons, and not simply because patients grind or clench. An unpleasant recollection, for instance, may result in a high reading, although it has nothing to do with bruxing. Moreover, as in the case of many other psychotherapeutic approaches, the training takes place in the daytime, when the patient is awake and when his behavior is under conscious control. It is not at all clear that such learning is transferable to the unconscious, sleeping, brain.

The main problem, though, is lack of evidence that EMG feedback does the patient any good. In one study, for example, subjects undergoing this treatment for two weeks, along with a program of listening to relaxation tapes, seemed to brux no less than control subjects (who received no treatment whatsoever) while they were receiving this treatment or six months after treatment ceased (Pierce and Gale, 1988).

Massed Negative Practice

Another controversial approach is the so-called massed negative practice, a scholarly variation of the folk principle of reverse psychology. Here the patient is told to voluntarily clench the jaw for five seconds, relax it for five seconds, and repeat this procedure five times in succession, six different times a day, for two weeks (Thompson, Blount, and Krumholtz, 1994). Alternatively, the duration of the clenching period may be individually tailored to each patient, with each clench continuing to the point of discomfort (Pierce and Gale, 1988).

This technique involves little or no cost and it does not interfere with the patient's sleep. But, by itself, this approach damages the teeth and may aggravate other bruxism symptoms (Feehan and Marsh, 1989, p. 181). Notwithstanding early enthusiastic clinical reports, at the moment the evidence for the effectiveness of this approach is meager at best. In one study, for example, subjects undergoing this treatment performed no better than controls while they were receiving this treatment or six months after treatment ceased (Pierce and Gale, 1988).

Exercise

Quinn (1995) and many others suggest isokinetic and stretching exercises of the mandible. Such exercises may or may not help alleviate bruxism, and they may perhaps be used to complement other approaches, but it seems unlikely that they could ever be used as the sole therapeutic approach.  Evidence that this approach is effective: non-existent.

Drugs

Both the stress and the brain malfunction etiological theories give at times rise to the use of anti-anxiety agents, muscle relaxers, and other drugs. Most authorities, however, feel that, at best, drugs in use now are of limited value in the treatment of the great majority of chronic bruxers, and that they often involve, moreover, untoward side effects.  Evidence that this approach is effective: non-existent.

Equilibration Therapy

Some people believe that bruxism is traceable to malocclusion (bad bite).  They therefore suggest eliminating this putative cause through orthodontic adjustment (=occlusal adjustment or equilibration). According to Ramfjord (1961), such adjustment was first used by Karolyi in 1901. But, to begin with, the role of malocclusion in causing bruxism is in doubt. Also, this technique is irreversible, for it involves the grinding down of some teeth (and artificially restoring others). Moreover, even if malocclusion triggered the bruxing habit, there are no guarantees that its removal will eliminate or ameliorate bruxing, for by now the habit may have become entrenched and self-sustaining. In view of these difficulties, and despite some spectacular claims in the older bruxism literature, it is perhaps safe to say that the majority of practitioners agree by now that "occlusal equilibration is costly and relatively ineffective" (Shatkin, 1992).   A recent review, for instance, concludes that "no reliable evidence has demonstrated that occlusal interference can cause nocturnal bruxism, or stop it, if the naturally occurring interferences are removed" (Clark et al., 1999).

Needless to say though, in severe and borderline cases of malocclusion, when equilibration would have been considered anyway, equilibration will continue to be used, and may constitute a part of a bruxism treatment program. But even then, this approach will need to be supplemented by other therapies aimed at eliminating what by now is probably an ingrained behavioral pattern.

Splints

By far the most common "treatment" regime for bruxism relies on the time-honored procedure of splint therapy (e.g., Karolyi, 1906, cited in Ramfjord, 1961, p. 23; Matthews, 1942). In the United States alone, some 3.6 million splints (aka nightguards, biteguards, occlusal splints, biteplates, removable appliances, or interocclusal orthopedic appliances) are annually prescribed by dentists in an effort to combat bruxism (1.6 million splints), myofacial pain (0.9 million), and TMJ pain (1.1 million)--a $1 billion industry (Pierce et al., 1995, by 2014, probably $2 billion). Much current research on the treatment of bruxism has been centered on the use of such dental appliances. Many patent applications describe splints for the treatment of bruxism (e.g., U.S. Pat. Nos. 5,666,973 and 5,823,193).

