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| REVIEW ARTICLE |
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| Year : 2015 | Volume
: 2
| Issue : 2 | Page : 55-62 |
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A systematic review of therapeutic modalities used in sleep bruxism
May Wathiq Al-Khudhairy
Department of Oral and Maxillofacial Surgery, Riyadh Colleges of Dentistry and Pharmacy, Riyadh, Saudi Arabia
| Date of Web Publication | 14-Jul-2015 |
Correspondence Address:
May Wathiq Al-Khudhairy
Department of Oral and Maxillofacial Surgery, Riyadh Colleges of Dentistry and Pharmacy, Riyadh
Saudi Arabia
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1658-6816.160757
Aim: Sleep bruxism (SB) has been present for over a century. There are many treatment modalities in the literature. The objective of this systematic review of randomized controlled clinical therapeutic trials of SB in adults diagnosed by clinical and/or electromyogram and/or polysomnography of SB is to elucidate the most effective of treatment modalities via documentation of the levels of evidence.
Materials and Method: This review conducted electronically on PubMed included only English Full text human clinical trials with or without randomization. Twenty-one articles were included in this review. The therapeutic modalities of SB were classified into behavioral therapy, appliance therapy, local pharmacotherapy, and systemic pharmacotherapy. Each article was further allotted a level of evidence.
Results: This review suggests that Oral appliances expressed the most positive outcome on SB episodes per hour of sleep.
Conclusion: There is still not sufficient evidence to support behavioral and pharmaco-therapeutic approach Keywords: Oral appliances, polysomnography, sleep bruxism, systematic review
How to cite this article:
Al-Khudhairy MW. A systematic review of therapeutic modalities used in sleep bruxism. Saudi J Oral Sci 2015;2:55-62 |
| Introduction | |  |
"Bruxomania" was first described in 1907. [1] Sleep bruxism (SB) has plagued the world over the years. It is defined as a repetitive jaw muscle activity characterized by grinding of the teeth or clenching of the jaw, a parasomnia, according to the International Classification of Sleep Disorders (ICSD-2), a sleep-related disorder, with a high incidence of sleep arousal. [2] SB has been associated with morning headaches, temporomandibular joint disorders (TMD), tooth wear, damage of dental restorations, and masseter muscle hypertrophy. [3] Daytime clenching or bruxing is a separate condition that is secondary to stress, certain medications (selective serotonin reuptake inhibitors) and/or a nervous tic. [3] The American Academy of Orofacial Pain defines SB as an oromotor parafunctional activity, which includes clenching, bracing, bruxing and gnashing of ones teeth. [4] The etiology of SB is multifactorial, including genetic, environmental, psychological, physiological, and pharmacological causes. Hence, its treatment ranges from behavioral modification; which includes patient education, promotion of sleep hygiene, habit control, relaxation, and meditation techniques in the forms of cognitive behavioral therapy, and biofeedback. Promotion of physical therapy in the form of massage, exercises, acupuncture, transcutaneous electrical neuromuscular stimulation, and contingent electrical nerve stimulation. An occlusal direction via the use of oral appliances; which range from occlusal splints, palatal splints, Mandibular orthopedic repositioning appliances (dual action for obstructive sleep apnea and SB), and nociceptive trigeminal inhibition appliance (NTI), and/or dental occlusal adjustments. Last but not least, a pharmacological approach via the use of local anesthetics, botulinum toxin injections, and oral administration of muscle relaxants, benzodiazepines, anticonvulsants, tricyclic antidepressants, etc. [5],[6]
The incidence of SB is inversely proportional to age, with its highest prevalence in children (14-20%), down to 13% in adolescence, further down to 3% in adults over age 60. [3],[4]
Diagnosis of SB is based on several factors; reports of grinding by the subject or ones sleep partner, clinical evidence of dental tooth wear, masseter muscle hypertrophy, history of morning headaches, and the diagnostic gold standard via laboratory polysomngraphy. [7]
The pattern of sleep in subjects with SB is pathognomonic of parasomnic events. According to Lavigne, most episodes of SB occur secondary to a wave of physiologic events following arousal from sleep. A momentary activation in the heart and brain (3-10 s), an increase in the jaw opening and suprahyoid muscle tones, followed by characteristic rhythmic jaw closing muscle contractions and occasional grinding of the teeth. [7]
