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Interleukin-1 as a genetic marker for periodontitis
Abstract
Periodontitis is considered to be a multifactorial disease. Studies have indicated that part of the clinical variability in periodontitis may be explained by genetic factors. Genes can affect the immunoinflammatory host response to bacterial challenge in the periodontal tissues by means of an overproduction of proinflammatory cytokines, such as interleukin-1 (IL-1). IL-1 plays an important role in the pathogenesis of periodontitis, through its involvement in the regulation of the host's inflammatory response and bone resorption. Therefore, the genes that encode for IL-1 production have recently received most attention as potential predictors of periodontal disease progression. Hence, the relationship between IL-1 genotype and periodontal disease has been investigated by a number of studies. This review article aimed to determine whether IL-1 could be regarded as a genetic marker for periodontitis by reviewing data concerning susceptibility, clinical parameters, and treatment strategies in relation to the IL-1 genotype. The review concluded that there is currently limited evidence to implicate a specific IL-1 genotype as a risk factor for chronic periodontitis in white populations. However, there is limited evidence that genetic variation in the IL-1B polymorphism could be a risk factor for aggressive periodontitis.
... It should be noted that periodontal medicine has substantially progressed in the last decades [19]. Clinical variability in periodontitis could be explained by genetic factors [20]. Thus, Ahmed Khan et al. [21] revealed the genetic association of the C-C motif chemokine ligand 2 rs1024611 polymorphism with periodontitis. ...
Periodontitis is a complex polymicrobial disease of the oral cavity that affects tooth-supporting tissues. It is caused by multiple factors, such as pathogenic bacteria, genetic predisposition, and host immune response factors. The pathogenesis of periodontal disease involves the complex interrelations among bacterial toxins, several populations of cells, and host cell-secreted inflammatory mediators. Generally, periodontitis is characterized by the formation of intricate and varied biofilms of microbes on the tooth surface, commonly known as dental plaque. Activation of defense cells is characterized by releasing inflammatory mediators, such as proteases, acidic metabolites, cytokines, interleukins, and chemokines, which destroy tissue and ultimately cause bone resorption. The individual periodontal condition has a significant impact on systemic homeostasis, and its disruption can cause the development of some metabolic disorders. This review article summarizes the latest studies on the pathogenesis of periodontitis and describes the role of inflammatory mediators and genetic polymorphism in individuals, as well as relationships with some metabolic conditions. The information is collected from PubMed, Scopus, ScienceDirect, SpringerLink, and clinicaltrials.gov.
A BSTRACT
Background
Periodontitis is a slow progressing infection and has profound systemic implications. The influence of various therapeutic drugs to inhibit inflammation and promote bone regeneration has been studied. Introduction of newer congeners of older drugs necessitates testing the efficacy of newer drugs for the said use.
Aim
The aim was to determine the effectiveness of newer nitroimidazoles and fluoroquinolones for controlling and eliminating periodontal pathology by binding to the targets.
Methods and Material
A total of 12 drugs were selected, and the chemical structure drugs used were retrieved form PubChem and development of 2d and 3d structures was done using chem draw software. Targets used were Gingipain K, FimA, Interleukin-1β, and Estrogen Receptor β. AutoDock version 4 software was used for in silico docking simulations. The binding free energy, inhibition constant, electrostatic energy, intermolecular energy, and total interaction surface are all provided by the docking tool. In this paper, the optimal docking pose for each target is chosen and presented.
Results
From the results of the study, it can be observed that gatifloxacin and ciprofloxacin have more affinity and interactions with all four targets were analyzed.
Conclusions
This study has effectively tested nitroimidazoles and fluoroquinolones comparatively and proposed that fluoroquinolones are more effective for blocking periodontitis.
Objectives
Plaque control by improved domestic oral hygiene is essential in periodontal treatment. However, changing treatment providers may interfere with building a dentist-patient relationship and in turn affect treatment success. The aim of this randomized, controlled, prospective short-term study was to determine the influence of either one or four different pre-graduate practitioners on patients’ oral hygiene parameters during active periodontal therapy.
Material and Methods
A total of 55 patients with periodontitis were allocated to two groups. Within the group “continuous treatment” (CT, n = 27), each patient was treated by one individual practitioner over the treatment period. For patients of the group “discontinuous treatment” (DT, n = 28), treatment in each session was performed by a different practitioner. Periodontal parameters (BOP, PBI, and PCR) were assessed at two timepoints: T1 (baseline) and T2 (end of active therapy).
Results
With CT, the PBI improved in 93% of the patients, compared to 71% with DT (p = 0.048). T1-T2 intragroup analysis showed a statistically significant improvement of all observed clinical parameters with no differences in ∆PBI, ∆BOP, and ∆PCR. Spearman’s correlation analysis revealed a weak correlation between PCR and BOP of CT only.
