This course was published in the January 2019 issue and expires January 2022. The authors have no commercial conflicts of interest to disclose. This 2 credit hour self-study activity is electronically mediated.
After reading this course, the participant should be able to:
- Define sleep bruxism, as well as its physiologic and etiologic mechanisms.
- Discuss the prevalence of sleep bruxism, and potential risk factors associated with this disorder.
- Explain the implications of sleep bruxism for oral health management.
Bruxism is an oral behavior defined as repetitive jaw-muscle activity characterized by clenching or grinding of the teeth and/or bracing or thrusting of the mandible.1 It is further described according to its circadian presentation: It may occur during waking hours (awake bruxism) or sleep (sleep bruxism).1 While the two share common risk factors and lead to similar consequences to the stomatognathic structures, they appear to have different pathophysiology and etiologic mechanisms.2 Awake bruxism mostly involves tooth clenching or tapping and jaw bracing, with or without tooth contact.3 Grinding is rarely noted during waking hours. Sleep bruxism is of particular interest in dentistry because of its potential role in dental restoration breakdown, tooth damage and wear, stomatognathic muscle pain, and temporomandibular joint disorders.4
According to the International Classification of Sleep Disorders (third edition), sleep bruxism is a sleep related movement disorder.5 It is defined as an involuntary trigeminal motor activity characterized by episodic and repetitive jaw muscle activity, with occasional tooth grinding or jaw clenching.5 The activity is associated with what is known as rhythmic masticatory muscle activity (RMMA).6 Reports have demonstrated that approximately 60% of “normal” or non-sleep-bruxing individuals exhibit RMMA; however, the frequency of RMMA in sleep bruxism has been shown to be three times greater.7
Sleep bruxism occurs primarily in non-rapid eye movement (NREM) sleep stages 1 and 2 (light sleep), with only 10% occurring during rapid eye movement sleep.7 In addition, the activity primarily manifests in the second and third cycles of sleep.8 Episodes will mostly occur in the transition from deep to light sleep.8
Previous research demonstrated that sleep bruxism occurs in association with physiological events that will precede, occur concurrently with, or follow RMMA.9 These events involve a temporary increase in the sympathetic nervous system tone approximately four to eight minutes prior to the event, resulting in sleep arousal, as well as tachycardia.8,10,11 An increase in the jaw opening muscle activity is observed approximately one second prior to RMMA. Also seen within approximately one second of the event is a rise in systolic and diastolic blood pressure, as well as fluctuations in breathing amplitude.12–14
Periodic arousals during sleep appear to be a normal response of the brain to environmental and internal physiologic stimuli.15 In normal sleepers, arousals occur between six and 14 times per hour of normal sleep. In NREM sleep, arousals tend to manifest in a structured and repetitive manner known as the cyclic alternating pattern (CAP),15 which consists of activation of electroencephalogram and electrocardiogram patterns every 20 to 60 seconds during NREM sleep.16 These events appear to be a mechanism for maintaining body homeostasis and protection during sleep. In fact, 80% of NREM sleep bruxism episodes take place in association with CAPs.17
It has been estimated that 8% to 31% of the general adult population and anywhere from 3.5% to 40.6% of the pediatric population are aware of teeth grinding during sleep.18,19 Reported prevalence varies depending on how sleep bruxism is defined and the methods used to determine the diagnosis. Most prevalence studies to date rely on self-report from surveys, which significantly limits the validity of the data. The reported prevalence of this condition is said to decrease with age, and ranges from 14% to 20% among children 11 years and younger to 13% among young adults (age 18 to 29), and 3% among those 60 and older.4 Sleep bruxism tends to be variable over time,20 as well as night to night,21 further confounding attempts to determine accurate epidemiological data. It appears that prevalence is no different in male and females.18 However, Baba et al22 noted that males might be more at risk. Although there are few reports on the progression or persistence of sleep bruxism, it appears it may be a persistent behavior over time.23
PATHOPHYSIOLOGY AND ETIOLOGY
Traditionally, dentistry has considered sleep bruxism to primarily have an anatomical etiology. Currently, there is no single clear pathophysiologic mechanism identified as responsible for these episodes. Most data would suggest they likely involve multiple mechanisms, including genetic and environmental factors. This section will focus on occlusal factors, genetics and environmental influences, psychosocial factors, and sleep related breathing disorders, as they relate to the genesis of sleep bruxism.
