INTRODUCTION
Bruxism, whether or not patients are conscious of it, remains one of the prevalent conditions encountered by dentists in their daily practice. In recent years, the phenomenon of bruxism has captured increasing interest among sleep specialists. The term “bruxing” originates from the Greek term brychein odontas translating to grinding one’s teeth [1]. “Bruxomania” was initially introduced in odontological literature as a potential causative factor for pyorrhea, being described as a purely psychological condition within the framework of occlusal neuroses [2].
Given this historical background, bruxism has traditionally been viewed as a stress-related oral parafunction that includes clenching, bracing, gnashing, and grinding of the teeth, whether during sleep or while awake [1]. Consequently, the primary focus of most clinicians has been on addressing the oral consequences of bruxism, such as tooth wear, tooth fractures, tooth mobility, failure of prostheses, masseter muscle hypertrophy, and orofacial pain, including temporomandibular disorders (TMD). Despite the absence of a clearly established understanding of the etiology and management of bruxism, purely peripheral factors, such as malocclusion, and solely psychological pathophysiology are no longer regarded as relevant in light of current evidence [3,4]. Instead, clinicians and researchers are now directing their attention toward the multifaceted etiology of bruxism, recognizing it as a significant topic in the medical community. Sleep bruxism (SB), previously categorized as a sleep-related movement disorder, was better understood through the use of polysomnography (PSG), which identified rhythmic masticatory muscle activity (RMMA) as a crucial biomarker of SB [5]. Currently, it is proposed that the definition of SB should be reconsidered. This viewpoint suggests that not all cases of SB ought to be classified as a disorder, considering that SB may possess physiological roles.
While SB is a long-standing concern, it presents numerous controversial issues such as diagnostic challenges, etiology, association with sleep disorders, orofacial pain, and treatment methodologies. Consequently, this review aims to delve into these topics through an extensive literature analysis, with the goal of augmenting clinicians’ comprehension of SB and aiding them in managing this complex condition. This involves examining the evolving concept of SB as both a disorder and a behavior.
MATERIALS & METHODS
To conduct a thorough review of the current literature on SB in adults, the author employed a targeted search strategy on PubMed. The selected keywords for this search included “sleep bruxism,” “polysomnography,” “obstructive sleep apnea,” “sleep disorders,” “pathophysiology,” “etiology,” and “prevalence.” The literature search, carried out up to 30 January 2024, initially yielded 283 references: 83 papers for [“Sleep Bruxism” AND “Polysomnography”], 48 papers for [“Sleep Bruxism” AND “Obstructive Sleep Apnea”], 69 papers for [“Sleep Bruxism” AND “Etiology”], 24 papers for [“Sleep Bruxism” AND “Pathophysiology”], 39 papers for [“Sleep Bruxism” AND “Prevalence], and 47 papers for [“Sleep Bruxism” AND “Sleep Disorders]. A total of 27 studies were excluded as duplicates from the search results.
The review of selected full-text English-language papers was conducted after screening titles and abstracts of all identified studies by H.K.K and H.R.S. Inclusion criteria included: 1) research with adult participants (aged over 18 years); 2) research focusing on SB diagnosis based on self-report, clinical examination, or PSG, excluding awake bruxism (AB); 3) studies employing observational studies, case-controlled studies, or randomized controlled clinical trials (RCT); and 4) systematic reviews or expert reviews. Seventy-three studies on children, 62 studies of specific publication types, including editorials and letters, and 47 studies without accessible full-text were excluded. Ultimately, 101 papers were included in this review.
RESULTS
Diagnosis and Assessment
Despite the growing interest in SB, diagnosing and assessing SB remains a significant challenge in both clinical and research domains. This section will discuss research findings related to the diagnosis and assessment of SB.
