Medications and addictive substances potentially inducing or attenuating sleep bruxism and/or awake bruxism

Abstract

Bruxism is a repetitive jaw‐muscle activity characterised by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible. It can occur during sleep, indicated as sleep bruxism, or during wakefulness, indicated as awake bruxism. Exogenous risk indicators of sleep bruxism and/or awake bruxism are, among others, medications and addictive substances, whereas also several medications seem to have the potential to attenuate sleep bruxism and/or awake bruxism. The objective of this study was to present a narrative literature on medications and addictive substances potentially inducing or aggravating sleep bruxism and/or awake bruxism and on medications potentially attenuating sleep bruxism and/or awake bruxism. Literature reviews reporting evidence or indications for sleep bruxism and/or awake bruxism as an adverse effect of several (classes of) medications as well as some addictive substances and literature reviews on medications potentially attenuating sleep bruxism and/or awake bruxism were used as starting point and guidelines to describe the topics mentioned. Additionally, two literature searches were established on PubMed. Three types of bruxism were distinguished: sleep bruxism, awake bruxism and non‐specified bruxism. Generally, there are insufficient evidence‐based data to draw definite conclusions concerning medications and addictive substances inducing or aggravating sleep bruxism and/or awake bruxism as well as concerning medications attenuating sleep bruxism and/or awake bruxism. There are insufficient evidence‐based data to draw definite conclusions concerning medications and addictive substances inducing or aggravating sleep bruxism and/or awake bruxism as well as concerning medications attenuating sleep bruxism and/or awake bruxism.

Research routes on improved sleep bruxism metrics: Toward a standardised approach

“…Furthermore, SB can also be relieved, exacerbated, or be secondary to different medications, e.g. clonidine and selective serotonin reuptake inhibitors (de Baat et al., 2020; Mayer et al., 2016; Melo et al., 2018). However, due to the low level of evidence, caution is required before generalising the associations between SB to comorbidities and/or use of medications to observed clinical manifestations that may be more prone to occur in more vulnerable individuals.…”

The neurophysiological basis of bruxism

“…Sleep bruxism cannot be eliminated because this would also eliminate GABA, and without GABA there is no sleep. Very little is known about the complex relationship between drugs and GABA release in the context of sleep; however, we cannot help but notice that some GABA agonist drugs (alcohol, phenethylamines (amphetamines and methylphenidate), heroin, anticonvulsants, and selective serotonin reuptake inhibitors) favor sleep bruxism while some GABA antagonists (clonidine, levodopa, clonazepam, gabapentin, hydroxyzine, and dopamine agonists) reduce it [ 32 , 33 ].…”

Is dopaminergic medication dose associated with self-reported bruxism in Parkinson’s disease? A cross-sectional, questionnaire-based study

“…Moreover, some risk factors for bruxism are more prevalent in patients with PD [27]. Examples of risk factors for bruxism are, amongst others, the presence of stress and depressive thoughts [28][29][30][31] and the use of specific types of medication, such as selective serotonin reuptake inhibitors (SSRI) [11,12]. All of these risk factors are more prevalent in patients with PD than in the general population [27].…”

“…Consequently, the number of bruxism episodes is expected to decrease by using levodopa [ 10 ]. The relation between medication usage and bruxism in otherwise healthy individuals has been studied before [ 11 , 12 ]. However, the results of studies on the effect of dopaminergic medication on bruxism are contradictory, some reporting decreases [ 10 , 13 , 14 ], others increases [ 15 ], and yet others no effect [ 12 , 16 , 17 ].…”