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.
Provides understanding of the pathophysiology and contemporary concepts of sleep bruxism.
Provides understanding of diagnosis of sleep bruxism.
Provides awareness of treatment strategies for sleep bruxism.
Provides awareness of links between sleep bruxism and other sleep-related conditions.
Bruxism is defined as a 'repetitive jaw-muscle activity characterised by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible' with 'two distinct circadian manifestations; either occurring during sleep (sleep bruxism) or during wakefulness (awake bruxism).'1
Sleep bruxism (SB) may lead to masticatory muscle hypertrophy, tooth surface loss, fracture of restorations or teeth, hypersensitive or painful teeth.2,3,4,5 The excessive forces on the teeth can contribute to alveolar bone resorption, which may be visible radiographically as generalised widening of the periodontal ligament space, and increased mobility which may be transient or permanent. In the presence of periodontal disease, the trauma from the occlusion may increase the rate of disease progression. Occlusal trauma cannot induce periodontal pocketing or attachment loss in teeth with a healthy periodontium.6 Investigations into the effects of SB on dental implants and implant-retained prostheses have found no increase in biological complications (for example, peri-implantitis), but increased risk of mechanical complications (for example, fracture of implants/prostheses).5
There is a wide variety in reported prevalence of bruxism (between 5–91%)3 as a result of the range of methodologies with differing reliabilities used to collect the data. However, the prevalence of SB is generally considered to be around 8–13% of the general population.7,8,9 SB is more common in children (14–18%) and lower in the elderly (around 3%).10 Awake bruxism (AB) is more common than SB: a 2013 systematic review reported a prevalence of 22.1–31%.9
Bruxism may be described as primary where there is no pre-existing causative medical condition, or secondary where it occurs as a result of a psychiatric or medical condition.11 Bruxism may involve a static clenching of the teeth, grinding, or a mixture of the two. This activity is accompanied by noise in around a third of sleep bruxists.10 Awake bruxism is more usually a static clenching without sounds;12 grinding whilst awake is generally only secondarily associated with medications or neurological disorders for example, dyskinesias.7
This article aims to provide an overview of the current understanding of sleep bruxism and its associated conditions, with discussion of best practice in diagnosis and management.
The aetiology of SB is the subject of some debate and is likely to be complex and multifactorial. It is now generally accepted that the pathophysiology of SB relates to activation of the central nervous system during sleep.4,13 There are various risk factors which can contribute to SB, including:13
Exogenous risk factors: smoking, heavy alcohol intake, caffeine, medications or illicit drugs14
Psychosocial factors: there is a common professional and patient perception that stress and anxiety exacerbate SB, although results of studies have varied7
Sleep disorders involving sleep arousal
The systemic nature of these risk factors strengthens the need to move away from previous concepts of bruxism as peripherally stimulated (that is, by features of the occlusion) and towards acceptance of central control of the condition. Bruxism has previously been viewed as a dysfunctional or parafunctional movement or pathological condition. Bruxism has in the past even been considered an 'occlusal disease' by some dentists,16 but despite these historical beliefs to the contrary, Lobbezoo, et al.3 found no evidence to support a causal role of occlusal factors in bruxism in a review of 46 papers.
Bruxism and sleep
Sleep bruxism is classified by the International Classification of Sleep Disorders as a sleep-related movement disorder.17 Sleep bruxism appears to occur as a reaction to micro-arousals during sleep: three to ten seconds-long episodes of increased heart rate and muscle tone, occurring eight to 15 times per hour in healthy subjects.7 Most SB episodes occur in clusters during these micro-arousals,7,18,19 and subjects with SB exhibit more micro-arousals than controls.10,18,20 Sleep bruxism may be concomitant with other sleep disorders for example, sleepwalking, sleep terrors and sleeptalking,7 which are also associated with arousal from sleep or 'confused wakening.'