Polygraphy and audiovisual evaluation of muscle activity is conducted in a sleep laboratory via an electromyogram (EMG) channel on the masseters. An ideal situation would include audiovisual recordings of the muscle activity from EMGs of the jaws and legs, electrocardiogram of heart rate, electroencephalogram of brain activity, and electrooculogram of eye movements during rapid eye movement (REM); all of which score to discriminate and diagnose unusual orofacial or oromandibular movements. [8]
Therefore, the gold standard for diagnosis of SB is the use of audio and video recordings together with sleep polygraphic recordings as this combination permits a more valid and reliable quantitative assessment of oromandibular activities. [8]
Three types of EMG signals can be scored for SB diagnosis; phasic, tonic, and mixed SB. Phasic episodes of SB (also known as rhythmic) occur in 88% of the time [8] involving three or more EMG bursts ranging from 0.25 to 2 s. [9] This type of SB, rhythmic, is more commonly seen in nocturnal teeth grinding and is perceived by their sleep partner. [8]
Tonic episodes of SB (also known as sustained) are not as frequent, occurring <10% of the time and are expressed by 1 EMG burst sustained longer than 2 s. Sustained SB are clinically expressed as nocturnal jaw clenchers [9] with associated tension-type headaches. They have fewer SB episodes per hour of sleep. [10] Mixed episodes of SB include a cocktail of phasic and tonic episodes. [8] The range of muscle activity in SB episodes is between 3 and 66 s with an approximate 9 s as an average. [11]
The disadvantage of laboratory sleep studies is the negative impact on subject compliance, expense, time consumption, and bias as sleep quality is not necessarily similar to ones home environment. The compromise to this is a double edged sword, where sensitivity and specificity are affected once the "gold standard" of SB diagnosis is substituted. There are home alternatives to the "gold standard" via a digital camera or an intraoral tooth contact sensor (attached to an occlusal appliance) or a mandibular movement sensor; which improve subject compliance, cost less and are simply more practical.
Objectives of the review
A systematic review of randomized controlled clinical therapeutic trials of SB in adults diagnosed by clinical and/or EMG and/or polysomnography of SB was performed to elucidate the most effective of treatment modalities via documentation of the levels of evidence.
| Materials and Methods | | |
Data collection was attained following a systematic review of the literature pursuing the protocol dictated by PRISMA [Figure 1]. Henceforth, a PubMed search was electronically conducted using keywords "treatment," and "SB." Furthermore, refinement of the search included only human clinical trials expressed in full text English articles. | Figure 1: PRISMA protocol used in this study to report articles for systematic review
Click here to view |
An initial 190 full-text articles in the English language were identified and screened that pertained to the treatment of SB in human. Of those, only 38 clinical trials were assessed for eligibility. Furthermore, 21 articles were deemed suitable to be incorporated into this qualitative review.
Levels of evidence were assigned as per criteria dictated by the center for evidence-based medicine [Table 1].
| Results | | |
The following classification system was improvised to extrapolate the needed information from the 21 articles included in this systematic review. It is as follows:
- Behavioral therapy in SB
- Appliance therapy of SB
- Local pharmacotherapy in SB
- Systemic pharmacotherapy of SB.
Behavioral therapy in sleep bruxism
Patient education, habit control, biofeedback, and cognitive behavioral therapy have been trending SB treatment since the early 1970s. A total of 3 behavioral therapy studies met the inclusion criteria set by PRISMA guideline [Table 2]. | Table 2: Studies evaluating the EMG activity of the temporalis muscle after biofeedback
Click here to view |
Appliance therapy of sleep bruxism
Appliance therapy of SB is common practice amongst dental practitioners in lieu of the damage to dental structures and restorations ensuing from untreated SB. A total of 12 studies using appliances met the inclusion criteria of this review. Varying degrees of success have been obtained with different types of appliances and the results of these studies are summarized in [Table 3]. | Table 3: Summary of diff erent types of appliances used for the management of SB
Click here to view |
Local pharmacotherapy in sleep bruxism
Botulinium toxin has gained popularity in the past decade; its use has had equivocal results. 2 studies met the inclusion criteria in this study [Table 4].
