No abstract

Given the observed associations with both heavy smoking and smokeless tobacco and a dose-response relationship, the present results support our hypothesis of a link between nicotine intake and bruxism.

Given the observed associations between alcohol drinking, binge drinking, passing-out due to excessive alcohol intake and coffee consumption, the results support our hypothesis of an independent association of both alcohol use, and coffee consumption with bruxism.

Objectives: The aim of the present study was to examine the role of genetic and environmental factors in the phenotypic variance of bruxism in a large population-based cohort of young adult twins in Finland.Methods: The material of the present study derives from the FinnTwin16 cohort study consisting of five birth cohorts of twin pairs born in 1975-1979 who completed a questionnaire (at mean age 24, range 23-27 years) with data on frequency of sleep-related bruxism in [2000][2001][2002]. We used quantitative genetic modeling, based on the genetic similarity of monozygotic and dizygotic twins, to estimate the most probable genetic model for bruxism, based on decomposition of phenotypic variance into components: additive genetic effects (A), dominant genetic effects (D), and non-shared environmental effects (E).Results: On average, 8.7% experienced bruxism weekly, 23.4% rarely, and 67.9% never, with no significant gender difference (p = .052). The best fitting genetic model for bruxism was the AE-model. Additive genetic effects accounted for 52% (95% CI 0.41-0.62) of the total phenotypic variance. Sex-limitation model revealed no gender differences.Conclusions: Genetic factors account for a substantial proportion of the phenotypic variation of the liability to sleep-related bruxism, with no gender difference in its genetic architecture.