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12.10 Sleep Bruxism
There has been a lack of consolidated knowledge to several kinds of physiological
and pathological motor occurrences within the orofacial and craniomandibular
regions that have frequently led to a no man’s land, with clear implications on the
design of both diagnostic and therapeutic algorithms and decisions seriously impacting patients’ outcomes. After brief description of the basic mechanisms subsidizing
the circadian and sleep-related motor control, an updated denition of sleep bruxism is provided within this section, as well as the current proposed classication.
12.10.1 Circadian andSleep-Related Motor Control
In humans, motor control is dictated by a complex, well-organized system linked
to oscillatory components associated with a central biological clock [183]. A background muscle activity represents the circadian dynamics of such control during
the day, which is progressively silenced during a typical No Rapid Eye Movement
(NoREM) - Rapid Eye Movement (REM) sleep cycle usually occurring during
nighttime [184]. The behavioral reduction in muscle activity during the nocturnal
phase results from both circadian and homeostatic inuences leading to a generalized inhibitory ow [185]. While this inhibition, which is evident mainly during
REM sleep, is expected, periodic phasic motoneuronal excitations leading to brief
movement moments do occur in the same physiological matrix [186]. Yet, abnormal/deviated patterns of motor inhibition, excitation, or both may also occur during
sleep as a cause of recurring motor phenomena, eventually leading to sleep-related
motor exacerbations [187]. Sleep bruxism is, in this context, a motor construct
derived from sleep. Wakeful bruxism is commonly considered another construct
which is arguably a less common circadian phenotype differing from the sleep
variant in several ways. Yet, considering circadian phenotypes linked to bruxism
may be more complex than simply separating according to the state of arousal from
which it derives. In a recent study, our team showed that a circadian prole of bruxism manifestations might symmetrically occur during the day, eventually with different clinical impacts depending on the moment in which is mostly perceived
[188]. One clear implication of such neglected circadian distribution is their
temporal relationship with some daily routines. For example, Bruxism perceived
near bedtime (awake bruxism), and during sleep (sleep bruxism) may interact with
mechanisms generating the onset and maintenance of insomnia.
12.10.2 Defining Bruxism
Sleep bruxism (SB) involves exacerbated activation of the masticatory muscles,
often resulting in a dynamic contact of teeth during sleep.
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Three denitions of sleep bruxism have been provided by the American Academy
of Sleep Medicine (AASM). The rst one, in 1990, was inscribed in the ICSD
within the parasomnias chapter, e.g., a disorder intruding on sleep but not associated
with complaints of insomnia or excessive sleepiness, as a stereotyped movement
disorder characterized by grinding or clenching of the teeth during sleep [189]. In
2005, the second edition of the ICSD integrated bruxism into the category of sleeprelated movement disorders, dening it as an oral parafunctional activity characterized by a sleep-dependent tooth grinding or jaw clenching, usually associated with
arousals [190].
However, several issues remained unsolved until 2013, when from a consensual meeting of experts, redened bruxism as “a repetitive jaw muscle activity
characterized by clenching or grinding of the teeth and/or bracing or trusting of
the mandible” [191]. The latest international consensus updated however the previous denition with the statement that SB is “a masticatory muscle activity during sleep that is characterized as rhythmic (phasic) or nonrhythmic (tonic) and not
a movement disorder or a sleep disorder in otherwise healthy individuals” [192].
L. D. AneybaLópez et al.
12.10.3 Epidemiological andDevelopmental Aspects
ofSleep Bruxism
Bruxism has been studied from the epidemiological point of view in large populations. Although, methodological constraints are related to subjectively reported
manifestations in most studies, both cross-sectional surveys and self-reports showed
that SB affects 15%–40% of children and 8%–10% of adults [193–198].
Pediatric bruxism can start as soon as the rst teeth erupt, and its prevalence rises
until the age of 6, reaching about 30% [199], lowering its frequency in adults (12%)
and advanced age (2%–4%) [194]. While there seems to be no difference in the
proportion of males and females affected, bias regarding potentially etiological factors cannot be discarded.
