Different application procedures of Nd:YAG laser as an adjunct to scaling and root planning in smokers with stage III grade C periodontitis: a single-blind, randomized controlled trial.

BACKGROUND: The aim of the present study was to evaluate whether different Nd:YAG laser applications as an adjunct to scaling and root planning (SRP) improve the healing response to periodontal therapy in smokers with periodontitis. METHODS: This clinical trial included eighty systemically healthy smokers with periodontitis. Patients were randomly allocated to a treatment group: SRP alone (group 1), SRP+low-level laser therapy (LLLT) with Nd:YAG laser (group 2), SRP+pocket debridement with ND:YAG laser (group 3), and SRP+combined pocket debridement and LLLT with Nd:YAG laser (group 4). Gingival index (GI), plaque index (PI), bleeding on probing (%), probing depth (PD), and clinical attachment level (CAL) were recorded, and gingival crevicular fluid (GCF) samples for metalloproteinase-8 (MMP-8) levels were collected at baseline, 1 month and 3 months after treatment. RESULTS: There were no significant differences between the treatment groups for the GI, PI, and BOP (%) parameters and MMP-8 levels at any time points (p > 0.05). For moderately deep pockets, PD and CAL reductions were significantly greater in all test groups compared to group 1 (p ˂ 0.05). For deep pockets, these reductions were significantly greater in group 2 and group 4 compared to group 1 (p ˂ 0.05). PD and CAL reductions were generally similar between test groups (p > 0.05) except PD reduction between baseline and 3 months in deep pockets (p ˂ 0.05). CONCLUSIONS: The findings of this clinical trial suggest that Nd:YAG laser applications may be beneficial on the healing response of smokers to non-surgical therapy compared to SRP alone.

Gingival crevicular fluid lipocalin-2 and semaphorin3A in stage III periodontitis: Non-surgical periodontal treatment effects.

BACKGROUND AND OBJECTIVE: Identification of biomarkers to assess individual risk and monitor periodontal health status is important. Research on lipocalin-2 (LCN2) and semaphorin3A (Sema3A) is lacking. This study aimed to evaluate gingival crevicular fluid (GCF) LCN2, Sema3A, and tumor necrosis factor-α (TNF-α) levels in periodontally healthy (H), gingivitis (G), and periodontitis (P) patients, and their changes following non-surgical periodontal therapy. METHODS: Sixty systemically healthy and non-smoker participants, diagnosed as periodontally healthy, gingivitis, and stage III grade C periodontitis, were recruited (n = 20/group). Clinical periodontal parameters were recorded and GCF samples were obtained at baseline from all groups; for group P, these were repeated one and three months following non-surgical periodontal treatment. GCF LCN2, Sema3A, and TNF-α levels were evaluated with enzyme-linked immunosorbent assay. RESULTS: GCF LCN2, Sema3A, and TNF-α total amounts were significantly higher in disease groups than group H (p < .001). Between P and G groups, only TNF-α levels were significantly different (p < .001). Non-surgical periodontal therapy resulted in significant improvement of all clinical parameters and significant decreases of GCF LCN2 and TNF-α levels, at both time points, compared with baseline (p < .001). Sema3A levels remained unchanged following treatment (p > .05). LCN2 and TNF-α levels were significantly positively correlated with clinical parameters. LCN2 (AUC [area under the curve] = 0.94) and TNF-α (AUC = 0.98) levels were similarly accurate in differentiating between periodontal disease (whether G or P) and healthy controls. CONCLUSIONS: LCN2 and TNF-α levels in GCF are correlated with clinical parameters and could prove useful as non-invasive screening tools for periodontitis.

Evaluation of galectin-3, peptidylarginine deiminase-4, and tumor necrosis factor-α levels in gingival crevicular fluid for periodontal health, gingivitis, and Stage III Grade C periodontitis: A pilot study.

