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Bruxism Management
Updated: Jan 27, 2017
 Author: Jeff Burgess, DDS, MSD; Chief Editor: Arlen D Meyers, MD,
MBA more...


Overview
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.
Definition
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. [1]
Behavior that occurs during the day is termed awake or diurnal bruxism
and can consist of semi-voluntary clenching or lateral tooth grinding
movement. Grinding or clinching that occurs at night is termed sleep
bruxism. [2]
Etiology
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. [3]
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. [4]
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. [5]
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. [9]
Diagnosis
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. [10]
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:
1. More than 4 bruxism episodes per hour
2. More than 6 bruxism bursts per episode and/or 25 bruxism bursts per
hour of sleep
3. 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. [13]
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 of 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. [14]
Management
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
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. [17]
A randomized controlled trial with 28 participants by Singh et al found
greater reduction in sleep bruxism episodes per hour after 3 months with
the mandibular advancement device when compared to the maxillary
occlusal splint, however, more discomfort was reported with the mandibular
advancement device. [18]
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.
Complications
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.
Pharmacology
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. [19]
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. [20]
Since that review, new evidence supports the use of clonazepam for
reducing nocturnal bruxism. [21] 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. [22]
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. [23]
As suggested in an article published in Clinical
Neuropharmacology, [24]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. [25] 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. [26]
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, [27] 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. [6] 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. [28]
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. [29]
Complications
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. [30, 31, 32, 33]
In a large case series, botulinum toxin A was injected into the masseter
muscles of 120 patients previously identified as bruxers. [34] . 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. [35]
The best support for the use of botulinum toxin A for bruxism comes from
the results of a randomized controlled trial involving 12
subjects. [36] 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. [37, 38]
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.
Occlusal Treatment
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. [39]