Nutrient insufficiencies and deficiencies involved in the pathogenesis of bruxism (Review)

Abstract

Stress has been well-documented to have a significant role in the etiopathogenesis of bruxism. Activation of the hypothalamic-pituitary-adrenal axis (HPA) and subsequent release of corticosteroids lead to increased muscle activity. Neurological studies have demonstrated that chronic stress exposure induces neurodegeneration of important neuronal structures and destabilization of the mesocortical dopaminergic pathway. These disruptions impair the abilities to counteract the overactivity of the HPA axis and disinhibit involuntary muscle activity, while at the same time, there is activation of the amygdala. Recent evidence shows that overactivation of the amygdala under stressful stimuli causes rhythmic jaw muscle activity by over activating the mesencephalic and motor trigeminal nuclei. The present review aimed to discuss the negative effects of certain vitamin and mineral deficiencies, such as vitamin D, magnesium, and omega-3 fatty acids, on the central nervous system. It provides evidence on how such insufficiencies may increase stress sensitivity and neuromuscular excitability and thereby reduce the ability to effectively respond to the overactivation of the sympathetic nervous system, and also how stress can in turn lead to these insufficiencies. Finally, the positive effects of individualized supplementation are discussed in the context of diminishing anxiety and oxidative stress, neuroprotection and in the reversal of neurodegeneration, and also in alleviating/reducing neuromuscular symptoms.

Keywords: bruxism; iron; magnesium; neurodegeneration; omega-3 fatty acids; vitamin D.

Figure 1

Effects of vitamin D, omega-3 fatty acids and magnesium on the mesocortical dopaminergic pathway (grey arrows). Vitamin D acts on the mesocortical dopaminergic pathway by protecting dopaminergic neurons (blue arrows). Omega-3 fatty acids suppress overactivity of the HPA axis and increase neurogenesis and synaptic activity in the hippocampus and N.Acc (orange arrows). Magnesium suppresses HPA and SAM axis overactivation by acting on the hypothalamus and LC, respectively (red arrows). Amy, amygdala; HPA, hypothalamic-pituitary-adrenal; HP, hippocampus; Hyp, hypothalamus; LC, locus coereleus; Mg, magnesium; N.Acc, nucleus accubens; SAM, sympathetic adrenal medullary; Vit.D. vitamin D; VTA, ventral tegmental area.

Figure 2

Schematic representation of events that lead from stress to jaw muscle activity. BLA, basolateral amygdala; CeA, central amygdala; GR, glucocorticoids; HP, hippocampus; Me5, mesencephalic trigeminal nucleus; MR, mineralocorticoid; N.Acc, nucleus accubens; NO, nitric oxide; VP, ventral pallidum; VTA, ventral tegmental area.