12.10.4 Risk Factors, Comorbidities, andGenetics
Every condition tending to supercialize sleep may pull the trigger for motor activation and therefore predispose to bruxism. Consequently, it is not surprising that
comorbid sleep disorders would be the main risk factors. Primary psychiatric and
neurological disturbances may also account as essential contributors.
Although obstructive sleep apnea alone has shown to signicantly increase SB
risk, an increase in arousals and circadian misalignment as frequent comorbidities
can also potentially trigger SB [200]. The co-occurrence of insomnia and sleep apnea
is frequent among population, showing a misalignment of the circadian clock [201],
in addition of sharing common pathophysiological pathways toward autonomic activation [201, 202]. Comorbid Insomnia and Sleep Apnea (COMISA) is also a putative
contributor to such oromotor phenomena. As recently reported, SB is common in
patients with COMISA [203] and therefore should be adequately assessed.
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The reasoning behind the interaction between SB and OSA is not enterally
understood and is still under debate. However, it was proposed a protective role of
the motor events during respiratory-related arousals [204] which has not yet been
conrmed [205].
Also, SB was proposed to be related substances intake. However, the cause–
effect relationship is lacking for many of those pharmacological agents and therefore evidence supporting specic medications as risk factors for bruxism is
low [206].
The relationship between SB and certain neurologic and psychiatric disorders
has not been established although their co-occurrence is frequent.
In children, some parasomnias and sleep-related behavioral issues mostly derived
from sleep-related dissociative states have been found to be prevalent in patients
with SB [17]. Also, psychosocial stressors in children and adults are frequent among
SB patients and exacerbated gastroesophageal reux has been found in the same
segment of ages [207].
There are also several tentative genetic-etiological contributors, such as the serotonin receptor encoding gene (HTR2A) and dopamine (DRD1) receptor gene, and
several polymorphisms seem to affect SB or being involved in its development,
pathogenesis, or its relationship with other sleep disorders [208].
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12.10.5 Treatment
The therapeutic success in bruxism treatment will depend on the clinical
approach taken; it is essential to adopt a new model from the perspective of the
individual rather than the partial vision of the teeth and their alterations, which
can offer answers about bruxism, understood as a dysfunctional muscular
activity with neurobiological origins that explain it beyond its evident peripheral effect.
The approach to the treatment of bruxism has varied according to the etiological
theories proposed in the past. Today, considering bruxism as a multifactorial parafunctional activity, treatment should be focused on etiological factors.
The therapeutic alternatives in the control of bruxism are independent for each
case since multiple conditions can cause this entity: However, personality type,
allergies, nutritional deciencies, malocclusions, central nervous system disorders,
drugs, deciency in oral proprioception, and genetic factors are some of the causes
for its development, so treatment should be focused mainly on the etiological factors. Although the trigger it is potentiated by certain emotional states such as anxiety and stress [209].
The functional evaluation of occlusion static and dynamic is of great importance
because it depends on any treatment’s success or failure. Although, we have multiple clinical studies, we still do not have sufcient scientic evidence for treating
bruxism.
Different treatment modalities have been applied (behavioral techniques, intraoral devices, medications, and stimulation); however, a clinical evaluation is essential to differentiate between awake bruxism and sleep bruxism and rule out any
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medical disorder or medication causing its presence (secondary bruxism). In some
cases, an overnight sleep study is necessary.
Below we will mention some of the treatments most frequently used in traditional practice for the control of bruxism within the dental ofce [210].
L. D. AneybaLópez et al.
12.11 Sleep Hygiene Measures
Modifying habits before sleeping and as relaxation techniques will be essential to
contribute to the joint therapy of bruxism, being the rst step in treatment.
