Smokers have a higher risk of inflammatory peri-implant disease than non-smokers.

AIM: To comparatively evaluate peri-implant health status in smokers and non-smokers. MATERIALS AND METHODS: A total of 142 implants (74 implants in non-smokers, 68 in smokers) in 43 smoker or non-smoker systemically healthy patients were included in the study. Demographic and clinical periodontal data were recorded and analysed by chi-square and Mann-Whitney U tests. RESULTS: Peri-implantitis and mucositis cases were significantly more frequent in the smokers than non-smokers (p = .001). Suppuration, bleeding and plaque scores around the implants were significantly higher in smokers than non-smokers (p = .001; p = .002; p < .0001, respectively). CONCLUSION: The present findings indicate that smokers have a higher risk of inflammatory peri-implant diseases. Therefore, more frequent recalls may be recommended in smokers with dental implants.

Is there an association between obstructive sleep apnea syndrome and periodontal inflammation?

OBJECTIVES: The aim of this study is to assess salivary, serum biomarkers, and subgingival bacteria as putative candidates in the potential association between obstructive sleep apnea syndrome (OSAS) and periodontal disease. MATERIALS AND METHODS: Fifty-two patients were grouped according to the severity of OSAS: 13 participants served as controls, 17 patients had mild-to-moderate OSAS, and 22 severe OSAS. Serum, saliva, and subgingival plaque samples were collected, and clinical periodontal parameters were recorded. Salivary, serum concentrations of interleukin-6 (IL-6), tumour necrosis factor (TNF-α), osteoprotegerin, soluble Receptor activator of nuclear factor kappa B ligand (sRANKL), and apelin were analysed by enzyme-linked immunosorbent assay. Bacterial counts were determined by real-time QPCR on plaque microbial DNA preparations. RESULTS: There was a significant change in the composition of microbes in plaque particularly in severe OSAS samples (p < 0.01). Statistical analyses indicated significantly higher salivary IL-6 levels in both OSAS groups compared to controls (p < 0.05). Salivary apelin levels were significantly higher in the severe OSAS group compared to the control group. Serum levels of these biomarkers and salivary osteoprotegerin, sRANKL levels were similar in the study groups. The incidence and duration of apnea positively correlated with clinical periodontal parameters (p < 0.05). CONCLUSION: OSAS appeared to alter the tested bacteria in plaque, correlate with increasing periodontal disease severity, have additive effect on salivary IL-6. CLINICAL RELEVANCE: OSAS is likely to associate with periodontal disease.

Is obesity a possible modifier of periodontal disease as a chronic inflammatory process? A case-control study.

BACKGROUND AND OBJECTIVE: This cross-sectional case-control study was conducted to provide a comparative evaluation of clinical periodontal measurements, together with serum levels of certain bioactive peptides and inflammatory cytokines, in relation to obesity. For this purpose, clinical periodontal measurements and the levels of serum leptin, adiponectin, interleukin-6 (IL-6), C-reactive protein and soluble intercellular adhesion molecule-1 of obese female individuals and their nonobese counterparts were compared. MATERIAL AND METHODS: Sixty obese (body mass index (BMI) > 30) and 31 nonobese (BMI < 30) female subjects were recruited for the present study. Before any periodontal intervention, serum samples were obtained and full-mouth clinical periodontal measurements were recorded at six sites per tooth. ELISA was used for the biochemical analysis. Data were tested statistically. RESULTS: Clinical attachment level was significantly higher in the obese group compared with the nonobese control group (p < 0.05). Serum levels of leptin and IL-6 were significantly higher in the obese group (p < 0.05). BMI correlated with the serum levels of inflammatory molecules (p < 0.05), but not with clinical periodontal parameters, in the obese group. CONCLUSION: In conclusion, obesity does not seem to have a prominent effect on clinical periodontal parameters but it does have many correlations with circulating inflammatory molecules. As suggested in the literature, increased levels of leptin and IL-6 in the obese group might be one explanation for a possible relationship between obesity and periodontal disease. A prospective study is warranted to clarify, in greater detail, the effects of obesity on periodontal health.

