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Genetic Control of GCF Exudation: Innate Immunity Genes and Periodontitis Susceptibility

Chronic periodontitis is a bacterial infection associated with dentally adherent biofilm (plaque) accumulation and age-related comorbidities. The disease begins as an inflammatory exudate from gingival margins, gingival crevicular fluid (GCF) in response to biofilm lysine. After a week of experiment...

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Autores principales: Lohinai, Zsolt M., Ruksakiet, Kasidid, Földes, Anna, Dinya, Elek, Levine, Martin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10532312/
https://www.ncbi.nlm.nih.gov/pubmed/37762554
http://dx.doi.org/10.3390/ijms241814249
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author Lohinai, Zsolt M.
Ruksakiet, Kasidid
Földes, Anna
Dinya, Elek
Levine, Martin
author_facet Lohinai, Zsolt M.
Ruksakiet, Kasidid
Földes, Anna
Dinya, Elek
Levine, Martin
author_sort Lohinai, Zsolt M.
collection PubMed
description Chronic periodontitis is a bacterial infection associated with dentally adherent biofilm (plaque) accumulation and age-related comorbidities. The disease begins as an inflammatory exudate from gingival margins, gingival crevicular fluid (GCF) in response to biofilm lysine. After a week of experimental gingivitis (no oral hygiene), biofilm lysine concentration was linearly related to biofilm accumulation (plaque index) but to GCF as an arch-shaped double curve which separated 9 strong from 6 weak GCF responders (hosts). Host DNA was examined for single nucleotide polymorphisms (SNPs) of alleles reported in 7 periodontitis-associated genes. Across all 15 hosts, an adenine SNP (A) at IL1B-511 (rs16944), was significant for strong GCF (Fisher’s exact test, p < 0.05), and a thymidine SNP (T) at IL1B+3954 (rs1143634) for weak GCF provided 2 hosts possessing IL6-1363(T), rs2069827, were included. The phenotype of IL1B+3954(T) was converted from weak to strong in one host, and of the non-T allele from strong to weak in the other (specific epistasis, Fisher’s exact test, p < 0.01). Together with homozygous alternate or reference SNPs at IL10-1082 or CD14-260 in 4 hosts, all hosts were identified as strong or weak GCF responders. The GCF response is therefore a strong or weak genetic trait that indicates strong or weak innate immunity in EG and controllable or uncontrollable periodontal disease, dental implant survival and late-life comorbidities.
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spelling pubmed-105323122023-09-28 Genetic Control of GCF Exudation: Innate Immunity Genes and Periodontitis Susceptibility Lohinai, Zsolt M. Ruksakiet, Kasidid Földes, Anna Dinya, Elek Levine, Martin Int J Mol Sci Article Chronic periodontitis is a bacterial infection associated with dentally adherent biofilm (plaque) accumulation and age-related comorbidities. The disease begins as an inflammatory exudate from gingival margins, gingival crevicular fluid (GCF) in response to biofilm lysine. After a week of experimental gingivitis (no oral hygiene), biofilm lysine concentration was linearly related to biofilm accumulation (plaque index) but to GCF as an arch-shaped double curve which separated 9 strong from 6 weak GCF responders (hosts). Host DNA was examined for single nucleotide polymorphisms (SNPs) of alleles reported in 7 periodontitis-associated genes. Across all 15 hosts, an adenine SNP (A) at IL1B-511 (rs16944), was significant for strong GCF (Fisher’s exact test, p < 0.05), and a thymidine SNP (T) at IL1B+3954 (rs1143634) for weak GCF provided 2 hosts possessing IL6-1363(T), rs2069827, were included. The phenotype of IL1B+3954(T) was converted from weak to strong in one host, and of the non-T allele from strong to weak in the other (specific epistasis, Fisher’s exact test, p < 0.01). Together with homozygous alternate or reference SNPs at IL10-1082 or CD14-260 in 4 hosts, all hosts were identified as strong or weak GCF responders. The GCF response is therefore a strong or weak genetic trait that indicates strong or weak innate immunity in EG and controllable or uncontrollable periodontal disease, dental implant survival and late-life comorbidities. MDPI 2023-09-18 /pmc/articles/PMC10532312/ /pubmed/37762554 http://dx.doi.org/10.3390/ijms241814249 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Lohinai, Zsolt M.
Ruksakiet, Kasidid
Földes, Anna
Dinya, Elek
Levine, Martin
Genetic Control of GCF Exudation: Innate Immunity Genes and Periodontitis Susceptibility
title Genetic Control of GCF Exudation: Innate Immunity Genes and Periodontitis Susceptibility
title_full Genetic Control of GCF Exudation: Innate Immunity Genes and Periodontitis Susceptibility
title_fullStr Genetic Control of GCF Exudation: Innate Immunity Genes and Periodontitis Susceptibility
title_full_unstemmed Genetic Control of GCF Exudation: Innate Immunity Genes and Periodontitis Susceptibility
title_short Genetic Control of GCF Exudation: Innate Immunity Genes and Periodontitis Susceptibility
title_sort genetic control of gcf exudation: innate immunity genes and periodontitis susceptibility
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10532312/
https://www.ncbi.nlm.nih.gov/pubmed/37762554
http://dx.doi.org/10.3390/ijms241814249
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