Effect of dopaminergic agonist group of drugs in treatment of sleep bruxism: A systematic review

Bhattacharjee, Bappaditya; Saneja, Ritu; Bhatnagar, Atul; Gupta, Pradeep Kumar

doi:10.1016/j.prosdent.2020.11.028

Cited by 7 publications

(5 citation statements)

References 37 publications

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“…Moreover, a neuroimaging study showed an imbalance on the expression of dopamine D2 receptors in patients with SB, confirmed by PSG 19 . Nonetheless, the evidence from clinical trials using dopaminergic agonist drugs is not clear 20 . Indeed, a recent systematic review did not find a significant effect of different dopaminergic agonist agents 20 .…”

Section: Bruxism and The Use Of Drugs And Psychoactive Substancesmentioning

confidence: 98%

“…20 Indeed, a recent systematic review did not find a significant effect of different dopaminergic agonist agents. 20 The physiology of the dopamine receptors and the differential degree of affinity of the dopaminergic agonist drugs add another layer of complexity on predicting the consequences of such drugs on the MMA. Moreover, it is still unclear the degree to which the effects of the dopaminergic agonists as increasing or decreasing jaw muscle activity during sleep are dependent on other medical comorbidities.…”

Section: B Ruxis M and The Us E Of Drug S And Psychoac Tive Subs Tan...mentioning

confidence: 99%

“…Nonetheless, the evidence from clinical trials using dopaminergic agonist drugs is not clear 20 . Indeed, a recent systematic review did not find a significant effect of different dopaminergic agonist agents 20 . The physiology of the dopamine receptors and the differential degree of affinity of the dopaminergic agonist drugs add another layer of complexity on predicting the consequences of such drugs on the MMA.…”

Section: Bruxism and The Use Of Drugs And Psychoactive Substancesmentioning

confidence: 99%

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Secondary bruxism: A valid diagnosis or just a coincidental finding of additional masticatory muscle activity? A narrative review of literature

Conti,

Cunha,

Conti

et al. 2023

J of Oral Rehabilitation

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IntroductionBruxism is defined as a repetitive masticatory muscle activity that can manifest it upon awakening (awake bruxism‐AB) or during sleep (sleep bruxism‐SB). Some forms of both, AB and SB can be associated to many other coexistent factors, considered of risk for the initiation and maintenance of the bruxism. Although controversial, the term ‘secondary bruxism’ has frequently been used to label these cases. The absence of an adequate definition of bruxism, the non‐distinction between the circadian manifestations and the report of many different measurement techniques, however, are important factors to be considered when judging the literature findings. The use (and abuse) of drugs, caffeine, nicotine, alcohol and psychoactive substances, the presence of respiratory disorders during sleep, gastroesophageal reflux disorders and movement, neurological and psychiatric disorders are among these factors. The scarcity of controlled studies and the complexity and interactions among all aforementioned factors, unfortunately, does not allow to establish any causality or temporal association with SB and AB. The supposition that variables are related depends on different parameters, not clearly demonstrated in the available studies.ObjectivesThis narrative review aims at providing oral health care professionals with an update on the co‐risk factors and disorders possibly associated with bruxism. In addition, the authors discuss the appropriateness of the term ‘secondary bruxism’ as a valid diagnostic category based on the available evidence.ConclusionThe absence of an adequate definition of bruxism, the non‐distinction between the circadian manifestations and the report of many different measurement techniques found in many studies preclude any solid and convincing conclusion on the existence of the ‘secondary’ bruxism.

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Section: Bruxism and The Use Of Drugs And Psychoactive Substancesmentioning

confidence: 98%

Section: B Ruxis M and The Us E Of Drug S And Psychoac Tive Subs Tan...mentioning

confidence: 99%

Section: Bruxism and The Use Of Drugs And Psychoactive Substancesmentioning

confidence: 99%

See 1 more Smart Citation

Secondary bruxism: A valid diagnosis or just a coincidental finding of additional masticatory muscle activity? A narrative review of literature

Conti,

Cunha,

Conti

et al. 2023

J of Oral Rehabilitation

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“…In this manner, it promotes the activation of the basolateral amygdala, which can in turn cause rhythmic jaw movement. If one considers that any malfunction at any point of the VTA-mesocortical-vSub-VP-N.Acc-Me5 pathway can cause bruxism, it is only logical to assume that this may provide an explanation as to why there is no specific medication that confers universal and consistently positive results; at the same time, the certainty of evidence produced by the majority of studies has been calculated in the range between very low and moderate ( 137 , 138 ). Similarly, the existence of neurological degeneration may constitute the reason why cognitive behavioral therapy is not successful as a bruxism management option, since it cannot reverse these neurological disturbances, at least not sooner than 6 months from the initiation of treatment ( 137 ).…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Neurobiology of bruxism: The impact of stress (Review)

