The aim of the present study was to evaluate surface alterations on titanium implant necks subsequent to different prophylaxis procedures. Fifty ITI implants were utilized. Forty implants were treated with 10 different prophylaxis procedures (ultrasonic scaler, plastic tip ultrasonic scaler, stainless steel curette, titanium curette, teflon curette, air powered system, abrasive rubber cups, polishing rubber cup and brush), and 10 implants were left as untreated controls. Surface alterations were studied on an area of 1 mm x 0.9 mm and quantified using optical microscopic, SEM and laser prophylometer analysis. The use of laser prophylometer provided an objective criterion for evaluation, expressing implant neck surface alterations in numeric values in terms of two roughness indexes, Ra and Rz. The results showed that, in comparison with the controls (Ra = 0.50; Rz = 3.98) the procedures investigated could be divided into 3 main groups: 1) Methods which altered the implant neck surface producing increased roughness (Ra = 0.68-2.08; Rz = 4.68-11.92); 2) Methods which left the implant neck surface unaltered (Ra = 0.44-0.57; Rz = 0.42-3.46); 3) Methods resulting in a smoothening of the implant neck surface (Ra = 0.36; Rz = 2.15). Group 1 included procedures that should be avoided. However, it appeared safe to apply the procedures of groups 2 and 3. To confirm these results, it will be necessary to evaluate the plaque- and calculus-removing efficacy from titanium neck implant surfaces in vivo.

Infective endocarditis (IE) is an inflammatory disease usually caused by bacteria entering the bloodstream and settling in the heart lining valves or blood vessels. Despite modern antimicrobial and surgical treatments, IE continues to cause substantial morbidity and mortality. Thus, primary prevention and enhanced diagnosis remain the most important strategies to fight this disease. In this regard, it is worth noting that for over 50 years, oral microbiota has been considered one of the significant risk factors for IE. Indeed, among the disparate recommendations from the American heart association and the European Society of Cardiology, there are good oral hygiene and prophylaxis for high-risk patients undergoing dental procedures. Thus, significant interest has grown in the role of oral microbiota and it continues to be a subject of research interest, especially if we consider that antimicrobial treatments can generate drug-resistant mutant bacteria, becoming a severe social problem. This review will describe the current knowledge about the relationship between oral microbiota, dental procedures, and IE. Further, it will discuss current methods used to prevent IE cases that originate from oral pathogens and how these should be focused on improving oral hygiene, which remains the significant persuasible way to prevent bacteremia and systemic disorders.

Mitochondrial dysfunction is a crucial contributor to heart diseases. Alterations in energetic metabolism affect crucial homeostatic processes, such asATP production, the generation of reactive oxygen species, and the release of pro-apoptotic factors, associated with metabolic abnormalities. In response to energetic deficiency, the cardiomyocytes activate the Mitochondrial Quality Control (MQC), a critical process in maintaining mitochondrial health. This process is compromised in cardiovascular diseases depending on the pathology’s severity and represents, therefore, a potential therapeutic target. Several potential targeting molecules within this process have been identified in the last years, and therapeutic strategies have been proposed to ameliorate mitochondria monitoring and function. In this context, physical exercise is considered a non-pharmacological strategy to protect mitochondrial health. Physical exercise regulates MQC allowing the repair/elimination of damaged mitochondria and synthesizing new ones, thus recovering the metabolic state. In this review, we will deal with the effect of physical exercise on cardiac mitochondrial function tracing its ability to modulate specific steps in MQC both in physiologic and pathologic conditions.

One of the possible complications of implant treatment is the occurrence of an implant fracture. Metal fatigue and biomechanical overload seem to be the most common causes of fractured implants. This study evaluated 4 implants (3 hollow cylinders and 1 hollow screw) which fractured after a mean loading period of 2.8 years. All implants had a 4 mm diameter and had been inserted in a posterior location. In 3 cases parafunctional habits were present. In all cases a vertical resorption of the peri-implant bone was present. The endosseous portion of the implant presented always a very high bone-implant contact percentage. Scanning electron microscopic examination showed that at least one of the implant holes was involved in the fracture line; no porosities or material defects were observed on the fractured surface of the implant. In hollow implants the holes could represent a site of less resistance.

No abstract

No abstract

Despite the availability of several therapies for the management of blood glucose in diabetic patients, most of the treatments do not show benefits on diabetic cardiomyopathy, while others even favor the progression of the disease. New pharmacological targets are needed that might help the management of diabetes and its cardiovascular complications at the same time. GRK2 appears a promising target, given its established role in insulin resistance and in systolic heart failure. Using a custom peptide inhibitor of GRK2, we assessed in vitro in L6 myoblasts the effects of GRK2 inhibition on glucose extraction and insulin signaling. Afterwards, we treated diabetic male mice (db/db) for 2 weeks. Glucose tolerance (IGTT) and insulin sensitivity (ITT) were ameliorated, as was skeletal muscle glucose uptake and insulin signaling. In the heart, at the same time, the GRK2 inhibitor ameliorated inflammatory and cytokine responses, reduced oxidative stress, and corrected patterns of fetal gene expression, typical of diabetic cardiomyopathy. GRK2 inhibition represents a promising therapeutic target for diabetes and its cardiovascular complications.

Background. Ergogenic nutritional supplementation is sought by professional athletes for improving physical performance; nevertheless, scientific evidence to support the chronic use of L-Arginine among water polo players is missing. Methods. Seventeen male professional water polo players were randomly assigned to assume 5 grams per day of L-Arginine ( n = 9 ) or placebo ( n = 8 ) for 4 weeks. The players’ fitness level was assessed in the maximal speed swimming test. Ear lobe blood samples taken before and after the effort for serum lactate content were analyzed. A speed-to-lactate ratio was generated at the baseline and after 4 weeks of treatment. We also tested the effects of L-Arginine in vitro, measuring NO production, mitochondrial respiration, and gene expression in human fibroblasts. Results. L-Arginine did not modify BMI, muscle strength, and maximal speed at 200 meters after 4 weeks. However, L-Arginine ameliorated oxidative metabolism to exercise as suggested by the statistically significant lower lactate-to-speed ratio, which was not observed in placebo-treated controls. In vitro, L-Arginine induced the expression of a key regulator of mitochondrial biogenesis (PGC1α) and genes encoding for complex I and increased the production of nitric oxide and the maximal oxygen consumption rate. Conclusions. Chronic L-Arginine is safe and effective in ameliorating the oxidative metabolism of professional water polo players, through a mechanism of enhanced mitochondrial function.