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Dental and Medical Problems

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doi: 10.17219/dmp/156400

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Language: English

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Cerón L, Pacheco M, Delgado Gaete A, Bravo Torres W, Astudillo Rubio D. Therapies for sleep bruxism in dentistry: A critical evaluation of systematic reviews [published online as ahead of print on November 28, 2022]. Dent Med Probl. doi:10.17219/dmp/156400

Therapies for sleep bruxism in dentistry: A critical evaluation of systematic reviews

Lissette Cerón1,A,B,C,D, Mishelle Pacheco1,A,B,C,D, Andrés Delgado Gaete2,A,C, Wilson Bravo Torres1,E,F, Daniela Astudillo Rubio1,E

1 Graduate Program in Oral Rehabilitation and Implant-Assisted Prosthetics, Faculty of Dentistry, University of Cuenca (Universidad de Cuenca), Ecuador

2 Department of Prostodontics, School of Dentistry, Catholic University of Cuenca (Universidad Católica de Cuenca), Ecuador

Abstract

The aim of the study was to evaluate the methodological quality and the risk of bias of systematic reviews with regard to the literature on therapies for sleep bruxism (SB) in dentistry, applying the AMSTAR 2 (A MeaSurement Tool to Assess systematic Reviews) qualitative guide, as well as the effectiveness of various kinds of treatment of SB. Initially, a total of 1,499 articles were obtained from 4 databases and 2 websites. Relevant articles were obtained from the PubMed, Scopus, Cochrane, and Embase databases as well as from Google Scholar and OpenGrey. Six systematic reviews that met the eligibility criteria were included. The methodological quality of all systematic reviews, assessed with the AMSTAR 2 tool, was critically low. Regarding treatment effectiveness, 5 systematic reviews reported on pharmacological management (botulinum toxin type A (BTX-A), clonazepam and clonidine), 2 reported on oral appliances (OAs) (stabilizing splints and mandibular advancement devices (MADs)) and 1 study addressed the effects of biofeedback (BF). The results of the therapies were diverse and confusing. The available research is not conclusive, and does not show clear evidence or a consensus on the part of researchers on the most effective treatment for the management of SB. More research of better methodological quality is needed in this area.

Keywords: treatment, sleep bruxism, teeth grinding, rhythmic masticatory muscle activity

Introduction

For decades, the term ‘bruxism’ has generated controversy in the academic and professional environment of dentistry due to the various definitions attributed to it and its alleged association with etiological factors that are currently considered to have no scientific relevance.

Various conceptualizations have been postulated for the definition of bruxism. Lobbezzo et al. in the 2013 international consensus defines sleep bruxism (SB) as “repetitive jaw-muscle activity characterized by clenching or grinding of the teeth and/or bracing or thrusting of the mandible”,1 the International Classification of Sleep Disorders – Third Edition (ICSD-3) classifies it as a sleep-related movement disorder,2 and Lobbezoo et al. in the 2018 international consensus updated the above definition of bruxism with other findings: (i) suggested separate definitions for SB and awake bruxism, the same being the chewing muscle activity that occurs during sleep (characterized as rhythmic or non-rhythmic) and during wakefulness (characterized by repetitive or sustained tooth contact and/or jaw effort or thrust); (ii) stated that bruxism should not be considered as a disorder, but as a behavior that may be a risk factor (and/or a protective factor) for certain clinical consequences in healthy individuals; and (iii) grouped the techniques for the diagnosis of bruxism into non-instrumental (self-reports) and instrumental (electromyography and polysomnography).3 Regarding the etiology of bruxism, in the past, it was associated with occlusal discrepancies, but nowadays, it is no longer considered as such,4 since several studies mention that SB is centrally regulated.1, 5 Despite these changes, the hypothesis of occlusal discrepancies has not been completely abandoned, which has led to confusion among clinicians in terms of making an accurate diagnosis, and therefore applying effective treatment – botulinum toxin type A (BTX-A),6, 7, 8 oral appliances (OAs),9 biofeedback (BF),10, 11 physical therapy,12, 13 or pharmacotherapy.14 Still, the efficacy of some of the abovementioned therapies for the management of bruxism has not been scientifically proven. There should be more randomized controlled clinical studies; in some cases, the authors even suggest conducting studies with larger samples and longer treatment periods to obtain results that would be reliable for clinical application. For this reason, as researchers, we feel the need to try to establish which therapies are really valid for the management of SB.

We have not found general studies that would evaluate the methodological quality of systematic reviews on this topic; therefore, this study will surely become a reference for future research. The aim of the present study was to evaluate the methodological quality of the literature and the risk of bias in the systematic reviews addressing therapies for SB by applying the AMSTAR 2 (A MeaSurement Tool to Assess systematic Reviews) qualitative guide15 as well as to assess the effectiveness of the therapies in terms of their clinical application. The research question was as follows: What is the methodological quality of studies analyzing the treatment of sleep bruxism and what is the effectiveness of various kinds of treatment?

Material and methods

Protocol and registration

This study was carried out in accordance with the PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses) 2020 Statement,16 and a general protocol based on the INPLASY (International Platform of Registered Systematic Review and Meta-analysis Protocols) guide for the registration of systematic review protocols (2021)17 was also executed. The record is publicly available under number 2021100080 and doi:10.37766/inplay2021.10.0080.

Eligibility criteria

The included studies were systematic reviews, with or without a meta-analysis, that evaluated the different kinds of treatment used in adult patients (aged 18 years or above) diagnosed with bruxism through poly­somnography, electro­myography and self-reports. No time or language restrictions were applied.

