Does smoking affect gingival crevicular fluid LL-37 levels following non-surgical periodontal treatment in chronic periodontitis?

OBJECTIVE: LL-37 contributes to maintaining the balance between health and disease. Smoking is a risk factor for periodontitis that impairs neutrophil functions. The aim of the present study was to comparatively evaluate gingival crevicular fluid (GCF) LL-37 levels in smoker and non-smoker chronic periodontitis (CP) patients and controls, as well as the effect of non-surgical periodontal treatment on GCF LL-37 levels. DESIGN: Thirty-one CP patients (16 smokers, 15 non-smokers) and thirty-one controls (16 smokers, 15 non-smokers) were included in the study. CP patients received non-surgical treatment. GCF LL-37 levels and periodontal parameters were assessed at baseline, 1 and 3 months after completion of non-surgical periodontal treatment. GCF LL-37 levels were analyzed by ELISA. RESULTS: No significant difference was observed in GCF LL-37 levels between smoker and non-smoker controls (p>0.05). Smoker CP group had significantly lower GCF LL-37 level than non-smoker CP group at baseline (p<0.05). GCF LL-37 levels significantly decreased in non-smoker CP group at first week, 1 and 3 months after completion of non-surgical periodontal treatment (p<0.05) although no significant decrease in GCF LL-37 levels was observed in smoker CP group (p>0.05). Periodontal parameters were correlated with GCF LL-37 levels in non-smoker CP group (p<0.05), but not in smoker CP group (p>0.05). CONCLUSIONS: GCF LL-37 levels do not seem to be affected from smoking in periodontal health. However, smoking might have a suppressive effect on GCF LL-37 levels in CP. Non-surgical treatment is effective in decreasing GCF LL-37 levels in non-smoker CP patients but not in smokers with CP.

Gene expression of transcription factor NFATc1 in periodontal diseases.

Periodontitis is a disease of infectious aetiology that causes inflammatory destruction of the tooth-supporting tissues. Activated T cells are central to the pathogenesis of the disease, by producing receptor activator of nuclear factor κB (NF-κB) ligand (RANKL) that stimulates bone resorption. Antigenic activation of T cells is regulated by the induction of transcription factor nuclear factor of activated T cells, cytoplasmic 1 (NFATc1). There is as yet no information on the potential involvement of NFATc1 in periodontal diseases. This study aimed to investigate NFATc1 gene expression levels in periodontal diseases, and analyse the potential correlation with RANKL expression and clinical periodontal parameters. In this cross-sectional study, gingival tissue biopsies were obtained from healthy (n = 10) and periodontally diseased (n = 58) sites. NFATc1 and RANKL gene expression levels in these samples were analysed by quantitative real-time polymerase chain reaction. Compared with healthy subjects, patients with gingivitis, chronic and aggressive periodontitis, exhibited higher NFATc1 expression, which proved to be statistically significant in the periodontitis groups. NFATc1 and RANKL expression levels strongly correlated with each other, and with clinical periodontal parameters. The increased expression of NFATc1 in periodontitis denotes a role for this transcription factor in the pathogenesis of the disease.

Periodontal infections and pre-term low birth weight: a case-control study.

OBJECTIVE: Pre-term delivery of low-birth-weight infants [pre-term low birth weight (PLBW)] remains a significant public health issue and a major cause of neonatal death and long-term health problems. There is a growing consensus that infections remote from fetal-placental unit may influence PLBW infants. Recent studies have suggested that maternal periodontal disease may be an independent risk factor for PLBW. The purpose of the present study was to evaluate the possible link between periodontal infections and PLBW by means of clinical and microbiological data in post-partum women with low socioeconomic level. METHODS: Clinical periodontal recordings comprising dental plaque, bleeding on probing, probing pocket depth and gingival recession were performed (six sites/tooth) in a total number of 181 women (53 cases and 128 controls) within 3 days post-partum. Subgingival plaque samples from mesio-or disto-buccal aspect of randomly selected one first molar and one incisor tooth have been obtained by paperpoints and were analysed by checkerboard DNA-DNA hybridization with respect to 12 bacterial species. In all analyses, the individual subject was the computational unit. Thus, mean values for all clinical parameters were calculated and bacterial scores from each individual sample were averaged. Statistical methods included Student's t-test, Fisher's exact test/chi(2) test, and multiple logistic regression analysis. RESULTS: The cases have gained significantly less weight during the pregnancy than did the controls (p<0.05). There were no statistically significant differences between the cases and controls with regard to the dental and periodontal parameters and the values of clinical periodontal recordings were found to be very similar (p>0.05). Mean and median scores (bacterial loads) of Porphyromonas gingivalis, Prevotella intermedia, Prevotella nigrescens, Actinobacillus actinomycetemcomitans, and Streptococcus intermedius in the subgingival plaque sampling sites were significantly higher in the controls than in the cases (p<0.05). The occurrence rates of P. intermedia, Fusobacterium nucleatum, Peptostreptococcus micros, Campylobacter rectus, Eikenella corrodens, Selenomonas noxia and S. intermedius were higher in the cases compared with the controls, but the differences were not statistically significant (p>0.05). According to the model created by the multiple logistic regression analysis, P. micros and C. rectus were found to significantly increase the risk of PLBW (p<0.01 and p<0.05 respectively), while P. nigrescens and A. actinomycetemcomitans decreased this risk (p<0.01). CONCLUSION: The present findings indicated that when subgingival bacteria were evaluated together, P. micros and C. rectus may have a role in increasing the risk for PLBW, although no single bacteria exhibited any relation with the risk of PLBW. Further studies are required to better clarify the possible relationship between periodontal diseases and PLBW.

