ReviewCureus2024
Exploring the Influence of Genetic Single-Nucleotide Polymorphism (SNPs) on Endodontic Pathologies: A Comprehensive Review.
Review in Cureus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Biomarkers for Treatment Response in Orthodontics: Molecular Mechanisms, Clinical Utility, and Future Directions.International journal of molecular sciences · 2026Review
- Review
- The potential associations of periapical lesions on endodontic microsurgery with guided bone regeneration: a retrospective analysis of 23 cases.Frontiers in medicine · 2026Article
- Prevalence of Glutathione-S-Transferase T and M Deletion Polymorphisms in Apical Periodontitis: a Two-Center Observational Study.Acta stomatologica Croatica · 2025Article
- The interleukin gene landscape: understanding its influence on inflammatory mechanisms in apical periodontitis.Molecular biology reports · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.