Nurgün Bıçakcı

Smoking and matrix metalloproteinases, neutrophil elastase and myeloperoxidase in chronic periodontitis.

OBJECTIVES To investigate possible relationship between smoking and serum concentrations of matrix metalloproteinase-8,-9 (MMP-8, MMP-9), tissue inhibitor of matrix metalloproteinases-1 (TIMP-1), neutrophil elastase (NE), myeloperoxidase (MPO) in chronic periodontitis (CP) patients relative to periodontally healthy subjects. METHODS Serum samples were obtained from 111 subjects before initiation of any periodontal intervention. Fifty-five CP patients (39 non-smokers, 16 smokers) and 56 periodontally healthy subjects (39 non-smokers, 17 smokers) were recruited. Serum concentrations of MMP-8 were determined by IFMA and MPO, MMP-9, TIMP-1, NE concentrations by ELISA. ANCOVA and Pearson correlation analysis was utilized for statistical analysis. RESULTS Serum MPO, NE concentrations were higher in smoker CP than non-smoker CP patients (P=0.002 and P<0.001, respectively), whereas these were similar in smoker, non-smoker periodontally healthy groups (P > 0.05). TIMP-1 concentration was higher in non-smoker CP than smoker CP group (P<0.05). MMP-9/TIMP-1 ratios were higher in smoker CP than non-smoker CP group (P=0.01). MMP-8 concentrations, MMP-8/TIMP-1 and MMP-9/TIMP-1 ratios in CP group were not significantly different from those in periodontally healthy group (P>0.05). CONCLUSIONS Our findings of significantly elevated serum MMP-9, MPO, NE together with decreased TIMP-1 in smoker CP patients than non-smokers support that smoking together with periodontal destruction may expose/predispose to cardiovascular diseases.

Is There an Interaction Between Polycystic Ovary Syndrome and Gingival Inflammation

BACKGROUND The aim of this study is to evaluate the gingival crevicular fluid (GCF), saliva, and serum concentrations of tumor necrosis factor-α (TNF-α), TNF-α receptor-1 (TNF-αR1), TNF-αR2, and interleukin-6 (IL-6) in non-obese females with polycystic ovary syndrome (PCOS) and either clinically healthy periodontium or gingivitis. METHODS Thirty-one females with PCOS and healthy periodontium, 30 females with PCOS and gingivitis, and 12 systemically and periodontally healthy females were included in the study. GCF, saliva, and serum samples were collected, and clinical periodontal measurements, body mass index, and Ferriman-Gallwey score (FGS) were recorded. Sex hormones, cortisol, and insulin levels were measured. TNF-α, TNF-αR1, TNF-αR2, and IL-6 were determined by enzyme-linked immunosorbent assay. Kruskal-Wallis followed by Bonferroni-corrected post hoc Mann-Whitney U tests were used to analyze the data. RESULTS The PCOS + gingivitis group revealed significantly higher GCF, saliva, and serum IL-6 concentrations than the PCOS + healthy group (P <0.0001). The two PCOS groups exhibited significantly higher saliva TNF-α concentrations than the control group (P = 0.024 and P = 0.013, respectively). The FGS index was significantly higher in the PCOS + gingivitis group than the PCOS + healthy group (P = 0.030). The PCOS + gingivitis group revealed significantly higher insulin concentration than the PCOS + healthy and control groups (P = 0.014 and P <0.0001, respectively). Serum TNF-α, TNF-αRs, and serum, GCF, and salivary IL-6 levels correlated with the clinical periodontal measurements. CONCLUSIONS PCOS and gingival inflammation appear to act synergistically on the proinflammatory cytokines IL-6 and TNF-α. Thus, PCOS may have an impact on gingival inflammation or vice versa. Additional studies are warranted to clarify the possible relationship between PCOS and periodontal disease.

Association between mannose-binding lectin levels and gene polymorphisms in chronic periodontitis and response to treatment

BACKGROUND The aims of the present study were: (1) to investigate mannose-binding lectin (MBL) gene exon-1 polymorphisms in Turkish subjects with chronic periodontitis (CP), (2) to assess the association between these polymorphisms and plasma MBL levels, (3) to determine the effects of MBL genotypes on the outcomes of non-surgical periodontal therapy. METHODS A total of 172 subjects were included in the present study. Genomic DNA was obtained from the peripheral blood of 83 CP patients and 89 periodontally healthy subjects. The MBL levels were measured by enzyme-linked immunosorbent assay (ELISA). The MBL gene exon-1 polymorphisms were genotyped by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. RESULTS Subjects homozygous for the frequent allele A had higher MBL plasma levels compared with rare allele B carriers. This difference in MBL plasma levels was statistically significant both in CP patients and healthy subjects. The distribution of MBL gene codon 54 genotypes and allele frequencies did not differ significantly between study groups. All study subjects were the MBL gene codon 52 and 57 frequent allele A carriers. Codon 54 B allele carriers had similar clinical periodontal parameters compared with AA genotypes after non-surgical periodontal therapy. CONCLUSIONS The present study failed to find any significant association between the MBL gene codon 54 polymorphisms and severe CP in a Turkish population. MBL gene rare allele carriers had lower MBL plasma levels in both study groups. It seems that MBL gene codon 54 B allele carriage may not influence the outcome of periodontal therapy.

Plasma Levels of C-Telopeptide Pyridinoline Cross-Links of Type I Collagen and Osteocalcin in Chronic Periodontitis

This study was planned to investigate whether chronic periodontitis patients exhibit different plasma concentrations of C-telopeptide pyridinoline cross-links of type I collagen (ICTP) and osteocalcin (OC) compared to the clinically healthy controls. Before initiation of any periodontal intervention, plasma samples and full-mouth clinical periodontal recordings were obtained from 58 otherwise healthy patients with chronic periodontitis and also from 47 systemically and periodontally healthy control subjects. Plasma ICTP levels were determined by radioimmunoassay and OC levels by enzyme-linked immunosorbent assay. Data were tested statistically using t test and ANOVA. The healthy control group exhibited significantly lower values in all clinical periodontal measurements (P < 0.001). There were no significant differences between the study groups in plasma ICTP and OC levels (P > 0.05). Within the limits of this study, it may be suggested that plasma levels of ICTP and OC may not provide distinguishing data between chronic periodontitis patients and clinically healthy subjects.