Evaluation of the relationship between smoking during pregnancy and subgingival microbiota.

BACKGROUND: Numerous studies have shown that smoking negatively affects periodontal health. Hormonal changes, which occur during pregnancy have also been reported to have adverse effects on the periodontal tissues or indirectly through alterations in the subgingival bacterial flora. At present, no knowledge exists concerning possible effects of smoking on the composition of subgingival plaque in pregnancy. The purpose of the present study was to evaluate the effects of smoking during pregnancy on the subgingival plaque bacteria most commonly associated with periodontal disease. METHODS: A total number of 181 women were examined within 72 h post-partum. Smoking status was recorded by means of a self-reported questionnaire and the study population was divided into three groups; non-smokers, light smokers, and heavy smokers. In each woman, two subgingival plaque samples were obtained from mesio- or disto-buccal aspect of randomly selected one molar and one incisor tooth by sterile paperpoints. Clinical periodontal recordings comprising presence of dental plaque, bleeding on probing (BOP), and probing pocket depth (PPD) were performed at six sites per each tooth at all teeth. Plaque samples were analysed by checkerboard DNA-DNA hybridization with respect to 12 bacterial species. In all analyses, the individual subject was the computational unit. Thus, mean values for all clinical parameters were calculated and bacterial scores from each individual sample were averaged. Statistical methods included chi2 test, Kruskal-Wallis test and Mann-Whitney U-test. RESULTS: Mean ages were similar in the study groups. Plaque, BOP and PPD recordings were lower in the heavy-smoker group, but the differences were not statistically significant (p>0.05). The detection rates and bacterial loads of the specific subgingival bacteria exhibited no significant differences between the groups. No correlation could be found between smoking status and detection rates and bacterial loads of various bacterial species. CONCLUSION: The present findings suggest that smoking during pregnancy does not have a significant effect on the composition of subgingival plaque bacteria.

Therapeutic versus prophylactic plus therapeutic administration of omega-3 fatty acid on endotoxin-induced periodontitis in rats.

BACKGROUND: The aim of the present study was 1) to evaluate the possible effects of therapeutic usage of omega-3 fatty acid on the gingival tissue levels of prostaglandin E2 (PGE2), prostaglandin F2alpha (PGF2alpha), platelet activating factor (PAF), and leukotriene B4 (LTB4) in endotoxin-induced periodontitis in rats and 2) to investigate whether prophylactic usage provides any additional benefits to therapeutic doses of omega-3 fatty acid. METHODS: Experimental periodontitis was induced by repeated injection of Escherichia coli lipopolysaccharide (LPS). Thirty-six adult male Sprague-Dawley rats were divided into four study groups: 1) saline controls; 2) LPS; 3) therapeutic omega-3 fatty acid (TO3); and 4) prophylactic plus therapeutic omega-3 fatty acid (P + TO3) groups. In TO3 group, omega-3 fatty acid was given for 15 days following induction of experimental periodontitis. In P + TO3 group, omega-3 fatty acid was started 15 days before baseline, and then periodontitis was induced at baseline and omega-3 fatty acid was continued for 15 days after baseline. On day 15 after baseline, all rats were anesthetized and sacrificed. PGE2, PGF2alpha, and LTB4 levels in gingival tissue samples were analyzed by enzyme immunoassay and PAF levels were analyzed by radioimmonoassay. Data were evaluated statistically by using parametric tests. RESULTS: LPS injection resulted in significant amount of bone loss (P<0.05). Neither therapeutic nor prophylactic plus therapeutic administration of omega-3 fatty acid with the doses and duration of therapy used in the present study was effective in preventing endotoxin-induced alveolar bone loss. TO3 group exhibited significant decreases in the gingival tissue levels of PGE2, PGF2alpha, LTB4, and PAF compared to the LPS group (P<0.05). PGE2 and PGF2alpha levels in TO3 group were similar to those of the saline group (P>0.05), while LTB4 and PAF levels were statistically higher than the saline group (P<0.05). Prophylactic plus therapeutic usage of omega-3 fatty acid provided similar levels of all these mediators to those of the saline controls (P>0.05). CONCLUSIONS: Therapeutic omega-3 fatty acid significantly reduced the gingival tissue levels of PGE2, PGF2alpha, LTB4, and PAF in experimental periodontitis. Furthermore, prophylactic usage of omega-3 fatty acid provided additional beneficial effects to the therapeutic administration by decreasing the gingival tissue levels of these mediators to levels of healthy tissue. These findings should be verified by longitudinal clinical trials investigating clinical and biochemical periodontal parameters to better define the possible role of omega-3 fatty acids in periodontal treatment.