Systemic pharmacotherapy of sleep bruxism
Pharamacotherapy for SB has been used for over three decades in the belief that if the cause (stress and psychosocial variables) is addressed, then the effect will be alleviated. The review found studies that used bromocriptine, clonazepam and clonidine that met the inclusion criteria. The results of these studies are summarized in [Table 4].
| Discussion | | |
Behavioral therapy
The result of this systematic review elaborated the importance of behavioral therapy in the form of biofeedback. Albeit few studies met the inclusion criteria [Table 2], it is imperative to be aware of its use.
One form of behavioral therapy is contingent electrical stimulation (CES) where the feedback is delivered to the skin, lip, and masticatory muscles via an electrical stimulus. This stimulus is generated secondary to detection of a grinding and/or clenching episode. During sleep, this stimulus is intended to interrupt the sleep cycle in order to stop the SB episode. [6]
All three studies provided a positive response to the decrease in the number of EMG episodes per hour of sleep. It should be noted that two of these studies, the author, [12],[13] has a financial interest in Medotech (Grindcare). In the study by Conti et al. [14] an interesting finding to the practicality of using this CES is its negative effect on sleep quality and the myofascial pain associated with the SB. There was no alteration in that aspect, which agrees with the known literature that sleep is important in controlling pain. [32] It is not the quantity of sleep as it is the quality of sleep that is of utmost importance. CES may alleviate the SB episodes of SB at the expense of their quality of sleep. It is interesting to elaborate that Conti et al. study [14] might have transformed the subjects into tonic SB having fewer SB episodes per hour of sleep and fewer grinding events; a model described by Lund, the pain adaptation model in which these subjects experience pain in their jaw and fatigue of their masticatory muscles which in turn decreases their parafunctional activities (SB). [33] To conclude, recent systematic reviews [5] with meta-analysis on CES biofeedback failed to show any effect on reducing SB episodes.
Appliance therapy
Most of the studies [15],[17],[21],[23],[25] confirmed SB in their study participants by laboratory polysomnography. Others [7],[16],[18],[20],[22] measured EMG activity at the subjects' home to confirm SB. The appliances used included a maxillary occlusal splint, mandibular advancement appliance, stabilization splint, palatal splint, nociceptive trigeminal inhibitory splint, and maxillary mandibular oral appliance. There was a statistically significant reduction [7],[16],[17],[18],[20],[21],[22],[23],[25] in SB episodes and/or decrease in EMG activity in the clenching muscles in most of the studies.
Van der Zaag et al. [15] evaluated Stabilization Splint verses a palatal splint, and the study yielded equivocal results. This confirms the subjective behavior of SB and confounders that affect its effective treatment.
Out of the 12 studies on appliance therapy, 2 [19],[24] compared appliance therapy verses other forms of therapy for SB.
Ommerborn et al. [19] recruited the subjects without any laboratory Polysomnography or EMG activity confirming their SB status, therefore, had a much larger sample (n = 57). The study evaluated appliance therapy verses behavioral therapy in the form of cognitive behavioral therapy "Bruxcore-Bruxism Monitoring Device). There was no statistical significance between either on the reduction of SB episodes. This might be due to the nature of the subjects recruited. They might by daytime clenchers and not true SB.
Madani et al. [24] compared stabilization splint to Gabapentin 300 mg/h in SB therapy and yielded statistically significant reduction in masseter muscle contraction. The gabapentin group had the added benefit of improved sleep.
