Chlorhexidine decreases the risk of ventilator-associated pneumonia in intensive care unit patients: a randomized clinical trial.

BACKGROUND AND OBJECTIVE: The aim was to evaluate whether oral swabbing with 0.2% chlorhexidine gluconate (CHX) decreases the risk of ventilator-associated pneumonia (VAP) in intensive care unit (ICU) patients. MATERIAL AND METHODS: Sixty-one dentate patients scheduled for invasive mechanical ventilation for at least 48 h were included in this randomized, double-blind, controlled study. As these patients were variably incapacitated, oral care was provided by swabbing the oral mucosa four times/d with CHX in the CHX group (29 patients) and with saline in the control group (32 patients). Clinical periodontal measurements were recorded, and lower-respiratory-tract specimens were obtained for microbiological analysis on admission and when VAP was suspected. Pathogens were identified by quantifying colonies using standard culture techniques. RESULTS: Ventilator-associated pneumonia developed in 34/61 patients (55.7%) within 6.8 d. The VAP development rate was significantly higher in the control group than in the CHX group (68.8% vs. 41.4%, respectively; p = 0.03) with an odds ratio of 3.12 (95% confidence interval = 1.09-8.91). Acinetobacter baumannii was the most common pathogen (64.7%) of all species identified. There were no significant differences between the two groups in clinical periodontal measurements, VAP development time, pathogens detected or mortality rate. CONCLUSION: The finding of the present study, that oral care with CHX swabbing reduces the risk of VAP development in mechanically ventilated patients, strongly supports its use in ICUs and indeed the importance of adequate oral hygiene in preventing medical complications.

Interleukin-17 and interleukin-18 levels in saliva and plasma of patients with chronic periodontitis.

BACKGROUND AND OBJECTIVE: This study was planned to investigate whether patients with chronic periodontitis exhibit different salivary and/or plasma concentrations of interleukin (IL)-17 and IL-18 compared with clinically healthy subjects. MATERIAL AND METHODS: Whole saliva and blood samples, together with full-mouth clinical periodontal recordings, were obtained from 22 otherwise healthy untreated nonsmokers with chronic periodontitis and from 21 systemically and periodontally healthy control subjects. The concentrations of IL-17 and IL-18 in saliva and plasma were determined using ELISAs. RESULTS: The healthy control group exhibited significantly lower values in all clinical periodontal measurements (p < 0.001). The salivary concentration of IL-17 was significantly lower, and that of IL-18 significantly higher, in patients from the chronic periodontitis group compared with healthy control subjects (p = 0.025 and p = 0.009, respectively). Plasma IL-17 and IL-18 concentrations were similar in the two study groups (p > 0.05). CONCLUSION: Within the limits of the present study, it may be suggested that an elevated salivary IL-18 level in untreated nonsmoker chronic periodontitis patients has the potential to be a biomarker for periodontal tissue destruction.

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.

Salivary osteocalcin levels are decreased in smoker chronic periodontitis patients.

OBJECTIVES: This study was planned to investigate whether smoker chronic periodontitis patients exhibit different salivary concentrations of C-telopeptide pyridinoline cross-links of type I collagen (ICTP) and osteocalcin (OC) compared to the non-smoker counterparts. METHODS: Whole saliva samples, full-mouth clinical periodontal recordings were obtained from 33 otherwise healthy chronic periodontitis patients and 36 systemically, periodontally healthy control subjects. Chronic periodontitis patients and healthy control subjects were divided into smoker and non-smoker groups according to their self reports. Salivary ICTP, OC levels were determined by Enzyme-linked Immunoassays. RESULTS: Healthy control groups exhibited significantly lower values in all clinical periodontal measurements (P < 0.001). Smoker periodontitis patients revealed similar clinical periodontal index values with non-smoker counterparts (P > 0.05). Chronic periodontitis patients exhibited significantly higher salivary OC levels than healthy controls (P < 0.05). Smoker periodontitis patients revealed lower salivary OC levels than non-smoker counterparts (P < 0.001). Log ICTP levels in non-smoker chronic periodontitis patients were higher than non-smoker controls (P < 0.05). Smoker healthy control group revealed higher log ICTP levels than non-smoker counterparts (P < 0.001). CONCLUSIONS: Within the limits of this study, it may be suggested that suppression of salivary osteocalcin level by smoking may at least partly explain the deleterious effects of smoking on periodontal status.

Plasma osteoprotegerin levels are decreased in smoker chronic periodontitis patients.

BACKGROUND: The aim of this study was to evaluate plasma levels of soluble receptor activator of nuclear factor-kappa B ligand (sRANKL) and osteoprotegerin (OPG) in smoker versus non-smoker chronic periodontitis patients. METHODS: Plasma samples were obtained from 13 smoker and 31 non-smoker systemically healthy chronic periodontitis patients, as well as 13 smoker and 29 non-smoker systemically and periodontally healthy subjects. Before commencing any periodontal intervention, venous blood samples were obtained and whole-mouth clinical periodontal measurements were recorded. sRANKL and OPG concentrations in plasma samples were determined by enzyme-linked immunosorbent assay (ELISA) technique. Data were tested statistically by student's t test, Wilcoxon matched pairs test, and Spearman's correlation analysis. RESULTS: All clinical periodontal measurements were significantly higher in chronic periodontitis groups than the healthy controls (p < 0.05). Smoker and non-smoker chronic periodontitis patients exhibited similar values in all clinical periodontal measurements and plasma sRANKL, OPG concentrations (p > 0.05). Smoker chronic periodontitis patients exhibited significantly lower (p = 0.007) plasma OPG concentrations and higher sRANKL/OPG ratio (p = 0.01) than smoker healthy controls. CONCLUSIONS: Within the limits of this study, periodontal inflammation in smoker chronic periodontitis patients seems to lower plasma osteoprotegerin levels and thereby increase the RANKL/OPG ratio, and possibly play a role in the increased susceptibility for alveolar bone destruction in smoker subjects.