International Journal of Community Medicine and Public Health, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 29, 2025

Periodontal disease is a complex, multifactorial condition characterized by chronic inflammation and progressive destruction of the tooth-supporting structures. Among its various forms, early-onset periodontitis particularly aggressive often associated with genetic predispositions. Genetic epigenetic factors play pivotal roles in shaping host susceptibility to this influencing immune responses, inflammatory regulation, tissue homeostasis. Single-nucleotide polymorphisms (SNPs) genes encoding cytokines, such as interleukin-1β tumor necrosis factor-alpha, are linked heightened amplifying damage accelerating progression. Additionally, like TLR2 TLR4 impair microbial recognition, promoting dysbiosis. Epigenetic modifications, including DNA methylation histone acetylation, further modulate gene expression, contributing dynamic interplay between predispositions environmental smoking or poor oral hygiene. Emerging research has also highlighted markers human leukocyte antigen (HLA) alleles matrix metalloproteinase (MMP) variants predictors severity therapeutic outcomes. These insights have driven development targeted therapies, inhibitors pro-inflammatory mediators, MMP inhibitors, potential miRNA-based interventions. High-throughput technologies, genome-wide association studies (GWAS), expanded understanding pathways involved periodontal disease. advances enable earlier detection personalized treatment strategies, offering mitigate progression reduce burden severe periodontitis. The integration into clinical practice marks significant step toward precision medicine, providing framework for tailored prevention interventions aimed at improving patient Future must continue explore these mechanisms uncover novel biomarkers refine approaches

Language: Английский