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Sleep bruxism: an overview for clinicians

Article in British dental journal official journal of the British Dental Association: BDJ online · September 2018
DOI: 10.1038/sj.bdj.2018.757

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Oral medicine CLINICAL

Sleep bruxism: an overview for clinicians

H. Beddis,*1 M. Pemberton2 and S. Davies3

Key points
Provides understanding of the Provides understanding of diagnosis of Provides awareness of treatment Provides awareness of links between
pathophysiology and contemporary sleep bruxism. strategies for sleep bruxism. sleep bruxism and other sleep-related
concepts of sleep bruxism. conditions.

Bruxism is characterised by clenching or grinding of the teeth due to contraction of the masseter, temporalis and other
jaw muscles. Bruxism may lead to masticatory muscle hypertrophy, tooth surface loss, fracture of restorations or teeth,
hypersensitive or painful teeth and loss of periodontal support. Sleep bruxism has previously been viewed as a dysfunctional
movement or pathological condition, whereas it is now accepted as a centrally controlled condition with various systemic
risk factors. It has been postulated that sleep bruxism may have a protective role during sleep, for example in relation
to airway maintenance or in stimulating saliva flow. A diagnosis of sleep bruxism may be made via patient report and
clinical interview, clinical examination, intraoral appliances or recording of muscle activity. Bruxism in itself does not require
treatment: management is only indicated where problems arise as a result of bruxism. Oral appliances primarily aim to
protect the dentition from damage caused by clenching/grinding, although they may reduce muscle activity. Irreversible
occlusal adjustments have no basis in evidence in the management of bruxism. Behavioural strategies include biofeedback,
relaxation and improvement of sleep hygiene. Administration of botulinum toxin (Botox) to the masticatory muscles appears
to reduce the frequency of bruxism, but concerns have been raised regarding possible adverse effects. Dentists should be
aware of the potential aetiology, pathophysiology and management strategies of sleep bruxism.

Introduction or painful teeth.2–5 The excessive forces on the be around 8–13% of the general population.7–9
teeth can contribute to alveolar bone resorp- SB is more common in children (14–18%)
Bruxism is defined as a ‘repetitive jaw-muscle tion, which may be visible radiographically and lower in the elderly (around 3%).10 Awake
activity characterised by clenching or grinding as generalised widening of the periodontal bruxism (AB) is more common than SB: a
of the teeth and/or by bracing or thrusting of ligament space, and increased mobility 2013 systematic review reported a prevalence
the mandible’ with ‘two distinct circadian which may be transient or permanent. In the of 22.1–31%.9
manifestations; either occurring during sleep presence of periodontal disease, the trauma Bruxism may be described as primary where
(sleep bruxism) or during wakefulness (awake from the occlusion may increase the rate of there is no pre-existing causative medical
bruxism).’1 disease progression. Occlusal trauma cannot condition, or secondary where it occurs as a
Sleep bruxism (SB) may lead to mastica- induce periodontal pocketing or attachment result of a psychiatric or medical condition.11
tory muscle hypertrophy, tooth surface loss, loss in teeth with a healthy periodontium.6 Bruxism may involve a static clenching of the
fracture of restorations or teeth, hypersensitive Investigations into the effects of SB on dental teeth, grinding, or a mixture of the two. This
implants and implant-retained prostheses have activity is accompanied by noise in around a
1
University of Leeds, Department of Restorative Dentistry, found no increase in biological complications third of sleep bruxists.10 Awake bruxism is more
Leeds Dental Institute, Leeds, LS2 9LU; 2University Dental
Hospital of Manchester, Oral Medicine, Higher Cambridge (for example, peri-implantitis), but increased usually a static clenching without sounds;12
street, Manchester, M15 6FH; 3TMD Clinic Manchester risk of mechanical complications (for example, grinding whilst awake is generally only second-
University Dental School, Manchester, M15 6FH
*Correspondence to: Hannah Beddis fracture of implants/prostheses).5 arily associated with medications or neurologi-
Email: H.Beddis@leeds.ac.uk There is a wide variety in reported preva- cal disorders for example, dyskinesias.7
Refereed Paper. lence of bruxism (between 5–91%)3 as a result This article aims to provide an overview of
Accepted 26 June 2018 of the range of methodologies with differing the current understanding of sleep bruxism
Published online 21 September 2018 reliabilities used to collect the data. However, and its associated conditions, with discussion
DOI: 10.1038/sj.bdj.2018.757
the prevalence of SB is generally considered to of best practice in diagnosis and management.