BACKGROUND: Comparing the gingival crevicular fluid (GCF) levels of galectin-3, peptidylarginine deiminase 4 (PAD4) and tumor necrosis factor-alpha (TNF-α) in individuals with stage III grade C periodontitis and gingivitis and with healthy periodontium was the purpose of this clinical research. METHODS: Sixty systemically healthy and non-smoker individuals consisting of stage III grade C periodontitis (group S3P/n = 20), gingivitis (group G/n = 20), and periodontally healthy (group HP/n = 20) were recruited for this research. Clinical parameters such as probing depth, clinical attachment level, gingival index, plaque index, and bleeding on probing were recorded in periodontal charts. Enzyme-linked immunosorbent assay method was used in evaluating the GCF levels of galectin-3, PAD4, and TNF-α for study groups. RESULTS: The GCF galectin-3 total amount was highest in group S3P compared with group G and group HP (P <0.05). Its total amount was also higher in group G compared with group HP (P <0.05). The GCF PAD4 total amount was higher in group S3P compared with group HP (P <0.05) but was similar with group G (P >0.05). Its total amounts were also similar in group G and group HP (P >0.05). The GCF TNF-α total amounts were similar in group S3P and group G (P >0.05) but significantly greater than the group HP (P ˂0.05). The GCF galectin-3, PAD4, and TNF-α concentrations were lower in the group S3P and group G compared with the group HP (P <0.05). There were significant positive correlations between GCF galectin-3 total amount and all clinical parameters (P ˂0.01) and also between GCF galectin-3 and TNF-α total amounts (P ˂0.01). There was no correlation between PAD4 and clinical parameters, or between PAD4 and TNF-α (P >0.05). CONCLUSIONS: Galectin-3 and PAD4 may be involved in the periodontal disease pathogenesis considering the elevated levels of these molecules in periodontal disease. These biomarkers may be used in the diagnosis of periodontal diseases.

Endocrine Disruptors and Polycystic Ovary Syndrome: Phthalates

Objective: We aimed to investigate a possible role of the endocrine disruptors phthalates, di-2-ethylhexyl phthalate (DEHP) and mono (2-ethylhexyl) phthalate (MEHP), in polycystic ovary syndrome (PCOS) aetiopathogenesis. We also wished to evaluate the relationship between phthalates and metabolic disturbances in adolescents with PCOS. Methods: A total of 124 adolescents were included. Serum MEHP and DEHP levels were determined by high-performance liquid chromatography. Insulin resistance was evaluated using homeostasis model assessment-insulin resistance, quantitative Insulin Sensitivity Check Index, fasting glucose/insulin ratio, Matsuda index, and total insulin levels during oral glucose tolerance test. Participants were further subdivided into lean and obese subgroups according to body mass index (BMI). Results: Sixty-three PCOS and 61 controls, (mean age 15.2±1.5; range: 13-19 years) were enrolled. Serum DEHP and MEHP concentrations were not significantly different between PCOS and control groups. The mean (95% confidence interval) values of DEHP and MEHP were 2.62 (2.50-2.75) µg/mL vs 2.71 (2.52-2.90) µg/mL and 0.23 (0.19-0.29) µg/mL vs 0.36 (0.18-0.54) µg/mL in PCOS and the control groups respectively, p>0.05. Correlation analysis, adjusted for BMI, showed that both phthalates significantly correlated with insulin resistance indices and serum triglycerides in adolescents with PCOS. Conclusion: Serum DEHP and MEHP concentrations were not different between adolescents with or without PCOS. However, these phthalates are associated with metabolic disturbances such as dyslipidemia and insulin resistance, independently of obesity, in girls with PCOS.

Assessment of saliva and gingival crevicular fluid soluble urokinase plasminogen activator receptor (suPAR), galectin-1, and TNF-α levels in periodontal health and disease.

