Normal sleep comprises two distinct states: NREM (non-rapid eye movement), which, based upon electroencephalography (EEG), is subdivided into three distinct stages (N1-3) and REM (rapid eye movement). A typical normal sleep pattern is where individuals progress from wakefulness to the NREM state, followed by the REM state and then cyclically alternating between REM and NREM stages. Overall, a night of sleep consists of approximately 75–80 % of NREM sleep and 20–25 % of REM sleep. Humans typically cycle through NREM/REM sleep stages at a rate of four to six times per sleep period with duration of each cycle being 90 to 110 min. NREM allows for physiological restoration and REM accommodates psychological restoration.

Young adult SB patients (20 to 40 years of age) without coexisting medical problems such as chronic pain or those experiencing OSA exhibit a normal sleep architecture [40]. When investigating the occurrence of SB during the sleep cycles at night, it has been found that SB events are higher in the second and third transition from NREM to REM sleep cycles as compared to the first and fourth cycles [41]. SB events are most frequently identified in the ascending period within a sleep cycle where there is a shift from deep NREM toward REM sleep associated with arousal activity and increase in sympathetic tone [42, 43]. Furthermore, it is important to appreciate that the manifestation of tooth grinding is preceded by a cascade of complex and well timed physiologic events (Table 5.3). Evidence regarding the pathophysiology of rhythmic masticatory muscle activity (RMMA) supports the hypothesis that this activity is associated with autonomic sympathetic cardiac activity and sleep arousals [6, 41, 44, 45]. Arousals are the response of the sleeping brain to external (environmental) and internal (physiological or pathological) stimuli [46]. The purpose of these arousals or active periods are that they are “windows” whereby the sleeping individual can readjust his/her body position, reset body temperature, and if any harmful event is perceived, can become fully awake, i.e., a fight or flight reaction could be triggered [47]. In normal healthy adults, sleep arousals occur between 6 and 14 times per hour of sleep and tend to occur at the end of a NREM period [48]. Approximately 80 % of SB events, i.e., repetitive jaw muscle contractions with or without tooth grinding, are observed during such recurrent arousal periods while the source of the genesis of the other 20 % is under investigation [49]. Evidence that SB and RMMA are associated with sleep arousal is supported by the observation that tooth grinding and RMMA can be evoked experimentally through manipulations that trigger arousal [2, 6, 22, 23, 50]. Interestingly, there does not appear to be any presence of arousals during RMMA events in normal adult volunteers who do not experience SB [45].

Catecholamines such as dopamine, norepinepherine, and serotonin have been suggested as being involved in SB pathophysiology [20, 40, 51]. Studies have reported that SB patients have elevated levels of catecholamines in their urine compared to controls, thus suggesting a link between stress and SB [52, 53]. In a pilot imaging study [54] involving dopamine, it was found that there was an asymmetric distribution of striatal dopamine binding sites in the brains of SB patients. However, the overall density of the striatal dopamine receptors was found to be within normal range in young adults with SB. In a clinical trial using l-dopa (a dopamine precursor), the results indicated an inhibitory effect on SB; however, when bromocriptine (a dopamine receptor agonist) was administered it did not result in any effect on SB events, and it failed to restore the imbalance of the striatal dopamine binding sites [55, 56].

The observation that smoking exacerbates tooth grinding provides indirect evidence for the role of the cholinergic system mediated through the nicotinic receptors as a mechanism for SB [57–59]. However, it remains to be determined if this occurrence is indeed due to the effect of nicotine receptor activation (increased vigilance and brain arousal), or if it increases the risk of SB as an oral habitual behavior.

