Changes in oxygen and carbon dioxide in the genesis of sleep bruxism: a mechanism study

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  • Suzuki Yoshitaka
    Center for Advanced Research in Sleep Medicine (CARSM), Dept. of Surgery, Hôpital du Sacré-Coeur de Montréal Faculty of Dental Medicine, Université de Montréal, Pavillon Roger-Gaudry Department of Stomatognathic Function and Occlusal Reconstruction, Graduate School of Biomedical Sciences, Tokushima University
  • Rompré Pierre
    Faculty of Dental Medicine, Université de Montréal, Pavillon Roger-Gaudry
  • Mayer Pierre
    Department of Medicine, Pulmonology and Sleep Clinic, Centre Hospitalier de l'Université de Montréal
  • Kato Takafumi
    Department of Oral Physiology, Osaka University Graduate School of Dentistry
  • Okura Kazuo
    Department of Stomatognathic Function and Occlusal Reconstruction, Graduate School of Biomedical Sciences, Tokushima University
  • Lavigne Gilles J.
    Center for Advanced Research in Sleep Medicine (CARSM), Dept. of Surgery, Hôpital du Sacré-Coeur de Montréal Faculty of Dental Medicine, Université de Montréal, Pavillon Roger-Gaudry Department of Stomatology, Centre Hospitalier de l'Université de Montréal

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<p>Purpose: Rhythmic masticatory muscle activity (RMMA), a biomarker of sleep bruxism (SB), has been associated with mild hypoxia and/or big breaths in some adults with non-sleep-disordered breathing. The purpose of this study was to investigate that concurrent oxygen and carbon dioxide fluctuations are among the physiological variables that contribute to RMMA onset.</p><p>Methods: Twelve subjects (5 female, 7 male, mean age: 43 ± 11) underwent polysomnography recording in a sleep laboratory. RMMA index and apnea-hypopnea index were calculated. Oxygen saturation (SpO2) was estimated by finger pulse oximeter and end-tidal CO2 (ETCO2) by nasal airflow cannula before and after RMMA onset. Given the expected response time delay between actual arterial hypoxemia and fingertip pulse detection, we adjusted the SpO2 desaturation onset to the onset of masseter muscle activity using a 17 s criterion based on ETCO2 shifts.</p><p>Results: SpO2 was slightly but significantly lower than at baseline (max: -0.6%) in the 6–4 s before RMMA onset and significantly higher in the 6–18 s after onset (0.9%; p < 0.05). Although ETCO2 before RMMA onset did not differ from baseline, it decreased at 8–10 s after onset (-1.7 mmHg: p < 0.05). No changes in SpO2 or ETCO2 in relation to RMMA onset reached a critical clinical threshold.</p><p>Conclusions: The mild transient hypoxia observed before RMMA onset was not associated with a change in ETCO2. The mild and brief oxygen fluctuations before RMMA onset may reflect a physiological response that seems to have little influence on SB genesis.</p>

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