A Hard Splint

(source: internet)

splint.gif (26646 bytes)

There are many variations of this appliance. The most common is the customized, hard acrylic, variety. Some dentists prefer a customized appliance made of soft, rubber-like, elastomeric material. One can also purchase prefabricated soft splints at a pharmacy. They cost much less than the custom-made ones, but they don’t provide as close a fit.

Another, far less popular, variation is the hydrostatic splint, a water-bearing pressure-equalizing appliance(see U.S. Pat. No. 4,211,008). This prefabricated splint does not require dental impressions or the manufacture of customized appliances. Instead, this disposable splint can be purchased through a dentist, ready-made for use, and is claimed to fit the mouths of most users.

The Hydrosplint aqualize.jpg (8870 bytes)

In practice, however, the pads often slip from under the teeth, the appliance wanders in the mouth, and may even be expelled during sleep. These shortcomings could be readily overcome by combining the idea of a hydrostatic splint with the taste-based appliance (see this link).  The pads would be attached to the sleeves, and could be connected to each other either along the contours of the appliance, as they do now, or directly.

The central question about all splints is: Just how effective are they?

Like other therapies, the splint has its fair share of aficionados. For example, in one study (which, however, lacked controls and hence could not rule out a placebo effect, and which, moreover, relied for the most part on subjective measures of improvement), long-term reductions in symptoms of bruxism were noted even in patients who wore the splint for six months (Sheikholeslam, Holmgren, and Riise, 1986). However, even in this highly favorable report of splint therapy, "the signs and symptoms recurred to the pre-treatment level within 1-4 weeks in about 80% of the patients."

Many other researchers feel that the splint does not diminish bruxing behavior, in the long term, nor alleviates most symptoms and consequences. They insist, in fact, that the splint only provides a measure of protection for the teeth, and, in the case of grinders, a moderation of the sound. And even this is purchased at a price: the splint is uncomfortable to wear, some patients remove it during sleep, and it may negatively affect one's bite, cause tooth decay, and lead to degenerative joint disease (Messing, 1992, p. 438).

The splint’s popularity can probably be ascribed to the gap between dental research and practice--most dentists are simply too overworked to keep up with the dental literature. Also, the splint provides some protection for the teeth, and most dentists are naturally more interested in protecting teeth than in such things as appearance or the temporomandibular joint. For a short while, too, the splint is often effective in treating the closely related TMDs (Messing, 1992, p. 395), and there is a tendency often, in both lay and professional circles, to think of these two conditions as more closely related than they actually are. Moreover, for a short while, the splint may be truly successful in stopping bruxism, a temporary effect that may lull patients and dentists alike to its limited value over the long term. Then there is the placebo effect: any kind of treatment seems better than no treatment at all. In one study of TMD patients, for instance, 64% reported a striking improvement of their condition following two mock equilibration sessions (cited in Biondi and Picardi, 1993, p. 90). In two other studies, the artificial temporary creation of gross biting abnormalities led to reductions of masseter EMG activity during sleep in 90% (Rugh, Barghi, and Drago, 1984) and 44% (Shiau and Syu, 1995) of the subjects. Because all positive views of splint therapies merely claim improvement, not cure or cessation of bruxing, the use of a double-blind design and control groups seems essential. Yet, this essential experimental design feature is lacking in most studies of splint therapy. Lastly, there is the belief that nothing can really be done to treat bruxism, or, if something can be done, that it involves a lot of hard work on the part of both patient and clinician, so one might as well lower one's sights and settle for a device with a proven, if temporary, track record.