Despite the positive impact of appliances on SB, there are few contrary ones, which is to be expected. Albeit randomized controlled trials, these studies fail to elaborate the exact mechanism precluding to SB reduction. Needless to say, oral appliances are amongst the most popular management techniques to address SB. They protect the teeth, reduce orofacial pain, and decrease the SB episodes per hour of sleep. [34],[35]
Local pharmacotherapy
Lee et al. [26] and Shim et al. [27] both expressed positive response via botulinum toxin A injection into the masseter [26],[27] and temporalis [27] muscles. There was a statistically significant decrease in EMG activity in the injected muscle but not necessarily a decrease in occurrence of the contraction. That is, the SB was still present, and this is in support of it being a centrally mediated phenomenon. Botulinum toxin A injected into the masseters and anterior temporalis muscles shows favorable results, however, one must take into consideration the muscle atrophy that occurs with repeated botulinum toxin A injections, cost and hour glass appearance post injection. It is important to note that Shim et al. [27] conducted the first study with Polysomnography to prove the positive therapeutic benefit of Botulinium Toxin A on SB.
Systemic pharmacotherapy
Two studies, Lobbezoo et al. [28] and Lavigne et al. [29] evaluated SB therapy with Bromocriptine, a dopamine D2 receptor agonist. These studies were conducted well over a decade ago at a time when Satoh and Harada [36] initially proposed a dopaminergic involvement responsible for SB. There was no statistical significant reduction in SB episodes per hour of sleep. The study with favorable results [28] had only 2 participants, which questions its reliability. In that study, more than half the initially recruited participants dropped out due to encountering severe adverse reactions to the bromocriptine. Furthermore, these adverse effects of this drug necessitate the prescription of a dopamine receptor antagonist peripherally such as Motillium (domperidone) [29] to counteract the side-effects of nausea, dizziness and palpitations. Hence, bromocriptine cannot be recommended in the treatment of SB.
Saletu et al. [30] evaluated benzodiazepine, Clonazepam 1 mg verses placebo in a sample that had comorbid movement disorders such as restless leg syndrome, periodic limb movements, insomnia amongst others. Despite the favorable results of statistically significant fewer SB episodes per hour of sleep, one must consider the bias since all other studies in this review excluded subjects having psychiatric, neurologic disorders, medications exacerbating SB and other parasomnias.
In a double-blind randomized control trial, Cara et al. [31] tested SB subjects with placebo or clonidine. There were contradictory results.
These studies all elaborate the multifactorial etiologic nature of SB, a central nervous system phenomenon that is fueled by stress and pain behavior more than to its structural components. [37],[38],[39]
| Conclusion | | |
The etiology of SB remains a gray area in the literature. Polysomnographic display of EMG activity of the clenching muscles is uniquely expressed by each SB subject. Hence, there are different ways that these SB subjects respond to treatment. Therefore, when reviewing the literature, it comes to no surprise that when certain approaches, appliances, and/or medications were prescribed the response was different by the SB subjects; where it was a successful therapeutic approach in one, it had no therapeutic effect in another. To this day, a century after its first mention in the literature, there is not one known therapy that has been proven to eliminate completely and/or cure SB. To conclude, the most promising findings are from those of oral appliances. Each subject should be addressed subjectively and approached in a step-wise manner, Biofeedback coined with appliance therapy and Botulinum Toxin injections might fair better than one specific treatment approach.
Financial support and sponsorship
Nil.
Conflict of interest
There are no conflicts of interest.
