- Author: Jeff Burgess, DDS, MSD; Chief Editor: Arlen D Meyers, MD, MBA more...
Evidence-based management of bruxism is hampered by the limited number of randomized controlled studies available for assessing the efficacy of various treatment strategies, the historical lack of understanding with respect to the etiology of the condition, and the changing diagnostic criteria by which bruxism is defined. Nonetheless, the literature contains references to a number of management strategies that may be useful in protecting the dentition, periodontium, and the jaw musculature and temporomandibular joint from this potentially destructive behavior.
The term bruxism is said to come from the Greek word "brychein," which means "to grind or gnash the opposing rows of upper and lower molar teeth." Per recent classification of sleep disorders, bruxism is defined as a sleep-related movement disorder. The Glossary of Prosthodontic Terms (GPT-8) defines bruxism as parafunctional tooth grinding habit consisting of involuntary rhythmic or spasmodic nonfunctional gnashing, grinding, or clenching of teeth.
Behavior that occurs during the day is termed awake or diurnal bruxism and can consist of semivoluntary clenching or lateral tooth grinding movement. Grinding or clinching that occurs at night is termed sleep bruxism.
Early theories suggesting that bruxism was related to general malocclusion have been disproven, although, in some isolated cases, tooth interferences may play a role in its onset.
What has emerged in the last 10 years from extensive research is a broader hypothesis defining the genesis and pathogenesis of bruxism. The factors that have found traction from these studies include genetic predisposition, sleep architecture (eg, micro arousals occurring during sleep), psychological factors such as distress and anxiety, environmental factors, CNS catecholaminergic levels, brain trauma, brain disease, drug effects (stimulatory drugs: ecstasy, caffeine, or serotonin reuptake inhibitors, anxiolytic medication, or dopaminergic drugs, etc), and autonomic nervous system function (pattern generation). Bruxism is also considered a natural behavior that stimulates salivation during sleep.
One experimental study involving induction of esophageal acidification has shown that bruxism episodes increase with acid stimulation, suggesting that reflux may cause bruxing behavior in individuals with this stomach abnormality.
Based on fMRI evidence (Lida T, et al. European Journal of Oral Science, 2010), light daytime tooth clenching is now known to be associated with activation of the bilateral sensorimotor cortex, supplementary motor area, dorsolateral prefrontal cortex, and the posterior parietal cortex. This suggests a more extensive cortical network than that occurring with finger behaviors, which were also evaluated in the study. The results provide further evidence for a complex central mechanism involved in bruxing behavior. Current sleep study evidence suggests that even before first tooth contact a series of physiological events occur which include activation of the autonomic cardiac system at minus 4 minutes, brain activity at minus four seconds, a rise in jaw opener muscle tone with 2 big breaths, and an increase in heart rate at minus one second. This particular sequence has been found to occur in close to 80% of rhythmic jaw movements associated with tooth grinding during sleep.
Other studies suggest that an imbalance in dopamine-mediated neural transmission may exist in some types of bruxism. For example, while short-term use of dopamine precursors such as L-dopa inhibits bruxism, long-term use of the L-dopa increases bruxism. Bromocriptine, a preferential dopamine D2 receptor agonist reduces bruxism episodes. Amphetamine and similar street drugs increase dopamine concentration and their use has been associated with bruxism. In at least one report smokers reported bruxism twice as frequently as nonsmokers, and nicotine is known to stimulate central dopaminergic activity. The SSRIs have an indirect effect on the dopaminergic system and are known to cause an increase in bruxism.[6, 7, 8, 2]
The role of psychosocial factors in the etiology of bruxism has been assessed by a recent systematic search of peer-reviewed papers (PubMed Database) dealing with bruxism and psychological/psychosocial factors. Forty-five papers were considered relevant. The authors of the article report that the reviewed studies showed an association between bruxism and anxiety, stress sensitivity, depression, and other personological characteristics. These findings appear to be contrary to sleep laboratory investigations, which do not support such associations. The totality of these reported studies and the sleep research suggests that, with respect to potential psychological or psychosocial causation, very distinct differences may exist with respect to these factors between subjects that grind their teeth during sleep and those who do so during the day.