In 1996, Lavigne et al. [6] initially tested the clinical validity of SB using PSG. The authors introduced SB research diagnostic criteria (SB-RDC): 1) a positive report of tooth grinding during sleep and 2) the detection of SB in a sleep laboratory. The laboratory criteria included: 1) >4 bruxism episodes per hour of sleep, and 2) >6 bruxism bursts per episode and/or >25 bruxism bursts per hour, plus at least one episode with tooth-grinding sounds [6]. The predictive values of SB-RDC for clinical diagnosis were 83.3% for bruxers and 81.3% for controls [6]. However, the validity of the RDC criteria for SB, particularly the binary cut-off point of 4 episodes, has been criticized due to concerns about variability in the frequency and severity of SB, especially in those cases that are inconsistent [7-9]. Given these concerns, the recommendation is that binary cut-off points for diagnosing SB should be avoided [10]. Nevertheless, the SB-RDC has represented a crucial advancement in understanding and diagnosing SB. Additionally, the intensity of SB was classified into low (2 episodes per hour), moderate (3–4 episodes per hour), and high (>4 episodes per hour) in the modified criteria [11].
In 2013, an international expert group reached a consensus to define bruxism as a repetitive jaw-muscle activity characterized by clenching or grinding of the teeth and/or bracing or thrusting of the mandible [12]. This expert group also introduced a graded diagnosis system consisting of three steps: 1) possible SB/AB based solely on self-report, 2) probable SB/AB based on both self-report and clinical examination, and 3) definite SB/AB based on self-report, clinical examination, and PSG [12]. This innovative diagnostic grading system suggests that bruxism may be a disorder necessitating diagnosis and appropriate treatment [12]. This paradigm-shifting consensus has propelled discussions about the characteristics of SB as a behavior, a risk factor, or a disorder [13]. Another key criticism of the 2013 grading system concerns its cumulative nature and reliance on instrumental assessment, which purportedly increases diagnostic precision. The primary concern is the lack of a direct correlation between the grading system and prognosis and treatment outcomes. This misalignment is particularly noticeable due to the poor consistency across different grading levels [13-15].
The issues raised were addressed in the revised expert consensus of 2018, which emphasized the objective of focusing on “grading the evidence of bruxism” predominantly as a behavior [10]. This modification contends that bruxism should not be classified as a disorder but rather considered a behavior that may serve as either a risk or a protective factor for certain clinical conditions [10]. The 2018 grading system categorizes SB/AB into three distinct categories: 1) possible SB/AB based exclusively on a positive self-report; 2) probable SB/AB contingent on a positive clinical examination, with or without a positive self-report; and 3) definite SB/AB reliant on a positive instrumental assessment, regardless of the presence of a positive self-report or clinical examination [10]. The revised system facilitates the diagnosis of cases with PSG-confirmed SB, even in the absence of a positive self-report or clinical examination.
The third edition of the International Classification of Sleep Disorders (ICSD-3), released in 2014, incorporated the grading concept of SB [5,12] and now includes SB as a sleep-related movement disorder [5]. Diagnosing SB requires reports of regular or frequent grinding sounds and the presence of one or more of the following: clinical signs and/or symptoms consistent with reports of tooth grinding during sleep [12]. These may include abnormal tooth wear, transient morning jaw muscle pain or fatigue, temporal headaches, or jaw locking upon awakening [5,12]. Despite the widespread usage of ICSD-3 criteria in diagnosing SB, the reliance on self-reports and observable signs and symptoms limits their validity for a definitive SB diagnosis. The diagnostic criteria for SB in the ICSD-3 show fair to moderate concordance with PSG diagnoses, exhibiting an area under the curve (AUC) that ranges from 0.55 to 0.75 [16]. Interestingly, no significant differences in self-reports were noted except for the high frequency of reported SB in the SB group compared to the control group diagnosed by PSG [16]. The most discriminative items for achieving an AUC of 0.75—with a specificity of 90%—were frequent reports (more than 4 times a week) of SB accompanied by transient morning jaw pain or fatigue [16].
Clinical indicators, such as self-reported teeth grinding and observed tooth wear, are associated with more frequent RMMA episodes [17]. However, a meta-analysis revealed disparities between self-reports, clinical assessments, and instrument-driven evaluations [18]. In this regard, the validity of portable electromyography (EMG) tools, such as bitestrip® and bruxoff® (http://www.bruxoff.com/en/), demonstrates relatively higher congruence with PSG (87.8% agreement for bitestrip; 83.3% sensitivity, 72% specificity for bruxoff) compared to self-reports and clinical examinations [19,20]. Nevertheless, it is advised against using these as standalone diagnostic tools due to the potential for high false-positive rates, particularly in patients with secondary SB [19,20].
