Objective: Problematic internet gaming in adolescents is associated with various negative outcomes, such as low self-esteem, depression, anxiety, and attention problems. We hypothesized that game coding education, by improving adolescents’ self-esteem, would be more effective than game literacy education in mitigating problematic internet gaming. Methods: A total of 126 adolescents who voluntarily applied for the game coding education and game literacy education program of the “Visiting Game Class” project operated by the Game Cultural Foundation participated in this study. We collected data on demographics, gaming patterns, and psychological status, including positive or negative perceptions of online games, depression, and anxiety. We designated those with scores higher than 40 on Young’s Internet Addiction Scale as the “problematic internet gaming” group. Results: Only game coding education was significantly effective in decreasing internet use, lowering depressive symptoms, and improving self-esteem. In the hierarchical logistic regression analysis, more frequent education time, coding education, stronger negative perceptions of gaming, and high self-esteem predicted decreased internet gaming among participants exhibiting problematic internet gameplay. Conclusion Game coding education effectively mitigates problematic gaming by improving adolescents’ self-esteem. Thus, it may be beneficial to increase education time and devise game education programs tailored to adolescents’ psychological status.

Growing evidence suggests close associations between periodontitis and atherosclerosis. To further understand the pathological relationships of these associations, we developed periodontitis with ligature placement around maxillary molars or ligature placement in conjunction with Porphyromonas gingivalis lipopolysaccharide injection at the ligature sites (ligature/P.g. LPS) in Apolipoprotein E knock out mice and studied the atherogenesis process in these animals. The mice were fed with high fat diet for 11 weeks and sacrificed for analyzing periodontitis, systemic inflammation, and atherosclerosis. Controls did not develop periodontitis or systemic inflammation and had minimal lipid deposition in the aortas, but mice receiving ligature or ligature/P.g. LPS showed severe periodontitis, systemic inflammation, and aortic plaque formation. The aortic plaque contained abundant macrophages and cells expressing both endothelial and mesenchymal cell markers. The severity of periodontitis was slightly higher in mice receiving ligature/P.g. LPS than ligature alone, and the magnitude of systemic inflammation and aortic plaque formation were also notably greater in the mice with ligature/P.g. LPS. These observations indicate that the development of atherosclerosis is due to systemic inflammation caused by severe periodontitis. In vitro, P.g. LPS enhanced the secretion of pro-inflammatory cytokines from macrophages and increased the adhesion of monocytes to endothelial cells by upregulating the expression of adhesion molecules from endothelial cells. Moreover, secretory proteins, such as TNF-α, from macrophages induced endothelial-mesenchymal transitions of the endothelial cells. Taken together, systemic inflammation induced by severe periodontitis might exacerbate atherosclerosis via, in part, causing aberrant functions of vascular endothelial cells and the activation of macrophages in mice.