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 CLINICAL Oral medicine

Aetiology Subjects with SB may also exhibit more whole with stimulating saliva flow during sleep.7
body movements (for example, twitches, jerks) Miyawaki et al. found that 57–59% of masti-
The aetiology of SB is the subject of some during sleep than controls,22 with studies finding catory muscle activity during sleep was associ-
debate and is likely to be complex and multi- that body movements were associated with SB in ated with swallowing activity; and that in SB
factorial. It is now generally accepted that the 65–78.9% of subjects23 and 93% of SB episodes.24 subjects 68% of swallowing activity occurred
pathophysiology of SB relates to activation of in conjunction with muscle activity compared
the central nervous system during sleep.4,13 Possible functions of sleep bruxism to only 10% in control subjects.19
There are various risk factors which can con- It has been hypothesised that there may be
tribute to SB, including:13 Bruxism is often considered as a disorder, or different types of bruxist activity: idiopathic;
• Exogenous risk factors: smoking, heavy a parafunction. A disorder is characterised by associated with airway patency; associated with
alcohol intake, caffeine, medications or lack of normal functioning of physical or mental sleep-related movement disorders; associated
illicit drugs14 processes, and a parafunction is a disordered with swallowing,20 so it may be the case that
• Psychosocial factors: there is a common function, for example, a normal function done all of these may co-exist in the same patient.
professional and patient perception that to an excessive extent, which has led to the con-
stress and anxiety exacerbate SB, although sideration by some of bruxism as a parafunction. Diagnosis of sleep bruxism
results of studies have varied7 However, the 2013 definition above includes
• Sleep disorders involving sleep arousal neither of these terms, with the rationale that it A diagnosis of bruxism may be made by the
• Comorbidities: other disorders including is uncertain that bruxism has no function. It has following:
obstructive sleep apnoea14 and gastro- been postulated that sleep bruxism may have a • Patient report and clinical interview
oesophageal reflux disorder.15 protective role during sleep, which may relate to • Clinical examination
airway maintenance1,25 or in stimulating saliva • Intraoral appliances
The systemic nature of these risk factors flow to lubricate the oropharynx.19 • Recording of muscle activity
strengthens the need to move away from • Electromyography (EMG)
previous concepts of bruxism as peripherally Airway maintenance • Polysomnography (PSG).
stimulated (that is, by features of the occlusion) Sleep bruxism activity has been shown to be
and towards acceptance of central control of the associated with an increase in respiration during Patient report and clinical interview
condition. Bruxism has previously been viewed an arousal episode, leading to a hypothesis that Suitable questions are given in Table 1.29,30 The
as a dysfunctional or parafunctional movement bruxism may have a role in reinstating or main- four questions in the Brux scale were developed
or pathological condition. Bruxism has in the taining airway patency during sleep.25 Muscle by van der Meulen et al., and form part of a larger
past even been considered an ‘occlusal disease’ activity during SB usually commences with tool (the Oral Parafunctions Questionnaire).31
by some dentists,16 but despite these historical activity of the suprahyoid muscles followed by The questions relating to awake bruxism may be
beliefs to the contrary, Lobbezoo, et al.3 found activity of the jaw-opening muscles and may used to help distinguish SB from other behav-
no evidence to support a causal role of occlusal therefore be responsible for mandibular protru- iours.5 However, diagnosis via questionnaire
factors in bruxism in a review of 46 papers. sion and airway opening.7 alone may be inaccurate, for example due to lack
The prevalence of SB appears to be increased of awareness of current behaviours (for example,
Bruxism and sleep in subjects with obstructive sleep apnoea (OSA), grinding noises in subjects sleeping alone).7 Up
but this relationship between SB is complex, to 80% of patients may be unaware of bruxism.32
Sleep bruxism is classified by the International with various contributing factors.26 Attempts Reports by sleeping partners of grinding noises
Classification of Sleep Disorders as a sleep- to elucidate a consistent temporal or causal during sleep are particularly suggestive of SB20
related movement disorder.17 Sleep bruxism relationship between the two have not been since normal orofacial muscle activity does not
appears to occur as a reaction to micro-arous- successful.14,26,27 cause noise. Lavigne found that this alone as a
als during sleep: three to ten seconds-long measure of bruxism had 78% sensitivity and
episodes of increased heart rate and muscle Swallowing and saliva stimulation 94% specificity following validation with PSG.23
tone, occurring eight to 15 times per hour in Gastro-oesophageal reflux (GORD) also
healthy subjects.7 Most SB episodes occur in appears to be a risk factor for with SB, and it has Painful TMD and bruxism
clusters during these micro-arousals,7,18,19 and been hypothesised that this association is via Whilst many patients are unaware of having SB,
subjects with SB exhibit more micro-arousals SB having a protective function stimulation of conversely some patients who do not have SB
than controls.10,18,20 Sleep bruxism may be saliva flow. Miyawaki et al. found that subjects may falsely believe they do have the condition,
concomitant with other sleep disorders for with SB had more episodes of GORD and that because they have been told by their dentist that
example, sleepwalking, sleep terrors and 60% of SB episodes occurred during reflux; and they do. This is probably based on the erroneous
sleeptalking,7 which are also associated with that administration of proton-pump inhibitor assumption by the dentist that painful mastica-
arousal from sleep or ‘confused wakening.’ medication led to a reduction in SB episodes tory muscles are caused by bruxism. A dentist
Around 60% of subjects without SB also compared to placebo and controls.15 may, therefore, conclude that a patient suffering
exhibit masticatory muscle activity during sleep, Swallowing activity during sleep has been from a painful temporomandibular disorder
but to a much lesser extent and without tooth noted exclusively following arousal episodes, (TMD) must be a bruxist. Whereas Smith
contact: SB is considered to be an extreme mani- and after around half of SB episodes, 28 carried out PSG in 53 patients with painful
festation of normal muscle activity during sleep.21 leading to a hypothesis that SB is associated TMD, of whom 74% self-reported having SB,

