Grevanny Ranny, Suhartono Antonius Winoto, Amin Almasyifa Herlingga Rahmasari, Auerkari Elza Ibrahim
Pediatric Dentistry Residency Program, Faculty of Dentistry, University of Indonesia, Jakarta, Indonesia.
Department of Oral Biology, Division of Forensic Odontology, Faculty of Dentistry, University of Indonesia, Jakarta 10430, Indonesia.
Iran J Med Sci. 2024 Nov 1;49(11):680-690. doi: 10.30476/ijms.2024.100801.3332. eCollection 2024 Nov.
Aggressive periodontitis is an inflammation of the periodontal tissue that usually affects adolescents and young adults aged <30 years, caused by attachment loss and fast bone degradation. The correlation between the epigenetic status and the initiation and progression of numerous acquired diseases was documented. Consequently, targeting epigenetic factors within periodontal tissues stands as an appealing prospect for both the diagnosis and treatment of periodontitis. In addition to the role of pathogenic bacteria and their products, alterations in gene expression due to extrinsic and intrinsic factors can cause disturbances in the host's immune response. Epigenetic changes, whether DNA methylation or microRNA (miRNA) dysregulation, can cause changes in gene expression in aggressive periodontitis and lead to more severe and rapid loss of the periodontal tissues. This study aimed to elucidate the relationships between oral hygiene, pathogenic bacteria, and genetics in periodontitis development to promote targeted prevention and treatment for enhanced oral health in individuals at risk of aggressive periodontitis. The method employed in this study entailed a comprehensive review and analysis of scholarly literature on the relationship between epigenetic mechanisms and the development of aggressive periodontitis. In conclusion, epigenetic regulation plays an important role in the pathogenesis of periodontitis through DNA methylation mechanisms that begin with Toll-like receptors (TLRs), cytokine signaling pathways, promoter genes, and progress to pro-inflammatory cells. When periodontal tissue inflammation occurs, miRNA inhibits protein translation from messenger ribonucleic acid (mRNA), which contributes to its aggressiveness.
侵袭性牙周炎是一种牙周组织炎症,通常影响30岁以下的青少年和年轻成年人,由附着丧失和快速的骨吸收引起。已有文献记载了表观遗传状态与多种后天性疾病的发生和发展之间的相关性。因此,针对牙周组织内的表观遗传因素是牙周炎诊断和治疗的一个有吸引力的前景。除了致病细菌及其产物的作用外,外在和内在因素引起的基因表达改变可导致宿主免疫反应紊乱。表观遗传变化,无论是DNA甲基化还是微小RNA(miRNA)失调,都可导致侵袭性牙周炎中的基因表达变化,并导致牙周组织更严重、更快的丧失。本研究旨在阐明口腔卫生、致病细菌和遗传学在牙周炎发展中的关系,以促进对有侵袭性牙周炎风险个体的针对性预防和治疗,从而增强口腔健康。本研究采用的方法是对关于表观遗传机制与侵袭性牙周炎发展之间关系的学术文献进行全面综述和分析。总之,表观遗传调控通过DNA甲基化机制在牙周炎发病机制中起重要作用,该机制始于Toll样受体(TLR)、细胞因子信号通路、启动子基因,并发展为促炎细胞。当牙周组织发生炎症时,miRNA抑制信使核糖核酸(mRNA)的蛋白质翻译,这导致了其侵袭性。