Around 60% of subjects without SB also exhibit masticatory muscle activity during sleep, but to a much lesser extent and without tooth contact: SB is considered to be an extreme manifestation of normal muscle activity during sleep.21 Subjects with SB may also exhibit more whole body movements (for example, twitches, jerks) during sleep than controls,22 with studies finding that body movements were associated with SB in 65–78.9% of subjects23 and 93% of SB episodes.24
Possible functions of sleep bruxism
Bruxism is often considered as a disorder, or a parafunction. A disorder is characterised by lack of normal functioning of physical or mental processes, and a parafunction is a disordered function, for example, a normal function done to an excessive extent, which has led to the consideration by some of bruxism as a parafunction. However, the 2013 definition above includes neither of these terms, with the rationale that it is uncertain that bruxism has no function. It has been postulated that sleep bruxism may have a protective role during sleep, which may relate to airway maintenance1,25 or in stimulating saliva flow to lubricate the oropharynx.19
Sleep bruxism activity has been shown to be associated with an increase in respiration during an arousal episode, leading to a hypothesis that bruxism may have a role in reinstating or maintaining airway patency during sleep.25 Muscle activity during SB usually commences with activity of the suprahyoid muscles followed by activity of the jaw-opening muscles and may therefore be responsible for mandibular protrusion and airway opening.7
The prevalence of SB appears to be increased in subjects with obstructive sleep apnoea (OSA), but this relationship between SB is complex, with various contributing factors.26 Attempts to elucidate a consistent temporal or causal relationship between the two have not been successful.14,26,27
Swallowing and saliva stimulation
Gastro-oesophageal reflux (GORD) also appears to be a risk factor for with SB, and it has been hypothesised that this association is via SB having a protective function stimulation of saliva flow. Miyawaki et al. found that subjects with SB had more episodes of GORD and that 60% of SB episodes occurred during reflux; and that administration of proton-pump inhibitor medication led to a reduction in SB episodes compared to placebo and controls.15
Swallowing activity during sleep has been noted exclusively following arousal episodes, and after around half of SB episodes,28 leading to a hypothesis that SB is associated with stimulating saliva flow during sleep.7 Miyawaki et al. found that 57–59% of masticatory muscle activity during sleep was associated with swallowing activity; and that in SB subjects 68% of swallowing activity occurred in conjunction with muscle activity compared to only 10% in control subjects.19
It has been hypothesised that there may be different types of bruxist activity: idiopathic; associated with airway patency; associated with sleep-related movement disorders; associated with swallowing,20 so it may be the case that all of these may co-exist in the same patient.
Diagnosis of sleep bruxism
A diagnosis of bruxism may be made by the following:
Patient report and clinical interview
Recording of muscle activity
Patient report and clinical interview
Suitable questions are given in Table 1.29,30 The four questions in the Brux scale were developed by van der Meulen et al., and form part of a larger tool (the Oral Parafunctions Questionnaire).31 The questions relating to awake bruxism may be used to help distinguish SB from other behaviours.5 However, diagnosis via questionnaire alone may be inaccurate, for example due to lack of awareness of current behaviours (for example, grinding noises in subjects sleeping alone).7 Up to 80% of patients may be unaware of bruxism.32 Reports by sleeping partners of grinding noises during sleep are particularly suggestive of SB20 since normal orofacial muscle activity does not cause noise. Lavigne found that this alone as a measure of bruxism had 78% sensitivity and 94% specificity following validation with PSG.23
Painful TMD and bruxism
Whilst many patients are unaware of having SB, conversely some patients who do not have SB may falsely believe they do have the condition, because they have been told by their dentist that they do. This is probably based on the erroneous assumption by the dentist that painful masticatory muscles are caused by bruxism. A dentist may, therefore, conclude that a patient suffering from a painful temporomandibular disorder (TMD) must be a bruxist. Whereas Smith carried out PSG in 53 patients with painful TMD, of whom 74% self-reported having SB, and found that only 17% had SB confirmed on PSG.33 Similarly, Raphael et al. carried out PSG in 124 women with myofascial pain and 46 matched controls. Significantly more subjects with painful TMD self-reported bruxism than controls (55% vs 15%), although there was no difference in prevalence of SB as diagnosed by PSG (around 10%). Interestingly, 39% of those with TMD pain had been told by their dentist that they had SB.34
Clinical observations suggestive of bruxism are listed in Table 1, although the currency or extent of bruxist activity is very difficult to gauge clinically. Many of the given observations, for example tooth surface loss (TSL), are subjective and/or may represent signs of historical bruxism.35
Studies have failed to demonstrate an association between tooth surface loss and bruxism36 or TMD.37 Tooth surface loss will be a combination of normal physiological functional wear, wear associated with bruxism, plus erosion from dietary or gastric sources. Tooth surface loss may be historical and cannot be used to indicate static clenching activity. Extent of tooth wear would be influenced by factors such as dietary and gastric acids, enamel quality and quantity and lack of posterior tooth support. As such, TSL is described as a weak indicator of bruxism.7 However 'bruxofacets',38 that is, tooth wear in an eccentric position of closure, may seem more convincing evidence of bruxism than wear in the intercuspal position. Tooth surface loss alone should not, therefore, be regarded as a reliable indicator of active bruxism, but should be used in conjunction with other clinical indicators.