OBJECTIVE: The aim of the study is to evaluate saliva and gingival crevicular fluid (GCF) levels of suPAR and galectin-1 in different periodontal health status and relationship between these molecules and TNF-α to understand the roles of these molecules in periodontal inflammation process. BACKGROUND: Soluble urokinase plasminogen activator receptor (suPAR) has been described as a biological marker of inflammation and immunological activation. Galectin-1, a member of the galectin family, is an anti-inflammatory cytokine. However, to date, levels of these two molecules in periodontal health and disease have not been well documented. METHODS: A total of 60 individuals, 20 with chronic periodontitis (group P), 20 with gingivitis (group G), and 20 with healthy periodontium (group H) were recruited for this study. Full-mouth clinical periodontal measurements were recorded in periodontal charts. GCF and whole saliva samples were collected to determine the levels of suPAR, galectin-1, and TNF-α in study groups using enzymelinked immunosorbent assay (ELISA) method. RESULTS: The GCF total amount of suPAR, galectin-1, and TNF-α in GCF was similar in group P and G (P > .05). The GCF total amounts of these molecules in GCF were higher in the group G and P compared to the group H (P < .05), whereas the GCF concentrations of suPAR and galectin-1 were lower in the group G and P compared to the group H (P < .05).The saliva concentration of suPAR was significantly higher in group P compared to the group G and H (P < .05). It was also higher in the group G compared to the group H but there is no significant difference between the groups (P > .05). Salivary galectin-1 levels were similar in the study groups (P > .05). CONCLUSION: Increased levels of GCF suPAR, galectin-1, and saliva suPAR in periodontal disease suggest that these molecules may play a role in the periodontal inflammation. suPAR and galectin-1 may be considered as potential biomarkers in periodontal disease.

Anti-inflammatory role of obestatin in autoimmune myocarditis.

Obestatin is a popular endogeneous peptide, known to have an autoimmune regulatory effect on energy metabolism and the gastrointestinal system. Studies regarding the anti-inflammatory effects of obestatin are scarce. The aim of this study was to show the anti-inflammatory effect of obestatin in an experimental model of autoimmune myocarditis in rats. Experimental autoimmune myocarditis was induced in Lewis rats by immunization with subcutaneous administration of porcine cardiac myosin, twice at 7-day intervals. Intraperitoneal pretreatment with obestatin (50 µg/kg) was started before the induction of myocarditis and continued for 3 weeks. The severity of myocarditis was evidenced by clinical, echocardiographic and histological findings. In addition, by-products of neutrophil activation, lipid peroxidation, inflammatory and anti-inflammatory cytokines were measured in serum. Obestatin significantly ameliorated the clinical and histopathological severity of autoimmune myocarditis. Therapeutic effects of obestatin in myocarditis were associated with reduced lipid peroxidation, suppression of polymorphonuclear leukocyte infiltration and enhancement of glutathione synthesis, inhibition of serum inflammatory and activation of anti-inflammatory cytokines. Histopathologically, the left ventricle was significantly dilated, and its wall thickened, along with widespread lymphocytic and histocytic infiltration. The myocardium was severely infiltrated with relatively large mononuclear cells. These histopathological changes were observed in lesser degrees in obestatin-treated rats. This study demonstrated a novel anti-inflammatory effect of obestatin in an experimental model of autoimmune myocarditis. Consequently, obestatin administration may represent a promising therapeutic approach for myocarditis and dilated cardiomyopathy in the future.

Cardioprotective effect of metformin against doxorubicin cardiotoxicity in rats.