The exclusion criteria embraced literature reviews, intervention studies, observational studies, in vitro laboratory research, randomized controlled clinical studies, abstracts, comments, case reports, protocols, personal opinions, expert opinions, letters, and posters. If a particular article of interest was not available, the author was contacted via e-mail; if after 3 attempts within an interval of 30 days there was no response, the study was excluded. In addition, studies in which methodology was not addressed, or studies using unspecified or non-validated dia­gnostic methods (self-reports) were also excluded.

Search strategy

An electronic search was conducted in February 2022 in 4 databases (PubMed, Scopus, Cochrane, and Embase). The gray literature was also searched through Google Scholar and OpenGrey. The retrieved articles were exported to a web application (Mendeley) and duplicate articles were eliminated. The search strategy used for each source of information is provided in Table 1. Study selection was carried out in 2 phases: phase 1 consisted of reading the title and the abstract; and phase 2 consisted of reading the full text (Figure 1).

The aforementioned procedures were performed by 2 reviewers independently, and in case of disagreement, a third reviewer was consulted.

Data collection process and data elements

Once duplicate studies were eliminated, 2 reviewers independently compiled the data in a table. Any disagreement was resolved by a third reviewer. After the selection of articles, the following information was extracted: author; year of publication; journal and its impact factor; population; interventions and comparators; design of the primary studies; and diagnostic methods for SB (Table 2).

Evaluation of methodological quality, quality of evidence and meta-bias

The evaluation of the methodological quality of the 6 included systematic reviews was performed by 2 reviewers independently by means of the AMSTAR 2 qualitative guide.15

The 6 systematic reviews were evaluated according to the PRISMA 2020 Statement,16 which consists of 27 items.

Data synthesis

The main results of the included systematic reviews were summarized, and only the primary studies that evaluated a decrease in the electromyographic activity with the use of instrumental tools were analyzed according to each treatment applied, discarding those whose diagnostic method was non-instrumental. A visual indication system (traffic light) was used, where green represented treatment with the best results, red represented treatment with the worst results, and yellow indicated that there were no differences between the compared groups (Table 3).

Results

Review and selection
of the primary studies

The search in the electronic databases identified 1,498 studies published between 2012 and 2022; after dupli­cates were eliminated, 1,431 remained. In addition, 1 article was found in the gray literature. In phase 1, the title and the abstract were reviewed, and 140 articles were selected; in phase 2, the texts were read in full, obtaining 18 articles, of which 6 systematic reviews were included for the qualitative synthesis. A total of 12 primary studies were identified within the systematic reviews. All systematic reviews were rated as critically low according to the AMSTAR 2 tool.15 More information on the evaluation of methodological quality can be found in Table 4.

Report on main findings

Of the 6 systematic reviews, 5 reported on the pharmacological management of bruxism. Four of them addressed the application of botulinum toxin type A (BTX-A), either into the temporalis or masseter muscle, unilaterally or bilaterally, with doses ranging from 8 IU to 80 IU. The information available on this topic is not conclusive, and although the results of some studies support the effectiveness of BTX-A in reducing the intensity of episodes of bruxism, there is not enough evidence to recommend this drug for the treatment of bruxism. One systematic review compared the effectiveness of clonazepam and clonidine with respect to placebo, showing a reduction in the episodes of bruxism; however, the follow-up period was limited.

Two systematic reviews reported on the effectiveness of OAs; comparison groups treated with stabilization splints and mandibular advancement devices (MADs) were included, and intermittent vs. continuous use and design were analyzed. The results of these investigations suggest that stabilization splints for intermittent use are the most recommended. Regarding MADs, both studies agree that they can significantly reduce bruxism and improve sleep quality, but can also cause muscle pain and temporomandibular disorders (TMDs).

Only 1 systematic review addressed the effects of BF. The findings of this study suggest a significant decrease in sleep bruxism events.

Discussion

Bruxism is a topic of interest in dentistry, so there is a need to provide scientifically proven information regarding its management. Several investigations have been carried out to confirm the safety and efficacy of various kinds of treatment aimed at solving bruxism. Systematic reviews are conducted to identify, evaluate and summarize research findings, and therefore they can provide reliable information and help guide clinical decision making. However, systematic reviews are not always carried out meticulously, and the risk of implicit bias can mislead readers and induce malpractice, as evidenced in our research, where the 6 included systematic reviews that met the eligibility criteria, when evaluated with the AMSTAR 2 tool,15 showed a low methodological quality; the critical points were not met in most of the investigations and the lack of homogeneity in terms of study design prevented us from performing any meta-analysis of the data.

Two of the included systematic reviews analyzed OAs, and reported diverse and confusing results, mainly due to the types of splints used, heterogeneous control groups and different observation periods. Manfredini et al. mention that almost all types of OAs for intermittent use are somehow effective in reducing the episodes of bruxism.19 However, Jokubauskas et al. indicate that although many studies support the efficacy of OA treatment for SB, the evidence is insufficient and the main role of OAs is protection against dental wear.20 Therefore, both authors support the idea of conducting future research with longer follow-up periods. Mainieri et al. reported that treatment with MADs resulted in a reduction in the activity of the chewing muscles, the signs and symptoms of SB, and occlusal strength as well as improvement in sleep quality, but 24% of their patients had to interrupt treatment due to TMDs, muscle pain and/or discomfort.21 In contrast, Saueressig et al. reported positive effects of MADs in the therapy of SB, without any signs or symptoms of TMDs.22

Another treatment for bruxism is the application of botulinum toxin, which has been referred to in a large number of studies. For example, Fernández-Núñez et al. concluded that its effectiveness was superior to any conventional treatment for SB, largely minimizing its symptoms.8 However, Long et al. revealed that botulinum toxin had the same efficacy as a nocturnal oral splint.23 De la Torre Canales et al. state that such disagreement is largely due to the lack of clinical protocols, the non-standardized dosage and different dilutions of the preparations among the different commercial brands used in each study.24 Regarding adverse effects, Lee et al.25 and Zhang et al.26 in their reviews reported the absence of adverse effects both at the time of treatment and after botulinum toxin injection, and if they were observed, they occurred in patients who received a dose higher than the established safe dose (≤100 IU) or who had a preexisting medical condition.25

