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.

PurposeNo definitive associations or causal relationships have been determined between obstructive sleep apnea-hypopnea (OSAH) and sleep bruxism (SB).The purpose of this study was to investigate, in a population reporting awareness of both OSAH and SB, the associations between each specific breathing and jaw muscle event. MethodsPolysomnography and audio-video data of 59 patients reporting concomitant OSAH and SB history were analyzed. Masseteric bursts after sleep onset were scored and classified into three categories: 1) sleep rhythmic masticatory muscle activity with SB (RMMA/SB), 2) sleep oromotor activity other than RMMA/SB (Sleep-OMA), and 3) wake oromotor activity after sleep onset (Wake-OMA).Spearman's rank correlation coefficient analyses were performed. Dependent variables were the number of RMMA/SB episodes, RMMA/SB bursts, Sleep-OMA, and Wake-OMA; and independent variables were apnea-hypopnea index (AHI), arousal index(AI), body mass index(BMI), gender, and age. ResultsAlthough all subjects had a history of both SB and OSAH, sleep laboratory results confirmed that these conditions were concomitant in only 50.8% of subjects. Moderate correlations were found in the following combinations 4 (p<0.05) ; RMMA/SB episode with AI, RMMA/SB burst with AI and age, Sleep-OMA burst with AHI, and Wake-OMA burst with BMI. ConclusionsThe results suggest that 1) sleep arousals in patients with concomitant SB and OSAH are not strongly associated with onset of RMMA/SB; 2) apnea-hypopnea events appear to be related to higher occurrence of other types of sleep oromotor activity, and not SB activity. SB genesis and OSAH activity during sleep are probably influenced by different mechanisms.

Clinicians and investigators need a simple and reliable recording device to diagnose or monitor sleep bruxism (SB). The aim of this study was to compare recordings made with an ambulatory electromyographic telemetry recorder (TEL-EMG) with those made with standard sleep laboratory polysomnography with synchronised audio-visual recording (PSG-AV). Eight volunteer subjects without current history of tooth grinding spent one night in a sleep laboratory. Simultaneous bilateral masseter EMG recordings were made with a TEL-EMG and standard PSG. All types of oromotor activity and rhythmic masseter muscle activity (RMMA), typical of SB, were independently scored by two individuals. Correlation and intra-class coefficient (ICC) were estimated for scores on each system. The TEL-EMG was highly sensitive to detect RMMA (0·988), but with low positive predictive value (0·231) because of a high rate of oromotor activity detection (e.g. swallowing and scratching). Almost 72% of false-positive oromotor activity scored with the TEL-EMG occurred during the transient wake period of sleep. A non-significant correlation between recording systems was found (r = 0·49). Because of the high frequency of wake periods during sleep, ICC was low (0·47), and the removal of the influence of wake periods improved the detection reliability of the TEL-EMG (ICC = 0·88). The TEL-EMG is sensitive to detect RMMA in normal subjects. However, it obtained a high rate of false-positive detections because of the presence of frequent oromotor activities and transient wake periods of sleep. New algorithms are needed to improve the validity of TEL-EMG recordings.

SUMMARYThere is some evidence suggesting that obstructive sleep apneahypopnea syndrome is concomitant with sleep bruxism. The aim of this study was to investigate the temporal association between sleep apneahypopnea events and sleep bruxism events. In an open observational study, data were gathered from 10 male subjects with confirmed obstructive sleep apnea-hypopnea syndrome and concomitant sleep bruxism. Polysomnography and audio-video recordings were performed for 1 night in a sleep laboratory. Breathing, brain, heart and masticatory muscle activity signals were analysed to quantify sleep and sleep stage duration, and number and temporal distribution of apnea-hypopnea events and sleep bruxism events. Apnea-hypopnea events were collected within a 5-min time window before and after sleep bruxism events, with the sleep bruxism events as the pivotal reference point. Two temporal patterns were analysed: (i) the interval between apneahypopnea events termination and sleep bruxism events onset, called T1; and (ii) the interval between sleep bruxism events termination and apnea-hypopnea events onset, called T2. Of the intervals between sleep bruxism events and the nearest apnea-hypopnea event, 80.5% were scored within 5 min. Most intervals were distributed within a period of <30 s, with peak at 0-10 s. The T1 interval had a mean length of 33.4 s and was significantly shorter than the T2 interval (64.0 s; P < 0.05). Significantly more sleep bruxism events were scored in association with the T1 than the T2 pattern (P < 0.05). Thus, in patients with concomitant obstructive sleep apnea-hypopnea syndrome and sleep bruxism, most sleep bruxism events occurred after sleep apnea-hypopnea events, suggesting that sleep bruxism events occurring close to sleep apneahypopnea events is a secondary form of sleep bruxism.