Genetic analysis of probable sleep bruxism and its associations with clinical and behavioral traits

Tommi Strausz; Satu Strausz; FinnGen; Tuula Palotie; Jari Ahlberg; Hanna M Ollila

doi:10.1093/sleep/zsad107

Genetic analysis of probable sleep bruxism and its associations with clinical and behavioral traits

Sleep. 2023 Oct 11;46(10):zsad107. doi: 10.1093/sleep/zsad107.

Authors

Tommi Strausz¹, Satu Strausz^{1

2}; FinnGen; Tuula Palotie^{3

4}, Jari Ahlberg³, Hanna M Ollila^{1

5

6

7}

Affiliations

¹ Institute for Molecular Medicine Finland, Helsinki Institute of Life Science, University of Helsinki, Helsinki, Finland.
² Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
³ Department of Oral and Maxillofacial Diseases, Head and Neck Center, Helsinki University Hospital, Helsinki, Finland.
⁴ Orthodontics, Department of Oral and Maxillofacial Diseases, Clinicum, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
⁵ Broad Institute of MIT and Harvard, Cambridge, MA, USA.
⁶ Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA.
⁷ Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

Abstract

Study objectives: Sleep bruxism (SB) can cause damage on teeth, headache and severe pain affecting both sleep and daily functioning. Yet despite the growing interest into bruxism, the underlying clinically relevant biological mechanisms remain unresolved. The aim of our study was to understand biological mechanisms and clinical correlates of SB including previously reported disease associations.

Methods: We used data from the FinnGen release R9 (N = 377 277 individuals) that are linked with Finnish hospital and primary care registries. We identified 12 297 (3.26%) individuals with International Classification of Diseases (ICD)-10 codes used for SB. In addition, we used logistic regression to examine the association between probable SB and its clinically diagnosed risk factors and comorbidities using ICD-10 codes. Furthermore, we examined medication purchases using prescription registry. Finally, we performed the first genome-wide association analysis for probable SB and computed genetic correlations using questionnaire, lifestyle, and clinical traits.

Results: The genome-wide association analysis revealed one significant association: rs10193179 intronic to Myosin IIIB (MYO3B) gene. In addition, we observed phenotypic associations and high genetic correlations with pain diagnoses, sleep apnea, reflux disease, upper respiratory diseases, psychiatric traits, and also their related medications such as antidepressants and sleep medication (p < 1e-4 for each trait).

Conclusions: Our study provides a large-scale genetic framework to understand risk factors for SB and suggests potential biological mechanisms. Furthermore, our work strengthens the important earlier work that highlights SB as a trait that is associated with multiple axes of health. As part of this study, we provide genome-wide summary statistics that we hope will be useful for the scientific community studying SB.

Keywords: FinnGen; Gastroesophageal Reflux; Genome-Wide Association Study; Obstructive Sleep Apnea; Pain; Population Register; Sleep Bruxism; Temporomandibular Joint Dysfunction Syndrome.

Grants and funding

HUS 4685/31/2016/Business Finland