Abstract

Several studies have addressed cytokine gene polymorphisms and their possible associations with periodontitis. We examined the association between salivary anti‐ and pro‐inflammatory mediator polymorphisms and initial periodontitis in Finnish adolescents, taking into account the effect of smoking. Salivary samples of 93 clinically examined adolescents from Eastern Finland were analyzed. Their oral health and smoking habits were recorded. Periodontal probing depth (PPD), and bleeding on probing (BOP) at four sites per tooth, root calculus (RC), and visible plaque index (VPI) were recorded from the index teeth. Salivary MMP‐8 median values were assessed. The sites with ≥4 mm PD were categorized as follows: PPD1 = one or more ≥4 mm pocket, PPD2 = two or more ≥4 mm pockets, and PPD3 = three or more ≥4 mm pockets. Genomic DNA was extracted from 300 μl of the saliva samples by genomic QIAamp® DNA Blood Mini Kit and genotyped for polymorphisms. Genetic variants for genotyping were selected from the following genes of interest: S100A8, FCGR2A, FCGR2B, IL10, MMP8, MMP3, MMP13, VDR, TLR4, MMP2, MPO, ELANE, IL1A, IL1B, IL1RN, CD28, MMP9, DDX39B, NFKBIL1, LTA, TNF, SOD2, IL6, TLR4, TIMP1, and SYN1. After false discovery rate control (FDR), polymorphisms in MMP3 (rs679620, rs520540, rs639752), CD28 (rs3116496), and VDR (rs2228570) associated (FDR q < 0.05) with deepened periodontal pockets. Smoking did not affect the results. Genetic polymorphisms of pro‐inflammatory mediators MMP3, CD28, and VDR seem to link to initial periodontitis.

Highlights

  • Periodontitis is a complex chronic low‐grade infection‐induced tissue destruction inflammatory disease involving environmental factors such as smoking

  • No statistical significant findings were observed between salivary matrix metalloproteinases (MMPs)‐8 median values and SPNs, which were analyzed in this study (Table 1)

  • The main finding of this study was that three MMP3 SNPs were associated as exposure agents with three or more at least 4‐mm deep periodontal pockets by the strict statistical analysis (FDR)

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Summary

Introduction

Periodontitis is a complex chronic low‐grade infection‐induced tissue destruction inflammatory disease involving environmental factors such as smoking. Other salivary inflammatory biomarker candidate genes for periodontitis are considered, such as myeloperoxidase (MPO‐463G/A) (Erciyas, Pehlivan, Sever, & Orbak, 2010) and calcium‐binding protein A8 (S100A8) (Sun et al, 2011), Vitamin D (1,25‐Dihydroxyvitamin D3) receptor (VDR) (Chen, Li, Zhang, & Wang, 2012; Laine et al, 2012), toll‐like receptor 2, 4 (Folwaczny, Glas, Török, Limbersky, & Folwaczny, 2004; Schröder & Schumann, 2005), and lymphotoxin alpha (LTA) (Vasconcelos et al, 2012) Studies on these cytokine and inflammatory mediator polymorphisms are rare, and the results are contradictory. Taking into account attachment loss and bleeding on probing, 10% of the subjects had initial periodontitis, and most of them were smokers (Heikkinen, 2011; Heikkinen et al, 2008). Heikkinen et al (2010, 2011, 2012 observed that smokers (25% of all participants) frequently harbored more periodontal bacteria than non‐smokers (66%), and smoking significantly decreased the values of the salivary biomarkers MMP‐8 and polymorphonuclear leukocytes (PMN) elastase in boys (Heikkinen et al, 2010; Heikkinen, 2011; Heikkinen et al, 2012)

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