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Biological sciences including genetics and epigenetics can be analyzed for how gene regulation affects the body’s immune response to an inflammatory disease such as periodontitis, commonly known as gum disease. Genetics and epigenetics can be defined as the processes by which genes were expressed or suppressed through polymorphism, (de)methylation, or (de)acetylation.
Studies note that specific environmental factors such as race, gender, diabetes, education, smoking, and body mass index (BMI) all increase the severity of periodontal disease. One quarter of chronic periodontitis patients tested for hyper/hypo methylation proved to be a significant factor in response to inflammatory disease. The authors concluded while it was not genetics alone that affected response or susceptibility to periodontitis, it was environmental factors that also regulated gene transcription. These regulations stimulated cytokines such as IL-1 and IL-6, which were noted in inflammatory destruction of periodontal tissues.
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Studies were conducted using different methods in the evaluation of genetic predisposition to periodontitis. Methods used were familial aggregation, twin studies, association studies, segregation, and linkage analysis. Familial aggregation studies focused on members of families who had a history of aggressive periodontitis. Familial studies conducted in Germany were reviewed by Hassell and Harris (1995) and concluded, “This aggregation within families strongly suggests a genetic predisposition.”
Read full, original post: How genetics and epigenetics link to periodontal disease: Research paper