The diagnosis of bruxism is descriptive in nature, contingent on the presence of symptoms such as acknowledged tooth grinding, pain in the TMJ or jaw musculature, temporal headache, tooth hypersensitivity or mobility, and poor sleep quality. These subjective symptoms are coupled with clinical signs such as abnormal tooth wear, tongue indentations, the presence of a linea alba along the biting plane of the buccal (cheek) mucosa, gum recession, masseter hypertrophy, and/or broken fillings or teeth.
Attempts have been made to provide a more formal definition of nocturnal bruxism based on sleep architecture and the number of episodes occurring during different phases of sleep. However, for some sleep variables their sensitivity and specificity is problematic. For example, rhythmic masticatory muscle activity (RMMA) has been reported to occur once or twice per hour in phases 1 and 2 of non-REM sleep for about 60% of nonbruxing individuals and 80% of patients as identified as bruxers. However, RMMA is also associated with other sleep disorders such as parasomnias, acid reflux, and obstructive sleep apnea and snoring so may not reliably differentiate bruxers from people with other sleep problems.
In another study sleep architecture, including the number of microarousals, K=complexes, K-alphas, EEG spindles, and the density of slow-wave activity was assessed in a small group of subjects and controls. Based on findings from this research, the authors concluded that, in bruxism patients, good sleep was characterized by a low incidence of K-complexes or K-alphas and by the absence of any difference in other sleep microstructure variables or SWA. The extent to which these variables predict bruxism has not been further assessed for diagnostic accuracy.
In diagnosing bruxism, particularly as a sleep disorder, their needs to be a well-defined exclusion criteria that separates bruxism from other sleep disorders such as sleep apnea, epilepsy, and REM disorder behaviors.
In an initial effort to establish a diagnostic criteria, Lavigne and colleagues have defined a set of polysomnographic diagnostic criteria, based on the analysis of 18 bruxers and 18 asymptomatic subjects. On the basis of this preliminary data, they have suggested several cut-off criteria for defining bruxism. According to Lavigne, a person defined as a bruxer should have the following:
- More than 4 bruxism episodes per hour
- More than 6 bruxism bursts per episode and/or 25 bruxism bursts per hour of sleep
- At least 2 episodes with grinding sounds
The validity of this suggested criteria has, to date, not been challenged by additional research with larger numbers and variable levels of bruxism severity, but, nonetheless, this first effort at establishing a sleep criteria may prove useful research and selective clinical situations.
Another possible criteria that might be considered in the diagnostic criteria includes micro-arousals defined by increased autonomic, cardiac, and respiratory activity which, according to one report, tends to repeat 8-14 times per hour of sleep in affected individuals.[11, 12]
Consequences of the Condition
Chronic bruxism, based on published reports, can cause mild-to-severe tooth wear, tooth cusp fracture, attached gingival recession, tooth mobility, fractured restorations, masticatory muscle pain, and temporomandibular disorders. Additionally, the literature includes other possible effects such as jaw opening limitation, temporal headache, ear symptoms (eg, plugging, tinnitus, subjective hearing loss), migraines, neck pain, insomnia, and depression.
In a retrospective analysis of parent report surveys, Insana and colleagues found a high prevalence of sleep-bruxism among preschool children (36.8%). In addition, in a subset preschoolers who received additional behavioral and neurocognitive assessments, bruxism was also associated with increased internalizing behaviors and increased health problems, which in turn were associated with decreased neurocognition. The researchers concluded that pediatric sleep-bruxism may serve as a warning sign for possible adverse health conditions, and the need for early intervention.
Effective management of bruxism relies on the recognition of potential causative factors associated with the condition. For example, since daytime or diurnal bruxism may be confounded by factors such as stress, distress, and other psychosocial parameters, considering interventions such as habit modification, relaxation therapy, biofeedback, or counseling may be appropriate.