The treatment for dental bruxism will depend on knowing what is causing this
problem. The dentist must determine the potential cause with precise questions and
a dental exam. Then, depending on the cause and the damage, the treatments applied
to treat dental bruxism aim to reduce pain, prevent tooth wear, and permanent damage to the jaw. These therapies can reduce the habit of clenching and grinding the
teeth, although they are often not a denitive solution. Splints are considered as the
initial treatment for the control of bruxism. However, it has been clinically observed
that the effects in the reduction of electromyographic events (EMG) of long-term
bruxism are transient.
One study compared occlusal splints versus doses of a gabapentin drug and
found that both treatments similarly reduced muscle activity associated with sleep
bruxism after 2months of therapy [211].
Traditional splints or dental protectors have been used to prevent dental bruxism
during sleep. Splints can make the pain go away while worn and help prevent the
damage this disorder can cause. However, they do not solve the problem since the
inconvenience reappears if they are no longer used. There are different types of
splints. Some t on the lower teeth and others on the upper ones. These protectors
are designed to keep the jaw in a more relaxed position.
Traditionally, splints or dental protectors have been used to prevent dental bruxism during sleep. Splints can make pain go away while they are worn and help
prevent the damage this disorder can cause. However, they do not solve the problem
since the inconvenience reappears if they are no longer used. There are different
types of splints, some t on the lower teeth and others on the upper ones. These
protectors are designed to keep the jaw in a more relaxed position.
12.11.1 Drug Therapy
Some experimental studies have been carried out on the use of medications in
patients with BS; however, more clinical research is still necessary for their use this
therapy in bruxism.
Lobbezzo etal. [212] used levodopa in severe bruxers, comparing them with a
placebo group. They observed a decrease in the number of sleep-related masticatory
events. Mohamed’s group [213] evaluated the use of amitriptyline in patients with
sleep bruxism and symptoms of temporomandibular disorder. The study showed
similar results, a decrease in masticatory events too.
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Huynh N etal. [214], showed the effect of 2 sympatholytic drugs, propranolol,
and clonidine, on sleep bruxism; the reduction of bruxism activity by 60% was
observed, but with signicant adverse effects such as dry mouth, morning hypotension, and suppression of REM sleep. Saletu et al. observed that in patients with
psychiatric and sleep comorbidities, clonazepam reduces bruxism and improves the
general quality of sleep [215].
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12.11.2 Botulinum Toxin
Botulinum toxin is one of the alternatives implemented for aesthetic use; it is used
for various treatments, including bruxism, reducing muscle strength in the masseter,
providing a reduction of bruxism events and activations in the brain during the night.
Bruxism has been evaluated with nocturnal polysomnography, showing a reduction of muscle contraction after 4 weeks, but without changes in the rhythm or
number of bruxism episodes per hour of sleep [216]. Lee etal. found similar results
after 8weeks after application of botulinum toxin [217]. There is a need for more e
scientic evidence for the use of botulinum toxin as an alternative treatment for
bruxism.
12.12 Role oftheDental Professional inDrug-Induced Sleep
Endoscopy (DISE)
Currently, the dentist’s role during DISE (Fig.12.24) is earning interest among our
otolaryngologist colleagues who perform these procedures while the patient is
under sedation.
Fig. 12.24 Dentist maneuvers during DISE procedures
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L. D. AneybaLópez et al.
The dentist with training in dental sleep medicine can participate during DISE,
trying to t diverse appliances using vertical dimension and protrusion to assign the
right tool to modify the airway.
It can also be combined with CPAP if it is eligible.
Several protocols are currently being developed for the role of the dentist during
the DISE nowadays [218].
Take-Home Message
• Oral appliances have been described as an efcacious treatment for OSA. Studies
have shown a decrease in the frequency and/or duration of Apneas, Hypopneas
RERAS and/or snoring, as well as in improving nocturnal oxygenation, improve-
ment of blood pressure, and quality of life. They may enhance CPAP adherence
when used nightly.
• However, their use is limited by side effects.
• Temporomandibular disorders and Bruxism are related to Obstructive sleep apnea.
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