In summary, a variety of diagnostic tools can be applied in the assessment of SB. Nevertheless, it is crucial to consider the evidence level when diagnosing SB. The use of binary cut-off points with PSG is discouraged, promoting the consideration of SB activities as a continuum rather than distinct categories. Further studies are necessary to advance the clinical application of these tools, improving their evidence basis and practical feasibility.
Epidemiology
Estimating the prevalence of SB is challenging due to the lack of awareness and the variability in how bruxism is defined. In a survey comprising 2019 adult participants, the prevalence of SB was reported at approximately 8% [21]. This prevalence varied based on the type of bruxism, with about 6% for the grinding type and around 20% displaying the clenching type [21].
A systematic review by Manfredini et al. [22], conducted in 2013, found that the prevalence of SB in adults was relatively consistent at 12.3% ± 3.1%. The same author also noted that the prevalence of SB is higher in children with a broader range of variability, from 3.5% to 40.6% [23]. This variation is mainly attributed to the reliance on parental reports and the children’s limited self-awareness. These two systematic reviews independently found no gender differences in the prevalence of SB, and noted that its occurrence tends to decline with age [22,23].
A 2019 umbrella review by Melo et al. [24] found that SB prevalence ranges from 3.5%–45.6% in children/adolescents and 1.1%–15.3% in adults. In a study consisting of 1042 individuals who completed a questionnaire and underwent PSG tests, 5.5% were positive for both the questionnaire and PSG, 7.4% were positive based only on PSG, and 12.5% were positive according to the questionnaire alone [25].
Previous epidemiologic studies suggest that interpreting the prevalence of SB requires careful consideration and may vary by age.
Orofacial Consequences of Sleep Bruxism and Their Evidence
Traditionally, SB has been primarily viewed as a disorder due to its potential to cause dental and musculoskeletal complications, such as damage to periodontal tissues, TMD, tooth wear, teeth fractures, dental implants, or restorations [26-28]. Although a systematic review [29] indicates an increased risk factor for dental implant failure in probable bruxers, several systematic reviews suggest a lack of evidence connecting SB to oral health disorders [26,27,30,31].
Most studies investigating the relationship between bruxism and tooth wear rely on self-reporting [27,32]. This reliance is due to the subjective nature of SB diagnosis based on self-reporting, which reflects not only the patient’s account but also their dentist’s opinion. Thus, many studies reporting a positive correlation between tooth wear severity and self-reported bruxism may be subject to bias [33].
Clinical and EMG features of subjects with possible SB and significant teeth attrition were compared to sex-/age-matched controls without tooth wear [34]. The study group reported a higher prevalence of self-reported and partner-reported SB and morning facial pain compared to controls. However, EMG activity showed no differences between the groups [34]. This finding suggests that the presence of tooth wear cannot be used as a direct biomarker for active SB [32,34].
In exploring the connection between SB and primary headaches, a systematic review conducted in 2014 included two studies [35]. These studies highlighted a significant elevation in the risk of tension-type headache (TTH) and migraine (odds ratio [OR] 3.12) associated with SB [36] and an increased risk of chronic migraine (OR 3.8) [37]. However, the systematic review concluded with insufficient scientific evidence to definitively establish these associations [35-37]. This was attributed to several limitations, such as the need for more stringent diagnoses of SB, dependence on self-reported data, and the inability to differentiate between AB and SB [38].
Two systematic reviews identified a positive relationship between self-reported SB and painful TMD and/or joint noise [31,38]. Yet, studies employing objective measures found that individuals with orofacial pain who are bruxers experienced fewer bruxism episodes than bruxers without pain [39], which supports the pain adaptation model [14,40].