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 Oral medicine CLINICAL

and found that only 17% had SB confirmed

Table 1 Questions to elicit patient reported history of bruxism, and suggestive clinical
on PSG.33 Similarly, Raphael et al. carried out indicators
PSG in 124 women with myofascial pain and
Are you aware of grinding your teeth during sleep?
46 matched controls. Significantly more subjects
with painful TMD self-reported bruxism than Questions to use during Has anyone told you that you grind your teeth during sleep?
controls (55% vs 15%), although there was no history‑taking On waking, do you have your jaws clenched or thrust forward?
difference in prevalence of SB as diagnosed by
On waking, do you experience pain or stiffness in the jaw muscles?
PSG (around 10%). Interestingly, 39% of those
with TMD pain had been told by their dentist How often do you clench your teeth during sleep?
that they had SB.34 How often do you grind your teeth during sleep?
‘Brux Scale’ questions.
van der Meulen et al.31 How often do you clench your teeth whilst awake?
Clinical examination
Clinical observations suggestive of bruxism are How often do you grind your teeth whilst awake?
listed in Table 1, although the currency or extent Masseteric hypertrophy
of bruxist activity is very difficult to gauge clini-
Muscle tenderness on palpation
cally. Many of the given observations, for example
tooth surface loss (TSL), are subjective and/or Wear facets on occlusal surfaces either within the normal envelope of
Factors on clinical examination movement of at eccentric jaw positions: termed ‘bruxofacets’
may represent signs of historical bruxism.35 suggestive of bruxism
Studies have failed to demonstrate an Shiny spots on restorations
association between tooth surface loss and Restorat ion or tooth fracture
bruxism36 or TMD.37 Tooth surface loss will be
Tongue scalloping and ridging on the cheek mucosa (‘linea alba’)
a combination of normal physiological func-
tional wear, wear associated with bruxism, plus
erosion from dietary or gastric sources. Tooth Table 2 Diagnostic criteria for sleep bruxism
surface loss may be historical and cannot be
Patient report/awareness of sounds of tooth-grinding during sleep, confirmed by a
used to indicate static clenching activity. Extent room-mate, plus:
of tooth wear would be influenced by factors The American At least one of the following:
such as dietary and gastric acids, enamel Academy of Sleep
1. Observation of abnormal tooth wear
Medicine17
quality and quantity and lack of posterior tooth 2. Report of masticatory muscle fatigue or pain on waking
support. As such, TSL is described as a weak 3. Masseteric hypertrophy
indicator of bruxism.7 However ‘bruxofacets’,38 Report of grinding noises by sleeping partner for at least 5 nights a week for the past
that is, tooth wear in an eccentric position of SB research diagnostic 3-6 months
closure, may seem more convincing evidence criteria (SB-RDC) One of: tooth wear into dentine with some loss of crown height; masseteric hyper‑
Lavigne, et al.7 trophy; positive PSG (at least 2 episodes of grinding noise per night, more than 4 SB
of bruxism than wear in the intercuspal episodes and more than 25 bruxism bursts per hour of sleep)
position. Tooth surface loss alone should not,
therefore, be regarded as a reliable indicator of
active bruxism, but should be used in conjunc- muscles. Recordings can be made using ambu- disorders and SB, although it is not without
tion with other clinical indicators. latory devices, so are also suitable for detection disadvantages relating to its complexity and
of AB as well as SB. requiring specialist equipment and is generally
Intraoral devices EMG cannot detect grinding noises, nor carried out in the sleep laboratory setting for
Some intra-oral appliances aim to detect SB, can it distinguish between bruxism and other research purposes only.35 This investigation is
such as via the incorporation of electric devices orofacial activities such as swallowing, talking, clearly outwith the scope of dental practice.
detecting forces applied during clenching/ lip biting/sucking, which represent around
grinding.36 The use of intra-oral appliances in 85% of EMG recordings in controls.23 Diagnostic protocols
diagnosis relies on patient tolerance and on the
assumption that the insertion of the device will Polysomnography All methods of SB diagnosis present limitations
not affect bruxist activity. The observation of wear Polysomnography (PSG) incorporates if used in isolation. The 2013 international
facets on intra-oral splints has been observed in various recordings including EMG, electro- consensus recommended that self-report only
the literature and anecdotally, although this has encephalogram, electrocardiogram (ECG) will provide a ‘possible’ diagnosis; a diagnosis
not been validated in detection of bruxism.38 and audio-visual recordings. These detailed based on this plus clinical examination will
evaluations allow arousal from sleep to be be ‘probable’ and that ‘definite’ diagnosis
Electromyography (EMG) assessed, and the presence of other sleep would require PSG or EMG recording.1,29 It is
EMG records the electrical activity of muscles disorders to be ruled out.38 Bruxist episodes acknowledged that PSG is the ‘gold standard,’
generated during movement, and will provide can be distinguished more readily from other but its complexity and expense render it
information on extent, duration and force of orofacial movements.23,38 PSG with audio- unsuitable for widespread use in the clinical
muscle activity. EMG uses sensors attached to visual recording is the ‘gold standard’ mode of setting.9,29,38 Certainly, a large proportion of
the skin overlying the masseter or temporalis assessment and diagnosis of sleep movement the literature uses questionnaire, interview or

