During the second half of he 20th century, the causes of Sleep Bruxism (SB) were believed to be stress and anxiety, occlusal interferences, dopamine activity in basal ganglia. Most previously existing hypotheses that tried to explain the origin of SB are now backed by some scientific evidence. The exception being the role of occlusal interference. It is probable that the origin of SB cannot be explained by a single or simple mechanism.
The first evidence of a genetic basis explaining a hereditary pattern of bruxism and related tooth wear was from questionnaire-based studies or from twin population analysis. These surveys demonstrated that 20% to 50% of subjects aware of tooth grinding had a direct relative who was also a tooth grinder. Identical (monozygotic) twins share the highest probability of presenting bruxism with high concordance.
The exact pathophysiology of SB is not known, but current evidence from experimental studies does suggest that rhythmic masticatory muscle activity (RMMA) and tooth grinding are secondary to the over-activation of the natural and ongoing physiologic activities linked to repetitive brief arousals during sleep. Evidence supporting and association between SB and stress, anxiety, and the hypothalamic-adrenal axis, however, is mixed at best, particularly when objective measures of RMMA are used. SB has been shown to be preceded by sudden shift in autonomic cardiac and respiratory activity, in addition to brain activity, suggesting that a brief and intense over-activation of the autonomic nervous system may be more closely tied to the pathophysiology of SB.