In a case-controlled study by Raphael et al. [41], involving 123 females with chronic myofascial TMD and 40 age-/sex-matched controls without TMD, sleep background EMG activity was examined. The findings revealed mild, consistent EMG activities in the masseter muscles among the pain group during sleep, suggesting that this masticatory muscle activity might contribute to the underlying mechanism of TMD pain [41].
A comparative study of patients diagnosed with TMD and SB confirmed via PSG included two groups: one with myofascial pain and an age-/sex-matched control group without myofascial pain [42]. The study found no significant differences in SB-related parameters [42], indicating the reduced importance of SB in orofacial pain context [43].
In a case-controlled study by Ahci et al. [44] using PSG, a significant correlation was found between temporomandibular joint (TMJ) sounds and the number of bruxism bursts. However, intra-articular pain in the TMJ was not related to SB parameters. A recent scoping review of SB and TMDs identified a low or negative correlation between instrument-assessed SB and TMDs [45]. The prevailing view that SB is a likely causative factor for TMD is now being challenged and requires further evaluation [44-46].
Conversely, recent findings from PSG studies have indicated a potential positive relationship between obstructive sleep apnea (OSA) and TMD [47-49]. These studies suggest that an ongoing increase in masticatory muscle activity during sleep may be associated with the relationship between OSA and TMD [50].
Currently, the evidence does not strongly support the negative impact of SB on orofacial health. To enhance understanding of this relationship, it is crucial to emphasize the need for rigorous study designs that include appropriate assessment tools and consider the heterogeneity of TMD subgroups.
Polysomnographic Features of SB
Understanding the variability in polysomnographic results is essential for interpreting data on SB. Prior research utilizing PSG to study SB has explored the presence of a first-night effect. A retrospective PSG analysis with SB subjects revealed no significant first-night effects [51]. Conversely, first-night effects due to considerable inter-night variability of SB were noted in a study investigating potential SB patients with home PSG [8]. A comparative PSG study showed the highest concordance rate in RMMA severity, ranked as follows: control (93.3%), low SB (76.9%), and moderate-high SB (60%). This indicates the varying impact of first-night effects depending on the severity of SB [9]. Therefore, verifying low RMMA frequency in suspected cases on the first night might necessitate multiple PSG tests.
Table 1 summarizes the findings of polysomnographic features in patients with SB. Numerous investigations have examined the influence of SB on sleep structure, sleep patterns, sleep stages, and sleep quality [52-60]. Current studies involving subjects with SB identified using PSG demonstrate that healthy individuals with SB generally exhibit a normal sleep macrostructure, with minor variations in specific sleep parameters [47,61-63]. Sleep efficiency and arousal index in patients with SB were within the normal range [53,54,64] or even higher than the non-SB group [59]. Lavigne et al. [52] noted differences in sleep microstructure parameters, except for K-complexes, supporting the concept that healthy individuals with SB are typically good sleepers.
Numerous studies have attempted to identify changes in rapid eye movement (REM) sleep in patients with SB [48-50,63], yet REM sleep does not appear to be significantly affected by SB [6,52,60]. Several studies, however, report inconsistent results. In a comparative study [64], although sleep recordings showed that sleep structures of SB groups showed similar sleep structure to controls, but the sleep stage dynamics of the SB group were different. Particularly, REM sleep and N2 were significantly more fragmented in the SB group, and the occurrence of RMMA was often preceded by extended periods of N3 [64]. This indicates a potential relationship between RMMA in SB and the regulation of REM sleep as well as the dissipation of homeostatic sleep pressure [64]. Moreover, Wieczorek et al. [53] observed a higher percentage of REM sleep, whereas Macaluso et al. [54] reported a decrease in REM sleep within the SB group.
The initiation of RMMA/SB episodes often correlates with transient autonomic arousals, leading to cortical activation [65-67]. Toyota et al. [66] discovered that the RMMA response to transient arousals varied according to the sleep stage, with the highest response in N1, and the lowest in N3 and REM. This observation is consistent with previous studies noted that RMMA mostly occurs in light non-REM (NREM) [6,54,66]. The authors proposed that RMMA may be particularly susceptible to arousal-related brainstem activation in SB compared to controls, suggesting that transient arousal serves as a physiological substrate rather than a direct trigger for RMMA [66].
