A FIELD-TRIAL OF TWO RESTORATIVE MATERIALS USED WITH ATRAUMATIC RESTORATIVE TREATMENT IN RURAL TURKEY: 24-MONTH RESULTS

Objective:

The purpose of this study was to investigate the clinical performance of high-strength glass ionomer cement (HSGIC) and resin-modified glass ionomer (RMGIC) in single and multiple surface carious cavities in the field conditions.

Material and Methods:

A split-mouth design, including ninety-one fillings placed on contra lateral molar pairs of 37 children, was used in permanent dentition. As filling materials, a HSGIC (Ketac Molar/3M ESPE) and a RMGIC (Vitremer/ 3M ESPE) were used with the Atraumatic Restorative Treatment (ART). Baseline and 6, 12 and 24-month evaluations of the fillings were made with standard-ART and USPHS criteria by two examiners with kappa values of 0.92 and 0.87 for both criteria.

Results:

According to the USPHS criteria, the retention rates of RMGIC and HSGIC restorations were 100% and 80.9% for single surface, and 100% and 41.2% for multiple surface restorations after 24 months, respectively. Irrespective of surface number, RMGIC was significantly superior to HSGIC (p= 0.004), according to both standard-ART and USPHS criteria.

Conclusion:

The results indicate that RMGIC may be an alternative restorative technique in comparison to high-strength GIC applications in ART-field-trials. However, further clinical and field trials are needed to support this conclusion.     

Annexin 1 mediates the rapid anti-inflammatory effects of neutrophil-derived microparticles

Polymorphonuclear leukocyte (PMN)-derived microparticles display inhibitory properties on target cells as assessed in vitro; since PMNs contain abundant amounts of the endogenous anti-inflammatory protein annexin 1 (AnxA1), we tested here whether biologically active AnxA1 could be present in PMN-derived microparticles. PMN adhesion to human umbilical vein endothelial cell (HUVEC) monolayers led to the generation of microparticles that contained AnxA1, as detected by Western blotting, flow cytometry, and mass spectrometry analyses. Addition of these microparticles to recipient PMNs prior to flow over HUVEC monolayers significantly inhibited cell adhesion, an effect abrogated by a neutralizing anti-AnxA1 antibody, or an antibody raised against the AnxA1 receptor, that is termed lipoxin A(4) receptor or ALX. Intravenous delivery of human PMN-derived microparticles markedly inhibited PMN recruitment to an air pouch inflamed with IL-1beta. This anti-inflammatory effect was also dependent on endogenous AnxA1, since injection of microparticles produced from wild-type PMNs (bone marrow derived), but not from AnxA1-null PMNs, inhibited IL-1beta-induced leukocyte trafficking. In conclusion, PMN-derived microparticles contain functionally active AnxA1 that confers them anti-inflammatory properties; generation of these microparticles in the microcirculation could promote inflammatory resolution by time-dependent dampening of cell recruitment.     

Prevention of maternal bacterial transmission on children's dental-caries-development: 4-year results of a pilot study in a rural-child population

AIM: Dental caries with its bacterial agent is an infectious disease, and shows a vertical transmission. The control of bacterial transmission of Mutans streptococci (MS) from mother to child has been studied, and its results on their children's caries development, and on their siblings' bacterial levels, have been analysed in a field-trial (for 4 years) in rural area. MATERIAL AND METHODS: In the same tribe, 8 mothers and their 11 children (test children [TC]), and then (following years) their 9 siblings (test sibling [TSb]), were followed for 4 years. The study started when the TC group had just started to erupt. Test mothers were subjected to a preventive regime. Examination of caries development as well as determination of plaque levels of MS in TC and TSb were carried out annually and at 6-month intervals. At the end of 4 years, two control groups (control children [CC] and control siblings [CSb]) resembling TC and TSb were selected from the other tribe living in the same village, and bacterial data and caries status were compared to both test groups. RESULTS: Microbial data demonstrated that the test children (p<0.01) and test siblings (p<0.05) had significantly low bacterial level in plaque samples. Accordingly, TC had significantly low dmf-t and -s number compared to corresponding control group (p<0.001 for dmf-t, p<0.0001 for dmf-s). CONCLUSION: The preventive regimen was applicable in rural southeastern Anatolia, where an introverted life style with a great tribal system is prevailing, any other preventive measures may have been practical or available, and babies are basically cared by mothers.     

