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Sleep bruxism ( SB) is a repetitive jaw-muscle activity characterised by clenching or grinding of the teeth during sleep. Sleep bruxism activity is characterised by rhythmic masticatory muscle activity ( RMMA). Many but not all RMMA episodes are associated with sleep arousal. The aim of this study was to evaluate whether transient oxygen saturation level change can be temporally associated with genesis of RMMA/ SB. Sleep laboratory or home recordings data from 22 SB (tooth grinding history in the absence of reported sleep-disordered breathing) and healthy subjects were analysed. A total of 143 RMMA/ SB episodes were classified in four categories: (i) no arousal + no body movement; (ii) arousal + no body movement; (iii) no arousal + body movement; (iv) arousal + body movement. Blood oxygen levels ( Sa O2) were assessed from finger oximetry signal at the baseline (before RMMA), and during RMMA. Significant variation in Sa O2 over time ( P = 0·001) was found after RMMA onset (+7 to +9 s). No difference between categories ( P = 0·91) and no interaction between categories and Sa O2 variation over time ( P = 0·10) were observed. Sa O2 of six of 22 subjects (27%) remained equal or slight increase after the RMMA/ SB onset (+8 s) compared to baseline; 10 subjects (45%) slightly decreased (drop 0·01-1%) and the remaining (27%) decreased between 1% and 2%. These preliminary findings suggest that a subgroup of SB subjects had (i) a minor transient hypoxia potentially associated with the onset of RMMA episodes, and this (ii) independently of concomitant sleep arousal or body movements. [ABSTRACT FROM AUTHOR]

Summary Rhythmic masticatory muscle activity (RMMA) is the characteristic electromyographic pattern of sleep bruxism (SB), a sleep-related motor disorder associated with sleep arousal. Sleep arousals are generally organised in a clustered mode known as the cyclic alternating pattern (CAP). CAP is the expression of sleep instability between sleep maintaining processes (phase A1) and stronger arousal processes (phases A2 and A3). This study aimed to investigate the role of sleep instability on RMMA/SB occurrence by analysing CAP and electroencephalographic (EEG) activities. The analysis was performed on the sleep recordings of 8 SB subjects and 8 controls who received sensory stimulations during sleep. Baseline and experimental nights were compared for sleep variables, CAP, and EEG spectral analyses using repeated measure ANOVAs. Overall, no differences in sleep variables and EEG spectra were found between SB subjects and controls. However, SB subjects had higher sleep instability (more phase A3) than controls ( P = 0·05). The frequency of phase A3 was higher in the pre-REM sleep periods ( P < 0·001), where peaks in RMMA/SB activity were also observed ( P = 0·05). When sleep instability was experimentally increased by sensory stimuli, both groups showed an enhancement in EEG theta and alpha power ( P = 0·04 and 0·02, respectively) and significant increases in sleep arousal and all CAP variables. No change in RMMA/SB index was found within either groups (RMMA/SB occurred in all SB subjects and only one control during the experimental night). These findings suggest that CAP phase A3 may act as a permissive window rather than a generator of RMMA/SB activity in predisposed individuals. [ABSTRACT FROM AUTHOR]