Rintakoski Katariina, Hublin Christer, Lobbezoo Frank, Rose Richard J, Kaprio Jaakko
Institute of Dentistry, University of Helsinki, Helsinki, Finland.
Twin Res Hum Genet. 2012 Dec;15(6):714-9. doi: 10.1017/thg.2012.54. Epub 2012 Sep 6.
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.
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 2000-2002. 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).
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% Cl 0.41--0.62) of the total phenotypic variance. Sex-limitation model revealed no gender differences.
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.
本研究旨在探讨遗传和环境因素在芬兰一个基于人群的大型年轻成年双胞胎队列中磨牙症表型变异中的作用。
本研究的材料来自芬兰双胞胎16队列研究，该研究由1975 - 1979年出生的五组双胞胎队列组成，他们在2000 - 2002年完成了一份问卷（平均年龄24岁，范围23 - 27岁），其中包含与睡眠相关磨牙症频率的数据。我们基于同卵双胞胎和异卵双胞胎的遗传相似性，使用定量遗传模型，通过将表型变异分解为以下成分：加性遗传效应（A）、显性遗传效应（D）和非共享环境效应（E），来估计磨牙症最可能的遗传模型。
平均而言，8.7%的人每周经历磨牙症，23.4%的人很少经历，67.9%的人从未经历，性别差异不显著（p = 0.052）。磨牙症的最佳拟合遗传模型是AE模型。加性遗传效应占总表型变异的52%（95%可信区间0.41 - 0.62）。性别限制模型显示无性别差异。
遗传因素在与睡眠相关磨牙症易感性的表型变异中占很大比例，其遗传结构不存在性别差异。