In the patient with sleep bruxism (which does not appear to be impacted by psychological or psychosocial factors), appropriate intervention might include appliance therapy and medication. In patients with medication or drug-induced bruxism, medication withdrawal or a change of medication type to one less likely to cause bruxism should be considered. If street drugs are involved, intervention should include drug and perhaps psychological counseling.
Bruxism occurring in patients with neurogenic abnormality (eg, Parkinson disease, dystonia, Huntington disease) might benefit from Botox injection of the muscles of mastication. Dietary counseling and management may be necessary in some cases as well (excessive caffeine use, tobacco use).
The health care provider attempting to manage bruxism should understand that nocturnal or sleep bruxism is not going to be cured by intervention. And the behavior is likely to decrease with age. Daytime bruxism can sometimes be effectively eliminated via intervention, suggesting a cure, but recrudescence of the condition is common.
The following sections outline the more commonly recommended management strategies for bruxism.
Appliance therapy has been extensively studied from 1966 to the present day, and several extensive reviews have been published in the last 10 years. Occlusal splints are generally appreciated to prevent tooth wear and injury and perhaps reduce night time clenching or grinding behavior rather than altering a causative malocclusion. In addition, they are unlikely to significantly reducing nocturnal behavior.
In one recent study, 32 potentially relevant RCTs were reviewed. Of these, only 5 were randomized controlled trials. Occlusal splints in these RCTs were compared to palatal splints, mandibular advancement devices, and transcutaneous electric nerve stimulation. They were compared via meta-analysis. Statistical differences were not found between the different procedures in terms of one common outcome variable, the arousal index. The authors conclude that based on this assessment, insufficient evidence exists to support splint therapy for treating sleep bruxism, at least with respect to this sleep factor. They further state that additional RCTs are warranted with attention to appropriate study methodology before final conclusions can be drawn regarding treatment efficacy.[15, 16]
Another study assessing 177 papers found that only 13% used a randomized clinical trial design, and, of those, little evidence-based recommendations were made by the authors regarding splints for the treatment of bruxism.
The type of appliance that has been studied and suggested as helpful in managing the consequences of nocturnal bruxism is the flat-planed stabilization splint, also called an occlusal bite guard, bruxism appliance, bite plate, and night guard. This appliance can vary in appearance and properties. It may be laboratory processed or constructed in the dental office and be fabricated from hard or soft material. The typical appliance covers either all of the maxillary or mandibular teeth. No determination has been made whether significant differences exist in terms of outcome between soft, hard, mandibular, or maxillary splints, but some clinicians feel that soft splints can increase clenching behavior in some patients. But even if no appreciable change occurs in nocturnal behavior consequent to splint therapy, the appliance serves to protect the dentition.
Appliances have also been used to retrain daytime clenching, but other less costly strategies may be equally or more efficacious in managing behavior modification of this daytime activity.
Some splints are made to cover only the anterior teeth, and when these are worn during the day as well as at night the posterior teeth can erupt. When this happens, the removal of the appliance then results in an anterior open bite that can be significant, necessitating the need for otherwise unnecessary orthodontic treatment. Soft splints have been linked to the development of malocclusion. Improper tooth cleaning during splint use can lead to dental caries, and, in some cases, appliance use may result in temporomandibular disorders (TMD). A less significant complication is the staining of teeth.
Historically, benzodiazepam–type drugs and muscle relaxants have been prescribed by clinicians in an attempt to reduce nocturnal bruxism. Given the past decade of brain research related to neurotransmitters associated with bruxism, a major focus of recent research has centered on additional potentially useful serotonergic and dopaminergic drugs for the management of sleep bruxism and also the use of acetylcholine-inhibiting formulations such as botulinum toxin.
