Exploring the Influence of Genetic Single-Nucleotide Polymorphism (SNPs) on Endodontic Pathologies: A Comprehensive Review

Abstract

A considerable portion of the global population is affected by pulpitis and periapical lesions. While the impact of infections caused by various microbes and host effector molecules in pulpal and periapical diseases is widely recognized, disease susceptibility and progression are also influenced by the dynamic interaction between host genetic factors and environmental influences. Apical periodontitis occurs as an inflammatory response to microorganisms present in the root canals of infected teeth. Initially functioning as the body’s defense mechanism, this response often progresses to chronic inflammation. Several studies have established associations between genetic polymorphisms and various dental conditions, including temporomandibular joint (TMJ) disorders, dental caries, orthognathic surgeries, open bite malocclusion, periapical periodontitis, pulp stones, pulpitis, periapical abscesses, local anesthesia complications, and endodontic treatment outcomes. Key findings from this review highlight the role of specific single-nucleotide polymorphisms (SNPs) in genes such as matrix metalloproteinase (MMP)1, MMP2, MMP3, interleukin (IL)-1β, IL-6, IL-17, and tumor necrosis factor-alpha (TNF-α), which influence inflammatory pathways and tissue remodeling. For example, SNPs in interleukin genes, such as IL-1β (-511 C/T), have been linked to an increased risk of apical periodontitis, while MMP gene polymorphisms contribute to tissue degradation in periapical lesions. This review underscores the importance of identifying genetic markers that drive disease progression and inflammatory processes in pulpal and periapical pathologies. A better understanding of these mechanisms can inform strategies for disease prevention, personalized treatment approaches, and improved endodontic outcomes.