A comprehensive PSG study investigating the relationship between simple snoring and SB [68] reported that 75.9% of patients with simple snoring exhibited SB, indicating a frequent co-occurrence of both conditions. Additionally, the bruxism episode index (BEI) showed a positive correlation with the maximum snore intensity [68]. Furthermore, Dumais et al. [69] identified a correlation between the oxygen desaturation index and BEI, suggesting SB as a physiological response that may protect against transient hypoxia.
In a study by Miki et al. [65], every RMMA episode coincided with a sleep arousal. Noteworthy, physical movements were more prevalent during arousals that included RMMA than those that did not [64], indicating that SB is frequently accompanied by body movements associated with arousal, in alignment with findings by Imai et al. [55].
Several studies have proposed that the disinhibition of trigeminal motor neurons or brief activation of the reticular activating system could lead to increased activity in autonomic and motor systems in individuals with SB [70,71]. However, the precise mechanism that triggers RMMA during micro-arousals remains unclear [62,63,71].
Etiology and Pathophysiology
Pathophysiological mechanisms of SB remain limited. While identifying the etiology of SB is more challenging, growing evidence supports the idea that SB is associated with complex factors centered on central rather than peripheral regulation [72,73]. Consequently, occlusal adjustment has been excluded as a treatment for SB.
Previous research has identified psychological factors, smoking, alcohol, medications (e.g., selective serotonin reuptake inhibitors), medical conditions (e.g., parkinsonism), and genetic predispositions as potential contributors to bruxism [4,56,74-77]. Nevertheless, the etiology of SB remains partially understood, partly due to the absence of a consistent definition of SB. This section will provide a brief review of recent evidence concerning the etiology of SB.
Experimental studies
Experimental evidence supports the protective physiologic role of masticatory muscle activities in patients with OSA [78], demonstrating that changes in the vertical position of the mandible and masseter muscle EMG activity consistently precede adjustments in airflow, as measured by nasal flow pressure (NFP). Specifically, mandibular depression correlated with a significant median reduction in NFP by 40.9% (p = 0.007) [78]. These findings underscore the critical role of mandibular movements in modulating airflow during sleep [78]. A classic study involving patients with OSA further highlighted the role of masseter muscle contractions in jaw stabilization for breathing [79]. These experimental studies affirm the strong association between masticatory muscle activities and respiratory regulation during sleep.
The genesis of RMMA
RMMA is more frequent and intense in those with SB, often marked by tooth grinding noise [58,71]. No significant difference in non-RMMA oromotor activities between SB and control groups has been observed [58]. Consequently, RMMA may serve as a biomarker for SB, potentially leading to dental complications in affected individuals [63].
Most episodes of RMMA are linked to sleep arousal [64-66]. This process often involves elevated sympathetic activity and increased EMG activity in the jaw-opening muscles [65-67] (Fig. 1). Additionally, several studies have suggested that sleep arousals may provide a “permissive window” for the initiation of RMMA episodes [71,80-82].
The relevance to sleep
The relationship of SB with sleep physiology has been extensively investigated. Currently, SB is widely recognized as associated with arousal phenomena. An arousal response signifies a substantial change in sleep depth, resulting in transitions to lighter sleep stages or complete awakening. Characterized by physiological changes, this response encompasses the complex interplay of neural, cardiovascular, and muscular systems, emphasizing the importance of specific brain regions and neurotransmitters in initiating and modulating these responses [73].
Most RMMA episodes are preceded by increased alpha EEG activity and tachycardia [83], highlighting the role of cortical and autonomic involvement in the initiation of SB. About 80% of RMMA episodes occur concurrently with the cyclic alternating pattern (CAP) [82,83]. CAP is defined by microarousal cycles lasting 20–40 seconds, which facilitate the dynamic organization of sleep and trigger motor events [50,82,84]. Motor episodes of SB are significantly correlated with CAP, including cortical arousal [84].