In 2003, the authors of a comprehensive review of the literature assessing the pharmacologic management of bruxism concluded, given the largely anecdotal reports published up to that time, that insufficient evidence-based data existed to draw conclusions regarding the effects of drugs associated with the dopaminergic, serotonergic, and adrenergic system on bruxism. They recommended more controlled, evidence-based research.
Since that review, new evidence supports the use of clonazepam for reducing nocturnal bruxism. In a placebo-controlled, single-blind, nonrandomized trial using polysomnography and psychometry, 10 subjects were given 1 mg clonazepam 30 minutes before lights out. The result was a significant improvement in the mean bruxism index (from 9.3 to 6.3/hour of sleep). Also, per the authors, significant improvement occurred in total sleep, total sleep time, sleep efficiency, sleep latency, and time awake during the total sleep period. Periodic leg movements also were noted to decrease significantly.
As for the effect of serotonergic medications on nocturnal bruxism, the evidence for efficacy is poor. In a placebo-controlled RCT, a serotonin precursor, L-tryptophan, was not found to be effective in reducing the behavior. The effect of antidepressant medications is mixed.
As suggested in an article published in Clinical Neuropharmacology, antidepressant drugs may exert deviating effects on bruxism: either they exacerbate the condition (selective serotonin reuptake inhibitors [SSRIs]) or they are inert in their effects (amitriptyline).
In a randomized, double-blind, crossover study on the effect of 25 mg of amitriptyline delivered over 4 weeks to 10 subjects with nocturnal bruxism, unilateral and cumulative electromyographic activity recorded on a home-use device failed to reveal differences between placebo and amitriptyline trials. The drug also did not appear to increase sleep duration. Even given the inherent problems with home monitoring devices with respect to reliability, the results do not support the use of amitriptyline for the management of bruxism.
Serotonin reuptake inhibitor medications (SSRIs) have been observed to increase bruxism. In these cases, a reduction in the dosage or withdrawal and substitution with another antidepressant may help to reduce behavior that is significant and pathologic. It should be appreciated that drug manipulation should not occur in the absence of physician consultation. Another approach to managing the patient with SSRI-induced bruxism is possible cotreatment with gabapentin.
In a reported case study involving onset of bruxism after use of venlafaxine therapy for depression, gabapentin was coprescribed for anxiety symptoms and was found to ameliorate the bruxing behavior completely.
Dopaminergic medication also appears to demonstrate potential utility in reducing nocturnal bruxism. In a double-blind, randomized, cross-over clinical trial described by F Lobbezoo and GJ Lavigne, 10 patients with sleep bruxism were assessed over 3 consecutive nights after being prescribed low doses of short-term L-dopa combined with benserazide. What was found was that L-dopa use produced a significant decrease in the average number of bruxism episodes per hour of sleep and the root-mean-square EMG level per burst of behavior (suggesting a normalization of the EMG activity pattern associated with sleep bruxism).
Low doses of the dopamine D1/D2 receptor agonist pergolide have also been reported to reduce bruxing behavior in a severe bruxism case.
The D2 receptor agonist bromocriptine was studied in 6 subjects using a double-blind, placebo-controlled polysomnographic and neuro-imaging study with a single crossover design. The bromocriptine subjects demonstrated a 20-30% greater reduction in bruxism episodes per hour of sleep, although the number of bursts per episode were not significant between groups. However, bromocriptine induced significantly lower root-mean squared EMG levels in this limited study, suggesting that the drug may be useful in treating bruxism.
In contrast, Huynh and Lavigne were not able to discern an effect of the use of a nonselective adrenergic beta-blocker, propranolol, on nocturnal bruxing behavior, although the latter drug was reported effective in reducing bruxism in patients taking antipsychotic medication.
Dentists are most likely to prescribe benzodiazepine and muscle relaxant drugs for the management of severe bruxism. Prescribing clinicians should be familiar with the general effects, side effects, and potential drug interactions involving these classes of medications. These medications should only be prescribed short term for maximum benefit.
In at least one study involving clonidine use for bruxism, the drug is reported to have caused severe morning hypotension in 20% of participants. In addition, long-term use of L-dopa has been associated with an increase in bruxing behavior.
