Background Heritability measures the ratio of the genetic component to the total phenotypic variance or, in other words, how much genetics can account for the difference in the distribution of disease seen in a population (Visscher et al. 2008). Therefore, this is a concept applied to a "population" rather than to specific individuals. Knowledge of disease heritability can help set boundaries on the potential of genetic variants to explain health and disease traits, inform genetic risk estimation, and estimate familial disease risk (Smith 1971). Heritability has traditionally been estimated by conducting twin or family studies with different analytic approaches (Tenesa and Haley 2013) and, more recently, by genome-wide association studies (GWASs). GWASs have been used to estimate the overall genetic contribution to physical characteristics (e.g., human height; Yang et al. 2010) and diseases (e.g., glioma; Kinnersley et al. 2015). However, most GWASs have sample sizes that allow them to effectively examine only common variants (>1% or 5% minor allele frequency), providing a lower bound for narrow-sense heritability (Kinnersley et al. 2015). The heritability of periodontal diseases, including gingivitis and periodontitis, was estimated in animal models (Miley et al. 2011; Hiyari et al. 2015) and in humans. Notably, studies of twins reported periodontitis heritability estimates that vary from around 0.3 to 0.5 (30% to 50%; Michalowicz, Aeppli, Virag, et al. 1991; Corey et al. 1993; Mucci et al. 2005). In contrast, other studies rejected the hypothesis of substantial heritability for periodontitis (Dowsett et al. 2002). Overall, there is still a high degree of uncertainty regarding how much of the observed variance in gingivitis and periodontitis is attributable to genetics. In the era of precision medicine (Divaris 2017), with a continuous effort to derive individual disease susceptibility assessments to inform prevention and 842510J DRXXX10.

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