Given the popularity of the splint, its immense profitablitiy to the dental establishment, and some of the claims that have been made about its effectiveness, it may be worth while to cite a few skeptics: "The most common treatment is a rubber device, worn over the teeth at night, called a mouthguard. This does not actually prevent or cure the bruxism, but it will prevent damage to the teeth when bruxism occurs" (Hartmann, 1994, p. 601). "Occlusal splints worn at night did not significantly reduce bruxing-clenching activity in bruxing subjects" (Kydd and Daly, 1985). Pierce and Gale (1988) found that bruxing decreased by about 50% during two weeks of splint therapy, but that, following withdrawal of treatment, it returned to baseline levels. Klineberg (1994) concludes that occlusal splints "will protect the teeth, but will not alter the habit in the long term." Splints, he says, become "worn when in use and wear and tear on the splint indicates continuation of the habit, even though patient[s] might report that they were no longer aware of clenching their teeth. The longer term effects of splint therapy indicate that clenching returns after the splint has been removed, or with continued use of it." (p. 15). According to Rugh et al. (1989), splint therapy is effective at first, but "the usual trend with longer treatment is to lose its effects. In other words, one usually sees a dramatic decrease or increase in EMG activity the first few nights of splint usage, followed by a gradual return to pretreatment EMG values." Perl (1994) says that "there is no way of preventing the clencher or bruxer from engaging in such parafunctional habits. Regardless, the clinician may be able to decrease the potential for destruction by adding a nightguard to the treatment protocol." Sheikholeslam, Holmgren, and Riise (1982) conclude that "when patients stopped wearing the splint, "signs and symptoms of nocturnal bruxism returned to the pre-treatment level within a period of 1-4 weeks in 80% of the patients. . . . Thus, the splint therapy in most cases must be regarded as a symptomatic treatment" (p. 142).  Dao and Lavigne (1998) say that although "splints may limit dental damage, their efficacy remains unestablished" (p. 355).  The comparative ineffectiveness of the traditional splint is also "borne out by the common clinical finding that patients may bite large teeth marks into night bite guards and frequently fracture appliances" (Trenouth, 1979).

Moreover, the use of such splints may sometimes adversely affect the patient's occlusion, e.g., cause an open bite (cf. Ahlin, 1991; Wiygul, 1991): "As with any technique, splint therapy has both positive and negative effects. If the complications are known and understood, they can be included in the treatment planning process and discussed with the patient before treatment begins. The most common complication of splint therapy is the creation of changes in the patient's occlusion" (Messing, 1991, p. 437). Another complication of splint therapy is decay under the splint, which may in turn cause caries and gum inflammation. Still another problem is severe degenerative joint disease (Messing, 438).

Splint-Induced Open Bite: After wearing a hard splint for a year, this patient can no longer bring his front teeth together
ob2.jpg (43528 bytes)

Magdaleno & Ginestal (2010) for example, studied the effects of a splint on three patients and reported that it led to "irreversible occlusal alterations."  On occasion, they concluded, "splints can provoke severe occlusal alterations and other complications, which are rarely alluded to in the literature.  Such splints are reported to negatively affect the condyle-disk relation in patients who exhibit disk displacement with reduction and to modify breathing features in patients with obstructive sleep apnea, although further studies are required to unequivocally demonstrate these findings. Finally, the splint seems to modify peripheral information at the level of the Central Nervous System, leading to modifications in corporal postural tone."  Lamentably, your good dentist is almost certainly unaware of these effects.  Ignorance in such cases is both bliss and good for business.  S/he can in good conscience prescribe the splint--just like your run-of-the-mill oncologist prescribes  ill-advised preventive mastectomies, thyroid removals, or chemotherapy to cancer patients.

To sum up, the splint may help slow down the destruction of teeth and it may moderate the sounds of grinding. In some patients, it may bring about a temporary reduction in bruxing, lowering it to about 50% of its former value. This effect, though real, may be nothing more than the well-known placebo effect, or it could be ascribable to the fact that the nighttime introduction of just about anything into the mouth temporarily alleviates bruxism symptoms. In a few patients, the splint may produce long-lasting improvements, although we are far from being sure about this more moderate claim. In other cases, it may intensify bruxism.