There is a common belief that stress and psychosocial variables contribute to SB. Studies suggest that children and adults reporting self-awareness of tooth grinding are more anxious, aggressive, and hyperactive [13, 17, 60–65]. However, the majority of these studies had methodological limitations resulting in rather weak evidence [66]. SB patients diagnosed by PSG displayed similar reaction times to vigilance as normal controls under an attention motor test condition [67]. Interestingly, the SB patients scored higher than the normal controls on anxiety regarding successful test performance. There is a suggestion among some studies that SB patients are more likely to deny the impact of life events due to their coping styles or personality [68, 69]. Additionally, in some case studies, masseter EMG activity increased during sleep following days with emotional or physical stressors; [70, 71] however, these findings were not consistent in all studies [72–74]. From these studies it can be concluded that there might exist a subgroup of SB patients whose response to life stressors includes excessive jaw motor activity and this reaction differs from that of normal individuals [66, 69, 75].

A genetic or familial predisposition for SB has been suggested by studies utilizing a questionnaire format or tooth wear examinations [76]. Twenty to 50 % of SB patients may have a family member who also reports tooth grinding during childhood [77–79]. Analyzing twin studies, it has been revealed that tooth grinding has greater concordance among monozygotic than dizygotic twins [80, 81]. Furthermore, the presence of SB in childhood persists in 86 % of adults [80]. In a large population-based cohort of young adult twins, it was reported that genetic factors accounted for 52 % of the total phenotypic variance [82]. In contrast, Michalowicz et al. [83], on the basis of a combined questionnaire and clinical study with almost 250 pairs of twins, concluded there was a lack of genetic correlation with SB. To date, no genetic variants or genetic inheritance patterns have been associated with SB. Yet, in a recent case-control study involving a Japanese population (non-related participants) it was found that the C allele carrier of the serotonin receptor 2A single nucleotide polymorphism (rs6313) was associated with an (OR = 4.25) increased risk of SB [84]. This finding is the first to identify a specific genetic component contributing to the etiology of SB. Despite this finding, it must be understood that SB is a multi-factorial disorder in which many other factors including other candidate genes are most likely involved in the etiology of this oral motor behavior or activity.

Historically, the dental profession was quite convinced that SB was directly related to occlusal factors, and early studies seemed to indicate that occlusal corrections diminished or stopped this activity [85–87]. However, later studies challenged the concept that occlusal factors such as occlusal disharmony or premature tooth contacts could be considered as principal initiating factors, while other studies showed that SB activity was not reduced by occlusal therapy [88–91]. There has also been a lack of correlation between dental morphology (dental arch, occlusion) and SB events among SB adult patients assessed by PSG [92]. Furthermore, the average tooth contact time, including meals, in healthy individuals is approximately 17.5 min/day [93]. Usually tooth contact is absent during sleep without motor activity, whereas it does occur in association with arousal, swallowing, and motor activity [94, 95]. Tooth contacts seem to occur in clusters approximately every 90 to 120 min during the night, suggesting that tooth contact is a consequence of jaw closing muscle activation within a sequence following arousal rather than a cause [95–97]. Interestingly, patients who are edentulous exhibit RMMA when they sleep while not wearing their dentures [98, 99]. In a study by Manfredini et al. [100], it was concluded that the role of various occlusal features such as interferences and centric slides, bite relationships, horizontal overlap, and midline discrepancies in the pathogenesis of SB is very minor and the contribution of occlusion to the differentiation between bruxers and non-bruxers is negligible.

Swallowing is a normal physiologic oropharyngeal motor activity occurring five to ten times/hour during sleep, which is a much lower rate as compared to wakefulness (60 times/hour during non-eating periods) [101]. This decreased rate of swallowing during sleep may be related to a decrease in salivary secretion and/or reflex sensitivity. Swallowing seems to occur predominantly in light NREM sleep in relation to arousals [44, 101]. Swallowing has also been found to occur with approximately 60 % of RMMA events in both SB patients and normal adult individuals [102]. Masseter bursts associated with RMMA occur when esophageal pH decreased in SB patients who did not experience sleep-related gastroesophageal reflux [39]. The relationship between swallowing, esophageal pH, microarousals, and salivation requires further investigation as it relates to sleep.