Occlusal Factors: In 1955, Bober24 reported the prevalence of sleep bruxism was higher in subjects with so-called malocclusions than in groups that had what he described as normal occlusion. More recent research has demonstrated the notion of peripheral causes, such as occlusion or other anatomical factors, is doubtful.4,25,26 In a double-blind, randomized controlled trial, 11 subjects had strips of gold foil glued either on a selected occlusal contact area or on the buccal surface of the same tooth (control). The foil was left in place for eight days. The active occlusal interference caused a significant reduction in the number and amplitude of sleep bruxism events. The authors noted that none of the subjects developed signs and/or symptoms of temporomandibular disorders throughout the study period.27 In addition, it has been demonstrated that elimination of occlusal interferences has no influence on jaw muscle activity during sleep.28,29 Based on these results, as well as data from more recent studies, it must be concluded the central nervous system, rather than peripheral factors, primarily regulates the genesis of sleep bruxism.30
Genetic and Environmental Factors: It is often thought that sleep bruxism is a hereditable trait, yet a specific gene has not yet been identified. A recent polysomnography-based study investigating familial aggregation in 111 individuals with sleep bruxism found that 37% had at least one first-degree relative who reported sleep bruxism.31 Other recent work has shown single nucleotide polymorphisms related to serotonergic neurotransmission and in the dopaminergic pathway gene DRD3 may play a role in the risk for this activity.32–34
Caffeine is known to be a central nervous system stimulant and has been shown to increase the risk of sleep bruxism by 1.5 times.35,36 Alcohol consumption, especially if in close proximity to sleeping, may not only negatively affect sleep architecture, it also affects serotonin and dopamine levels in the central nervous system. This activity may be at least partially responsible for the initiation or exacerbation of sleep bruxism.37,38 Compared to nonsmokers, smokers have been shown to have a twofold greater risk for the disorder (potentially via stimulation of the dopamine system).36–38
Certain pharmacologic agents are also known to induce or enhance sleep bruxism. These are typically selective serotonin reuptake inhibitors and amphetamines, as well as illegal substances, such as 3,4-methylenedioxymethamphetamine and cocaine.36,37 A recent systematic review reported that duloxetine, paroxetine, venlafaxine, barbiturates and methylphenidate may be associated with sleep bruxism.39
Psychosocial Factors: Studies have suggested that children and adults reporting self-awareness of tooth grinding are more anxious, aggressive and hyperactive.35,40–42 Other psychological factors, such as nervousness, competitive behaviors, emotional lability and poor coping mechanisms, have been associated with sleep bruxism.43–46 Giraki et al47 found that subjects with high sleep bruxism activity tend to feel more stressed at work and in daily life. However, studies by Watanabe et al,48 as well as van Selms et al,49 failed to demonstrate a relationship between these episodes and stress (anticipated and experienced). In light of these conflicting reports, conclusions concerning the role of stress in sleep bruxism should be viewed cautiously.
Sleep Related Breathing Disorders: Sleep bruxism has often been found to be associated with sleep disordered breathing (SDB).50–52 It has been suggested that sleep bruxism may play a protective role in restoring normal airway patency and respiration after a respiratory event.51,53 While some reports have demonstrated a significant reduction in these episodes in patients treated for SDB with adenotonsillectomy,54 mandibular advancement devices55,56 or a continuous positive airway pressure machine,57 the association appears mostly related to the occurrence of arousals during sleep resulting from the respiratory event.52 The absence of consistent RMMA at the end of abnormal respiratory events suggests other factors are involved in the genesis of sleep bruxism.58 In addition, in individuals with concomitant SDB and sleep bruxism, 54% of the sleep bruxism events occurred within 0 to 10 seconds following the respiratory event, 25.5% occurred preceding the event, and 19.5% occurred without any temporal relationship to a respiratory event.59,60 Due to the frequent comorbidity of these two entities, further studies are needed to clarify the nature of this apparent link.
Sleep bruxism is a sleep related movement disorder that may affect a significant portion of the population. To date, prevalence data is based largely on questionnaires and subjective reports. This activity appears to differ from awake bruxism in etiopathology and should therefore be specified when discussing these behaviors. Due to the clinical consequences of sleep bruxism, dentistry considers this disorder to be of significant importance. Throughout the dental and sleep literature, there are numerous hypotheses to explain the etiology and pathophysiology of sleep bruxism. At present, a multifactorial etiological explanation has accepted that genetics, environmental and psychosocial factors, sleep related breathing disorders, and neurochemical mechanisms might all play a role. The long-held belief in dentistry that sleep bruxism is significantly related to anatomical or peripheral factors currently lacks evidentiary support. Further investigation is needed to better define this behavior and, ultimately, establish appropriate evidence-based therapies when deemed necessary.
- Lobbezoo F, Ahlberg J, Glaros AG, et al. Bruxism defined and graded: an international consensus. J Oral Rehabil. 2013;40:2–4.
- Carra M. Sleep-related bruxism. Curr Sleep Med Rep. 2018;4:28–38.
- Shetty S, Pitti V, Satish Babu CL, Surendra Kumar GP, Deepthi BC. Bruxism: a literature review. J Indian Prosthodont Soc. 2010;10:141–148.
- Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K. Bruxism physiology and pathology: an overview for clinicians. J Oral Rehabil. 2008;35:476–494.
