The Role of Polymorphisms at the Interleukin-1, Interleukin-4, GATA-3 and Cyclooxygenase-2 Genes in Non-Surgical Periodontal Therapy

Int J Mol Sci. 2022 Jun 30;23(13):7266. doi: 10.3390/ijms23137266.

Abstract

Periodontitis is a multifactorial disease. The aim of this explorative study was to investigate the role of Interleukin-(IL)-1, IL-4, GATA-3 and Cyclooxygenase-(COX)-2 polymorphisms after non-surgical periodontal therapy with adjunctive systemic antibiotics (amoxicillin/metronidazole) and subsequent maintenance in a Caucasian population. Analyses were performed using blood samples from periodontitis patients of a multi-center trial (ClinicalTrials.gov NCT00707369=ABPARO-study). Polymorphisms were analyzed using quantitative real-time PCR. Clinical attachment levels (CAL), percentage of sites showing further attachment loss (PSAL) ≥1.3 mm, bleeding on probing (BOP) and plaque score were assessed. Exploratory statistical analysis was performed. A total of 209 samples were genotyped. Patients carrying heterozygous genotypes and single-nucleotide-polymorphisms (SNP) on the GATA-3-IVS4 +1468 gene locus showed less CAL loss than patients carrying wild type. Heterozygous genotypes and SNPs on the IL-1A-889, IL-1B +3954, IL-4-34, IL-4-590, GATA-3-IVS4 +1468 and COX-2-1195 gene loci did not influence CAL. In multivariate analysis, CAL was lower in patients carrying GATA-3 heterozygous genotypes and SNPs than those carrying wild-types. For the first time, effects of different genotypes were analyzed in periodontitis progression after periodontal therapy and during supportive treatment using systemic antibiotics demonstrating a slight association of GATA-3 gene locus with CAL. This result suggests that GATA-3 genotypes are a contributory but non-essential risk factor for periodontal disease progression.

Keywords: Cyclooxygenase-2; GATA-3; Interleukin-1; Interleukin-4; antibiotics; periodontal therapy; periodontitis; polymorphisms; risk factor.

Publication types

  • Multicenter Study

MeSH terms

  • Anti-Bacterial Agents
  • Cyclooxygenase 2* / genetics
  • GATA3 Transcription Factor* / genetics
  • Humans
  • Interleukin-1* / genetics
  • Interleukin-4* / genetics
  • Periodontitis* / genetics
  • Polymorphism, Single Nucleotide

Substances

  • Anti-Bacterial Agents
  • GATA3 Transcription Factor
  • IL4 protein, human
  • Interleukin-1
  • Interleukin-4
  • Cyclooxygenase 2
  • PTGS2 protein, human

Associated data

  • ClinicalTrials.gov/NCT00707369