Vagus nerve controls resolution and pro-resolving mediators of inflammation

Resolution of inflammation is now recognized as a biosynthetically active process involving pro-resolving mediators. Here, we show in zymosan-initiated peritoneal inflammation that the vagus nerve regulates local expression of netrin-1, an axonal guidance molecule that activates resolution, and that vagotomy reduced local pro-resolving mediators, thereby delaying resolution. In netrin-1^+/− mice, resolvin D1 (RvD1) was less effective in reducing neutrophil influx promoting resolution of peritonitis compared with Ntn1^+/+. Netrin-1 shortened the resolution interval, decreasing exudate neutrophils, reducing proinflammatory mediators, and stimulating the production of resolvins, protectins, and lipoxins. Human monocytes incubated with netrin-1 produced proresolving mediators, including resolvins and lipoxins. Netrin-1 and RvD1 displayed bidirectional activation in that they stimulated each other’s expression and enhanced efferocytosis. These results indicate that the vagus nerve regulates both netrin-1 and pro-resolving lipid mediators, which act in a bidirectional fashion to stimulate resolution, and provide evidence for a novel mechanism for local neuronal control of resolution.Acute inflammation is part of the complex response to tissue injury and infection by invading microorganisms. In the initial phase of the acute inflammatory response, immune cells extravasate and migrate to the site of inflammation guided by chemokines and eicosanoid mediators (Serhan et al., 2008; Tabas and Glass, 2013). In the resolution phase, specialized lipid mediators (SPM) endowed with novel pro-resolving properties are biosynthesized, which stimulates active resolution of tissue insult (Serhan and Savill, 2005). The resolution phase limits excessive neutrophil infiltration into affected organs, namely cessation of PMN influx and the clearance of apoptotic PMN and cellular debris by macrophages (Mϕ; Serhan and Savill, 2005). Excessive PMN within tissues can give rise to sustained local inflammation via further tissue destruction that often leads to the eventual loss of organ function (Asfaha et al., 2001; Serhan and Savill, 2005; Charo and Ransohoff, 2006; Tabas and Glass, 2013).Neuronal guidance proteins present in peripheral tissues contribute to the local control of leukocyte migration and inflammation (Wu et al., 2001; Rao et al., 2002; Mirakaj et al., 2011a). Netrin-1 is one of these neuronal proteins, which acts as a chemoattractant in axonal migration (Colamarino and Tessier-Lavigne, 1995; van Gils et al., 2012). Recently, netrin-1 was found to direct leukocyte traffic during acute inflammation in peripheral organs (Ly et al., 2005; Rosenberger et al., 2009; Mirakaj et al., 2010, 2011b; Aherne et al., 2012). With an acute inflammatory response, complete resolution of tissue inflammation is the ideal outcome for affected tissues to regain function (Bannenberg et al., 2005; Serhan and Savill, 2005; Serhan and Petasis, 2011). Although netrin-1 clearly exerts antiinflammatory and protective properties (Ly et al., 2005; Rosenberger et al., 2009; Mirakaj et al., 2010, 2011b; Aherne et al., 2012), whether netrin-1 serves to stimulate endogenous resolution programs remained to be explored. In this regard, resolution and eventual homeostasis are achieved via limiting further infiltration of neutrophils (PMN), as well as promoting local clearance via Mϕ phagocytosis of cellular debris, apoptotic cells, and/or invading organisms (Serhan and Savill, 2005) orchestrated by novel local chemical mediators, i.e., resolvins, that possess this defining action (Serhan et al., 2002; Serhan and Petasis, 2011). Tracey (2002) uncovered neuronal reflex circuits that sense peripheral inflammation and provide regulatory feedback via specific nervous signals that regulate immune responses (Olofsson et al., 2012).Because it is now clear that endogenous antiinflammation and pro-resolution are not equivalent processes in that pro-resolving mediators both stop/limit PMN entry and enhance nonphlogistic phagocytosis by Mϕ (Serhan and Savill, 2005; Serhan and Petasis, 2011), we questioned whether the vagus nerve, netrin-1 expression, and local endogenous resolution programs are linked and impact the resolution of acute inflammation. Here, we report a new circuit involving the vagus nerve, netrin-1, and local lipid mediators that control the resolution of inflammation.