OBJECTIVE: The clinical use of doxorubicin, which is a strong antineoplastic agent, is limited due to its cardiotoxic side effects. Metformin is a drug with antihyperglycemic effects, and it has been shown to have a cardioprotective effect on left ventricular function in experimental animal models of myocardial ischemia. The present study investigated the cardioprotective effect of metformin in rats with doxorubicin cardiotoxicity. METHODS: Wistar albino rats were used in the study. Forty male, 10-week-old Wistar albino rats were randomly divided four groups. The control group rats were intraperitoneally administered saline solution twice a week, four doses in total. The doxorubicin group rats received doxorubicin (4 mg/kg, twice a week, cumulative dose: 16 mg/kg) intraperitoneally. The metformin group rats received metformin (250 mg/kg/day, every day for 14 days) via gavage. The doxorubicin + metformin group rats received doxorubicin and metformin at the same dose. Left ventricular functions were evaluated by using M-mode echocardiography one day after the last dose of doxorubicin. Heart tissue samples were histopathologically examined. Cardiomyocyte apoptosis was detected using in situ terminal deoxynucleotide transferase assay (TUNEL). Serum brain natriuretic peptide and C-type natriuretic peptide levels were measured. Catalase, superoxide dismutase, glutathione peroxidase, and tumor necrosis factor alpha levels were analyzed in the heart tissue. The assumptions of equality of variances and normal distribution were checked for all variables (Shapiro-Wilk test and Q-Q graphics).To identify intergroup differences, one-way variant analysis or the Kruskal-Wallis test was used. A p<0.05 value was accepted as statistically significant. RESULTS: Our results showed that doxorubicin treatment caused significant deterioration in left ventricular functions by echocardiography, histological heart tissue damage, and increase in cardiomyocyte apoptosis. Doxorubicin + metformin group showed protection in left ventricular function, elimination of histopathologic change, and reduced of cardiomyocyte apoptosis. CONCLUSION: The present study provided evidence that metformin has cardioprotective effects against doxorubicin cardiotoxicity.

The endocrine disruptor bisphenol A may play a role in the aetiopathogenesis of polycystic ovary syndrome in adolescent girls.

AIM: Experimental in vitro studies have shown that bisphenol A affects steroidogenesis, folliculogenesis and ovarian morphology. The aim of this study was to investigate the role of the endocrine disruptor bisphenol A in the aetiopathogenesis of polycystic ovary syndrome (PCOS) in adolescents and its relationship with metabolic parameters, insulin resistance and obesity in this population. METHODS: A total of 112 girls with PCOS and 61 controls between 13 and 19 years of age were enrolled in the study. Serum bisphenol A levels were measured by high-pressure liquid chromatography. An oral glucose tolerance test was also performed. RESULTS: Adolescents with PCOS had markedly increased serum bisphenol A levels (mean: 1.1 ng/mL 95% CI: 1.0-1.2) than controls (mean: 0.8 ng/mL 95% CI: 0.6-0.9, p = 0.001). When we compared the subgroups according to obesity, the main factor determining the significant increase in bisphenol A was the presence of PCOS, but not obesity (p = 0.029). Bisphenol A was significantly correlated with total testosterone (r = 0.52), free testosterone (r = 0.44), dehydroepiandrosterone sulphate (r = 0.37) and Ferriman-Gallwey score (r = 0.43) (p < 0.05). CONCLUSION: Adolescents with PCOS had higher serum bisphenol A levels than controls, independent of obesity. Bisphenol A concentrations were significantly correlated with androgen levels, leading us to consider that bisphenol A might play a role in the aetiopathogenesis of PCOS in adolescents.

The effects of dexmedetomidine on early stage renal functions in pediatric patients undergoing cardiac angiography using non-ionic contrast media: a double-blind, randomized clinical trial.

