Neurobiological Mechanisms Involved in Sleep Bruxism

Abstract

Sleep bruxism (SB) is reported by 8% of the adult population and is mainly associated with rhythmic masticatory muscle activity (RMMA) characterized by repetitive jaw muscle contractions (3 bursts or more at a frequency of 1 Hz). The consequences of SB may include tooth destruction, jaw pain, headaches, or the limitation of mandibular movement, as well as tooth-grinding sounds that disrupt the sleep of bed partners. SB is probably an extreme manifestation of a masticatory muscle activity occurring during the sleep of most normal subjects, since RMMA is observed in 60% of normal sleepers in the absence of grinding sounds. The pathophysiology of SB is becoming clearer, and there is an abundance of evidence outlining the neurophysiology and neurochemistry of rhythmic jaw movements (RJM) in relation to chewing, swallowing, and breathing. The sleep literature provides much evidence describing the mechanisms involved in the reduction of muscle tone, from sleep onset to the atonia that characterizes rapid eye movement (REM) sleep. Several brainstem structures (e.g., reticular pontis oralis, pontis caudalis, parvocellularis) and neurochemicals (e.g., serotonin, dopamine, gamma aminobutyric acid [GABA], noradrenaline) are involved in both the genesis of RJM and the modulation of muscle tone during sleep. It remains unknown why a high percentage of normal subjects present RMMA during sleep and why this activity is three times more frequent and higher in amplitude in SB patients. It is also unclear why RMMA during sleep is characterized by co-activation of both jaw-opening and jawclosing muscles instead of the alternating jaw-opening and jaw-closing muscle activity pattern typical of chewing. The final section of this review proposes that RMMA during sleep has a role in lubricating the upper alimentary tract and increasing airway patency. The review concludes with an outline of questions for future research.

Mécanismes physiologiques et neurochimiques impliqués dans le bruxisme du sommeil

“…De nombreux travaux ont montré que le bruxisme peut apparaître pendant toutes les phases du sommeil, mais de façon prédominante dans le stade 2, soit au cours du sommeil lent léger [10,27,32] . Au cours d'études, les auteurs ont pu remarquer que des changements d'ondes cérébrales apparaissaient avant un épisode de bruxisme, témoignant d'une activité corticale accrue [27,28,29] .…”

“…De part les composantes corticales et autonomes qui accompagnent l'épisode de bruxisme, on associe le bruxisme au phénomène de microéveil : le bruxisme du sommeil serait une réaction d'éveil exagérée, accompagnée par des manifestations physiologiques (salivation, déglutition) et pathologiques (apnée, mouvements pério-diques) diverses. [10] . De même, une forte dose de L-Dopa favorise la parafonction tandis qu'une faible dose a un effet bénéfique.…”

“…De même, une forte dose de L-Dopa favorise la parafonction tandis qu'une faible dose a un effet bénéfique. Ce phénomène est compatible avec d'autres agonistes dopaminergiques qui possèdent une action bidirectionnelle [10] . En 1997, Lobbezoo et coll.…”

“…Dans une étude décrivant des phé- nomènes de bruxisme apparus chez quatre patients sous ISRS, Bostwick et Jaffee montrent que la prise de buspirone, agoniste de la séroto-nine, entraîne la disparition des signes [3] . Par contre, l'utilisation d'un précurseur de la séroto-nine (le tryptophane) ou d'un inhibiteur de sa réab-sorption (l'amytriptyline) n'entraîne ni augmentation ni diminution du bruxisme [10,26] .…”

“Age is associated with self-reported sleep bruxism, independently of tooth loss.” A critical commentary

“…Nevertheless the contrary occurs. It was found that several neurochemicals (e.g., serotonin, dopamine, gamma aminobutyric acid, and noradrenaline) are involved in both the genesis of rhythmic jaw movements (e.g., bruxism) and the modulation of muscle tone during sleep [9]. With age physiological changes occur.…”