Genetic polymorphisms and bruxism: A scoping review.

BACKGROUND

Recent studies have highlighted the multifactorial nature of bruxism, with behavioral, psychosocial, and physiological factors, including genetic predisposition, contributing to its development. However, the role of genetic markers in determining susceptibility to bruxism remains poorly understood, with limited studies offering significant findings.

OBJECTIVES

To identify the current knowledge to investigate the susceptibility of genetic markers for sleep (SB) and/or awake bruxism (AB).

MATERIALS AND METHODS

Seven electronic databases and two grey literature platforms were searched up to January 2024. We included studies that related different types of genes and/or genetic polymorphisms with different types of bruxism, regardless of age or sex of the participants. To be included the study must have described the form of detection of bruxism.

RESULTS

A total of 21 reports were included. Of these, 16 were primary research reports. The remaining five articles consisted of four systematic reviews and a literature review incorporating a systematic mapping process, and network visualization. Within the pool of 16 primary study reports, seven focused on the association of genetic polymorphisms with both SB and AB, while seven concentrated solely on the association with SB. One primary study reported results related to probable AB and one article did not specify the bruxism type. Regarding all the studied genes and polymorphisms, significant association results were obtained for 15 polymorphisms from 11 different genes. Self-reported SB was associated with genes from the serotonergic (5HTR2A) and dopaminergic pathways (DRD2, DRD3, and ANKK1), as well as genes encoding enzymes (COMT and MMP9) and proteins (ACTN3 and ANKK1). Instrumentally reported SB was linked only to the reverse telomerase gene (TERT). Self-reported AB was associated with the ACTN3 and ANKK1 genes.

CONCLUSION

This review identified 30 genes and 56 polymorphisms variations potentially associated with either SB or AB. However, few presented significant results regarding positive associations, mostly acting at neurotransmitter pathways. The authors recommend further studies to determine the susceptibility of genetic markers as a risk factor for bruxism.