BACKGROUND: In this study we aimed to investigate the effects of dexmedetomidine on early stage renal function in pediatric patients undergoing cardiac angiography. METHODS: 60 pediatric patients between 6 and 72 months of age undergoing cardiac angiography were included in the study. Patients were divided into two groups. The patients in both groups were administered 1 mg · kg(-1) ketamine, 1 mg · kg(-1) propofol as bolus and followed by 1 mg · kg(-1) · h(-1) ketamine and 50 µg · kg(-1) · min(-1) propofol infusion. Additionally, a loading dose of 1 µg · kg(-1) dexmedetomidine given over 10 min followed by 0.5 µg · kg(-1) · h(-1) dexmedetomidine infusion to patients in group D. The patients were evaluated for NGAL, creatinine, renin, endothelin-1, TAS and TOS blood levels before the procedure and 6th and 24th h after the procedure. pRIFLE criteria were used to define CIN and its incidence in the study. RESULTS: According to pRIFLE criteria contrast-induced acute kidney injury developed in 3 (10%) of the patients in group D and 11 (36.7%) of the patients in group C (P = 0.029, risk ratio = 0.27; 95% CI: 0.084-0.88). In patients who developed CIN, Endothelin-1 levels in groups C and D were significantly higher than baseline levels at 6th, 24th and 6th h, respectively. Renin levels were significantly increased at 6th and 24 th( ) h in patients with CIN in both groups. CONCLUSIONS: Dexmedetomidine may be beneficial in protecting against contrast-induced nephropathy during pediatric angiography by preventing the elevation of vasoconstrictor agents such as plasma endothelin-1 and renin.

Assessment of paraoxonase 1, xanthine oxidase and glutathione peroxidase activities, nitric oxide and thiol levels in women with polycystic ovary syndrome.

OBJECTIVE: To investigate whether there is any relation between oxidative stress and the antioxidant system in the development of polycystic ovary syndrome (PCOS) by measuring serum nitric oxide (NO) levels and xanthine oxidase (XO) activity (a generator of reactive oxygen species) and antioxidant status by measuring serum thiol levels and glutathione peroxidase (GSHPx) and paraoxonase 1 (PON1) activities. DESIGN: Prospective case-control study. SETTING: University hospital in Turkey. SAMPLE: Thirty women with polycystic ovary syndrome and 20 age- and sex-matched healthy control subjects were included. METHODS: Serum XO, PON1 and GSHPx activity and NO and thiol levels were determined by spectrophotometric methods. MAIN OUTCOME MEASURES: Activity of serum XO, PON1 and GSH, as well as NO and thiol levels. RESULTS: Serum XO activities were higher in women with PCOS than in the control women (p<0.001). The PON1 activity was lower in women with PCOS than in the control women (p<0.001). No significant difference was found between NO and thiol levels and GSHPx activities of women with PCOS and the control women (p>0.05). Serum PON1 activities were negatively correlated with serum XO activities and NO levels. CONCLUSION: Increased oxidant XO activity and decreased lipid antioxidant PON1 activity, along with the observed negative correlation between these parameters, suggests that women with PCOS are under oxidative stress and that there is XO-mediated lipid peroxidation, which may be related to increased atherosclerosis seen in later life in such women.

Melatonin promotes fracture healing in the rat model.

OBJECTIVES: In this study, we investigated the effect of melatonin on fracture healing in the rat tibia model by using biochemical and histopathologic methods. MATERIALS AND METHODS: In this study 80 male Sprague-Dawley rats were randomized into two groups, a control group (Group 1) and melatonin group (Group 2) with eight rats per group according to the day of sacrifice (Days 1, 3, 7, 14 and 28). The fractures were produced by the manual breakage using plate-bending devices, placed at the distal 3(rd) of the right tibia. Group 2 received 30 mg/kg/day melatonin and group 1 1% alcohol in saline 5 ml/kg/day intraperitoneally during the experiment. Plasma Malondialdehyde (MDA) levels, activity of superoxide dismutase (SOD) and myeloperoxidase (MPO) were measured biochemically. The fracture healing was evaluated using a five-point scale defined by Allen et al. RESULTS: Malondialdehyde levels in group 2 decreased at days 3, 7, 14, and 28 compared to control values (p<0.05). Superoxide dismutase activity in group 2 decreased at days 3, 7 and 14, and returned to the 1(st) day value after 28 days. Myeloperoxidase values in group 2 decreased at days 1, 3, and 7 (p<0.001). Histopathological specimens of healed tibias showed two animals with complete cartilaginous union, five with incomplete bony union and one with complete bony union in the group 2. In contrast, in the group 1, six rats showed complete cartilaginous union and two showed incomplete cartilaginous union (p<0.05). CONCLUSION: The administration of melatonin maybe beneficial in suppressing the effects of free oxygen radicals and regulating antioxidant enzyme activity in the fracture healing process.