| References | | |
| 1. | Marie MM, Pietkiewicz M. Bruxomania (gritting of the teeth). Rev Stomatol 1907;14:107-16.  |
| 2. | American Academy of Sleep Medicine. International Classification of Sleep Disorders: Diagnostic and Coding Manual. Revised. 2 nd ed. Westchester: American Academy of Sleep Medicine; 2005. |
| 3. | Huynh N, Manzini C, Rompré PH, Lavigne GJ. Weighing the potential effectiveness of various treatments for sleep bruxism. J Can Dent Assoc 2007;73:727-30. |
| 4. | De Leeuw R, editor. The American academy of orofacial pain. In: Orofacial Pain. Guidelines for Assessment, Diagnosis and Management. 4 th ed. Chicago: Quintessence; 2008. |
| 5. | Wang LF, Long H, Deng M, Xu H, Fang J, Fan Y, et al. Biofeedback treatment for sleep bruxism: A systematic review. Sleep Breath 2014;18:235-42. |
| 6. | Ilovar S, Zolger D, Castrillon E, Car J, Huckvale K. Biofeedback for treatment of awake and sleep bruxism in adults: Systematic review protocol. Syst Rev 2014;3:42. |
| 7. | Dubé C, Rompré PH, Manzini C, Guitard F, de Grandmont P, Lavigne GJ. Quantitative polygraphic controlled study on efficacy and safety of oral splint devices in tooth-grinding subjects. J Dent Res 2004;83:398-403. |
| 8. | Lavigne GJ, Kato T, Kolta A, Sessle BJ. Neurobiological mechanisms involved in sleep bruxism. Crit Rev Oral Biol Med 2003;14:30-46. |
| 9. | Kato T, Thie NM, Huynh N, Miyawaki S, Lavigne GJ. Topical review: Sleep bruxism and the role of peripheral sensory influences. J Orofac Pain 2003;17:191-213. |
| 10. | Schwartz BS, Stewart WF, Simon D, Lipton RB. Epidemiology of tension-type headache. JAMA 1998;279:381-3. |
| 11. | Kardachi BJ, Clarke NG. The use of biofeedback to control bruxism. J Periodontol 1977;48:639-42. [ PUBMED] |
| 12. | Jadidi F, Castrillon E, Svensson P. Effect of conditioning electrical stimuli on temporalis electromyographic activity during sleep. J Oral Rehabil 2008;35:171-83. |
| 13. | Jadidi F, Castrillon EE, Nielsen P, Baad-Hansen L, Svensson P. Effect of contingent electrical stimulation on jaw muscle activity during sleep: A pilot study with a randomized controlled trial design. Acta Odontol Scand 2013;71:1050-62. |
| 14. | Conti PC, Stuginski-Barbosa J, Bonjardim LR, Soares S, Svensson P. Contingent electrical stimulation inhibits jaw muscle activity during sleep but not pain intensity or masticatory muscle pressure pain threshold in self-reported bruxers: A pilot study. Oral Surg Oral Med Oral Pathol Oral Radiol 2014;117:45-52. |
| 15. | Van der Zaag J, Lobbezoo F, Wicks DJ, Visscher CM, Hamburger HL, Naeije M. Controlled assessment of the efficacy of occlusal stabilization splints on sleep bruxism. J Orofac Pain 2005;19:151-8. |
| 16. | Landry ML, Rompré PH, Manzini C, Guitard F, de Grandmont P, Lavigne GJ. Reduction of sleep bruxism using a mandibular advancement device: An experimental controlled study. Int J Prosthodont 2006;19:549-56. |
| 17. | Harada T, Ichiki R, Tsukiyama Y, Koyano K. The effect of oral splint devices on sleep bruxism: A 6-week observation with an ambulatory electromyographic recording device. J Oral Rehabil 2006;33:482-8. |
| 18. | Baad-Hansen L, Jadidi F, Castrillon E, Thomsen PB, Svensson P. Effect of a nociceptive trigeminal inhibitory splint on electromyographic activity in jaw closing muscles during sleep. J Oral Rehabil 2007;34:105-11. |
| 19. | Ommerborn MA, Schneider C, Giraki M, Schäfer R, Handschel J, Franz M, et al. Effects of an occlusal splint compared with cognitive-behavioral treatment on sleep bruxism activity. Eur J Oral Sci 2007;115:7-14. |
| 20. | Van Selms MK, Lobbezoo F, Visscher CM, Naeije M. Myofascial temporomandibular disorder pain, parafunctions and psychological stress. J Oral Rehabil 2008;35:45-52. |