Periodontal health and serum, saliva matrix metalloproteinases in patients with mild chronic obstructive pulmonary disease.

BACKGROUND AND OBJECTIVES: The present case-control study aimed to evaluate comparatively the salivary and serum levels of matrix metalloproteinases (MMP)-8 and- 13 and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) in patients with mild chronic obstructive pulmonary disease (COPD) and non-COPD controls. MATERIAL AND METHODS: Clinical periodontal measurements were recorded before any periodontal intervention in 36 patients with mild COPD and 20 non-COPD controls admitted to Ege University Department of Chest Diseases COPD outpatient clinic (Izmir, Turkey). Salivary and serum levels of MMP-8, MMP-13, and TIMP-1 were determined by immunofluorometric assay (IFMA) and enzyme-linked immunosorbent assay (ELISA). Data were analyzed with non-parametric statistical tests. RESULTS: Patients with COPD were significantly older than the control group (p < 0.05). The COPD group showed significantly higher serum levels of MMP-8 IFMA, MMP-8/TIMP-1 IFMA than the control group (p < 0.005). By ELISA, serum MMP-8, MMP-8/TIMP-1, TIMP-1, and MMP-13 levels were similar in both groups (p > 0.05). Salivary MMP-8, MMP-13, and TIMP-1 levels were similar in both groups (p > 0.05). CONCLUSIONS: The present findings suggest that immunodetection of MMP-8 is dependent on the selected techniques and even with mild COPD some systemic inflammatory markers such as MMP-8 tend to increase. However, the present clinical periodontal and biochemical findings do not provide support for the previously proposed interaction between COPD and periodontal diseases.

Periodontal diseases and stress: a brief review.

Periodontal diseases are common chronic inflammatory diseases caused by pathogenic microorganisms colonising the subgingival area and inducing local and systemic elevations of pro-inflammatory cytokines resulting in tissue destruction. Apparition and evolution of periodontal diseases are influenced by many local or systemic risk factors. Psychological stress has been suggested as one of them and may negatively influence the outcome of periodontal treatment. However, mechanisms explaining the possible relationship between stress and increased susceptibility to periodontal disease remain poorly understood. Several stress markers are found in blood and saliva of patients with periodontal diseases and influence the development of periodontal diseases by several mechanisms including modifications of the inflammatory response and changes in the composition of the dental biofilm. The aim of this review is to provide an insight into the relationship between psychological stress and periodontal diseases.

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.

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.

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.

Crevicular fluid matrix metalloproteinase-8, -13, and TIMP-1 levels in type 2 diabetics.

OBJECTIVES: To evaluate whether type 2 diabetes mellitus (DM) enlarged and if so the quantum of such increase in the gingival crevicular fluid (GCF) levels of matrix metalloproteinase-8 (MMP-8), MMP-13 and tissue inhibitor of metalloproteinases-1 (TIMP-1). METHODS: Subjects (n = 73) were divided into five groups as follows: 12 DM patients with gingivitis (DM-G), 12 DM patients with periodontitis (DM-P), 12 systemically healthy patients with gingivitis (H-G), 13 systemically healthy patients with periodontitis (H-P) and 24 periodontally, systemically healthy volunteer subjects (H-C). Full-mouth clinical periodontal measurements were performed at six sites per tooth. Gingival crevicular fluid samples were obtained from two sites representing the clinical periodontal diagnosis in single-rooted teeth. Gingival crevicular fluid levels of MMP-8, MMP-13 and TIMP-1 were analysed by immunofluorometric MMP assay (IFMA), enzyme-linked immunosorbent assay (ELISA). Data were tested statistically by parametric tests. RESULTS: All clinical periodontal measurements were similar in both diabetic and systemically healthy patients with periodontal disease (all P > 0.05). Total amounts of MMP-8 in GCF samples were significantly lower in H-C group than DM-G, DM-P, H-P groups (all P < 0.05). Matrix metalloproteinase-13, TIMP-1 total amounts were similar in study groups (P > 0.05). Diabetes mellitus patients exhibited similar levels of MMP-8, MMP-13, TIMP-1 with systemically healthy gingivitis/periodontitis patients (P > 0.05). CONCLUSIONS: Within the limits of this study, DM does not seem to significantly affect GCF levels of MMP-8, MMP-13, TIMP-1 or clinical periodontal status.

