Osteoarthritis year in review 2016: genetics, genomics and epigenetics

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Osteoarthritis year in review 2016: genetics, genomics and epigenetics J.B.J. van Meurs  Osteoarthritis and Cartilage  Volume 25, Issue 2, Pages 181-189 (February 2017) DOI: 10.1016/j.joca.2016.11.011 Copyright © 2016 Terms and Conditions

Fig. 1 Genetics of OA. Rare mutations in monogenetic disorders (single causal gene) are in general found in a single family and have a large effect size, resulting in early-onset OA. By contrast, late onset OA is a complex trait and is caused by a large number of common DNA variants together with environmental factors. The effect size of these common variants are in general small, and can vary between individuals in the population. Osteoarthritis and Cartilage 2017 25, 181-189DOI: (10.1016/j.joca.2016.11.011) Copyright © 2016 Terms and Conditions

Fig. 2 A: Identified genetic loci for each of the joint sites with genome-wide significant (p < 5 × 10−8) or genome-wide suggestive (p < 10−7) evidence. Shown are the gene names that are annotated nearest to the DNA variant associated. Some of the hip or knee associated loci, show only association in a certain subgroup: Total Joint Replacment (TJR); Total hip replacement (THR); Total knee replacement (TKR); * Only significant in the Asian population. B: Number of identified genetic loci according to the number of cases in the discovery GWAS analysis. Red: OA; blue: Schizophrenia Osteoarthritis and Cartilage 2017 25, 181-189DOI: (10.1016/j.joca.2016.11.011) Copyright © 2016 Terms and Conditions