Studies that analyzed the effects of centrally acting drugs show very good results in the treatment of SB. It refers, among others, to clonazepam, used not only as an anticonvulsant, since its mechanism of action is also relaxation and sedation at the muscular level, mood stabilization, and relieving insomnia/anxiety.27 In the study by Saletu et al., 21 patients diagnosed with BS received 1 mg of clonazepam per day, which showed efficacy in the polysomnographic study, with a statistically significant reduction of BS as compared to placebo.14 However, seve­ral authors mention that it is necessary to be cautious with this type of medication, since after a period of use of 2–4 weeks, it could cause dependence.28, 29 Clonidine has an antihypertensive effect by acting as a selective agonist of the α2 receptor, which influences the sympathetic–parasympathetic balance as well as the sleep structure and motor activities during sleep.30 It is also used to treat migraine, chronic pain, psychiatric disorders, and SB.27 Polysomnographic records have shown that clonidine is effective in reducing SB significantly.31

Recently, a group of researchers have evaluated the effect of 100 mg opipramol (a single dose), which shows positive effects in reducing SB. This information could be useful for researchers who delve into this topic of great interest, taking into consideration a larger population with a control group and long-term follow-up periods.32

It has also been suggested that bruxism is a risk factor for developing TMDs, since an increase in the activity of the masticatory muscles could cause joint overload and myofascial pain. However, almost all studies that point to such an association used non-validated methods to diagnose bruxism, which indicates a possible diagnostic bias that could have increased the level of significance of the discussed association.33, 34, 35 Studies such as those by Smardz et al.36 and Wieckiewicz et al.37 showed through their results that the relationship between SB and TMDs was not statistically significant, clearly indicating that SB is not related to TMDs, nor does it increase the risk of the appearance of any specific diagnosis of TMDs. These studies support the importance of using scientifically proven methods for making an accurate diagnosis, and thus choosing the optimal treatment.

Regarding BF, it is a subject that is still under debate, as there are studies, such as those by Lobbezoo et al.38 and Jokubauskas et al.,11 which show positive effects, i.e., a reduction in the episodes of bruxism in the short term; however, the authors suggest more well-designed longitudinal studies with larger samples.

In general, with our study, we were able to demonstrate that, due to the lack of scientific evidence of good methodological quality, there is still controversy and confusion about SB. A lot of misinformation has been provided about its pathophysiology in countless articles; dentists commonly relate it to peripheral factors – dental, occlusal and skeletal, believing that occlusal corrections decrease or stop this sleep activity.39, 40 Yet, Manfredini et al. in their research questioned occlusal disharmony or premature contacts as an etiological factor, concluding that the contribution of occlusion was not statistically significant in patients with and without bruxism.4 Similarly, in a study by Ommerborn et al., a review of the functional and occlusal role was made, and no relationship was found with regard to the occlusal parameters, or skeletal or orofacial anatomy, that could explain bruxism events; on the contrary, the authors found that the role of psychology, neurotransmitters and micro-arousals as central factors prevailed.41 Obviously, as in any pathology, whether an associated disorder occurs or not depends on the adaptive capacity of the person, e.g., coping with pain or stress, and genetic predisposition.41 Therefore, SB is no longer considered to be simply related to dental occlusion factors, but it is known to have a central origin, which involves biological factors (e.g., neurochemical factors, such as dopamine and other neurotransmitters, genetics and sleep disorders), physiological factors (e.g., brain activity, muscle activity, and cardiac and respiratory functions, etc.)and psychological factors (e.g., stress sensitivity, personality traits and anxiety).5, 42, 43, 44, 45, 46, 47 This has resulted in a major transformation in our understanding of BS.

Therefore, it is important to know how SB is generated and to be aware of the different stages of sleep that a person normally goes through. Sleep ideally should last 7–8 h, starting with wakefulness, continuing with non-REM (rapid eye movement) sleep (N1, N2, N3) until the depth of sleep or REM sleep increases, and this cycle is repeated several times during the night. However, there are moments in which the individual goes to wakefulness, and these brief periods are known as micro-arousals. The term ‘micro-arousal’ refers to a response or a sudden change in sleep during which the individual reaches a lighter sleep, and then there is an interruption of sleep for at least 3 s, characterized by an increase in brain, auto­nomic, cardiac, and muscular activity, without a complete return to consciousness.48 Taking micro-arousals as a reference, associated pathologies can be identified, such as obstructive sleep apnea (OSA), which consists in the interruption of sleep due to the lack of air in an attempt to breathe again.49, 50 Several studies have considered the possible association between SB and OSA, as SB may be a motor reflex of the central nervous system in response to a sleep arousal and OSA leads to sleep arousals.51, 52, 53 Another pathology associated with bruxism is gastroesophageal reflux (GER), which occurs when gastric acid passes from the stomach into the esophagus, and once it exceeds the adaptive capacity of the epithelium, it generates symptoms or histological damage.54 Li et al. showed a strong association between bruxism and symptomatic GER, and recommended that the GER status be taken into consideration as a fundamental part of the diagnosis of bruxism.55

Previous studies identified that also hypoxia,56 increased body mass index (BMI),57 hypertension,1, 57, 58 excessive daytime sleepiness59 and snoring60 acted as independent risk factors for SB; in this study we did not investigate these issues, and another type of study could be conducted in the future to clarify them.