There appears to be an interaction between airway patency and jaw motor activity during sleep. During sleep, due to a decrease in oropharyngeal muscle tonicity, the jaw is open for 90 % of the total sleep time [94]. Narrowing of the upper airway during sleep occurs as the mandible and the tongue collapse into the pharynx [103]. The reduction in this space is exacerbated when sleeping in the supine position as a result of gravitational forces. Intriguingly, 75 % of RMMA events also occur in the supine position [102]. Khoury et al. [104] reported that an increase in the amplitude of respiration was observed with a simultaneous and significant increase in the activation of the suprahyoid (jaw opening) muscles when RMMA events occur. This increase in respiratory amplitude preceding RMMA, however, seems more likely to be associated with an autonomic drive during arousals rather than to function as an opening of the upper airway after an apneic event. Furthermore, studies have shown that RMMA events rarely present after apneic events [105]. Therefore, it remains to be demonstrated whether or not SB is a reactive-protective mechanism of the upper airway to overcome upper airway collapse.

A primary feature of SB is tooth grinding noise. When clinically assessing the presence of SB it is imperative to differentiate tooth grinding noise due to SB from that of other oral sounds emitted from the mouth and throat during sleep such as snoring, grunting, groaning, vocalization, tongue clicking, lip smacking, or temporomandibular joint noise [106]. Additionally, sounds made from the bed itself due to movements and sleeping position changes also must be taken into account. Clearly, it is very difficult for a tooth grinding history to be reliably elicited from the patients who do not have a sleep partner or who are edentulous. In certain individuals, fluctuation in grinding history may be associated with jaw muscle symptoms or other risk factors such as stressors and medication use [58, 107, 108]. Therefore, tooth grinding noise should not be used as the sole determinant of SB activity.

The severity of tooth wear can be assessed according to published criteria [109, 110]. However, it is not possible to separate patients with SB from those without by observing tooth wear factors [111], as tooth wear may be produced by other etiologic factors (oral habits, food consistency, acid reflux, alimentary disorders, etc.); therefore, occlusal attrition cannot be considered an accurate indicator of this habit being currently performed [112]. Menapace et al. [113] reported that tooth wear was present in 100 % of SB patients but also in 40 % of asymptomatic individuals. Abe et al. [114] determined that SB patients (young adults) present with greater tooth wear as compared to controls (no report of any history of tooth grinding or sleep laboratory evidence of SB) but tooth wear was not able to discriminate between different sub-groups (moderate/high versus low) of SB patients. Furthermore, SB cannot be assumed to exist if there is no current report of tooth grinding as witnessed by a sleep partner, since the tooth wear may have occurred years before the SB activity.

Muscle pain (myalgia) and dysfunction symptoms related to SB may be quite different than those related to concomitant disorders. SB patients most frequently report myalgia on awakening in the morning, whereas masticatory myofascial pain intensifies as the day progresses [115, 116]. Other orofacial symptoms associated with TMD such as limitation in opening, TMJ noise, and arthralgia can be present concomitantly [117]. Although studies have suggested an association between self-reported SB and TMD, causation has not been clearly established [116, 118]. Furthermore, PSG studies have been unable to confirm such a link [119–121]. Raphael et al. [122] in a case-control study (124 vs. 46; all females) investigating the association between SB and myofascial TMD, using two-night laboratory PSG monitoring, found no statistically significant differences in SB rates among cases (9.7 %) compared to controls (10.9 %). They concluded there was no relationship between SB and myofascial TMD, but their study did not address the possibility that SB could be involved in the initial onset or triggering of myofascial TMD. Their findings merely emphasized that treatment aimed at reducing SB among those who already have chronic myofascial TMD may be inappropriate, since myofascial TMD patients do not brux at excessive rates while asleep. Other studies, using PSG and masseter EMG recordings, have reported that SB patients with orofacial pain report significantly less bruxism episodes per hour of sleep and less EMG activity in the masticatory muscles during sleep than pain free controls [123, 124]. It appears the association between orofacial pain symptoms and SB may be somewhat dependent on poor sleep, as pain and sleep have a bidirectional association [116, 125, 126].