Extra-short implants in the prosthetic rehabilitation of the posterior maxilla.

AIM: To compare clinical outcomes of 'extra-short' and regular bone level implants in the posterior maxilla for 12 months after loading. MATERIALS AND METHODS: Twenty-three systemically healthy, non-smoking patients received 30 extra-short, 24 regular bone level implants. Acrylic stents were fabricated for each patient for correct implant positioning. Implant lengths were 4-6 mm in the test, 8/10 mm in the control group. Radiographic evaluation was performed at baseline, 6, and 12 months after loading. Crestal bone level (CBL), CBL change (CBLC), true crown length (TCL), implant/crown ratio (ICR) and residual bone height (RBH) below maxillary sinus floor were calculated digitally. Data were tested statistically. RESULTS: Residual bone height was significantly lower, and TCL and ICR were higher in the test than the control group (P < 0.0001). CBL measurements at baseline were 0.19 ± 0.18 mm and 0.31 ± 0.37 mm and at 12 months, 0.24 ± 0.24 mm and 0.41 ± 0.31 mm, respectively in the test and control groups. CBL values at 12 months were significantly lower in the test than the control group (P < 0.05). CBLCs were similar at all times (P > 0.05). No correlation was found between the CBLC and implant/prosthetic parameters. CONCLUSION: Extra-short and regular implants might provide similar clinical outcomes in prosthetic rehabilitation of atrophic maxilla, during 12 months follow-up.

Root coverage with coronally advanced flap:6-year follow-up.

AIM: The aim of this study was to evaluate the long-term stability of root coverage without a regular control programme after coronally advanced flap (CAF) procedures in isolated gingival recessions. MATERIAL AND METHODS: Recession defects were treated with CAF using microsurgery technique. Probing depth, clinical attachment level, keratinized gingival width, plaque index, papilla bleeding index, recession depth, recession width and root surface area was evaluated at baseline, and then postoperative 6-month and 6-year follow-up sessions. Percentages of root coverage and complete root coverage rates were also calculated. RESULTS: In total, 12 defects in 12 patients of the 36 defects in 30 patients were available for analysis at the 6-year follow-up examination (66.7% of the initial sites could be reached). Percentage of mean root coverage was 95.06% at 6-month and 69.27% at 6-year and the difference was statistically significant (P < 0.05). Complete root coverage rate decreased from 75% (at 6-month) to 50% (at 6-year), but the difference was not statistically significant (P > 0.05). CONCLUSION: Within the limits of this long-term follow-up study, there seems to be a rather high risk for relapse after root coverage with CAF possibly due to the lack of regular recalls and persistent traumatic tooth brushing habits.

Tobacco-induced suppression of the vascular response to dental plaque.

Cigarette smoking presents oral health professionals with a clinical and research conundrum: reduced periodontal vascular responsiveness to the oral biofilm accompanied by increased susceptibility to destructive periodontal diseases. This presents a significant problem, hampering diagnosis and complicating treatment planning. The aim of this review is to summarize contemporary hypotheses that help to explain mechanistically the phenomenon of a suppressed bleeding response to dysbiotic plaque in the periodontia of smokers. The influence of smoke exposure on angiogenesis, innate cell function, the production of inflammatory mediators including cytokines and proteases, tobacco-bacteria interactions, and potential genetic predisposition are discussed.

Diamond burs versus curettes in root planing: a randomized clinical trial.