Taking into account all the background described above, researchers saw the need to update information about SB, and it is in the 2018 consensus where SB is defined as the activity of the masticatory muscles during sleep (chara­cterized as rhythmic or non-rhythmic) and where it is considered as a behavior.3 According to its clinical consequences, it was classified as: (i) a risk factor if it presents one or more negative consequences for oral health, such as severe masticatory muscle pain or joint pain, increasing the likelihood of developing a disease, without necessarily inducing it; (ii) a protective factor if it provides one or more positive health outcomes, as in the case of OSA, where the upper airway can be prevented from collapsing or its patency can be restored during sleep, or in the case of GER, where increased salivation reduces the risk of harmful chemical tooth wear; or (iii) it is neither a risk factor or a protective factor, i.e., it is only considered a motor activity of multifactorial etiology, with no consequences at the level of oral health; it is extremely important not to overdiagnose it as a pathology, since its intensity or frequency does not mean pathogenicity.61, 62, 63, 64

Conclusions

Taking the limitations of the present study into consideration, the following conclusions can be drawn: the methodological quality of the studies included in this research, after being analyzed with AMSTAR 2, proved criti­cally low; the authors recommend future research studies of better methodological quality so that the results can be applied in clinical practice. The use of centrally acting drugs, such as clonazepam and clonidine, demonstrated efficacy in reducing the episodes of SB; however, caution is recommended in their administration because of adverse effects. Treatment with botulinum toxin, OAs and BF did not demonstrate short-term efficacy; therefore, prospective studies with a longer duration are recommended. The difficulty involved in treating SB is that it does not always need to be controlled, as in most cases, it should not be considered a pathology according to the current literature. It can be a risk factor or a protective factor; therefore, treatment should not be focused on SB as such, but on investigating the pathologies, comorbidities or associated factors that lead to its onset.

Ethics approval and consent to participate

Not applicable.

Data availability

The datasets generated and/or analyzed during the current study are available from the corresponding author on reasonable request.

Consent for publication

Not applicable.

Tables


Table 1. Search strategy used for each of the sources of information

Source
of information

Search strategy

PubMed

(““bruxism”” [MeSH Terms] OR ““sleep bruxism”” [MeSH Terms]) AND ((““systematic review”” [Publication Type] OR ““systematic review as topic”” [MeSH Terms] OR ““systematic review”” [All Fields]) OR ((““review”” [Publication Type] OR ““literature review as topic”” [MeSH Terms] OR ““review”” [All Fields]) AND (““publications”” [MeSH Terms] OR ““literature”” [MeSH Terms])) OR (““literature review as topic”” [MeSH Terms]))

Scopus

(TITLE-ABS-KEY (“bruxism sleep”) OR TITLE-ABS-KEY (“bruxism”) AND TITLE-ABS-KEY (“systematic review”))

Cochrane

(“systematic review” OR “systematic reviews” OR “systematic literature review” OR “systematic literature reviews” OR “meta analysis” OR “meta synthesis” OR “systematic” OR “review” OR “reviews”) AND (“bruxism” OR “sleep bruxism” OR “bruxist”) AND (“therapy” OR “adult” OR “treatment” OR “effectiveness”) in Title Abstract Keyword

Embase

(‘bruxism’/exp OR ‘bruxism’ OR ‘sleep bruxism’/exp OR ‘sleep bruxism’ OR ‘awake bruxism’) AND (‘systematic review’/exp OR ‘systematic review’ OR ‘integrative review’/exp OR ‘integrative review’ OR ‘meta-analysis’/exp OR ‘meta analysis’ OR ‘overview’ OR ’review’/exp OR ‘review’ OR ‘systematic literature review’ OR ‘rapid review’/exp OR ‘rapid review’)

Google Scholar

“treatment bruxism” AND “systematic review”

OpenGrey

“treatment” AND “bruxism”

Table 2. Summary of the overall descriptive characteristics of the included systematic reviews

Author, year, country, journal with its IF

Population

Interventions (I) and comparators (C)

Primary study design

Diagnostic methods
for bruxism

Ågren et al.18
2020, Sweden
J Oral Rehabil
IF = 3.837

bruxism
patients

BTX-A (I)
placebo (C)

RCT, prospective
or retrospective studies

instrumental
approaches

Fernández-Núñez et al.8
2019, Spain
Med Oral Patol Oral Cir Bucal
IF = 2.555

bruxism
patients

BTX-A (I)
placebo,
occlusal splints, medications
or cognitive-behavioral therapy (C)

RCT

instrumental
and non-instrumental approaches

Manfredini et al.19
2015, Italy
J Oral Rehabil
IF = 3.837

bruxism
patients

SB diagnosis (I)
the comparison was based on the description
of the condition and features
of the passive or active control group

RCT and uncontrolled before–after studies

instrumental
approaches

Jokubauskas et al.20
2018, Lithuania
J Oral Rehabil
IF = 3.837

bruxism
patients

occlusal splints and MADs (I)
nociceptive trigeminal inhibitory splint, BF (C)

RCT,
before–after crossover

instrumental
approaches

Long et al.23
2012, China
Int Dent J
IF = 2.512

bruxism
patients

BTX-A (I)
placebo or other interventional procedures (C)

RCT and non-randomized studies

instrumental
and non-instrumental approaches

De la Torre Canales et al.24
2017, Brazil
Clin Oral Investig
IF = 3.623

bruxism
patients

BTX-A (I)
other treatment (C)

RCT, prospective
and before–after

instrumental
and non-instrumental approaches

IF – impact factor; BTX-A – botulinum toxin type A; SB – sleep bruxism; MADs – mandibular advancement devices; BF – biofeedback; RCT – randomized controlled trial.
Table 3. Results regarding the efficacy of therapies for sleep bruxism (SB) represented graphically by color, with green and red representing the best and the worst treatment, respectively, and yellow indicating that there were no differences between the compared groups