| 21. | Landry-Schönbeck A, de Grandmont P, Rompré PH, Lavigne GJ. Effect of an adjustable mandibular advancement appliance on sleep bruxism: A crossover sleep laboratory study. Int J Prosthodont 2009;22:251-9. |
| 22. | Amorim CF, Vasconcelos Paes FJ, de Faria Junior NS, de Oliveira LV, Politti F. Electromyographic analysis of masseter and anterior temporalis muscle in sleep bruxers after occlusal splint wearing. J Bodyw Mov Ther 2012;16:199-203. |
| 23. | Arima T, Tomonaga A, Toyota M, Inoue SI, Ohata N, Svensson P. Does restriction of mandibular movements during sleep influence jaw-muscle activity? J Oral Rehabil 2012;39:545-51. |
| 24. | Madani AS, Abdollahian E, Khiavi HA, Radvar M, Foroughipour M, Asadpour H, et al. The efficacy of gabapentin versus stabilization splint in management of sleep bruxism. J Prosthodont 2013;22:126-31. |
| 25. | Takahashi H, Masaki C, Makino M, Yoshida M, Mukaibo T, Kondo Y, et al. Management of sleep-time masticatory muscle activity using stabilisation splints affects psychological stress. J Oral Rehabil 2013;40:892-9. |
| 26. | Lee SJ, McCall WD Jr, Kim YK, Chung SC, Chung JW. Effect of botulinum toxin injection on nocturnal bruxism: A randomized controlled trial. Am J Phys Med Rehabil 2010;89:16-23. |
| 27. | Shim YJ, Lee MK, Kato T, Park HU, Heo K, Kim ST. Effects of botulinum toxin on jaw motor events during sleep in sleep bruxism patients: A polysomnographic evaluation. J Clin Sleep Med 2014;10:291-8. |
| 28. | Lobbezoo F, Soucy JP, Hartman NG, Montplaisir JY, Lavigne GJ. Effects of the D2 receptor agonist bromocriptine on sleep bruxism: Report of two single-patient clinical trials. J Dent Res 1997;76:1610-4. |
| 29. | Lavigne GJ, Soucy JP, Lobbezoo F, Manzini C, Blanchet PJ, Montplaisir JY. Double-blind, crossover, placebo-controlled trial of bromocriptine in patients with sleep bruxism. Clin Neuropharmacol 2001;24:145-9. |
| 30. | Saletu A, Parapatics S, Anderer P, Matejka M, Saletu B. Controlled clinical, polysomnographic and psychometric studies on differences between sleep bruxers and controls and acute effects of clonazepam as compared with placebo. Eur Arch Psychiatry Clin Neurosci 2010;260:163-74. |
| 31. | Carra MC, Macaluso GM, Rompré PH, Huynh N, Parrino L, Terzano MG, et al. Clonidine has a paradoxical effect on cyclic arousal and sleep bruxism during NREM sleep. Sleep 2010;33:1711-6. |
| 32. | Rompré PH, Daigle-Landry D, Guitard F, Montplaisir JY, Lavigne GJ. Identification of a sleep bruxism subgroup with a higher risk of pain. J Dent Res 2007;86:837-42. |
| 33. | Lund JP. Pain and control of muscles. In: Orofacial Pain and Tempromandibular Disorders. New York: Raven Press; 1995. p. 103-15.re. |
| 34. | Dao TT, Lavigne GJ, Charbonneau A, Feine JS, Lund JP. The efficacy of oral splints in the treatment of myofascial pain of the jaw muscles: A controlled clinical trial. Pain 1994;56:85-94. |
| 35. | Okeson JP. Management of Temporomandibular Disorders and Occlusion. 5 th ed. St. Louis: Mosby; 2003. p. 428. |
| 36. | Sato T, Harada Y. Depression of the H-reflex during tooth grinding in sleep. Physiol Behav 1972;9:893-4. [ PUBMED] |
| 37. | DeBoever JA, Carlsson GE. Etiology and differential diagnosis. In: Zarb GA, Carlsson GE, Sessle BJ, Mohl ND, editors. Temporomandibular Joint and Masticatory Muscle Disorders. Copenhagen: Munksgaard; 1994. p. 171-87. |
| 38. | Lobbezoo F, Lavigne GJ. Do bruxism and temporomandibular disorders have a cause-and-effect relationship? J Orofac Pain 1997;11:15-23. |
| 39. | Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally, not peripherally. J Oral Rehabil 2001;28:1085-91. |
[Figure 1]
[Table 1], [Table 2], [Table 3], [Table 4]
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