- AASM. International classification of sleep disorders (ICSD-3). Available at: https://learn.aasm.org/Public/Catalog/Details.aspx?id=%2FgqQVDMQIT%2FED y86PWgqgQ%3D%3D&returnurl=%2fUsers%2fUserOnlineCourse.aspx%3f LearningActivityID%3d%252fgqQVDMQIT%252fEDy86PWgqgQ%253d%253d. Accessed December 12, 2018.
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- Lavigne GJ, Rompré PH, Poirier G, Huard H, Kato T, Montplaisir JY. Rhythmic masticatory muscle activity during sleep in humans. J Dent Res. 2001;80:443–448.
- Huynh N, Kato T, Rompré PH, et al. Sleep bruxism is associated to micro-arousals and an increase in cardiac sympathetic activity. J Sleep Res. 2006;15:339–346.
- Lavigne GJ, Huynh N, Kato T, et al. Genesis of sleep bruxism: motor and autonomic-cardiac interactions. Arch Oral Biol. 2007;52:381–384.
- Carra MC, Rompré PH, Kato T, et al. Sleep bruxism and sleep arousal: an experimental challenge to assess the role of cyclic alternating pattern. J Oral Rehabil. 2011;38:635–642.
- Kato T, Montplaisir JY, Guitard F, Sessle BJ, Lund JP, Lavigne GL. Evidence that experimentally induced sleep bruxism is a consequence of transient arousal. J Dent Res. 2003;82:284–288.
- Dumais IE, Lavigne GJ, Carra MC, Rompré PH, Huynh NT. Could transient hypoxia be associated with rhythmic masticatory muscle activity in sleep bruxism in the absence of sleep-disordered breathing? A preliminary report. J Oral Rehabil. 2015;42:810–818.
- Nashed A, Lanfranchi P, Rompré P, et al. Sleep bruxism is associated with a rise in arterial blood pressure. Sleep. 2012;35:529–536.
- Khoury S, Rouleau GA, Rompré PH, Mayer P, Montplaisir JY, Lavigne GJ. A significant increase in breathing amplitude precedes sleep bruxism. Chest. 2008;134:332–337.
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- Carra MC, Macaluso GM, Rompré PH, et al. Clonidine has a paradoxical effect on cyclic arousal and sleep bruxism during NREM sleep. Sleep. 2010;33:1711–1716.
- Manfredini D, Winocur E, Guarda-Nardini L, Paesani D, Lobbezoo F. Epidemiology of bruxism in adults: a systematic review of the literature. J Orofac Pain. 2013;27:99–110.
- Manfredini D, Restrepo C, Diaz-Serrano K, Winocur E, Lobbezoo F. Prevalence of sleep bruxism in children: a systematic review of the literature. J Oral Rehabil. 2013;40:631–642.
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- Lavigne GJ, Guitard F, Rompré PH, Montplaisir JY. Variability in sleep bruxism activity over time. J Sleep Res. 2001;10:237–244.
- Baba K, Haketa T, Clark GT, Ohyama T. Does tooth wear status predict ongoing sleep bruxism in 30-year-old Japanese subjects? Int J Prosthodont. 2004;17:39–44.
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- Bober H. Grundlagen der therapie der hatiptformen des (nachtlichen) zahneknirschens. Oesterreichische Zeitschrift Fur Stomatologie. 1955;52:450–453.
- 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.
- Lobbezoo F, Rompré PH, Soucy JP, et al. Lack of associations between occlusal and cephalometric measures, side imbalance in striatal D2 receptor binding, and sleep-related oromotor activities. J Orofac Pain. 2001;15:64–71.
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- Lobbezoo F, Ahlberg J, Manfredini D, Winocur E. Are bruxism and the bite causally related? J Oral Rehabil. 2012;39:489–501.
- Khoury S, Carra MC, Huynh N, Montplaisir J, Lavigne GJ. Sleep bruxism-tooth grinding prevalence, characteristics and familial aggregation: a large cross-sectional survey and polysomnographic validation. Sleep. 2016;39:2049–2056.
- Oporto GHt, Bornhardt T, Iturriaga V, Salazar LA. Genetic polymorphisms in the serotonergic system are associated with circadian manifestations of bruxism. J Oral Rehabil. 2016;43:805–812.
- Abe Y, Suganuma T, Ishii M, et al. Association of genetic, psychological and behavioral factors with sleep bruxism in a Japanese population. J Sleep Res. 2012;21:289–296.
- Oporto GHt, Bornhardt T, Iturriaga V, Salazar LA. Single nucleotide polymorphisms in genes of dopaminergic pathways are associated with bruxism. Clin Oral Investig. 2018;22:331–337.
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- Bertazzo-Silveira E, Kruger CM, Porto De Toledo I, et al. Association between sleep bruxism and alcohol, caffeine, tobacco, and drug abuse: a systematic review. J Am Dent Assoc. 2016;147:859–866,e4.
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- 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;22:251–259.
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Featured image by PIYAPONG THONGCHAROEN/ISTOCK/GETTY IMAGES PLUS
From Decisions in Dentistry. January 2019;5(1):28–31.