The role of K-events
The clinical relevance of the K-complex, a waveform identified in stage N2 of NREM sleep, has been examined in sleep medicine. Prior research suggested that the K-complex might be connected to sleep disorders, such as movement disorders [85], sleep arousal [86], and sleep protection [87]. Based on historical evidence, the involvement of the K-complex in SB has been investigated [48]. The findings indicated a lower incidence of K-events, including K-complex and K-alphas, in the SB group as opposed to the controls, implying that K-events may not be linked with SB [52].
The role of SpO2
Suzuki et al. [88] examined the factors contributing to the onset of RMMA. They observed that SpO2 levels were significantly lower than baseline 4–6 seconds prior to RMMA onset and significantly increased 6–18 seconds after the onset [88]. The researchers hypothesized that mild but significant hypoxia preceding RMMA onset might represent a physiological response mechanism.
The role of neurotransmitters
It is well established that a variety of neurotransmitters play significant roles in regulating sleep processes and SB [7,70,89]. Gamma-aminobutyric acid (GABA) and various catecholamines, including dopamine, serotonin, adrenaline, and acetylcholine, are implicated in the modulation of SB [7,70,89]. Research on neurotransmitters involved with SB predominantly comprises case reports and studies investigating the effects of medications targeting these neurotransmitters, thus examining their impact on SB. Due to the inconsistent findings and limited evidence regarding the role of neurotransmitters in SB, refer to the review paper by Lavigne et al. [7] for a more detailed description of the findings on SB and catecholamines.
Evolving Perspectives on SB
Over time, research has increasingly illuminated potential positive health benefits associated with SB. Additionally, nocturnal teeth grinding may promote oral lubrication and thereby help to alleviate complications arising from acid reflux [90].
The first author of the paper published in 2013, “Bruxism Defined and Graded: An International Consensus [12],” along with colleagues [13], has provided a critical analysis. This commentary suggests that SB should primarily be viewed as a behavior rather than a disorder. Based on the neurophysiologic understanding that SB involves activating the reticular activating system through various neurotransmitters, SB should not be considered merely as a parafunction represented by an abnormal activity [89].
In contemporary sleep medicine, although SB is categorized as a sleep-related movement disorder [5], there is consensus that SB, characterized by rhythmic or non-rhythmic masticatory muscle activity during sleep, should not be classified as a movement or sleep disorder in otherwise healthy individuals [10].
These recent insights collectively challenge the conventional view of SB as a pathological disorder. Instead, they promote a re-evaluation of SB, suggesting it may serve physiologic or protective roles in healthy individuals.
Comorbidities of SB: SB and Systemic Diseases
A systematic review conducted in 2022 discovered that SB is more prevalent in individuals with sleep disorders such as OSA, restless leg syndrome, gastroesophageal reflux disease (GERD), REM behavior disorder, Parkinson’s disease, and sleep-related epilepsy than in the general populations [91]. The review proposed sleep arousal as a common factor contributing to these associated sleep disorders [65,91].
Many previous studies have explored the association between OSA and SB. The prevalence of SB, ranging from 33.3% to 53.7%, is significantly higher than that seen in the general population [48,91]. Cortical arousal and transient hypoxemia are believed to contribute to the initiation of bruxism episodes [47,49,69,88].
Several investigations have explored the potential link between Parkinson’s disease and SB, suggesting that the loss of dopaminergic neurons and the resultant dopamine imbalance may play a role in the pathogenesis of both PD and SB [7,89,90]. Additionally, SB is more prevalent among GERD patients, potentially serving as a protective mechanism against chemical tooth erosion by stimulating salivation in these individuals [90].
In conclusion, the association between SB and various systemic diseases is well-documented; therefore, clinicians should be vigilant regarding SB in patients with SB-related disorders.
Management of Sleep Bruxism
Pharmacologic approach
Previous research has indicated that clonazepam, which enhances the inhibitory actions of GABA, and clonidine, a central α2-receptor agonist, can effectively manage SB. These medications have demonstrated a 40%–60% reduction in jaw motor events in SB patients [92,93].