BACKGROUND: This study compares diamond burs and curettes by clinical, microbiological, biochemical and scanning electron microscopic parameters and treatment time data in the non-surgical periodontal treatment of patients with chronic periodontitis. METHODS: Two quadrants of each of the 12 patients received root planing with diamond burs, whereas the other two quadrants were treated with curettes. Clinical periodontal measurements were recorded at baseline and then 1, 3 and 6 months after completion of non-surgical periodontal treatment. Subgingival plaque and gingival crevicular fluid samples were obtained at baseline and 1-month control. Twenty-one hopeless teeth received root planing with diamond burs or curettes or no treatment and then extracted for microscopic evaluations. RESULTS: Clinical periodontal parameters improved similarly with both treatment modalities. Microbiological analyses revealed similar findings for the bacterial load (16S gene copy numbers) and ratio of each bacterium to the total bacterial count at baseline and 1-month control. Cytokine levels in the gingival crevicular fluid samples exhibited differences between the two treatments. Scanning electron microscopic analyses indicated that diamond burs were better in terms of calculus removal and loss of tooth substance indices but roughness index values were better for curettes. CONCLUSIONS: Diamond burs provide findings comparable with curettes in root planing.

Differentiation of Chronic and Aggressive Periodontitis by FTIR Spectroscopy.

Without longitudinal clinical data, it is difficult to differentiate some cases of chronic periodontitis (CP) and aggressive periodontitis (AgP). Furthermore, both forms of disease are exacerbated by tobacco use. Therefore, this cross-sectional study was planned, primarily, to determine the ability of Fourier-transform infrared (FTIR) spectroscopy to distinguish CP and AgP patients by analysis of human saliva samples and, secondarily, to assess the potential confounding influence of smoking on discriminating disease-specific spectral signatures. FTIR spectra were collected from patients with a clinical diagnosis of CP (n = 18; 7 smokers) or AgP (n = 23; 9 smokers). Self-reported smoking status, which may be unreliable, was confirmed by salivary cotinine analysis. Spectral band area analysis and hierarchical cluster analyses were performed to clarify if the 2 periodontitis groups as well as smoker and nonsmoker patients could be differentiated from each other. Significant variations in lipid, amino acid, lactic acid, and nucleic acid content were found between nonsmoker CP and AgP groups. Although significantly lower lipid, phospholipid, protein, amino acid, lactic acid, and nucleic acid content was noted in the smoker AgP group compared with the nonsmoker AgP group, in the CP group, phospholipid, protein, amino acid, and lactic acid content was significantly lower for smokers compared with the nonsmokers. Based on these variations, nonsmoker CP and AgP patients were discriminated from each other with high sensitivity and specificity. Successful differentiation was also obtained for the smoker CP and AgP groups. Thiocyanate levels successfully differentiated smokers from nonsmokers, irrespective of periodontal status, with 100% accuracy. Differentiation of AgP and CP forms, concomitant with determination of smoking status, may allow the dental health professional to tailor treatment accordingly.

Evaluation of transforming growth factor-beta 1 level in crevicular fluid of cyclosporin A-treated patients.

BACKGROUND: The aim of the present study was to investigate the level of transforming growth factor-beta 1 (TGF-beta 1) in gingival crevicular fluid (GCF) samples of cyclosporin A (CsA)-treated patients and to compare the results with control groups. METHODS: Fourteen renal transplant patients exhibiting severe CsA-induced gingival overgrowth, 10 patients with chronic gingivitis, and 10 subjects with clinically healthy periodontium were included in the study. In CsA-treated patients, GCF samples were harvested from sites exhibiting gingival overgrowth (CsA GO+) and sites not exhibiting gingival overgrowth (CsA GO-). The TGF-beta 1 levels in a total of 96 GCF samples from the 34 participants were analyzed by enzyme-linked immunosorbent assay. The results were expressed in terms of total amount (pg/2 sites) and concentration (ng/ml). RESULTS: TGF-beta 1 total amounts in CsA GO+ and CsA GO- sites were similar and significantly higher than that of healthy sites (P < 0.02 and P < 0.01, respectively). The total amount of TGF-beta 1 was also higher in gingivitis sites compared to the healthy sites, but the difference was not statistically significant (P > 0.05). CsA GO+ and CsA GO- sites exhibited higher total amount and concentration of TGF-beta 1 than that of gingivitis sites, but the differences were insignificant (P > 0.05). CONCLUSIONS: The results of the present study support the theory that CsA increases the synthesis of TGF-beta 1 in GCF. However, since the difference between CsA GO+ and CsA GO- sites was not statistically significant, it seems unlikely that GCF TGF-beta 1 level is the sole factor responsible for the CsA-induced gingival overgrowth. Complex interactions between various mediators of inflammation and tissue modeling are possibly involved in the pathogenic mechanisms of this side effect.