Thus, the splint may or not stop bruxism for a while, it partially protects the teeth, and it moderates grinding sounds. For most patients, it accomplished little else. A patient may wear this uncomfortable appliance for years and years, perhaps risking an open bite where none existed before (a minor inconvenience, to be sure, but still annoying--try to eat artichoke leaves, a hard salami slice, or sunflower seeds with lower and upper front teeth that cannot come together), and still destroy her teeth, still develop headaches, still change her appearance for the worse, still develop TMD. Given these shortcomings, even the most enthusiastic advocates of splint therapy would have to concede that, at the very least, something else is required to treat the millions of chronic bruxers whose condition is getting worse despite faithfully wearing this appliance for years.

References

Ahlin J. H. (1991). Clinical application of remoldable appliances for craniomandibular disorder. Cranio Clinics International, 1, 65-79.

Biondi, M., & Picardi, A. (1993). Temporomandibular joint pain-dysfunction syndrome and bruxism: etiopathogenesis and treatment from a psychosomatic integrative viewpoint. Psycother Psychosom, 59, 84-98.

Blount, R. L., Drabman, N. W., Wilson, W., & Stewart, D. (1982). Reducing severe diurnal bruxism in two profoundly retarded females. Journal of Applied Behavior Analysis, 15, 565-71.

Clark, G. T., Koyano, M. S., & Browne, P. A. (1993). Oral motor disorders in humans. CDA Journal 21, 19-30.

Clark GT, Tsukiyama Y, Baba K, & Watanabe, T.  (1999).  Sixty-eight years of experimental occlusal interference studies: what have we learned? Journal of Prosthetic Dentistry, 82(6):704-13.

Clarke, J. H. and Reynolds, P. J. Suggestive hypnotherapy for nocturnal bruxism: a pilot study. 1991. American Journal of Clinical Hypnosis 33(4): 248-53.

Dao, T. T & Lavigne, G. J. 1998. Oral splints: the crutches for temporomandibular disorders and bruxism?Crit Rev Oral Biol Med, 9(3):345-61.

Ellison, J. M. , and Stanziani P. (1993). SSRI-associated nocturnal bruxism in four patients. Journal of Clinical Psychiatry, 54, 432-434.

Feehan, M. & Marsh, N. (1989). The reduction of bruxism using contingent EMG audible biofeedback: A case study. Journal of Behavioural Therapy and Experimental Psychiatry, 20, 179-183.

Golan, H. 1989. Temporomandibular joint disease treated with hypnosis. American Journal of Clinical Hypnosis, 31: 269-274.

Hartmann, E. (1994). Bruxism. In M. H. Kryger, T. Roth, & W. C. Dement (Eds). Principles and Practice of Sleep Medicine (2nd ed., pp. 598-601). Philadelphia: W. B. Saunders.

Horowitz, L. G. Freedom from Teeth Grinding and Night Clenching. Rockport: Tetrahedron, 1989.

Kaplan, A. A., Goldman J. R. General Concepts of Treatment. In Kaplan, A. S. and Assael, L. A. 1992. Temporomandibular Disorders. Philadelphia: Saunders, pp. 388-394.

Klineberg, I. Bruxism: aetiology, clinical signs and symptoms. 1994. Australian Prosthodontic Journal 8: 9-17.

Kydd, W. L. and Daly, C. Duration of Nocturnal tooth contacts during bruxing. 1985. Journal of Prosthetic Dentistry, 53(5): 717-721.

LaCrosse, M. B. Understanding change: Five-year follow-up of brief hypnotic treatment of chronic bruxism. 1994. American Journal of Clinical Hypnosis 36(4): 276-181.

Lehvila, P. Bruxism and magnesium: Literature Review and Case Reports. Proc. Finn. Dent. Soc. 70: 217-224, 1994.

Lerman, M. D. (1987). The hydrostatic splint: new muscle-directed TMJ-PDS treatment technique. CDS Review, 80, 30-34.