Systematic
review

Primary study

Treatment

Intervention
group
(IG)

Control
group
(CG)

Reported results

Diagnostic
method

Ågren et al.18
Fernández-Núñez et al.8
Manfredini et al.19
Long et al.23
De la Torre Canales et al.24

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(1):16–23.
doi:10.1097/PHM.0b013e3181bc0c78

BTX-A

p < 0.001*
for IG as compared to placebo (CG)

EMG

Ågren et al.18

Ondo WG, Simmons JH, Shahid MH, Hashem V,
Hunter C, Jankovic J. Onabotulinum toxin-A injections for sleep bruxism: A double-blind, placebo-controlled study. Neurology. 2018;90(7):e559–e564.
doi:10.1212/WNL.0000000000004951

p = 0.090
for both IG
and placebo (CG)

EMG

Manfredini et al.19
De la Torre Canales et al.24

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(3):291–298. doi:10.5664/jcsm.3532

p < 0.001*
for both IG
and placebo (CG)

EMG

Manfredini et al.19

Sato M, Iizuka T, Watanabe A, et al. Electromyogram biofeedback training for daytime clenching and its effect on sleep bruxism. J Oral Rehabil.
2015;42(2):83–89. doi:10.1111/joor.12233

BF

p < 0.050*
for IG as compared to placebo (CG)

EMG

Valiente López M, van Selms MK, van der Zaag J, Hamburger HL, Lobbezoo F. Do sleep hygiene measures and progressive muscle relaxation influence sleep bruxism? Report of a randomised controlled trial. J Oral Rehabil. 2015;42(4):259–265. doi:10.1111/joor.12252

sleep hygiene instructions and Jacobson’s relaxation techniques

p > 0.050
for both IG
and information
on the condition of SB (CG)

PSG

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(2):163–174. doi:10.1007/s00406-009-0034-0

clonazepam

p = 0.010*
for IG as compared to placebo (CG)

PSG

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(12):1711–1716. doi:10.1093/sleep/33.12.1711

clonidine

p = 0.020*
for IG as compared to placebo (CG)

PSG

Madani AS, Abdollahian E, Khiavi HA, et al.
The efficacy of gabapentin versus stabilization
splint in management of sleep bruxism.
J Prosthodont. 2013;22(2):126–131.
doi:10.1111/j.1532-849X.2012.00914.x

hard stabilization splint

p < 0.050*
for both IG
and gabapentin (CG)

PSG

Matsumoto H, Tsukiyama Y, Kuwatsuru R, Koyano K. The effect of intermittent use of occlusal splint devices on sleep bruxism: A 4-week observation with a portable electromyographic recording device. J Oral Rehabil. 2015;42(4):251–258. doi:10.1111/joor.12251

stabilization splint for continuous use

p < 0.050*
for intermittent use (CG) as compared to continuous use (IG)

EMG

Jokubauskas et al.20

Dalewski B, Chruściel-Nogalska M, Frączak B. Occlusal splint versus modified nociceptive trigeminal inhibition splint in bruxism therapy: A randomized, controlled trial using surface electromyography. Aust Dent J. 2015;60(4):445–454. doi:10.1111/adj.12259

mandibular occlusal splints

p > 0.050
for both IG and modified nociceptive trigeminal inhibitory splint (CG)

EMG

Singh PK, Alvi HA, Singh BP, et al. Evaluation of various treatment modalities in sleep bruxism. J Prosthet Dent. 2015;114(3):426–431. doi:10.1016/j.prosdent.2015.02.025

reinforced adjustable MADs

p > 0.050
for both IG and occlusal splints (CG)

PSG

Gu WP, Yang J, Zhang FM, Yin XM, Wei XL, Wang C. Efficacy of biofeedback therapy via a mini wireless device on sleep bruxism contrasted with occlusal splint: A pilot study. J Biomed Res. 2015;29(2):160–168. doi:10.7555/JBR.28.20130145

maxillary occlusal splint and vibratory feedback

p = 0.001*
for IG as compared to maxillary occlusal splint without vibration (CG)

PSG

EMG – electromyography; PSG – polysomnography; * statistically significant.
Table 4. AMSTAR 2 (A MeaSurement Tool to Assess systematic Reviews) – critical appraisal tool for systematic reviews that include randomized or non-randomized studies of healthcare interventions, or both

