Sleep & breathing = Schlaf & Atmung · 2026
Cannabinoids and sleep bruxism: mechanistic rationale, polysomnographic evidence, and future research directions.
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Metello Neves Leonardo Brigido, Dos Santos Daniel Domingues, Couto Neto Mario Pereira, Pereira Francisco Jose, Laino Paulo Henrique, Baldessarini Bruno Luiz, Lima Bernardo Correia, Grillo Ricardo
Аннотация
PURPOSE: Sleep bruxism (SB) is masticatory muscle activity during sleep, most often studied through its polysomnographic marker, rhythmic masticatory muscle activity (RMMA). Cannabinoids have attracted interest for their analgesic, anxiolytic and sleep-modulating properties, but whether they influence SB, and whether such modulation would benefit patients, remains unclear. This review examines cannabidiol (CBD), tetrahydrocannabinol (THC) and cannabinol (CBN) in relation to sleep, arousal and masticatory muscle activity, and separates what has been demonstrated from what is inferred.
METHODS: We searched PubMed/MEDLINE, Embase and Web of Science for records published between 1 January 2004 and 14 June 2026, with searches last run on 14 June 2026. Cannabinoid terms were crossed with sleep terms and with bruxism terms, and searched independently for mechanistic literature. Seminal earlier work was retrieved by hand-searching reference lists. Each source was classified by level and directness of evidence.
RESULTS: Meta-analytic evidence indicates that cannabis administration at therapeutic doses does not consistently alter total sleep time, sleep onset latency, sleep efficiency or sleep staging. A randomised polysomnographic trial of CBN missed its primary endpoint (wake after sleep onset); in uncorrected secondary and tertiary analyses, 300 mg reduced the electroencephalographic arousal index and sleep onset latency and increased N2 sleep. Preclinical polysomnography supports a hypnotic action of CBN and of its brain-penetrant metabolite, with partial tolerance within two weeks. One randomised trial reported that topical CBD reduced a portable device bruxism index and masseter activity in patients with SB and painful temporomandibular disorders, through a proposed local mechanism involving myorelaxation and analgesia. The entire direct clinical evidence base comes from a single research group, and no study has measured RMMA by polysomnography under any cannabinoid.
CONCLUSION: Two distinct pathways could link cannabinoids to SB, one peripheral and one central, and neither has been demonstrated in patients with SB. The clinically relevant question is not whether a cannabinoid lowers a motor activity index, but whether it improves outcomes that matter in patients whose SB carries consequences. Trials combining polysomnography, masseter electromyography and patient-centred outcomes are required before any clinical recommendation.
TRIAL REGISTRATION: Not applicable (narrative review).
METHODS: We searched PubMed/MEDLINE, Embase and Web of Science for records published between 1 January 2004 and 14 June 2026, with searches last run on 14 June 2026. Cannabinoid terms were crossed with sleep terms and with bruxism terms, and searched independently for mechanistic literature. Seminal earlier work was retrieved by hand-searching reference lists. Each source was classified by level and directness of evidence.
RESULTS: Meta-analytic evidence indicates that cannabis administration at therapeutic doses does not consistently alter total sleep time, sleep onset latency, sleep efficiency or sleep staging. A randomised polysomnographic trial of CBN missed its primary endpoint (wake after sleep onset); in uncorrected secondary and tertiary analyses, 300 mg reduced the electroencephalographic arousal index and sleep onset latency and increased N2 sleep. Preclinical polysomnography supports a hypnotic action of CBN and of its brain-penetrant metabolite, with partial tolerance within two weeks. One randomised trial reported that topical CBD reduced a portable device bruxism index and masseter activity in patients with SB and painful temporomandibular disorders, through a proposed local mechanism involving myorelaxation and analgesia. The entire direct clinical evidence base comes from a single research group, and no study has measured RMMA by polysomnography under any cannabinoid.
CONCLUSION: Two distinct pathways could link cannabinoids to SB, one peripheral and one central, and neither has been demonstrated in patients with SB. The clinically relevant question is not whether a cannabinoid lowers a motor activity index, but whether it improves outcomes that matter in patients whose SB carries consequences. Trials combining polysomnography, masseter electromyography and patient-centred outcomes are required before any clinical recommendation.
TRIAL REGISTRATION: Not applicable (narrative review).