The neurophysiological basis of bruxism

Mesencephalic trigeminal nucleus (MTN) neurons innervate the stretch receptors of the jaw elevator muscles and periodontal ligament mechanoreceptors, Bruxism activates the MTN. We analyzed how MTN cells are structured, their anatomy and physiology, and the effects of their activation. To induce and maintain sleep, gamma-aminobutyric acid (GABA), an inhibitor neurotransmitter, is released from the ventro-lateral preoptic area of the hypothalamus and acts on the ascending reticular activating system (ARAS) nuclei. The GABA neurotrasmitter induces the entry of chlorine into cells, hyperpolarizing and inhibiting these. MTN cells, on the contrary, are depolarized by GABA, as their receptors are activated upon GABA binding. They “let out” chlorine and activate ARAS cells. MTN cells release glutamate, an excitatory neurotransmitter onto their target cells, in this case onto ARAS cells. During wakefulness, ARAS activation causes cerebral cortex activation; instead, during sleep (sleep bruxism), ARAS activation avoids an excessive reduction in ARAS neurotransmitters, including noradrenaline, dopamine, serotonin, acetylcholine and glutamate. These neurotransmitters, in addition to activating the cerebral cortex, modulate vital functions such as cardiac and respiratory functions. Polysomnography shows that sleep bruxism is always accompanied by cardiac and respiratory activation and, most importantly, by brain function activation. Bruxism is not a parafunction, and it functions to activate ARAS nuclei.