Long, J, H., Jr. (1998). A device to prevent jaw clenching. Journal of Prosthetic Dentistry, 79, 353-4.

Magdaleno, F. & Ginestal, E. (2010).  Side effects of stabilization occlusal splints: a report of three cases and literature reviewCranio. 28(2):128-35.

Matthews, E. (1942). A treatment for the teeth-grinding habit. Dental Record, 62, 154-155.

Messing, S. G. (1992). Splint Therapy. In A. S. Kaplan & L. A. Assael. Temporomandibular Disorders (pp. 395-454). Philadelphia: Saunders.

Miguel, A. M. V, Montplaisir, J., Rompre, P. H., Lund, J. P., & Lavigne G. J. (1992). Bruxism and other orofacial movements during sleep. Journal of Craniomandibular Disorders, 6, 71-81.

Murray, B. A psychologist investigates what sets people’s teeth on edge. 1998. APA Monitor Online, 29 (6).

Perl, M. L. (1994). Parafunctional habits, nightguards, and root form implants. Implant Dentistry, 3, 261-3.

Ploceniak, C. Bruxism and magnesium, my clinical experiences since 1980. Revue de Stomatologie et de Chirurgie Maxillo-Faciale, (French; English abstract in Medline). 1990. 91 Suppl. 1:127

Quinn, J. H. Mandibular exercises to control bruxism and deviation problems. 1995. Cranio 13(1): 30-34.

Ramfjord, S. P. (1961). Bruxism, a clinical and electromyographic study. Journal of the American Dental Association, 2, 21-44.

Rijsdijk, B. A., Van Es R. J., Zonneveld, F. W., Steenks, M. H., & Koole, R. (1998). Botulinum toxin type A treatment of cosmetically disturbing masseteric hypertrophy. Nederlands Tijdschrift voor Geneeskunde, 142, 529-32.

Rugh, J. D., Barghi, N. and H. Drago, C. J. Experimental occlusal discrepancies and nocturnal bruxism. 1984. Journal of Prosthetic Dentistry 51: 548-553.

Rugh, J. D., Graham, G. S., Smith, J. C., & Ohrbach, R. K. (1989). Effects of canine versus molar occlusal splint guidance on nocturnal bruxism and craniomandibular symptomatology. Journal of Craniomandibular Disorders, 3, 203-210.

Shatkin, A. J. Bruxism and Bruxomania. 1992. Rhode Island Dental Journal 25(4): 7-10.

Sheikholeslam, A. Holmgren, K. and Riise, C. 1986. A clinical and electromyographic study of the long-term effects of an occlusal splint of the temporal and masseter muscles in patients with functional disorders and nocturnal bruxism. Journal of Oral Rehabilitation 13: 137-145.

Shiau, Y. Y., Syu, J. Z. Effect of working side interferences on mandibular movement in bruxers and non-bruxers. Journal of Oral Rehabilitation, 1995, 22: 145-151.

Thompson, B. H., Blount, B. W., & Krumholtz, T. S. (1994). Treatment approaches to bruxism. American Family Physician, 49, 1617-22.

Trenouth, M. J. (1979). The relationship between bruxism and temporomandibular joint dysfunction as shown by computer analysis of nocturnal tooth contact patterns. Journal of Oral Rehabilitation, 6, 81-87.

Van Dongen, C. A. (1992). Update and literature review of bruxism. Rhode Island Dental Journal, 25, 11-16.

Watson, T. S. (1993). Effectiveness of arousal and arousal plus overcorrection to reduce nocturnal bruxism. Journal of Behavior Therapy and Experimental Psychiatry 24, 181-185.

Wiygul, J. P. (1991). Maxillary full-coverage appliance. Cranio Clinics International, 1, 39-53.

Yustin, D., Neff, P., Rieger, M. R., and Hurst, T. Characterization of 86 bruxing patients and long-term study of their management with occlusal devices and other forms of therapy. 1993. Journal of Orofacial Pain 7: 54-60.

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