Systematic
review

Q1

Q2

Q3

Q4

Q5

Q6

Q7

Q8

Q9

Q10

Q11

Q12

Q13

Q14

Q15

Q16

Overall confidence

Ågren et al.18
2020

×

×

×

critically
low

Fernández-Núñez et al.8
2019

×

×

×

critically
low

Manfredini et al.19
2015

×

×

×

critically
low

Jokubauskas et al.20
2018

×

×

×

critically
low

Long et al.23
2012

×

×

×

critically
low

De la Torre Canales et al.24
2017

×

×

×

critically
low

Answers marked as colors: green – yes; yellow – partial yes; red – no; green-gray – no meta-analysis (×).
Questions:
Q1: Did the research questions and the inclusion criteria for the review comprise the components of PICO?
Q2: Did the report of the review contain an explicit statement that the review methods had been established prior to conducting the review, and did the report justify any significant deviations from the protocol?*
Q3: Did the review authors explain their selection of the study designs for inclusion in the review?
Q4: Did the review authors use a comprehensive literature search strategy?*
Q5: Did the review authors perform study selection in duplicate?
Q6: Did the review authors perform data extraction in duplicate?
Q7: Did the review authors provide a list of the excluded studies and justify the exclusions?*
Q8: Did the review authors describe the included studies in adequate detail?
Q9: Did the review authors use a satisfactory technique for assessing the risk of bias (RoB) in individual studies that were included in the review?*
Q10: Did the review authors report on the sources of funding for the studies included in the review?
Q11: If meta-analysis was performed, did the review authors use appropriate methods for the statistical combination of the results?
Q12: If meta-analysis was performed, did the review authors assess the potential impact of RoB in individual studies on the results of the meta-analysis or other evidence synthesis?
Q13: Did the review authors account for RoB in the primary studies when interpreting/discussing the results of the review?*
Q14: Did the review authors provide a satisfactory explanation for, and discussion of, any heterogeneity observed in the results of the review?
Q15: If they performed quantitative synthesis, did the review authors carry out an adequate investigation of publication bias (small study bias) and discuss its likely impact on the results of the review?*
Q16: Did the review authors report any potential sources of conflict of interest, including any funding they received for conducting the review?
Rating overall confidence in the results of the review:
High: No or one non-critical weakness – the systematic review provides an accurate and comprehensive summary of the results of the available studies that address the question of interest.
Moderate: More than one non-critical weakness** – the systematic review has more than one weakness, but no critical flaws; it may provide an accurate summary of the results of the available studies that were included in the review.
Low: One critical flaw with or without non-critical weaknesses – the systematic review has a critical flaw and may not provide an accurate and comprehensive summary of the available studies that address the question of interest.
Critically low: More than one critical flaw with or without non-critical weaknesses – the review has more than one critical flaw and should not be relied on to provide an accurate and comprehensive summary of the available studies.
* domains considered critical for AMSTAR II; ** multiple non-critical weaknesses may diminish confidence in the review and it may be appropriate to move the overall appraisal down from moderate to low confidence.

Figures


Fig. 1. Study selection flowchart

References (64)

