Cannabinoids and sleep bruxism: mechanistic rationale, polysomnographic evidence, and future research directions.

Metello Neves L.; Dos Santos D.; Couto Neto M.; Pereira F.; Laino P.; Baldessarini B.; Lima B.; Grillo R. · Sleep & breathing = Schlaf & Atmung · 2026

**Background & Methods** This is a narrative review examining the mechanistic rationale and evidence for cannabinoids (CBD, THC, CBN) in treating sleep bruxism (SB), assessed primarily through polysomnographic markers including rhythmic masticatory muscle activity (RMMA). A systematic search of PubMed/MEDLINE, Embase, and Web of Science was conducted from January 2004 through June 2026, with sources classified by level and directness of evidence. **Key Findings** - Meta-analytic evidence demonstrates that therapeutic-dose cannabis administration does not consistently alter total sleep time, sleep onset latency, sleep efficiency, or sleep staging patterns. - A randomized polysomnographic trial of CBN (300 mg) failed its primary endpoint (wake after sleep onset) but showed in secondary analyses reduced electroencephalographic arousal index, decreased sleep onset latency, and increased N2 sleep; preclinical data support CBN's hypnotic action with partial tolerance developing within two weeks. - A single randomized trial reported that topical CBD reduced portable bruxism device indices and masseter muscle activity in patients with sleep bruxism and painful temporomandibular disorders, attributed to proposed local myorelaxant and analgesic mechanisms rather than central effects. **Dosage & Administration** CBN: 300 mg (oral, from randomized trial). CBD: topical application (specific dosage not detailed). Other cannabinoids evaluated at "therapeutic doses" but specific dosing not uniformly reported across studies. **Safety & Adverse Effects** Not reported. The review does not detail adverse event profiles from included studies. **Evidence Quality** This narrative review identifies critical evidence gaps limiting clinical recommendations. The entire direct clinical evidence for cannabinoids and bruxism derives from a single research group. Notably, no study has measured RMMA by polysomnography under any cannabinoid condition. Two theoretically plausible pathways linking cannabinoids to SB exist (peripheral myorelaxation and central arousal modulation), but neither has been demonstrated in patients with SB. The authors emphasize that the clinically relevant question extends beyond motor activity reduction to whether cannabinoids improve patient-centered outcomes in individuals experiencing consequences from SB. Future trials must integrate polysomnography, masseter electromyography, and validated patient-centered outcome measures before clinical recommendations can be justified.

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