The protective effect of melatonin on nicotine-induced myocardial injury in newborn rats whose mothers received nicotine.

OBJECTIVE: Nicotine, one of the most dangerous substances in tobacco, can pass the placenta and affect the fetal hemodynamics. The aim of this study was to evaluate the protective effects of melatonin on hearts of nicotine exposed newborn rats whose mothers received nicotine. METHODS: This is an experimental, randomized, controlled study. Study groups were composed of five groups of rats; high-dose nicotine (HDN), HDN+melatonin (HDNM), low-dose nicotine (LDN), LDN+melatonin (LDNM), control. Myocardial and plasma malondialdehyde (MDA), nitric oxide(NO), glutathione peroxidase (GSHPx) and superoxide dismutase (SOD) were analyzed and myocardial tissue was examined histopathologically. Comparisons of groups were done with Kruskal-Wallis one-way analysis test. All pairwise multiple comparisons and the comparisons between control and other groups were done with Dunn's nonparametric multiple comparison test. RESULTS: Plasma and tissue MDA levels among groups were different (p=0.001 for plasma MDA and p=0.001 for tissue MDA). Plasma MDA levels of HDN, HDNM, LDN, and tissue MDA levels of HDN and LDN were significantly higher than in control group (p<0.05 for plasma MDA and for tissue MDA). Plasma and tissue NO levels among groups were also different (p=0.011 for plasma NO and p=0.001 for tissue NO). Plasma NO of LDN group was higher than of LDNM group, and plasma NO of LDNM group was lower than in control group (p<0.05). Tissue NO levels of HDN and LDN groups were higher than of control group (p<0.05). There was no difference between plasma GSHPx levels among groups (p=0.221) but statistically significant different was detected between tissue GSHPx levels among groups (p=0.001). Tissue GSHPx level was found lower in HDN group than in control group (p<0.05). Tissue GSHPx level of LDNM group was higher than of LDN group, and tissue GSHPx level of HDNM group was higher than of HDN group (p<0.05). A difference was found between plasma and tissue SOD among groups (p=0.005 for plasma SOD and p=0.001 for tissue SOD). Plasma SOD of LDN group was significantly lower than of HDNM and LDNM groups (p<0.05). Tissue SOD analyzes revealed lower levels in HDN and LDN groups than in control group (p<0.05). Severe cardiomyopathy was determined in HDN and LDN groups (p<0.05). CONCLUSION: Nicotine exposure depletes myocardial antioxidant enzymes and increases free radicals and lipid peroxidation products. Melatonin particularly prevents the nicotine-induced cardiac injury as an antioxidant.

Effect of melatonin in the prevention of post-operative adhesion formation in a rat uterine horn adhesion model.

BACKGROUND: Our main aim was to investigate the effects of melatonin (ME), possibly the most powerful free-radical scavenger, on the prevention of i.p. adhesion formation in rat uterine horn. Our secondary aim was to determine whether different methods of administration of ME were beneficial. METHODS: Animals were randomly assigned into seven groups, each consisting of 13 rats. Measured serosal injury was created using a standard technique. While control and two sham groups were not given ME, two of the remaining four groups were given a single dose of 10 mg/kg (2 mg) of ME i.p. immediately after injury and 30 min prior to injury respectively. In the two other groups, ME treatment was continued daily for 5 days. All animals were killed 2 weeks after surgery and adhesions were determined and scored by a examiner blinded to the test. RESULTS: The extent, severity and total scores of adhesion were found to be significantly reduced in all of the ME treatment groups when compared with control and sham groups. There were no statistically significant differences between the treatment groups. CONCLUSIONS: This study showed that even single dose ME therapy was effective in the prevention of post- operative i.p. adhesion formation.