Oğuzhan Aksu

Lipoxin A4 and Neutrophil/Lymphocyte Ratio: A Possible Indicator in Achieved Systemic Risk Factors for Periodontitis

Background The aim of this study was to evaluate the serum lipoxin A4 (LXA4) and neutrophil/lymphocyte (Ne/Ly) ratio in individuals with achieved systemic risk factors for periodontitis. Material/Methods One hundred and eighty volunteers (69 male, 111 female) who were categorized as systemically healthy control, diabetes, hyperlipidemia, obese and menopause were recruited for this cross-sectional study. Sociodemographic characteristics and oral health behaviors were recorded via questionnaire. Clinical periodontal parameters, including plaque index (PI), gingival index (GI), probing pocket depth (PD), clinical attachment level (CAL), sulcus bleeding index (SBI) and decayed, missing, and filled teeth index (DMFT), were assessed. Systemic parameters and LXA4 levels were evaluated in serum samples. Results Clinical periodontal parameters and DMFT were higher in subjects with achieved systemic risk factors than in healthy subjects. The systemically healthy with periodontitis group had higher serum LXA4 levels than the systemically healthy with non-periodontitis group (P<0.05). The Ne/Ly ratio was higher in the hyperlipidemic group with periodontitis than in the hyperlipidemic group with non-periodontitis (P<0.05). In the control group, serum LXA4 levels were positively correlated with the PD, CAL and SBI. Conclusions In the presence of periodontitis, an increase in LXA4 levels and the Ne/Ly ratio in hyperlipidemic patients could contribute to the hypothesis that these parameters could be an indicator in periodontitis and its systemic risk factors.

Caffeic acid phenethyl ester protects against amphotericin B induced nephrotoxicity in rat model.

The present study was conducted to investigate whether caffeic acid phenethyl ester (CAPE), an active component of propolis extract, has a protective effect on amphotericin B induced nephrotoxicity in rat models. Male Wistar-Albino rats were randomly divided into four groups: (I) control group (n = 10), (II) CAPE group (n = 9) which received 10 μmol/kg CAPE intraperitoneally (i.p.), (III) amphotericin B group (n = 7) which received one dose of 50 mg/kg amphotericin B, and (IV) amphotericin B plus CAPE group (n = 7) which received 10 μmol/kg CAPE i.p. and one dose of 50 mg/kg amphotericin B. The left kidney was evaluated histopathologically for nephrotoxicity. Levels of malondialdehyde (MDA), nitric oxide (NO), enzyme activities including catalase (CAT), and superoxide dismutase (SOD) were measured in the right kidney. Histopathological damage was prominent in the amphotericin B group compared to controls, and the severity of damage was lowered by CAPE administration. The activity of SOD, MDA, and NO levels increased and catalase activity decreased in the amphotericin B group compared to the control group (P = 0.0001, P = 0.003, P = 0.0001, and P = 0.0001, resp.). Amphotericin B plus CAPE treatment caused a significant decrease in MDA, NO levels, and SOD activity (P = 0.04, P = 0.02, and P = 0.0001, resp.) and caused an increase in CAT activity compared with amphotericin B treatment alone (P = 0.005). CAPE treatment seems to be an effective adjuvant agent for the prevention of amphotericin B nephrotoxicity in rat models.

Investigation of pulmonary involvement in inflammatory bowel disease in an experimental model of colitis.

Background/Aims: Inflammatory bowel disease (IBD) may also involve various extra-intestinal organs. Clinical studies have found asymptomatic/symptomatic pulmonary involvement in 1% to 6% of patients with IBD. The present study histopathologically investigated pulmonary involvement in an experimental model of colitis in order to demonstrate pulmonary tissue involvement in IBD and to expose potential etiological factors. It also explored the relation between inflammation and tissue concentrations of vascular endothelial growth factor (VEGF) and tumor necrosis factor α (TNF-α). Methods: The study comprised 24 male Wistar albino rats. The rats were divided into four groups of six rats each. Acute colitis was induced in two separate groups using either the dextran sulphate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) method, while the other two groups were used as controls for each model of colitis. Wallace scoring was used for macroscopic assessment of colitis, and the lungs were histopathologically examined. Concentrations of VEGF and TNF-α in pulmonary tissue were measured by the enzyme-linked immunosorbent assay method. Results: The number of animals that had alveolar hemorrhage was significantly higher in the TNBS-induced colitis and DSS-induced colitis groups compared to their own control groups (p = 0.015 and p = 0.015, respectively). VEGF and TNF-α concentrations in pulmonary tissues were significantly increased in both the TNBS colitis and DSS colitis groups compared to their own control groups (p = 0.002 and p = 0.004, respectively; and p = 0.002 and p = 0.002, respectively). Conclusions: The present study demonstrated that significant and serious histopathological changes directly associated with colitis occur in the lungs in IBD.

Is gastroesophageal reflux contribute to the development chronic cough by triggering pulmonary fibrosis.

BACKGROUND/AIMS Previous studies have shown that the prevalence of abnormal acid reflux in fibrotic lung disease patients is high, and in particular, patients with secondary pulmonary fibrosis show higher esophageal acid exposure than normal controls. There are also some findings that, in patients with pathological reflux, pulmonary fibrosis may develop. The aim of this study is to investigate if pulmonary fibrosis is involved in the pathogenesis of chronic cough due to Gastroesophageal Reflux. MATERIALS AND METHODS A prospective study was performed in twenty-one patients with chronic cough due to gastroesophageal reflux who was diagnosed as reflux esophagitis by upper gastrointestinal endoscopy, histology, and in ten healthy controls without GER or any lung disease. All participitants underwent laryngoscopic examination and gastroesophageal scintigraphy with late lung imaging. Bronchoalveolar lavage fluid total and differential cell counts, T and B cell subsets, and the concentrations of IL- 1β and TNF-α were measured. RESULTS Reflux extending into the proximal esophagus was noted in 52.5%, and posterior laryngitis was present in 90.5% of the patients. No evidence of pulmonary aspiration was noted in the patients with reflux on scintigraphic examination. No significant difference was found between the GER and control groups in terms of cellular content, IL-1β and TNF-α levels or mean T cell subsets and B cell counts in bronchoalveolar lavage fluid. Forced expiratory volume in one second, forced vital capacity FEV1/FVC, total lung capacity, and carbon monoxide diffusion capacity values were within normal limits in the gastroesophageal reflux group. CONCLUSION Our findings do not support the hypothesis that gastroesophageal reflux leads to chronic cough by triggering alveolar epithelial injury and subsequent pulmonary fibrosis.