Dental implants with locking taper connection versus screwed connection: microbiologic and scanning electron microscope study.

The aim of this study is to carry out an analysis of the Fixture-Abutment Interfaces (FAI), comparing different connection systems, to evaluate the role of geometric discrepancy, which is present between the abutment and the fixture, in favoring the permeability to bacterial colonization. Two types of commercially available FAI were studied, 16 screwed FAI (Sweden-Martina Italia) (4 of Ø 3.8 mm, 4 of Ø 4.7 mm, 4 of Ø 5.7 mm and 4 of Ø 6.7 mm) and 4 FAI (Bicon) (Ø 3.5mm). The assays were carried out in vitro, placing the different dental implants in contact with broth culture of Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa and Streptococcus pyogenes to test the infiltration inside the FAI. Furthermore, scanning electron microscope (SEM) analysis was carried out to evaluate the gap at the fixture-abutment interface. In all the locking taper FAI and in the screwed FAI with a diameter of 3.8 mm there was no trace of bacterial infiltration of the species examined. In the screwed FAI with a diameter of 4.7 mm, 5.7 mm and 6.7 mm there was an increasing level of bacterial infiltration in relationship to the diameter. Therefore, this paper shows that there exists an important correlation between the diameter of the screwed implant and the permeability to microbic infiltration that is directly proportional to the diameter of the implant

Nitric Oxide-mediated cytotoxic effect induced by zoledronic acid treatment on Human Gingival Fibroblasts

Zoledronic acid (ZA) belongs to bisphosphonates (BPs), drugs administered to treat resorptive bone diseases. Although ZA is largely used in the clinical practice, significant adverse effects of ZA, such as osteonecrosis of the jaw (ONJ), were recorded. The aim of this work was to evaluate the role of Nitric Oxide (NO) in the in vitro response of Human Gingival Fibroblasts (HGFs) to 1, 5, 10 and 100μM ZA. HGFs morphology was evaluated through phase contrast microscopy and live/ dead staining; MTT and ELISA assays were applied to measure cell viability, Collagen Type I and IL6 secretion. ROS production and mitochondrial membrane potential were evaluated by flow cytometry; NO production and NOS activity by spectrophotometric analysis; eNOS and nNOS expression by fluorescence microscopy. Viable fibroblasts are evidenced in control sample while floating dead cells and cells close to detachment phase in ZA treated sample along with decreased level of Collagen Type I. Control sample shows higher number of viable cells respect to ZA treated one and ROS production increases when ZA is added. Released NO in ZA treated sample appears higher and NO overproduction is related to increased nNOS activity. IL 6 secretion level is higher in ZA treated sample than in control one. Our results suggest ROS involvement in NO overproduction, due to nNOS recruitment, both at low and high doses. In turn, NO release seems to be able to trigger the inflammatory response only when high doses are administered

Periodontitis: from local infection to systemic diseases.

Periodontitis is a chronic infectious disease, characterized by the progressive loss of the teeth's supporting tissues, affecting almost 40% of the entire adult population. An imbalance between a localized gram-negative infection and an exaggerated host inflammatory response plays a pivotal role in determining gingival tissue damage. Recent evidence suggests that the effect of periodontitis might not be limited just to the oral cavity but it might have systemic consequences. Indeed periodontitis has also been associated with a moderate systemic inflammatory response. Although the mechanisms behind this association remain unclear, periodontitis might represent one distant source of low-grade systemic inflammation. This association could explain the increased risk of future cardiovascular diseases observed, the impaired metabolic control in diabetes subjects and the adverse pregnancy outcomes observed in populations suffering from periodontitis. In this review we describe the pathophysiological processes involved in periodontitis and briefly review the evidence produced to support an association between periodontitis and systemic diseases.Link_to_subscribed_fulltex