Associations between <scp><i>CD14</i></scp> −159 <scp>C</scp>&gt;<scp>T</scp> polymorphism and chronic/aggressive periodontitis susceptibility

Zhang, H; Zhou, Lian; Han, Yan; Cai, Qi; Li, D; Pan, Yongsheng; Wang, Lei

doi:10.1111/odi.12096

Cited by 10 publications

(9 citation statements)

References 31 publications

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“…CD14 was absent in the saliva of individuals with active caries lesions (Bergandi et al. ) and no associations were confirmed with the periodontitis trait (Zhang et al., , Zheng et al., , Han et al. ).…”

Section: Resultsmentioning

confidence: 99%

Host genetics role in the pathogenesis of periodontal disease and caries

Nibali

Iorio

et al. 2017

J Clinic Periodontology

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Background: This study aimed to produce the latest summary of the evidence for association of host genetic variants contributing to both periodontal diseases and caries. Materials and Methods: Two systematic searches of the literature were conducted in Ovid Medline, Embase, LILACS and Cochrane Library for large candidate gene studies (CGS), systematic reviews and genome-wide association studies reporting data on host genetic variants and presence of periodontal disease and caries. Results: A total of 124 studies were included in the review (59 for the periodontitis outcome and 65 for the caries outcome), from an initial search of 15,487 titles. Gene variants associated with periodontitis were categorized based on strength of evidence and then compared with gene variants associated with caries. Several gene variants showed moderate to strong evidence of association with periodontitis, although none of them had also been associated with the caries trait. Conclusions: Despite some potential aetiopathogenic similarities between periodontitis and caries, no genetic variants to date have clearly been associated with both diseases. Further studies or comparisons across studies with large sample size and clear phenotype definition could shed light into possible shared genetic risk factors for caries and periodontitis. Inflammatory periodontal diseases and caries are the most common bacteria-mediated diseases of mankind despite being highly preventable. Periodontal diseases are characterized by an inflammatory reaction against members of the oral microbiota (Curtis 2015) and, among them, Periodontitis (PD) leads to apical migration of the epithelial attachment and resorption of connective tissue and alveolar bone, often resulting in early tooth loss. Heritability has long been thought to play an important role in the predisposition to periodontitis (Baer 1971). Genetic factors are now thought to determine about half the variance of periodontitis risk in the population (Michalowicz et al. 1991). Common single-nucleotide polymorphisms (SNPs) able to affect gene activity or protein production, with an effect on structural factors of the periodontium or on the host response to microbial challenge, are among possible risk factors for periodontitis. LuigiHowever, despite research dating back nearly two decades (Kornman et al. 1997), no single gene variant has yet clearly emerged as definitely predisposing to periodontitis.Caries leads to continued localized mineral loss from the dental enamel and as it progresses, subclinical mineral losses become visible (white spot lesions) and eventually unsupported enamel collapses (cavities) (Vieira 2016). Caries is traditionally described as the interplay among a susceptible host, microbiota and diet (Keyes 1960 (Hunt et al. 1944). Depending on the surrogate measure of the disease employed, genetics explain 25-64% of the variance of the disease seen in the population (reviewed in Vieira et al. 2014).Since both periodontitis and caries are bacteria-mediated oral diseases and depen...

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Section: Resultsmentioning

confidence: 99%

Host genetics role in the pathogenesis of periodontal disease and caries

Nibali

Iorio

et al. 2017

J Clinic Periodontology

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“…7 Besides, a meta-analysis of genetic variations also found that a point mutation in CD14, an actor in innate immune response, is associated with some forms of periodontitis. 8 In this context, the modulation of different immune system actors, modulated by gene regulation mechanisms, clearly plays an important role in periodontitis progression and susceptibility to progression. 9 Epigenetic mechanisms, that is, DNA methylation, histone modification, and miRNA, orchestrate such gene regulation; additionally, DNA methylation in blood has been shown to allow for the detection of treatment response's predictors in several immune diseases.…”

Section: Introductionmentioning

confidence: 99%

ZNF718, HOXA4, and ZFP57 are differentially methylated in periodontitis in comparison with periodontal health: Epigenome‐wide DNA methylation pilot study

