# Sleep Bruxism and Hypobaric Hypoxia Exposure: Exploring the Physiological Association

## TL;DR

This paper explores how high-altitude hypoxia may influence sleep bruxism through physiological and molecular changes.

## Contribution

The paper reviews the novel association between hypobaric hypoxia and sleep bruxism, focusing on shared physiological and molecular mechanisms.

## Key findings

- Sleep bruxism is linked to GER and autonomic dysregulation, which are also seen in hypobaric hypoxia.
- Hypoxia exposure triggers oxidative stress and sleep alterations that may worsen bruxism severity.
- TRPV1 and HIF-1α activation are implicated in the neurophysiological mechanisms of bruxism under hypoxia.

## Abstract

Sleep bruxism (SB) is a masticatory muscle activity during sleep which can be categorized as primary, when it remains unclear whether the phenomenon is directly linked to a specific disorder, or if it only coexists, and secondary, when it is proven to be associated with a particular disorder, treatment or lifestyle and bruxism that is part of the signs of a disorder. In this way, SB is associated with various factors, including obstructive sleep apnea and gastroesophageal reflux (GER), where evidence suggests SB has a protective role in airway patency, potentially triggered by microarousals and autonomic instability, especially under hypoxia conditions. Since hypobaric hypoxia exposition—generated by high-altitude exposure—produces a decrease in the partial pressure of oxygen, it triggers alterations in cardiac rhythm and gastric function, which could be associated with physiological alterations mentioned in SB. Therefore, the aim of this review is to determine the effect of hypobaric hypoxia exposure on the physiological and molecular alterations during sleep bruxism. Method: The SANRA-guided narrative review synthesized recent human and animal studies on hypoxia’s physiological and molecular effects in sleep bruxism. In conclusion, SB is associated with GER and autonomic dysregulation, which are present in hypobaric hypoxia conditions, where respiratory disturbances, microarousals, and increased muscle activity are associated with SB. High-altitude exposure triggers oxidative stress, genetics, and sleep alteration, which exacerbate its severity. Moreover, neurophysiological and molecular mechanisms, including TRPV1 and HIF-1α activation, are implicated. Finally, polysomnography remains the gold standard for diagnosis; however, studies at high altitude are needed to confirm this association.