Some intra-oral appliances aim to detect SB, such as via the incorporation of electric devices detecting forces applied during clenching/grinding.36 The use of intra-oral appliances in diagnosis relies on patient tolerance and on the assumption that the insertion of the device will not affect bruxist activity. The observation of wear facets on intra-oral splints has been observed in the literature and anecdotally, although this has not been validated in detection of bruxism.38
EMG records the electrical activity of muscles generated during movement, and will provide information on extent, duration and force of muscle activity. EMG uses sensors attached to the skin overlying the masseter or temporalis muscles. Recordings can be made using ambulatory devices, so are also suitable for detection of AB as well as SB.
EMG cannot detect grinding noises, nor can it distinguish between bruxism and other orofacial activities such as swallowing, talking, lip biting/sucking, which represent around 85% of EMG recordings in controls.23
Polysomnography (PSG) incorporates various recordings including EMG, electroencephalogram, electrocardiogram (ECG) and audio-visual recordings. These detailed evaluations allow arousal from sleep to be assessed, and the presence of other sleep disorders to be ruled out.38 Bruxist episodes can be distinguished more readily from other orofacial movements.23,38 PSG with audio-visual recording is the 'gold standard' mode of assessment and diagnosis of sleep movement disorders and SB, although it is not without disadvantages relating to its complexity and requiring specialist equipment and is generally carried out in the sleep laboratory setting for research purposes only.35 This investigation is clearly outwith the scope of dental practice.
All methods of SB diagnosis present limitations if used in isolation. The 2013 international consensus recommended that self-report only will provide a 'possible' diagnosis; a diagnosis based on this plus clinical examination will be 'probable' and that 'definite' diagnosis would require PSG or EMG recording.1,29 It is acknowledged that PSG is the 'gold standard,' but its complexity and expense render it unsuitable for widespread use in the clinical setting.9,29,38 Certainly, a large proportion of the literature uses questionnaire, interview or examination techniques, and a combination of these is sufficient for diagnosis in the clinical setting; it is only for research purposes that a 'definite' diagnosis would be beneficial.
A number of diagnostic protocols have been used in the literature, but not all are validated.37
Two sets of criteria are given in Table 2. The SB-RDC have a sensitivity of 83.3% and specificity of 81.3% for detecting moderate-severe SB (occurring >5 nights/week).7 Other clinical signs which can be associated with SB include cheek ridging, tongue scalloping or restoration/tooth fracture.
It is important to note that the clinical signs lack specificity for SB and alternative causes should be considered.5 For example, tooth wear is a multifactorial condition which may also be due to erosion or abrasion; or may be historic.
In the authors' opinion, a reasonable course of action for the clinical setting would be to take into account plausible patient reports (that is, not just based upon having been told by a previous dentist) plus observation of a combination of the clinical signs listed in Table 1.
Management of sleep bruxism
It is important to note that SB itself does not require treatment; management is only indicated where problems arise as a result of SB. There is little high-quality evidence available on which to base SB management.39 The reader is directed to an extensive review of management strategies by Lobbezoo et al.,35 which was updated in a systematic review by Manfredini et al.39 Irreversible adjustment of the occlusal surfaces of teeth in management of bruxism is not supported by the literature.35
Oral appliances primarily aim to protect the dentition from damage caused by clenching/grinding. Evidence for their effects on muscle activity is conflicting, with some studies finding reduction in muscle activity during their use40,41 and others finding an increase in some subjects.42 Oral splints are also used in the management of temporomandibular disorders, where their therapeutic effect may be independent of their effect on SB.
Soft vacuum-formed splints are easy to construct and fit, although they are difficult to adjust and anecdotally may exacerbate bruxism in some cases.43 These may deteriorate fairly rapidly and are often recommended as a more short-term strategy; hard acrylic splints may be more effective in reducing bruxism.35
Stabilisation splints may reduce muscle activity and will prevent the unwanted consequences of bruxism, for example, grinding noises, tooth wear and associated pain.40 These splints should be constructed with full occlusal coverage and provide balanced occlusal contact across the arch, with canine guidance on excursions. Ideally, the occlusion should be provided in the retruded contact position.