  1. Lobbezoo F, Ahlberg J, Glaros AG, et al. Bruxism defined and graded: An international consensus. J Oral Rehabil. 2013;40(1):2–4. doi:10.1111/joor.12011
  2. Sateia MJ. International classification of sleep disorders – third edition: Highlights and modifications. Chest. 2014;146(5):1387–1394. doi:10.1378/chest.14-0970
  3. Lobbezoo F, Ahlberg J, Raphael KG, et al. International consensus on the assessment of bruxism: Report of a work in progress. J Oral Rehabil. 2018;45(11):837–844. doi:10.1111/joor.12663
  4. Manfredini D, Visscher CM, Guarda-Nardini L, Lobbezoo F. Occlusal factors are not related to self-reported bruxism. J Orofac Pain. 2012;26(3):163–167. PMID:22838000.
  5. Klasser GD, Rei N, Lavigne GJ. Sleep bruxism etiology: The evolution of a changing paradigm. J Can Dent Assoc. 2015;81:f2. PMID:25633110.
  6. Patel J, Cardoso JA, Mehta S. A systematic review of botulinum toxin in the management of patients with temporomandibular disorders and bruxism. Br Dent J. 2019;226(9):667–672. doi:10.1038/s41415-019-0257-z
  7. Sendra LA, Montez C, Vianna KC, Barboza EP. Clinical outcomes of botulinum toxin type A injections in the management of primary bruxism in adults: A systematic review. J Prosthet Dent. 2021;126(1):33–40. doi:10.1016/j.prosdent.2020.06.002
  8. Fernández-Núñez T, Amghar-Maach S, Gay-Escoda C. Efficacy of botulinum toxin in the treatment of bruxism: Systematic review. Med Oral Patol Oral Cir Bucal. 2019;24(4):e416–e424. doi:10.4317/medoral.22923
  9. Riley P, Glenny AM, Worthington HV, et al. Oral splints for patients with temporomandibular disorders or bruxism: A systematic review and economic evaluation. Health Technol Assess. 2020;24(7):1–224. doi:10.3310/hta24070
  10. Wang LF, Long H, Deng M, et al. Biofeedback treatment for sleep bruxism: A systematic review. Sleep Breath. 2014;18(2):235–242. doi:10.1007/s11325-013-0871-y
  11. Jokubauskas L, Baltrušaitytė A. Efficacy of biofeedback therapy on sleep bruxism: A systematic review and meta-analysis. J Oral Rehabil. 2018;45(6):485–495. doi:10.1111/joor.12628
  12. de Paula Gomes CA, El Hage Y, Amaral AP, Politti F, Biasotto-Gonzalez DA. Effects of massage therapy and occlusal splint therapy on electromyographic activity and the intensity of signs and symptoms in individuals with temporomandibular disorder and sleep bruxism: A randomized clinical trial. Chiropr Man Ther. 2014;22(1):43. doi:10.1186/s12998-014-0043-6
  13. Amorim CS, Espirito Santo AS, Sommer M, Marques AP. Effect of physical therapy in bruxism treatment: A systematic review. J Manipulative Physiol Ther. 2018;41(5):389–404. doi:10.1016/j.jmpt.2017.10.014
  14. 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(2):163–174. doi:10.1007/s00406-009-0034-0
  15. Shea BJ, Reeves BC, Wells G, et al. AMSTAR 2: A critical appraisal tool for systematic reviews that include randomised or non-randomised studies of healthcare interventions, or both. BMJ. 2017;358:j4008. doi:10.1136/bmj.j4008
  16. Page MJ, McKenzie JE, Bossuyt PM. The PRISMA 2020 statement: An updated guideline for reporting systematic reviews. Rev Esp Cardiol. 2021;74(9):790–799. doi:10.1016/j.recesp.2021.06.016
  17. International Platform of Registered Systematic Review and Meta-analysis Protocols (INPLASY). INPLASY’s guidance for registering systematic review protocols (2021). https://inplasy.com. Accessed December 10, 2021.
  18. Ågren M, Sahin C, Pettersson M. The effect of botulinum toxin injections on bruxism: A systematic review. J Oral Rehabil. 2020;47(3):395–402. doi:10.1111/joor.12914
  19. Manfredini D, Ahlberg J, Winocur E, Lobbezoo F. Management of sleep bruxism in adults: A qualitative systematic literature review. J Oral Rehabil. 2015;42(11):862–874. doi:10.1111/joor.12322
  20. Jokubauskas L, Baltrušaitytė A, Pileičikienė G. Oral appliances for managing sleep bruxism in adults: A systematic review from 2007 to 2017. J Oral Rehabil. 2018;45(1):81–95. doi:10.1111/joor.12558
  21. Mainieri VC, Saueressig AC, Fagondes SC, Teixeira ER, Seitenfus Rehm DD, Grossi ML. Analysis of the effects of a mandibular advancement device on sleep bruxism using polysomnography, the BiteStrip, the sleep assessment questionnaire, and occlusal force. Int J Prosthodont. 2014;27(2):119–126. doi:10.11607/ijp.3675
  22. Saueressig AC, Mainieri VC, Grossi PK, et al. Analysis of the influence of a mandibular advancement device on sleep and sleep bruxism scores by means of the BiteStrip and the Sleep Assessment Questionnaire. Int J Prosthodont. 2010;23(3):204–213. PMID:20552084.
  23. Long H, Liao Z, Wang Y, Liao L, Lai W. Efficacy of botulinum toxins on bruxism: An evidence-based review. Int Dent J. 2012;62(1):1–5. doi:10.1111/j.1875-595X.2011.00085.x
  24. De la Torre Canales G, Câmara-Souza MB, do Amaral CF, Rodrigues Garcia RC, Manfredini D. Is there enough evidence to use botulinum toxin injections for bruxism management? A systematic literature review. Clin Oral Investig. 2017;21(3):727–734. doi:10.1007/s00784-017-2092-4
  25. 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(1):16–23. doi:10.1097/PHM.0b013e3181bc0c78
  26. Zhang LD, Liu Q, Zou DR, Yu LF. Occlusal force characteristics of masseteric muscles after intramuscular injection of botulinum toxin A (BTX-A) for treatment of temporomandibular disorder. Br J Oral Maxillofac Surg. 2016;54(7):736–740. doi:10.1016/j.bjoms.2016.04.008
  27. de Baat C, Verhoeff M, Ahlberg J, et al. Medications and addictive substances potentially inducing or attenuating sleep bruxism and/or awake bruxism. J Oral Rehabil. 2021;48(3):343–354. doi:10.1111/joor.13061
  28. Quagliato LA, Freire RC, Nardi AE. Risks and benefits of medications for panic disorder: A comparison of SSRIs and benzodiazepines. Expert Opin Drug Saf. 2018;17(3):315–324. doi:10.1080/14740338.2018.1429403
  29. Soyata AZ, Oflaz S. Gabapentin treatment in bruxism associated with fluoxetine. J Clin Psychopharmacol. 2015;35(4):481–483. doi:10.1097/JCP.0000000000000337
  30. 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(12):1711–1716. doi:10.1093/sleep/33.12.1711
  31. Sakai T, Kato T, Yoshizawa S, et al. Effect of clonazepam and clonidine on primary sleep bruxism: A double-blind, crossover, placebo-controlled trial. J Sleep Res. 2017;26(1):73–83. doi:10.1111/jsr.12442