Hernández

Hernández-Castañeda

Pieschacón

et al. 2021

J of Periodontal Research

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Objective: To investigate the differences in the epigenomic patterns of DNA methylation in peripheral leukocytes between patients with periodontitis and gingivally healthy controls evaluating its functional meaning by functional enrichment analysis. Background:The DNA methylation profiling of peripheral leukocytes as immunerelated tissue potentially relevant as a source of biomarkers between periodontitis patients and gingivally healthy subjects has not been investigated.Methods: A DNA methylation epigenome-wide study of peripheral leukocytes was conducted using the Illumina MethylationEPIC platform in sixteen subjects, eight diagnosed with periodontitis patients and eight age-matched and sex-matched periodontally healthy controls. A trained periodontist performed the clinical evaluation.Global DNA methylation was estimated using methylation-sensitive high-resolution melting in LINE1. Routine cell count cytometry and metabolic laboratory tests were also performed. The analysis of differentially methylated positions (DMPs) and differentially methylated regions (DMRs) was made using R/Bioconductor environment considering leukocyte populations assessed in both routine cell counts and using the FlowSorted.Blood.EPIC package. Finally, a DMP and DMR intersection analysis was performed. Functional enrichment analysis was carried out with the differentially methylated genes found in DMP.Results: DMP analysis identified 81 differentially hypermethylated genes and 21 differentially hypomethylated genes. Importantly, the intersection analysis showed that zinc finger protein 718 (ZNF718) and homeobox A4 (HOXA4) were differentially hypermethylated and zinc finger protein 57 (ZFP57) was differentially hypomethylated in periodontitis. The functional enrichment analysis found clearly immune-related ontologies such as "detection of bacterium" and "antigen processing and presentation." Conclusion:The results of this study propose three new periodontitis-related genes: ZNF718, HOXA4, and ZFP57 but also evidence the suitability and relevance of studying leukocytes' DNA methylome for biological interpretation of systemic immunerelated epigenetic patterns in periodontitis. | 711 HERNÁNDEZ Et al.

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“…Several studies have analysed the association between different CD14 polymorphisms and chronic periodontitis (CP), but the results have been conflicting. The meta‐analysis performed by Zhang et al 14 showed an association between the CD14 ‐260C/T polymorphism and decreased risk of mild‐to‐moderate, but not severe, periodontitis. In contrast, Zheng et al found no relationship between this variant and periodontitis 15 .…”

Section: Introductionmentioning

confidence: 99%

Association of the CD14 ‐260C/T polymorphism with plaque‐induced gingivitis depends on the presence of Porphyromonas gingivalis

Bartošová

Linhartová

Musilová

et al. 2021

Int J Paed Dentistry

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Background Plaque‐induced gingivitis is the most prevalent periodontal disease associated with pathogenic biofilms. The host immune system responds to pathogens through pattern recognition receptors (PRRs), such as Toll‐like receptors (TLRs) and their co‐receptor cluster of differentiation 14 (CD14). Aim This study investigated the association between the functional polymorphism in the CD14 gene and the dental plaque microbiota in children with gingivitis. Design A total of 590 unrelated children (307 with plaque‐induced gingivitis and 283 controls, aged 13‐15 years) were enrolled in this case‐control study. Dental plaque was processed using a ParoCheck® 20 detection kit. The CD14 ‐260C/T (rs2569190) polymorphism was determined with the PCR‐RFLP method. Results Gingivitis was detected in 64.2% of boys and 35.8% of girls (P < .001). Children with gingivitis had a significantly higher occurrence of dental caries (P < .001). No significant differences in the CD14 ‐260C/T allele and genotype distribution among individuals with or without gingivitis in the whole cohort were found. Children with gingivitis and P gingivalis, however, were significantly more frequent carriers of the CT and TT genotypes than children with gingivitis without P gingivalis or healthy controls (P < .05). Conclusions The CD14 ‐260C/T polymorphism acts in cooperation with P gingivalis to trigger plaque‐induced gingivitis in Czech children.

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Associations between CD14 −159 C>T polymorphism and chronic/aggressive periodontitis susceptibility

Abstract: The present meta-analysis provided confirmative evidence that CD14 -159 C>T was involved in the development of periodontitis.

Cited by 10 publications

References 31 publications

Host genetics role in the pathogenesis of periodontal disease and caries

Host genetics role in the pathogenesis of periodontal disease and caries

ZNF718, HOXA4, and ZFP57 are differentially methylated in periodontitis in comparison with periodontal health: Epigenome‐wide DNA methylation pilot study

Association of the CD14 ‐260C/T polymorphism with plaque‐induced gingivitis depends on the presence of Porphyromonas gingivalis

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