Masseter muscle hypertrophy may be bilaterally manually palpated. If these muscles are hypertrophic, the volume of muscle tissue increases approximately two times while the teeth are clenched in comparison to a relaxed state [2]. However, masseter muscle hypertrophy does not strictly imply sleep muscle activity as it can also occur as a result of awake clenching [127].

As previously discussed, awake bruxism or AB is considered a distinct nosologic entity from SB. AB, based upon self-report studies, tends to be mainly a reactive process and is induced or exaggerated by stressors and/or anxiety or hyperactivity [107, 128]. SB patients often report an awareness of AB, with patients who have mild SB more often being cognizant of AB and stress than those with severe SB [26]. Physiologic recordings in subjects with and without orofacial pain while experiencing natural stress (before an examination) or during experimental stress (mental calculations) revealed increases in muscle tone, heart rate and/or voluntary chewing/clenching [129–131]. The clinical consequences associated with AB may deleteriously impact dental structures (natural dentition and prosthetic devices) and/or involve pain and dysfunction of the jaw musculature and joints [120, 132–134].

Headache is a common finding in the general adult population with a lifetime prevalence of 85–95 % [135]. Headache is also a problem in children, with as many as 70 % of children being affected at least once in childhood [136, 137]. The prevalence of reported headache-related complaints among SB patients is also high (60–90 % of SB patients) [138–140]. Children who have migraine headaches have been shown to have a high prevalence of sleep disturbances, including snoring and SB [141]. Furthermore, it has been reported that 30–50 % of SB adult patients complain of headache either in the morning (most frequently) or during the day [142]. In a descriptive PSG study, it was reported that within a SB patient population spanning from 23 to 67 years of age, 65 % reported morning headaches [143]. The exact mechanisms underlying the possible interactions between SB and headache requires further investigation, but this is a difficult challenge due to the high prevalence of headaches in general.

SB may be a possible cause of tension-type headaches if patients wake with facial and/or temporal skull area pain, with pain typically subsiding as the day progresses [24, 71, 121]. These morning headaches may be explained as a post-exercise soreness in the temporalis muscles [144]. SB patients may report waking up in the middle of the night with pain and tension in facial and cranial areas following sustained SB events. In a study by Kampe et al. [62], 14 % of SB patients reported pain at night, while 31 % reported pain during both at night and daytime. It is important to recognize that nocturnal pain and headaches that may be induced by SB can be confused with similar symptoms experienced by fibromyalgia patients, which include muscle tenderness areas and morning stiffness, fatigue, and poor sleep [145, 146].

A cause and effect relationship between SB and SDB, which is a combination of upper airway resistance syndrome and OSA, has yet to be established despite frequent claims of an association among these entities [17]. However, other studies have shown a correlation between habitual snoring and SB [147]. In a PSG study, increased masticatory EMG activity including RMMA was detected in approximately 50 % (10/21) of adult patients) with OSA [22]. In another PSG study investigating sleep disorders among a group of 53 myofascial pain patients (75 % met self-report criteria for SB, but only 17 % met PSG criteria for active SB), two or more sleep disorders were diagnosed in 43 % of those patients; insomnia disorder (36 %) and OSA (28.4 %) demonstrated the highest frequencies [119]. In another PSG study involving 119 patients between the ages of 2–16 years referred to a pediatric sleep center for snoring, SB was identified in 70 patients [148]. There have been clinical observations and some studies that have provided indirect evidence of a relationship between SB and SDB by reporting a decrease in SB after the patients have undergone treatments (adenotonsillectomy and continuous positive airway pressure) for the underlying sleep disorder [149–151]. These findings support the hypothesis that RMMA may be a sleep oromotor activity that assists in reinstating airway patency following a respiratory obstruction [104, 152]. It is important to note that the association between apnea/hypopnea and arousals is opposite to the association between SB and arousals; apneic events trigger arousals, while RMMA is triggered during arousals [105]. Nonetheless, several studies failed to show a temporal association between apneic events and RMMA; instead, tonic masseter muscle activity is frequently found at the termination of apneic events [22, 29, 153]. Overall, the factors responsible for the induction of increased RMMA frequency in patients with SB require further investigation.

