SummaryIn 2013, consensus was obtained on a definition of bruxism as repetitive masticatory muscle activity characterised by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible and specified as either sleep bruxism or awake bruxism. In addition, a grading system was proposed to determine the likelihood that a certain assessment of bruxism actually yields a valid outcome. This study discusses the need for an updated consensus and has the following aims: (i) to further clarify the 2013 definition and to develop separate definitions for sleep and awake bruxism; (ii) to determine whether bruxism is a disorder rather than a behaviour that can be a risk factor for certain clinical conditions; (iii) to re-examine the 2013 grading system; and (iv) to develop a research agenda. It was concluded that: (i) sleep and awake bruxism are masticatory muscle activities that occur during sleep (characterised as rhythmic or non-rhythmic) and wakefulness (characterised by repetitive or sustained tooth contact and/or by bracing or thrusting of the mandible), respectively; (ii) in otherwise healthy individuals, bruxism should not be considered as a disorder, but rather as a behaviour that can be a risk (and/or protective) factor for certain clinical consequences; (iii) both non-instrumental approaches (notably self-report) and instrumental approaches (notably electromyography) can be employed to assess bruxism; and (iv) standard cut-off points for establishing the presence or absence of bruxism should not be used in otherwise healthy individuals; rather, bruxism­related masticatory muscle activities should be assessed in the behaviour’s continuum.

To date, there is no consensus about the definition and diagnostic grading of bruxism. A written consensus discussion was held among an international group of bruxism experts as to formulate a definition of bruxism and to suggest a grading system for its operationalisation. The expert group defined bruxism as a repetitive jaw-muscle activity characterised by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible. Bruxism has two distinct circadian manifestations: it can occur during sleep (indicated as sleep bruxism) or during wakefulness (indicated as awake bruxism). For the operationalisation of this definition, the expert group proposes a diagnostic grading system of 'possible', 'probable' and 'definite' sleep or awake bruxism. The proposed definition and grading system are suggested for clinical and research purposes in all relevant dental and medical domains.

The clinical validity of diagnostic criteria for sleep orofacial motor activity--more specifically, bruxism--has never been tested. Polysomnographic recordings from 18 bruxers and 18 asymptomatic subjects, selected according to American Sleep Disorders Association criteria, were analyzed (1) to discriminate sleep bruxism from other orofacial motor activities and (2) to calculate sensitivity, specificity, and predictive values of research criteria. Clinical observations and reports revealed that all 18 bruxers reported frequent tooth-grinding during sleep. Tooth wear was noted in 16 out of 18 bruxers and jaw discomfort reported by six of them. These findings were present in none of the controls. The analysis of polysomnographic data showed that the asymptomatic subjects presented a mean of 1.7 +/- 0.3 bruxism episodes per hour of sleep (sustained or repetitive bursting activity in jaw closer muscles), while bruxers had a significantly higher level of activity: 5.4 +/- 0.6. Controls exhibited 4.6 +/- 0.3 bruxism bursts per episode and 6.2 (from 0 to 23) bruxism bursts per hour of sleep, whereas bruxers showed, respectively, 7.0 +/- 0.7 and 36.1 (5.8 to 108). Bruxism-like episodes with at least two grinding sounds were noted in 14 of the 18 bruxers and in one control. The two groups exhibited no difference in any of the sleep parameters. Based on the present findings, the following polysomnographic diagnostic cut-off criteria are suggested: (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, and (3) at least 2 episodes with grinding sounds. When the polysomnographic bruxism-related variables were combined under logistic regression, the clinical diagnosis was correctly predicted in 81.3% of the controls and 83.3% of the bruxers. The validity of these clinical research criteria needs now to be challenged in a larger population, over time, and in subjects presenting various levels of severity of sleep bruxism.

