Decontamination using a desiccant with air powder abrasion followed by biphasic calcium sulfate grafting: a new treatment for peri-implantitis.

Peri-implantitis is characterized by inflammation and crestal bone loss in the tissues surrounding implants. Contamination by deleterious bacteria in the peri-implant microenvironment is believed to be a major factor in the etiology of peri-implantitis. Prior to any therapeutic regenerative treatment, adequate decontamination of the peri-implant microenvironment must occur. Herein we present a novel approach to the treatment of peri-implantitis that incorporates the use of a topical desiccant (HYBENX), along with air powder abrasives as a means of decontamination, followed by the application of biphasic calcium sulfate combined with inorganic bovine bone material to augment the intrabony defect. We highlight the case of a 62-year-old man presenting peri-implantitis at two neighboring implants in positions 12 and 13, who underwent access flap surgery, followed by our procedure. After an uneventful 2-year healing period, both implants showed an absence of bleeding on probing, near complete regeneration of the missing bone, probing pocket depth reduction, and clinical attachment gain. While we observed a slight mucosal recession, there was no reduction in keratinized tissue. Based on the results described within, we conclude that the use of HYBENX and air powder abrasives, followed by bone defect grafting, represents a viable option in the treatment of peri-implantitis

Oestrogen replacement therapy reduces total plasma homocysteine and enhances genomic DNA methylation in postmenopausal women

Although oestrogen replacement therapy (ERT), which can affect the risk of major cancers, has been known to reduce total plasma homocysteine concentrations in postmenopausal women, the mechanisms and subsequent molecular changes have not yet been defined. To investigate the effect of ERT on homocysteine metabolism, thirteen healthy postmenopausal women were enrolled in a double-blind, placebo-controlled, randomized, cross-over study consisting of two 8-week long phases, placebo and conjugated equine oestrogen (CEE; 0·625 mg/d). Concentrations of total plasma homocysteine, vitamin B6and serum folate and vitamin B12were measured by conventional methods. Genomic DNA methylation was measured by a new liquid chromatography/MS method and promoter methylation status of the oestrogen receptor (ER)α,ERβandp16genes was analysed by methylation-specific PCR after bisulfite treatment. The CEE phase demonstrated a significantly decreased mean of total plasma homocysteine concentrations compared with the placebo phase (8·08 μmol/l (6·82–9·39)v.9·29 (7·53–11·35),P < 0·05) but there was no difference in the blood concentrations of the three B vitamins. The CEE phase also showed a significantly increased genomic DNA methylation in peripheral mononuclear cells compared with the placebo phase (2·85 (SD0·12) ng methylcytosine/μg DNAv.2·40 ± (SD0·15)P < 0·05). However, there was no difference in promoter methylation in theERα,ERβandp16genes. This study demonstrates that decreased homocysteinaemia by CEE therapy parallels with increased genomic DNA methylation, suggesting a potential new candidate mechanism by which ERT affects the risk of cancers and a possible new candidate biomarker for the oestrogen-related carcinogenesis through folate-related one-carbon metabolism

Successful management of peri-implantitis around short and ultrashort single-crown implants: a case series with a 3-year follow-up

Introduction and Aim. In case of peri-implantitis, resective surgery is contraindicated for short and ultrashort implants, limiting the treatment options to regenerative surgery or to implant removal. 'is retrospective case series presents the clinical and radiographic outcomes of a surgical regenerative procedure to treat peri-implantitis around short and ultrashort implants. Materials and Methods. The study is a retrospective evaluation of patients suffering from peri-implantitis and those who underwent access flap surgery, concomitant chemical and mechanical decontamination of implant surface, and bone grafting using a self-hardening mixture of bone substitutes and biphasic calcium sulfate. No membranes were applied to cover the grafting material, and primary tension-free closure was achieved. The retrospective protocol was reviewed and approved by the Ethics Committee for Clinical Sperimentation (CESC) of Verona and Rovigo, Italy (based in the University of Verona) (Prog. 1863CESC. Date of approval: 2018-07-04). Results. 15 patients (17 implants) have been diagnosed with peri-implantitis after a mean follow-up of 24 months after loading. Implant length was between 5 and 8 mm. 8 patients (10 implants) had a history of periodontitis. At baseline, the mean PD (probing pocket dept) at the deepest site was 8.12 mm, with an average mBI (modified bleeding index) of 2.35 and a mean BD (bone defect depth) of 3.04 mm. At the 3-year follow-up, the CSR was 100%, the mean mBI was 0.88 (average reduction: - 1.47), the mean PD was 3.35 mm (mean PD reduction: 4.77 mm), and the mean bone defect was reduced by 1.74 mm, with a mean bone fill of 55%. Conclusions. The results of the present case series suggest that if accurate surface decontamination is achieved, high survival rate and good clinical and radiographic results can be obtained after 3 years. However, only the histological examination could confirm the growth of new bone in direct contact with the implant surface or if the grafted material only fills the space left by the peri-implant defect

Gene sequence variations of the platelet P2Y12 receptor are associated with coronary artery disease