Botulinum toxin A
The most recent advocated pharmacological approach to managing the pathological effects of nocturnal and diurnal bruxism is injection of the muscles of mastication with botulinum toxin A. This neurotoxin inhibits the release of acetylcholine from the neuromuscular junction, essentially rendering the muscle incapable of activity. This approach to therapy may find its greatest application in the treatment of severe bruxism associated with coma, brain injury, amphetamine abuse, Huntington disease, autism, and Parkinson disease but is also being used to treat more minor cases of bruxism as well.[29, 30, 31, 32]
In a large case series, botulinum toxin A was injected into the masseter muscles of 120 patients previously identified as bruxers. . A standardized dosage and location criteria was used for each patient. Follow-up occurred at 15 days, and participants were asked about the effects and potential complications via a short questionnaire. The author reports that 30% of the patients reported fair results, 65.8% declared good, and 4.2% declared an excellent result, and that no one reported significant side effects. Although the methodology associated with this study is significantly flawed, the results of this case series suggest a possible use of Botox in managing bruxism.
Other case studies appear to support the efficacy of Botox injection. In a study in which 19 patients were injected with botulinum toxin type A, none reported unwanted side effects. The duration of the effect of botox was from 13-26 weeks, and the final dose ranges varied from 25-40 IU per muscle.
The best support for the use of botulinum toxin A for bruxism comes from the results of a randomized controlled trial involving 12 subjects. Botulinum toxin was injected into both masseters of 6 subjects, and saline injected into the masseters of 6 others (as a control), and the 2 groups were compared for nocturnal electromyographic (EMG) activity at 4, 8, and 12 weeks. This study's results were published in the American Journal of Physical Medicine and Rehabilitation in 2010. Masseter muscle bruxism events were found to decrease significantly following toxin injection, while in both groups the EMG activity of the temporalis muscle remained similar for bruxism events.
Subjective bruxing symptoms were observed to decrease in both groups after injection, which represents a rather interesting finding suggesting that the needling or injury from saline independent of toxin could induce a perceived decrease in bruxism behavior. The authors conclude that this data supports the safe use of Botox in treating bruxism.
Complications include bleeding, spot tenderness, bruising, toxic reactions, and infection.
Relaxation, Behavioral Strategies, Sleep Hygiene
The use of relaxation strategies such as meditation, hypnosis, guided imagery, self-monitoring, habit retraining, cognitive behavioral intervention, and biofeedback in the management of nocturnal bruxism have not been validated by sound scientific studies (eg, RCTs and studies using nocturnal polysomnography and psychometry). Nonetheless, because these interventions are noninvasive and have been shown to be effective in controlling other forms of habitual behavior, they may have utility in treating diurnal or daytime behavior. Hypnosis appears partially supported by a number of case reports suggesting that long-term effects might be possible in such management. Other relaxation techniques, including meditation, are theorized to reduce stress and improve self-esteem and self control.[36, 37]
Improvement in the quantity and quality of sleep is also understood generally to reduce the episodes of bruxism. As a result, some physical medicine approaches such as cardiovascular toning programs, TENS, acupuncture, manual massage, and a few alternative naturopathic approaches have also been suggested for the management of bruxism. None have been studied appropriately to allow reasonable comment on their efficacy.
A review article that is to be published in the journal Med Oral Patol Oral Cir Bucal (the full article has been released in advance of publication) reviews concepts associated with sleep bruxism, including appropriate intervention. The author, José-Luis de la Hoz-Aizpurua and associates, note that with respect to the occlusion as a cause of bruxism, “the scientific literature has repeatedly proved that this theory lacks scientific validity.” However, in cases in which it can be determined that a specific tooth interference may be initiating bruxing behavior, the offending biting contact should be adjusted to remove the irritant. This does not mean that all the teeth should be adjusted to accommodate a theoretical ideal occlusal position based on unsupported hypotheses.
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