Sleep architecture as a candidate for phenotyping sleep bruxism: A narrative physiological review

Abstract

BackgroundSleep bruxism (SB), an oral behaviour in otherwise healthy individuals, is characterised by frequent rhythmic masticatory muscle activity (RMMA) during sleep. RMMA/SB episodes occur over various sleep stages (N1‐N3 and rapid eye movement (REM)), sleep cycles (non‐REM to REM), and frequently with microarousals. It currently remains unclear whether these characteristics of sleep architecture are phenotype candidates for the genesis of RMMA/SB.ObjectivesThis narrative review investigated the relationship between sleep architecture and the occurrence of RMMA as a SB phenotype candidate.MethodsPubMed research was performed using keywords related to RMMA/SB and sleep architecture.ResultsIn non‐SB and SB healthy individuals, RMMA episodes were most frequent in the light non‐REM sleep stages N1 and N2, particularly during the ascending phase of sleep cycles. The onset of RMMA/SB episodes in healthy individuals was preceded by a physiological arousal sequence of autonomic cardiovascular to cortical activation. It was not possible to extract a consistent sleep architecture pattern in the presence of sleep comorbidities. The lack of standardisation and variability between subject complexified the search for specific sleep architecture phenotype(s).ConclusionIn otherwise healthy individuals, the genesis of RMMA/SB episodes is largely affected by oscillations in the sleep stage and cycle as well as the occurrence of microarousal. Furthermore, a specific sleep architecture pattern cannot be confirmed in the presence of sleep comorbidity. Further studies are needed to delineate sleep architecture phenotype candidate(s) that contribute to the more accurate diagnosis of SB and treatment approaches using standardised and innovative methodologies.

Inflammatory Markers and Sleep Architecture in Sleep Bruxism—A Case-Control Study

“…However, it needs to be kept in mind that tooth wear is not a pathognomonic sign of active SB [58]. Another already mentioned phenomenon linked with SB was the alteration of sleep architecture [56]. It is expressed as shorter total sleep duration and shorter nonrapid eye movement (NREM) and rapid eye movement (REM) sleep, and higher arousals during REM and NREM sleep [53,59], and what is first made evident by this study-the restriction of N3 sleep stage.…”

“…Diagnosis of SB should activate the screening for hypertension to provide early and optimal treatment, preventing long-term cardiovascular events [55]. Sleep fragmentation is another negative appearance observed in patients with SB [56]. Depending on the clinical setting, however, SB can potentially be a harmful as well as a protective behavior [10].…”