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 CLINICAL Oral medicine

examination techniques, and a combination of Stabilisation splints may reduce muscle reflexes which maintain airway patency, or
these is sufficient for diagnosis in the clinical activity and will prevent the unwanted con- posterior displacement of the tongue and jaw
setting; it is only for research purposes that a sequences of bruxism, for example, grinding by the splint.
‘definite’ diagnosis would be beneficial. noises, tooth wear and associated pain.40 These Further research investigating the effects of
A number of diagnostic protocols have been splints should be constructed with full occlusal stabilisation splint therapy in OSA is required.
used in the literature, but not all are validated.37 coverage and provide balanced occlusal It may be prudent to warn patients of this risk,
Two sets of criteria are given in Table 2. The contact across the arch, with canine guidance and exercise caution in provision of a stabi-
SB-RDC have a sensitivity of 83.3% and speci- on excursions. Ideally, the occlusion should be lisation splint to those with an existing OSA
ficity of 81.3% for detecting moderate-severe provided in the retruded contact position. diagnosis until after consultation with their
SB (occurring >5 nights/week).7 Other clinical Partial coverage anterior splints (for sleep apnoea physician.
signs which can be associated with SB include example, the nociceptive trigeminal inhibition,
cheek ridging, tongue scalloping or restora- or NTI, splint) have been used in bruxism to Behavioural intervention
tion/tooth fracture. reduce muscle activity via reducing maximum A variety of behavioural strategies have been
It is important to note that the clinical signs clenching force. These should be used with described, including biofeedback, relaxation
lack specificity for SB and alternative causes caution and with careful monitoring due to and improvement of sleep hygiene.
should be considered.5 For example, tooth wear the risks of tooth mobility or over-eruption Biofeedback aims to provide immediate
is a multifactorial condition which may also be of uncovered teeth and resultant occlusal information to the patient about their
due to erosion or abrasion; or may be historic. changes. 40,44 Over-eruption and occlusal behaviour, enabling its reduction. Biofeedback
In the authors’ opinion, a reasonable course changes are a risk with all splints with only has been used for awake and sleep bruxism.
of action for the clinical setting would be to partial occlusal coverage when worn for long Techniques include: EMG with auditory,
take into account plausible patient reports (that periods of time and this potential should be vibratory or electric stimulatory feedback;
is, not just based upon having been told by a guarded against.45 occlusal splints which release a bad taste on
previous dentist) plus observation of a com- A wide range of over-the-counter splints clenching/grinding; and devices intending
bination of the clinical signs listed in Table 1. are readily available via the internet or from to arouse a patient from sleep during an SB
non-dental outlets. This raises some concerns episode.35 There is no long-term evidence
Management of sleep bruxism because of unsubstantiated manufacturers’ for the efficacy of biofeedback strategies, and
claims of efficacy, risks of unwanted tooth concerns exist that techniques causing sleep
It is important to note that SB itself does movement from partial coverage and other disruption may lead to excessive daytime
not require treatment; management is only adverse effects.46 sleepiness.50