Awake bruxism is defined as the awareness of jaw clenching. Its prevalence is reported to be 20% among the adult population. Awake bruxism is mainly associated with nervous tic and reactions to stress. The physiology and pathology of awake bruxism is unknown, although stress and anxiety are considered to be risk factors. During sleep, awareness of tooth grinding (as noted by sleep partner or family members) is reported by 8% of the population. Sleep bruxism is a behaviour that was recently classified as a 'sleep-related movement disorder'. There is limited evidence to support the role of occlusal factors in the aetiology of sleep bruxism. Recent publications suggest that sleep bruxism is secondary to sleep-related micro-arousals (defined by a rise in autonomic cardiac and respiratory activity that tends to be repeated 8-14 times per hour of sleep). The putative roles of hereditary (genetic) factors and of upper airway resistance in the genesis of rhythmic masticatory muscle activity and of sleep bruxism are under investigation. Moreover, rhythmic masticatory muscle activity in sleep bruxism peaks in the minutes before rapid eye movement sleep, which suggests that some mechanism related to sleep stage transitions exerts an influence on the motor neurons that facilitate the onset of sleep bruxism. Finally, it remains to be clarified when bruxism, as a behaviour found in an otherwise healthy population, becomes a disorder, i.e. associated with consequences (e.g. tooth damage, pain and social/marital conflict) requires intervention by a clinician.

One hundred thirty-three cases of restless legs syndrome (RLS), diagnosed with criteria recently formulated by an international study group, were studied by questionnaire and with all-night polysomnographic recordings. Results show that RLS starts at a mean age of 27.2 years and before age 20 in 38.3% of patients. Symptoms often appear in one leg only and also involve upper limbs in about half of all cases. Most patients (94%) report sleep-onset insomnia or numerous nocturnal awakenings due to RLS symptoms. A strong relationship was found between these complaints and polysomnographic findings; increasing sleep latency and number of awakenings and decreasing sleep efficiency were associated with worsening symptoms. Periodic leg movements in sleep (index > 5 movements/h sleep) were found in 80.2% of patients. This study shows that this percentage is increased when 2 recording nights are considered (most severe score). Eighty patients of 127 (63%) reported the presence of RLS in at least one of their first-degree relatives. In these families, 221 of 568 first-degree relatives (39%) were reported by the patients to be affected with RLS.

Sleep bruxism (SB) is reported by 8% of the adult population and is mainly associated with rhythmic masticatory muscle activity (RMMA) characterized by repetitive jaw muscle contractions (3 bursts or more at a frequency of 1 Hz). The consequences of SB may include tooth destruction, jaw pain, headaches, or the limitation of mandibular movement, as well as tooth-grinding sounds that disrupt the sleep of bed partners. SB is probably an extreme manifestation of a masticatory muscle activity occurring during the sleep of most normal subjects, since RMMA is observed in 60% of normal sleepers in the absence of grinding sounds. The pathophysiology of SB is becoming clearer, and there is an abundance of evidence outlining the neurophysiology and neurochemistry of rhythmic jaw movements (RJM) in relation to chewing, swallowing, and breathing. The sleep literature provides much evidence describing the mechanisms involved in the reduction of muscle tone, from sleep onset to the atonia that characterizes rapid eye movement (REM) sleep. Several brainstem structures (e.g., reticular pontis oralis, pontis caudalis, parvocellularis) and neurochemicals (e.g., serotonin, dopamine, gamma aminobutyric acid [GABA], noradrenaline) are involved in both the genesis of RJM and the modulation of muscle tone during sleep. It remains unknown why a high percentage of normal subjects present RMMA during sleep and why this activity is three times more frequent and higher in amplitude in SB patients. It is also unclear why RMMA during sleep is characterized by co-activation of both jaw-opening and jawclosing muscles instead of the alternating jaw-opening and jaw-closing muscle activity pattern typical of chewing. The final section of this review proposes that RMMA during sleep has a role in lubricating the upper alimentary tract and increasing airway patency. The review concludes with an outline of questions for future research.

No abstract

Rhythmic Masticatory Muscle Activity (RMMA) is frequently observed during sleep in normal subjects and sleep bruxers. We hypothesized that some normal subjects exhibit RMMA at a lower frequency than sleep bruxers. Polysomnographic data from 82 normal subjects were compared with data from 33 sleep bruxers. RMMA episodes were defined as three or more consecutive bursts of masseter EMG activity, with or without tooth-grinding. Such episodes were observed in nearly 60% of normal subjects. A lower frequency of episodes was noted in normal subjects than in bruxers. Sleep organization was similar between groups. Bruxers had twice as many masseter muscle bursts per episode and episodes of higher amplitude compared with controls with RMMA. The high prevalence of RMMA observed in normal subjects suggests that this activity is related to certain sleep-related physiological functions, including autonomic activation.