A double-blind, crossover, placebo-controlled trial with PSG recordings of primary SB assessed the effects of clonazepam and clonidine [94]. Clonidine decreased the number of RMMA episodes by 30% compared to placebo and clonazepam [94], and also lowered heart rate during NREM sleep [92]. Conversely, clonazepam failed to show beneficial effects on SB, including autonomic activities, and the occurrence of microarousals and RMMA episodes, in contrast to findings reported by Saletu et al. [92]. This suggests that modulation of autonomic activity might play a more pivotal role in the genesis of RMMA episodes in primary SB.
Despite limited evidence regarding the role of dopaminergic agonists in SB [95], short-term administration of levodopa and dopamine agonists has been observed to suppress bruxism activity in controlled PSG studies. Nevertheless, prolonged use of levodopa is acknowledged as a risk factor for exacerbating bruxism [73].
Four RCTs indicated the effectiveness of botulinum toxin type A (BTX-A) in reducing the number, duration, and peak amplitude of EMG bursts during SB events [96].
Behavioral approach
In a randomized controlled trial, there were no intervention effects of sleep hygiene instructions combined with progressive muscle relaxation on SB variables and sleep variables in both the SB and control groups [97]. Cognitive-behavioral therapy, which aims to manage the psychological stress associated with SB, showed inconsistent effectiveness in reducing SB activity [96]. Biofeedback therapy, which utilizes EMG feedback during sleep to regulate excessive muscle activity, is believed to potentially decrease SB-related EMG activity [96]. Further investigation into the long-term effects and potential adverse events of biofeedback therapy is warranted.
Oral appliance
A meta-analysis has shown that oral appliances (OAs) designed for mandibular advancement to a certain degree effectively mitigate SB [98]. Notably, an RCT revealed that a mandibular advancement appliance, adjusted to a minimum of 25% advancement, significantly reduces SB episodes with less discomfort than 50%–75% advancement [98].
Two systematic reviews have suggested that various types of OAs, including the maxillary occlusal splint, mandibular stabilization splint, and palatal splint, tend to reduce SB events [96,99]. However, the majority of the included studies did not demonstrate statistical significance over control, and the level of evidence was low.
In summary, a systematic review [96] concluded that treatments such as BTX-A injections, clonazepam, and clonidine might potentially reduce SB. The review also indicated that nearly all types of OAs could be somewhat effective in reducing SB. Nevertheless, the current evidence for a standard treatment for SB remains insufficient, except for the use of OAs.
CONCLUSION
Based on the available literature, PSG findings from prior studies suggest an association between SB and sleep arousal. As SB is generally not associated with adverse health outcomes, it should not be regarded as a pathology or disorder in individuals who are otherwise healthy. A more balanced clinical approach is currently needed, which acknowledges.
The current evidence supporting diagnostic criteria for detecting pathologic SB is inadequate. Therefore, a differential diagnosis should be considered for individuals with SB who also report sleep disturbances or have related medical conditions. Clinicians managing patients with SB should be cognizant of the possible comorbid sleep disorders and pursue collaborations with sleep physicians.
In managing SB, it is essential to recognize that there is no universal treatment that fits all cases. Many SB instances require no intervention as they do not represent a pathological condition. However, when SB is associated with potentially detrimental orofacial outcomes or related medical conditions, a comprehensive evaluation and customized management strategy are crucial.
Due to the daily variability of SB, using a dichotomous cut-off for the number of bruxism events may not be necessarily effective in diagnosing and managing bruxism [100]. This suggests that relying solely on numerical thresholds may not accurately assess the actual impact of the condition due to the daily fluctuation of bruxism. Therefore, a comprehensive and multifaceted approach to assessing bruxism is required for the accurate diagnosis and effective management of health issues related to bruxism.
In 2024, a preeminent group of SB experts introduced the “Standardised Tool for the Assessment of Bruxism” [101]. Designed to facilitate a multi-dimensional evaluation of bruxism, including its status, comorbidities, etiology, and consequences, this tool aims to provide a deeper understanding of bruxism patients. This allows for effective screening for comorbidities associated with SB and informing targeted management strategies. Moreover, further research is needed to discriminate between pathological and physiological SB to personalize treatment and prevent unnecessary interventions.
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