indicated where problems arise as a result Sleep hygiene measures include: avoidance of
of SB. There is little high-quality evidence The use of occlusal appliances in caffeine close to bedtime; keeping the bedroom
available on which to base SB management.39 subjects with obstructive sleep well-ventilated and quiet; relaxing close to
The reader is directed to an extensive review apnoea bedtime; and relaxation techniques before
of management strategies by Lobbezoo et al.,35 Some evidence, albeit of limited quality, sleep.51 These measures aim to reduce any
which was updated in a systematic review by has suggested that stabilisation splints may influence of psychological stress on SB, although
Manfredini et al.39 Irreversible adjustment of aggravate obstructive sleep apnoea – a disorder a randomised controlled trial with 16 partici-
the occlusal surfaces of teeth in management characterised by partial or completed airway pants by Valiente Lopez et al. found that sleep
of bruxism is not supported by the literature.35 obstruction during sleep.47 A small randomised hygiene and relaxation had no effect on SB.51
controlled trial with ten participants by It is possible that a common behavioural
Occlusal splints Nikolopoulou et al. also found that wearing a intervention in subjects who brux or snore is
Oral appliances primarily aim to protect the stabilisation splint increased the mean number an intervention by a sleep partner.
dentition from damage caused by clenching/ of apnoeic episodes, although the effect size
grinding. Evidence for their effects on muscle was small.48 Pharmacological interventions
activity is conflicting, with some studies A small sample of ten patients with OSA Drug therapy includes the use of benzodi-
finding reduction in muscle activity during underwent overnight PSG while wearing azepines, anticonvulsants, beta-blockers,
their use40,41 and others finding an increase stabilisation splints in a pilot study by serotonergic and dopaminergic agents, anti-
in some subjects.42 Oral splints are also used Gagnon et al.49 Whilst there was no statisti- depressants, muscle relaxants and a number
in the management of temporomandibular cally significant change in the overall mean of others. 35,52 A Cochrane review found
disorders, where their therapeutic effect may number of hypopneic/apnoeic episodes, this insufficient evidence to support the use of
be independent of their effect on SB. number increased in six subjects, and reduced this approach,53 and it is recommended that
Soft vacuum-formed splints are easy to in one. There was a statistically significant 40% this should only be considered when other
construct and fit, although they are difficult increase in snoring. Splint usage also signifi- conservative strategies have failed, and in
to adjust and anecdotally may exacerbate cantly increased the percentage of apnoeic conjunction with medical practitioners.35
bruxism in some cases.43 These may deteriorate episodes occurring whilst lying on the side or Administration of botulinum toxin (Botox) to
fairly rapidly and are often recommended as a stomach. The authors hypothesised that these the muscles of mastication appears to reduce
more short-term strategy; hard acrylic splints these observations may have been because the frequency of bruxism and a review by
may be more effective in reducing bruxism.35 the splint may have a negative effect on the Long et al. found equal efficacy to occlusal

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BRITISH DENTAL JOURNAL | VOLUME 225 NO. 6 | SEPTEMBER 28 2018501

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