Conclusions
In the present study, improvement of all parameters was comparable between the groups. PBI, as a parameter displaying patient’s domestic plaque control compliance, improved in more patients from CT than DT. This is possibly indicating an advantage of continuous treatment by one single practitioner.
Clinical relevance
Treatment by either a single practitioner or by multiple, constantly changing practitioners might influence patients’ compliance to modify their behaviour when medically necessary.
Aim:
To assess the efficacy of vitamin E oral spray in pregnancy.
Materials & methods:
This was a retrospective study aimed to evaluate efficacy of vitamin E oral spray (vitamin E acetate in a medium chain tryglicerides vehicle - patented formulation) starting from the first trimester of pregnancy, with a control group.
Results:
A total of 100 women were included in the study and were compared with a matched control group. Only 25/200 women reported to have at least one teeth cleaning during pregnancy. Women who received the oral spray had a significantly lower risk of preterm birth compared with the control group, and lower risk of periodontal diseases.
Conclusion:
Use of oil-based vitamin E oral spray in pregnancy is associated with a decreased risk of periodontal diseases and therefore preterm birth.
Objective:
The aim of this study was to compare IL-1β levels in gingival crevicular fluid (GCF) from healthy and periodontitis sites of IL-1B(3954)-Single Nucleotide Polymorphism (SNP) positive and IL-1B(3954)-SNP negative periodontitis subjects in association with their bacterial profiles.
Background:
Susceptibility to periodontitis has been associated with several risk factors, including allelic variants at multiple gene loci. Variations in the IL-1 gene cluster have been linked with increased risk for periodontitis. IL-1B(3954)-SNP has been previously associated with increased levels of IL-1β in GCF or periodontal tissues in chronic periodontitis patients, as well as higher levels of specific periodontal pathogens. There is insufficient evidence to conclude if IL-1B gene polymorphisms affect the susceptibility to periodontitis by ultimately modulating the levels of IL-1β in GCF, the subgingival microbial profile or both.
Materials and methods:
GCF, subgingival plaque, and buccal epithelial cells were collected from 32 individuals with periodontitis. GCF IL-1β levels were measured by an enzyme-linked immunosorbent assay (ELISA). Bacterial plaque samples were analyzed for 11 periodontal pathogens using polymerase chain reaction (PCR) analysis with specific primers for the 16SrRNA gene of each bacterium. IL-1B(3954)-SNP status was determined by identifying the carriers of the polymorphic T allele.
Results:
A significant association was shown between IL-1B(3954)-SNP and IL-1β GCF levels (amount and concentration). The concomitant presence of two or three red complex bacterial species was associated with increased IL-1β GCF levels in periodontitis sites (site-level analysis). The concurrent presence of all three red complex periodontal pathogens and IL-1B(3954)-SNP was associated with the highest IL-1β GCF levels in periodontitis sites.
Conclusions:
Our results indicate an independent association of both IL-1B(3954)-SNP and red complex bacterial species with increased IL-1β levels in GCF of periodontitis sites. A better understanding of the interaction between genetics, bacteria, and inflammation is essential to develop more effective diagnostic, prognostic, and therapeutic tools for periodontitis.
Platelet-rich fibrin (PRF) provides a scaffold for cell migration and growth factors for promoting wound healing and tissue regeneration. Here, we report using PRF in periodontal healing after open flap debridement (OFD) in canine periodontitis. A split-mouth design was performed in twenty dogs. Forty periodontitis surgical sites were randomly categorized into 2 groups; OFD alone and OFD with PRF treatment. Clinical parameters of periodontal pocket depth, gingival index, and the cemento-enamel junction-alveolar bone levels/root length ratio were improved in the OFD + PRF group. The OFD + PRF group also demonstrated a dramatically decreased inflammatory score compared with the OFD group. Collagen accumulation was improved in the OFD + PRF group at later time points compared with baseline. PRF application also significantly reduced inflammatory cytokine expression (TNFA and IL1B), and promoted the expression of collagen production-related genes (COL1A1, COL3A1, and TIMP1) and growth factors (PDGFB, TGFB1, and VEGFA). These findings suggest that PRF combined with OFD provides a new strategy to enhance the overall improvement of canine periodontitis treatment outcomes, especially in terms of inflammation and soft tissue healing. Therefore, PRF use in treating periodontitis could play an important role as a regenerative material to improve canine periodontitis treatment.
Background:
Periodontitis is a chronic inflammation of periodontal supporting tissue caused by local factors. Periodontal surgery can change the gene expression of peripheral blood mononuclear cells. However, little is known about the potential mechanism of surgical treatment for periodontitis.