In a study of healthy young adults, it was reported that a significant relationship between decreased esophageal pH and RMMA, short EMG bursts and tooth clenching seems to occur when the person is sleeping mainly in a supine position. Of note, only about 10 % of the episodes of decreased esophageal pH (defined as a rapidly decreasing intraesophageal pH with a decrease of more than 0.4 per 2 s) included clenching episodes and the number of clenching episodes was independent of various sleep positions [154]. More specifically, it was found that RMMA is a secondary event to gastroesophageal reflux occurring via sleep arousal and often associated with swallowing [39]. Furthermore, RMMA events including SB were induced by esophageal acidification [155]. It has been proposed that preventing gastroesophageal reflux and avoiding sleeping in a supine position might be effective in decreasing the frequency of SB [154]. Overall, the physiologic link between SB, the increase in salivation and the association with gastroesophageal reflux requires further investigation.

SB is frequently reported to dentists or physicians by the patient and/or bed partner and parents. Given a positive report about tooth grinding, the diagnosis of SB is usually clinical, based on the observation of the following signs and symptoms: abnormal tooth wear, hypertrophy of masseter muscles, fatigue, discomfort or pain of jaw muscles [156]. However, none of these clinical findings is a direct proof of current SB activity. Tooth wear for example, although widely reported as the distinctive dental sign of bruxism in general may be related to many other factors that can influence the presence of attrition and erosion on dental surfaces.

There is an intraoral appliance (Bruxocore^TM) that indirectly assesses the mechanical impact of SB on the dentition [157, 158]. This appliance covers the upper dentition and is worn for a few weeks while the patient is sleeping, and the surface area and volume of attrition on the appliance are evaluated. When this technique is employed, it has been found that jaw muscle activities during sleep are not always correlated with the degree of wear. Therefore, to reliably and accurately diagnose SB, electronic recording and documenting devices are utilized with strict criteria to detect and classify SB activity. It is also important that the presence of other conditions such as orofacial pain, headache, and SDB be assessed in patients with SB by questionnaire at the time of initial examination.

Attempts have been made to monitor SB activity in natural home settings using ambulatory monitoring. Despite the obvious benefits of these devices such as lower cost and being used in the natural environment, the specificity of SB motor activity assessment remains a limitation [2]. In the absence of simultaneous audio-visual recording, it is difficult to exclude the presence of non-SB-specific orofacial movements during sleep such as swallowing and scratching [159]. A novel portable EMG device (Grindcare®) has been designed to provide online recording of EMG activity, online processing of EMG signals to detect a particular oromotor activity (tooth grinding/tooth clenching), and also for use as a biofeedback device. Encouraging results have been reported from several studies where this device has been utilized due its ability to detect EMG events associated with SB, and to exclude orofacial movements unrelated to SB (grimaces, swallowing, etc.) [160, 161]. In a systematic review assessing the diagnostic accuracy of ambulatory monitoring devices compared to PSG in the measurement of SB, it was concluded that the validity of portable instrumental diagnostic approaches is not sufficient to support any non-PSG techniques employed as a stand-alone diagnostic method in the research setting, with the possible exception of the Bruxoff® device which needs to be further confirmed with future investigations [162].

Although a variety of tools have been developed to assess jaw muscle activity during sleep, the gold standard for SB diagnosis remains a full night PSG audio-video recording (highly controlled but in an unnatural environment). This is the only protocol, which allows the simultaneous monitoring of sleep electroencephalographic, electrocardiographic, electromyographic, and respiratory signals during sleep. However, PSG recordings are not routinely performed for clinical SB diagnosis, as they are both costly and time consuming. A PSG investigation may be indicated in cases of SB associated with other signs and symptoms suggestive of other sleep disorders, especially SDB. In these cases, the patient should be referred to a sleep physician for further investigations and diagnosis.