Partial coverage anterior splints (for example, the nociceptive trigeminal inhibition, or NTI, splint) have been used in bruxism to reduce muscle activity via reducing maximum clenching force. These should be used with caution and with careful monitoring due to the risks of tooth mobility or over-eruption of uncovered teeth and resultant occlusal changes.40,44 Over-eruption and occlusal changes are a risk with all splints with only partial occlusal coverage when worn for long periods of time and this potential should be guarded against.45
A wide range of over-the-counter splints are readily available via the internet or from non-dental outlets. This raises some concerns because of unsubstantiated manufacturers' claims of efficacy, risks of unwanted tooth movement from partial coverage and other adverse effects.46
The use of occlusal appliances in subjects with obstructive sleep apnoea
Some evidence, albeit of limited quality, has suggested that stabilisation splints may aggravate obstructive sleep apnoea – a disorder characterised by partial or completed airway obstruction during sleep.47 A small randomised controlled trial with ten participants by Nikolopoulou et al. also found that wearing a stabilisation splint increased the mean number of apnoeic episodes, although the effect size was small.48
A small sample of ten patients with OSA underwent overnight PSG while wearing stabilisation splints in a pilot study by Gagnon et al.49 Whilst there was no statistically significant change in the overall mean number of hypopneic/apnoeic episodes, this number increased in six subjects, and reduced in one. There was a statistically significant 40% increase in snoring. Splint usage also significantly increased the percentage of apnoeic episodes occurring whilst lying on the side or stomach. The authors hypothesised that these these observations may have been because the splint may have a negative effect on the reflexes which maintain airway patency, or posterior displacement of the tongue and jaw by the splint.
Further research investigating the effects of stabilisation splint therapy in OSA is required. It may be prudent to warn patients of this risk, and exercise caution in provision of a stabilisation splint to those with an existing OSA diagnosis until after consultation with their sleep apnoea physician.
A variety of behavioural strategies have been described, including biofeedback, relaxation and improvement of sleep hygiene.
Biofeedback aims to provide immediate information to the patient about their behaviour, enabling its reduction. Biofeedback has been used for awake and sleep bruxism. Techniques include: EMG with auditory, vibratory or electric stimulatory feedback; occlusal splints which release a bad taste on clenching/grinding; and devices intending to arouse a patient from sleep during an SB episode.35 There is no long-term evidence for the efficacy of biofeedback strategies, and concerns exist that techniques causing sleep disruption may lead to excessive daytime sleepiness.50
Sleep hygiene measures include: avoidance of caffeine close to bedtime; keeping the bedroom well-ventilated and quiet; relaxing close to bedtime; and relaxation techniques before sleep.51 These measures aim to reduce any influence of psychological stress on SB, although a randomised controlled trial with 16 participants by Valiente Lopez et al. found that sleep hygiene and relaxation had no effect on SB.51
It is possible that a common behavioural intervention in subjects who brux or snore is an intervention by a sleep partner.
Drug therapy includes the use of benzodiazepines, anticonvulsants, beta-blockers, serotonergic and dopaminergic agents, antidepressants, muscle relaxants and a number of others.35,52 A Cochrane review found insufficient evidence to support the use of this approach,53 and it is recommended that this should only be considered when other conservative strategies have failed, and in conjunction with medical practitioners.35 Administration of botulinum toxin (Botox) to the muscles of mastication appears to reduce the frequency of bruxism and a review by Long et al. found equal efficacy to occlusal splints, whilst recommending that further studies are required to determine efficacy and long-term outcomes.54 There are concerns that Botox administration can lead to osteopenic changes in the condyles and the sites of muscle attachment.55
Sleep bruxism occurs in 8–13% of the general population. Bruxism may lead to damage to teeth and restorations. Dentists should be aware of the potential aetiology, pathophysiology and management strategies in order to better advise patients.
Bruxism is now generally accepted as a centrally controlled phenomenon, and may be associated with other conditions leading to arousal from sleep. As such, dental interventions may be unlikely to reduce the frequency or severity of SB
Diagnosis of SB in the clinical setting should be made on the basis of patient history and clinical examination. For research purposes additional PSG recording should be considered
SB per se is not an indication for treatment
Dental management of SB should be directed at protecting the oral structures from the effects of SB. The primary aim of oral splints in SB is to protect the dentition. They may reduce muscle activity but evidence is conflicting
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) may reduce bruxism, but concerns have been raised regarding possible adverse effects.