Aim:
To explore the potential molecular mechanism of surgical treatment for periodontitis.
Methods:
First, based on the expression profiles of genes related to surgical treatment for periodontitis, a set of expression disorder modules related to surgical treatment for periodontitis were obtained by enrichment analysis. Subsequently, based on crosstalk analysis, we proved that there was a significant crosstalk relationship between module 3 and module 5. Finally, based on predictive analysis of multidimensional regulators, we identified a series of regulatory factors, such as endogenous genes, non-coding RNAs (ncRNAs), and transcription factors, which have potential regulatory effects on periodontitis.
Results:
A total of 337 genes related to surgical treatment for periodontitis were obtained, and 3896 genes related to periodontitis were amplified. Eight expression modules of periodontitis were obtained, involving the aggregation of 2672 gene modules. These modules are mainly involved in G-protein coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger, and adenylate cyclase-modulating G-protein coupled receptor signaling pathway. In addition, eight endogenous genes (including EGF, RPS27A, and GNB3) were screened by network connectivity analysis. Finally, based on this set of potential dysfunction modules, 94 transcription factors (including NFKB1, SP1, and STAT3) and 1198 ncRNAs (including MALAT1, CRNDE, and ANCR) were revealed. These core regulators are thought to be involved in the potential molecular mechanism of periodontitis after surgical treatment.
Conclusion:
Based on the results of this study, we can show biologists and pharmacists a new idea to reveal the potential molecular mechanism of surgical treatment for periodontitis, and provide valuable reference for follow-up treatment programs.
Aim:
The aim of this systematic review was to evaluate the number of articles in the area of personalized medicine specific to dentistry.
Materials and methods:
Electronic search using three databases was performed using PubMed, Embase, and Scopus search.
Results:
Results suggest that there is a definite need for more awareness and research pertaining to this specific area.
Conclusion:
With this background, the authors have written a comprehensive review on applications of personalized medicine in various branches of dentistry.
Observational studies demonstrate that women with severe periodontitis have a higher risk of adverse pregnancy outcomes like preterm birth and low birthweight. Standard treatment for periodontitis in the form of scaling and root planing during the second trimester failed to reduce the risk of preterm or low birthweight. It is premature to dismiss the association between periodontitis and adverse pregnancy outcomes because one explanation for the failure of scaling and root planing to reduce the risk of adverse pregnancy outcomes is that periodontal pathogens spread to the placental tissue prior to periodontal treatment. In the placenta, orally derived organisms could cause direct tissue damage or mediate a maternal immune response that impairs the growth of the developing fetus. Sequencing studies demonstrate the presence of organisms derived from the oral microbiome in the placenta, but DNA-based sequencing studies should not be the only technique to evaluate the placental microbiome because they may not detect important shifts in the metabolic capability of the microbiome. In humans, polymerase chain reaction and histology have detected periodontal pathogens in placental tissue in association with multiple adverse pregnancy outcomes. We conclude that both placental and oral microbiomes may play a role in periodontitis-associated adverse pregnancy outcomes. However, the measure to determine the association between periodontal pathogens in the placenta and adverse pregnancy outcomes should be the amount and prevalence, not the mere presence of such microorganisms. Placental colonization with periodontal pathogens thus potentially represents the missing link between periodontitis and adverse pregnancy outcomes.
Interleukin-1β (IL-1β) is a prominent pro-inflammatory cytokine that is implicated in a variety of autoimmune diseases and plays an important role in host defense against infections. IL-1β activity increases with its increasing binding capacity to IL-1 receptors (IL-1Rs). Thus, numerous studies have targeted the discovery of molecules modulating the interactions between IL-1β and IL-1R1. We have conducted an IL-1R1 structure-based virtual screening to identify small molecules that could alter IL-1β activity, using in silico computational analysis. Sixty compounds from commercial libraries were predicted to bind to IL-1R1, and their influence on cytokine production in IL-1β-stimulated gingival fibroblasts (GFs) was determined. Of these, only (2-(1,2-diphenyl-1H-indol-3-yl)ethanamine (DPIE) showed a synergistic increase in inflammatory molecules and cytokine production (IL-6, IL-8, and COX-2) at both mRNA and protein levels in IL-1β-stimulated GFs. The enhancing activity of DPIE in IL-1β-induced cytokine production increased in a dose-dependent manner without cytotoxicity. This pattern was also observed in IL-1β-stimulated primary human periodontal ligament cells (PDLs). Furthermore, we measured the impact of DPIE on the IL-1β–IL-1R1 system using surface plasmon resonance and demonstrated that DPIE increased the binding affinity of IL-1β to IL-1R1. These data indicate that DPIE boosts IL-1β signaling by enhancing the binding of IL-1β to IL-1R1 in oral primary cells.
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