Biochemical analysis of total collagen content and collagen types I, III, IV, V and VI in gingiva of various periodontitis categories.

Collagen is one of the chief components of the extracellular matrix of gingival connective tissue, where five different types have been identified to date. The molecular mechanism of collagen loss in periodontitis still needs to be explored. In the present study total collagen content was investigated in gingival connective tissue of adult periodontitis (AP) as well as early onset periodontitis patients (EOP) and clinically healthy subjects. Furthermore, collagen type I, III, IV, V andVI content was evaluated in gingival biopsies obtained from periodontitis patients. There was a statistically significant difference between AP (25.1 +/- 8.1 microg/mg) and EOP (15.6 +/- 4.0microg/mg) groups with regard to the total collagen content (P < 0.05). In the clinically healthy control group the total collagen content was 20.7 +/- 4.6microg/mg. Moreover, the distribution of collagen types exhibited variations in pooled homogenates of each periodontitis group. The total collagen loss seemed to be greater in the EOP patients than in the AP patients. When the ratio of fibril forming collagens to nonfibrillar collagens was evaluated, it seems to be decreased in AP patients in comparison to EOP patients. The findings of the present study suggest that different collagen types present in various periodontitis categories may be related with diverse pathogenic mechanisms acting in these diseases.

Fatty acid profiles in smokers with chronic periodontitis.

We hypothesized that tobacco smoke induces alterations to the 3-OH fatty acids present in lipid A in a manner consistent with a microflora of reduced inflammatory potential. Whole saliva samples and full-mouth clinical periodontal recordings were obtained from persons with (22 smokers; 15 non-smokers) and without (14 smokers; 15 non-smokers) chronic periodontitis. Clear differences in the contributions of multiple saturated 3-OH fatty acid species were noted in the group with disease compared with healthy individuals. Increases in the long-chain fatty acids associated with anaerobic bacterial periodontopathogens, particularly 3-OH-C(i17.0) (146.7%, relative to controls), were apparent. Significant reductions in the 3-OH fatty acids associated with the consensus (high potency) enteric LPS structure (3-OH-C(12.0) and 3-OH-C(14.0); 33.3% and 15.8% reduction, respectively) were noted in smokers compared with non-smokers with chronic periodontitis. Thus, smoking is associated with specific structural alterations to the lipid-A-derived 3-OH fatty acid profile in saliva that are consistent with an oral microflora of reduced inflammatory potential. These findings provide much-needed mechanistic insight into the established clinical conundrum of increased infection with periodontal pathogens but reduced clinical inflammation in smokers.

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.

Gingival status, crevicular fluid tissue-type plasminogen activator, plasminogen activator inhibitor-2 levels in pregnancy versus post-partum.

BACKGROUND: This study was conducted to evaluate a possible link between periodontal status of pregnant women and the plasminogen activator system in gingival crevicular fluid (GCF). METHODS: GCF samples were obtained from four interproximal sites of anterior teeth in 43 women during the second trimester and also after delivery. Full mouth dental plaque, bleeding on probing (BOP) and probing depth (PD) values were recorded at six sites/tooth in each subject. GCF levels of tissue type plasminogen activator (t-PA) and its inhibitor, plasminogen activator-inhibitor-2 (PAI-2) were determined by ELISA. Data comparisons between pregnancy and post-partum were made by Wilcoxon signed rank test. RESULTS: The number of pockets with a PD>4 mm and total volume of GCF sampled were reduced significantly after delivery (p=0.000 and p=0.013, respectively). No significant differences were detected in GCF concentrations of t-PA or PAI-2 between pregnancy and post-partum. CONCLUSIONS: Our results suggest that GCF t-PA and PAI-2 concentrations are not affected by pregnancy. Reductions in PD values and GCF volume following delivery indicate a resolution of oedema in gingival tissues, possibly related to hormonal changes due to the ending of pregnancy.