<p>Abstract</p> <p>Background</p> <p>The platelet P2Y₁₂receptor plays a key role in platelet activation. The H2 haplotype of the P2Y₁₂receptor gene (<it>P2RY12</it>) has been found to be associated with maximal aggregation response to adenosine diphosphate (ADP) and with increased risk for peripheral arterial disease. No data are available on its association with coronary artery disease (CAD).</p> <p>Methods </p> <p>The H2 haplotype of the <it>P2RY12 </it>was determined in 1378 unrelated patients of both sexes selected according to the presence of significant coronary artery disease (CAD group) or having normal coronary angiogram at cardiac catheterization (CAD-free group). Significant coronary artery disease was angiographically determined, and was defined as a greater than 50% visually estimated luminal diameter stenosis in at least one major epicardial coronary artery.</p> <p>Results</p> <p>In the studied population 71.9% had CAD (n = 991) and 28.1% had normal coronary angiogram (n = 387). H2 haplotype carriers were more frequent in the CAD group (p = 0.03, OR = 1.36, 95%CI = 1.02–1.82). The H2 haplotype was significantly associated with CAD in non-smokers (p = 0.007, OR = 1.83 95%CI = 1.17–2.87), but not in smokers. The association remained significant after adjustment for other covariates (age, triglycerides, HDL, hypertension, diabetes) by multivariate logistic regression (p = 0.004, OR = 2.32 95%CI = 1.30–4.15).</p> <p>Conclusion</p> <p>Gene sequence variations of the P2Y₁₂receptor gene are associated with the presence of significant CAD, particularly in non-smoking individuals.</p

Endothelial Cells' Activation and Apoptosis Induced by a Subset of Antibodies against Human Cytomegalovirus: Relevance to the Pathogenesis of Atherosclerosis

Human cytomegalovirus (hCMV) is involved in the pathogenesis of atherosclerosis. We have previously shown in patients with atherosclerosis that antibodies directed against the hCMV-derived proteins US28 and UL122 are able to induce endothelial cell damage and apoptosis of non-stressed endothelial cells through cross-rection with normally expressed surface molecules. Our aim was to dissect the molecular basis of such interaction and to investigate mechanisms linking innate immunity to atherosclerosis.We analysed the gene expression profiles in endothelial cells stimulated with antibodies affinity-purified against either the UL122 or the US28 peptides using the microarray technology. Microarray results were validated by quantitative PCR and by detection of proteins in the medium. Supernatant of endothelial cells incubated with antibodies was analysed also for the presence of Heat Shock Protein (HSP)60 and was used to assess stimulation of Toll-Like Receptor-4 (TLR4). Antibodies against UL122 and US28 induced the expression of genes encoding for adhesion molecules, chemokines, growth factors and molecules involved in the apoptotis process together with other genes known to be involved in the initiation and progression of the atherosclerotic process. HSP60 was released in the medium of cells incubated with anti-US28 antibodies and was able to engage TLR4.Antibodies directed against hCMV modulate the expression of genes coding for molecules involved in activation and apoptosis of endothelial cells, processes known to play a pivotal role in the pathogenesis of atherosclerosis. Moreover, endothelial cells exposed to such antibodies express HSP60 on the cell surface and release HSP60 in the medium able to activate TLR4. These data confirm that antibodies directed against hCMV-derived proteins US28 and UL122 purified from patients with coronary artery disease induce endothelial cell damage and support the hypothesis that hCMV infection may play a crucial role in mediating the atherosclerotic process

Combined Effect of Hemostatic Gene Polymorphisms and the Risk of Myocardial Infarction in Patients with Advanced Coronary Atherosclerosis

BACKGROUND: Relative little attention has been devoted until now to the combined effects of gene polymorphisms of the hemostatic pathway as risk factors for Myocardial Infarction (MI), the main thrombotic complication of Coronary Artery Disease (CAD). The aim of this study was to evaluate the combined effect of ten common prothrombotic polymorphisms as a determinant of MI. METHODOLOGY/PRINCIPAL FINDINGS: We studied a total of 804 subjects, 489 of whom with angiographically proven severe CAD, with or without MI (n = 307; n = 182; respectively). An additive model considering ten common polymorphisms [Prothrombin 20210G>A, PAI-1 4G/5G, Fibrinogen beta -455G>A, FV Leiden and "R2", FVII -402G>A and -323 del/ins, Platelet ADP Receptor P2Y12 -744T>C, Platelet Glycoproteins Ia (873G>A), and IIIa (1565T>C)] was tested. The prevalence of MI increased linearly with an increasing number of unfavorable alleles (chi(2) for trend = 10.68; P = 0.001). In a multiple logistic regression model, the number of unfavorable alleles remained significantly associated with MI after adjustment for classical risk factors. As compared to subjects with 3-7 alleles, those with few (/=8) alleles had an increased MI risk (OR 2.49, 95%CIs 1.03-6.01). The number of procoagulant alleles correlated directly (r = 0.49, P = 0.006) with endogenous thrombin potential. CONCLUSIONS: The combination of prothrombotic polymorphisms may help to predict MI in patients with advanced CAD

Homocysteine and Coronary Heart Disease: Meta-analysis of MTHFR Case-Control Studies, Avoiding Publication Bias

Robert Clarke and colleagues conduct a meta-analysis of unpublished datasets to examine the causal relationship between elevation of homocysteine levels in the blood and the risk of coronary heart disease. Their data suggest that an increase in homocysteine levels is not likely to result in an increase in risk of coronary heart disease