  32. Wieckiewicz M, Martynowicz H, Wieczorek T, et al. Consecutive controlled case series on effectiveness of opipramol in severe sleep bruxism management – preliminary study on new therapeutic path. Brain Sci. 2021;11(2):146. doi:10.3390/brainsci11020146
  33. Huhtela OS, Näpänkangas R, Joensuu T, Raustia A, Kunttu K, Sipilä K. Self-reported bruxism and symptoms of temporomandibular disorders in Finnish university students. J Oral Facial Pain Headache. 2016;30(4):311–317. doi:10.11607/ofph.1674
  34. Aguilera AB, Lopez LG, Aguilera EB, et al. Relationship between self-reported sleep bruxism and pain in patients with temporomandibular disorders. J Oral Rehabil. 2014;41(8):564–572. doi:10.1111/joor.12172
  35. Sierwald I, John MT, Schierz O, et al. Association of temporomandibular disorder pain with awake and sleep bruxism in adults. J Orofac Orthop. 2015;76(4):305–317. doi:10.1007/s00056-015-0293-5
  36. Smardz J, Martynowicz H, Michalek-Zrabkowska M, et al. Sleep bruxism and occurrence of temporomandibular disorders-related pain: A polysomnographic study. Front Neurol. 2019;10:168. doi:10.3389/fneur.2019.00168
  37. Wieckiewicz M, Smardz J, Martynowicz H, Wojakowska A, Mazur G, Winocur E. Distribution of temporomandibular disorders among sleep bruxers and non-bruxers – a polysomnographic study. J Oral Rehabil. 2020;47(7):820–826. doi:10.1111/joor.12955
  38. Lobbezoo F, Ahlberg J, Glaros AG, et al. Bruxism defined and graded: An international consensus. J Oral Rehabil. 2013;40(1):2–4. doi:10.1111/joor.12011
  39. García DN, Cabrera LG, Reyes OR, Méndez DN. Tendencias contemporáneas de las bases fisiopatológicas del bruxismo. Medisan. 2014;18(8):1149–1156. https://doaj.org/article/03c406924a014bd6b0602c850ab3c827. Accessed December 10, 2021.
  40. Reyes BH, Díaz Gómez SM, Hidalgo SH, Nodarse RL. Bruxismo: panorámica actual. Arch Méd Camagüey. 2017;21(1):913–930. http://revistaamc.sld.cu/index.php/amc/article/view/4817/2664. Accessed December 10, 2021.
  41. Ommerborn MA, Giraki M, Schneider C, et al. Effects of sleep bruxism on functional and occlusal parameters: A prospective controlled investigation. Int J Oral Sci. 2012;4(3):141–145. doi:10.1038/ijos.2012.48
  42. Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally, not peripherally. J Oral Rehabil. 2001;28(12):1085–1091. doi:10.1046/j.1365-2842.2001.00839.x
  43. Oyarzo JF, Valdés C, Bravo R. Etiología, diagnóstico y manejo de bruxismo de sueño. Rev Méd Clín Las Condes. 2021;32(5):603–610. https://doaj.org/article/0dbed79825e64eb19efa2c5e191b6438. Accessed December 10, 2021.
  44. Carra MC, Huynh N, Lavigne G. Sleep bruxism: A comprehensive overview for the dental clinician interested in sleep medicine. Dent Clin North Am. 2012;56(2):387–413. doi:10.1016/j.cden.2012.01.003
  45. Koyano K, Tsukiyama Y, Ichiki R, Kuwata T. Assessment of bruxism in the clinic. J Oral Rehabil. 2008;35(7):495–508. doi:10.1111/j.1365-2842.2008.01880.x
  46. Manfredini D, Serra-Negra J, Carboncini F, Lobbezoo F. Current concepts of bruxism. Int J Prosthodont. 2017;30(5):437–438. doi:10.11607/ijp.5210
  47. Kuhn M, Türp JC. Risk factors for bruxism. Swiss Dent J. 2018;128(2):118–124. PMID:29533049.
  48. McNamara P, Johnson P, McLaren D, Harris E, Beauharnais C, Auerbach S. REM and NREM sleep mentation. Int Rev Neurobiol. 2010;92:69–86. doi:10.1016/S0074-7742(10)92004-7
  49. Maspero C, Giannini L, Galbiati G, Rosso G, Farronato G. Obstructive sleep apnea syndrome: A literature review. Minerva Stomatol. 2015;64(2):97–109. PMID:25747430.
  50. Patel SR. Obstructive sleep apnea. Ann Intern Med. 2019;171(11):ITC81–ITC96. doi:10.7326/AITC201912030
  51. Tachibana M, Kato T, Kato-Nishimura K, Matsuzawa S, Mohri I, Taniike M. Associations of sleep bruxism with age, sleep apnea, and daytime problematic behaviors in children. Oral Dis. 2016;22(6):557–565. doi:10.1111/odi.12492
  52. Hosoya H, Kitaura H, Hashimoto T, et al. Relationship between sleep bruxism and sleep respiratory events in patients with obstructive sleep apnea syndrome. Sleep Breath. 2014;18(4):837–844. doi:10.1007/s11325-014-0953-5
  53. da Costa Lopes AJ, Abrahão Cunha TC, Magalhães Monteiro MC, Serra-Negra JM, Cabral LC, Simamoto PC Jr. Is there an association between sleep bruxism and obstructive sleep apnea syndrome? A systematic review. Sleep Breath. 2020;24(3):913–921. doi:10.1007/s11325-019-01919-y
  54. Ohmure H, Oikawa K, Kanematsu K, et al. Influence of experimental esophageal acidification on sleep bruxism: A randomized trial. J Dent Res. 2011;90(5):665–671. doi:10.1177/0022034510393516
  55. Li Y, Yu F, Niu L, Long Y, Tay FR, Chen J. Association between bruxism and symptomatic gastroesophageal reflux disease: A case–control study. J Dent. 2018;77:51–58. doi:10.1016/j.jdent.2018.07.005
  56. 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(11):810–818. doi:10.1111/joor.12323
  57. Martynowicz H, Dymczyk P, Dominiak M, et al. Evaluation of intensity of sleep bruxism in arterial hypertension. J Clin Med. 2018;7(10):327. doi:10.3390/jcm7100327
  58. Nashed A, Lanfranchi P, Rompré P, et al. Sleep bruxism is associated with a rise in arterial blood pressure. Sleep. 2012;35(4):529–536. doi:10.5665/sleep.1740
  59. Câmara-Souza MB, Costa de Figueredo OM, Rodrigues Garcia RC. Association of sleep bruxism with oral health-related quality of life and sleep quality. Clin Oral Investig. 2019;23(1):245–251. doi:10.1007/s00784-018-2431-0
  60. Michalek-Zrabkowska M, Wieckiewicz M, Macek P, et al. The relationship between simple snoring and sleep bruxism: A polysomnographic study. Int J Environ Res Public Health. 2020;17(23):8960. doi:10.3390/ijerph17238960
  61. Polmann H, Réus JC, Massignan C, et al. Association between sleep bruxism and stress symptoms in adults: A systematic review and meta-analysis. J Oral Rehabil. 2021;48(5):621–631. doi:10.1111/joor.13142
  62. Polmann H, Domingos FL, Melo G, et al. Association between sleep bruxism and anxiety symptoms in adults: A systematic review. J Oral Rehabil. 2019;46(5):482–491. doi:10.1111/joor.12785
  63. Bertazzo-Silveira E, Kruger CM, De Toledo IP, et al. Association between sleep bruxism and alcohol, caffeine, tobacco, and drug abuse: A systematic review. J Am Dent Assoc. 2016;147(11):859–866.e4. doi:10.1016/j.adaj.2016.06.014
  64. Melo G, Dutra KL, Filho RR, et al. Association between psychotropic medications and presence of sleep bruxism: A systematic review. J Oral Rehabil. 2018;45(7):545–554. doi:10.1111/joor.12633