Pavlou,

Spandidos,

Zoumpourlis

et al. 2024

Biomed Rep

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Bruxism is a non-functional involuntary muscle activity that affects more than one-third of the population at some point in their lives. A number of factors have been found to be related to the etiopathogenesis of bruxism; therefore, the condition is considered multifactorial. The most commonly accepted factor is stress. Stress has long been considered to increase muscle tone and to reduce the pain threshold. Current evidence indicates that exposure to chronic stress, distress and allostatic load ignite neurological degeneration and the attenuation of critical neuronal pathways that are highly implicated in the orofacial involuntary muscle activity. The present review discusses the negative effects that chronic stress exerts on certain parts of the central nervous system and the mechanisms through which these changes are involved in the etiopathogenesis of bruxism. The extent of these morphological and functional changes on nerves and neuronal tracts provides valuable insight into the obstacles that need to be overcome in order to achieve successful treatment. Additionally, particular emphasis is given on the effects of bruxism on the central nervous system, particularly the activation of the hypothalamic-pituitary-adrenal axis, as this subsequently induces an increase in circulating corticosterone levels, also evidenced by increased levels of salivary cortisol, thereby transforming bruxism into a self-reinforcing loop.

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“…The search of bruxism etiology seems to never end [12,13]. There have been proposed theories focusing on the genetic origin [14,15], psychosocial factors [16], and vulnerability to stress or anxiety [17], the role of various neurotransmitters: serotonin [18], dopamine [19], gamma aminobutyric acid (GABA), and noradrenaline [18]. There has been even an observed link between dietary fiber intake and the prevalence of sleep bruxism [20].…”

Section: Introductionmentioning

confidence: 99%

Inflammatory Markers and Sleep Architecture in Sleep Bruxism—A Case-Control Study

Fulek,

Wieckiewicz,

Szymanska-Chabowska

et al. 2024

JCM

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Background: Sleep bruxism (SB) is a common sleep-related movement behavior with a multifaceted etiology and a deficiently understood pathophysiology. A recent hypothesis suggests a link between SB and systemic inflammation. The scope of the study was to determine whether bruxers have altered sleep structure and different levels of inflammatory parameters compared to nonbruxers. Methods: A total of 83 adults underwent full-night polysomnography. The polysomnograms were evaluated using the American Academy of Sleep Medicine (AASM) guidelines. Then, the blood samples were obtained from the participants by venipuncture and the analyses were performed. The study group was divided based on bruxism episode index (BEI) into two groups: BEI ≤ 4 and BEI > 4. Results: In comparison with nonbruxers, the oxygen desaturation index (ODI) was significantly higher in severe bruxers (7.5 ± 11.08 vs. 3.33 ± 5.75, p < 0.005), as well as the arousal parameters (7.77 ± 4.68 vs. 4.03 ± 2.97, p < 0.001), and the mean oxygen desaturation (3.49 ± 0.69 vs. 3.01 ± 0.67, p < 0.05). Moreover, the differences in sleep architecture and deprivation of the deep sleep phase were observed, the non-REM sleep stage 3 was significantly shorter in severe bruxers (p < 0.03). Differences were also noted in non-REM sleep stage 1 and REM sleep phase. In the investigated group, there were no statistical differences in inflammatory cytokines levels between bruxers and nonbruxers. Conclusions: Sleep bruxism is associated with sleep structure alterations and may be associated with deep sleep phase deprivation. The inflammatory markers are not linearly correlated with the severity of sleep bruxism expressed as BEI.

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Effect of dopaminergic agonist group of drugs in treatment of sleep bruxism: A systematic review

Cited by 7 publications

References 37 publications

Secondary bruxism: A valid diagnosis or just a coincidental finding of additional masticatory muscle activity? A narrative review of literature

Secondary bruxism: A valid diagnosis or just a coincidental finding of additional masticatory muscle activity? A narrative review of literature

Neurobiology of bruxism: The impact of stress (Review)

Inflammatory Markers and Sleep Architecture in Sleep Bruxism—A Case-Control Study

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