Retrospective Clinical Evaluation of RMGIC/GIC Class V Restorations.

The aim of this retrospective study was to evaluate the clinical performance of glass-ionomer cement (GIC) and resin-modified glass-ionomer cement (RMGIC) materials in Class V carious cervical lesions restored by dental students. Ninety-six (96) restorations performed with either GIC (Fuji IX) (n = 39) or RMGIC (Fuji II LC) (n = 57) were evaluated using the modified USPHS criteria by two independent investigators at two follow-up evaluations (two years apart). The Fisher statistical test was used to compare USPHS criteria and examine significant differences, with a significance level set at p < 0.05. The Kaplan-Meier algorithm was used to calculate the survival probability. The overall success rate of Class V restorations was 72.9% at the second follow-up evaluation, with restorations ranging in age from 2.5 to 3.5 years. The RMGIC (Fuji II LC) restorations exhibited a significantly higher overall success rate compared to the GIC (Fuji IX) restorations (p = 0.0104). Significant differences were observed in retention (p = 0.0034) and color match (p = 0.0023).

Five-Year Clinical Performance of Complex Class II Resin Composite and Amalgam Restorations-A Retrospective Study.

The aim of this retrospective study was to investigate the clinical performance of posterior complex resin composite (RC) and amalgam (AM) restorations after a five-year period. One hundred and nineteen complex Class II restorations placed by dental students were evaluated using the USPHS criteria. Data were analyzed using Chi-square, Mann-Whitney, and Wilcoxon tests at a 0.05 level of significance. After five years, the percentages of clinically satisfactory complex Class II RC and AM restorations were 78% and 76.8%, respectively. The main reasons for the failure of AM restorations included secondary caries (Bravo-10.1%), defective marginal adaptation (Charlie-8.7%), and fracture of the tooth (Bravo-7.2%). RC restorations presented failures related to the fracture of the restoration (Bravo-16%) and defective marginal adaptation (Charlie-8.2%). There was a significantly higher incidence of secondary caries for AM restorations (AM-10.1%; RC-0%; p = 0.0415) and a higher number of fractures for RC restorations (AM-4.3%; RC-16%; p = 0.05). Regarding anatomy, AM restorations presented a significantly higher number of Alfa scores (49.3%) compared to RC restorations (22.4%) (p = 0.0005). The results of the current study indicate that complex class II RC and AM restorations show a similar five year clinical performance.

Matrix metalloproteinase 9 is associated with peritoneal membrane solute transport and induces angiogenesis through ß-catenin signaling.

Background: For patients using peritoneal dialysis (PD), the peritoneal membrane can develop fibrosis and angiogenesis, leading to ultrafiltration failure, chronic hypervolemia and increased risk of technique failure and mortality. Matrix metalloproteinases (MMPs), and specifically the gelatinases (MMP2 and MMP9), may be involved in peritoneal membrane injury. Methods: From stable PD patients, mesothelial cells were assayed for MMP gene expression. MMP9 was overexpressed in mouse peritoneum by adenovirus, and MMP9 -/- mice were subjected to transforming growth factor ß (TGF-ß)-induced peritoneal fibrosis. Results: MMP9 mRNA expression correlated with peritoneal membrane solute transport properties. Overexpression of MMP9 in the mouse peritoneum induced submesothelial thickening and angiogenesis. MMP9 induced mesothelial cell transition to a myofibroblast phenotype measured by increased alpha smooth muscle actin and decreased E-cadherin expression. Angiogenesis was markedly reduced in MMP9 -/- mice treated with an adenovirus expressing active TGF-ß compared with wild-type mice. TGF-ß-mediated E-cadherin cleavage was MMP9 dependent, and E-cadherin cleavage led to ß-catenin-mediated signaling. A ß-catenin inhibitor blocked the angiogenic response induced by AdMMP9. Conclusions: Our data suggest that MMP9 is involved in peritoneal membrane injury possibly through cleavage of E-cadherin and induction of ß-catenin signaling. MMP9 is a potential biomarker for peritoneal membrane injury and is a therapeutic target to protect the peritoneal membrane in PD patients.

Genetic Polymorphisms and Peritoneal Membrane Function.

BACKGROUND: Outcomes for peritoneal dialysis (PD) patients are affected by the characteristics of the peritoneal membrane, which may be determined by genetic variants. We carried out a systematic review of the literature to identify studies which assessed the association between genetic polymorphisms, peritoneal membrane solute transport, and clinical outcomes for PD patients. METHODS: The National Library of Medicine was searched using a variety of strategies. Studies which met our inclusion criteria were reviewed and data abstracted. Our outcomes of interest included: high transport status peritoneal membrane, risk for peritonitis, encapsulating peritoneal sclerosis (EPS), patient and technique survival. We combined data from studies which evaluated the same genetic polymorphism and the same outcome. RESULTS: We evaluated 18 relevant studies. All studies used a candidate gene approach. Gene polymorphisms in the interleukin (IL)-6 gene were associated with peritoneal membrane solute transport in several studies in different ethnic populations. Associations with solute transport and polymorphisms in endothelial nitric oxide synthase and receptor for advanced glycation end product genes were also identified. There was evidence of a genetic predisposition for peritonitis found in 2 studies, and for EPS in 1 study. Survival was found to be associated with a polymorphism in vascular endothelial growth factor and technique failure was associated with a polymorphism in the IL-1 receptor antagonist. CONCLUSIONS: There is evidence that characteristics of the peritoneal membrane and clinical outcomes for PD patients have genetic determinants. The most consistent association was between IL-6 gene polymorphisms and peritoneal membrane solute transport.

Gremlin promotes peritoneal membrane injury in an experimental mouse model and is associated with increased solute transport in peritoneal dialysis patients.

The peritoneal membrane becomes damaged in patients on peritoneal dialysis (PD). Gremlin 1 (GREM1) inhibits bone morphogenic proteins (BMPs) and plays a role in kidney development and fibrosis. We evaluated the role of gremlin in peritoneal fibrosis and angiogenesis. In a cohort of 32 stable PD patients, GREM1 concentration in the peritoneal effluent correlated with measures of peritoneal membrane damage. AdGrem1, an adenovirus to overexpress gremlin in the mouse peritoneum, induced submesothelial thickening, fibrosis, and angiogenesis in C57BL/6 mice, which was associated with decreased expression of BMP4 and BMP7. There was evidence of mesothelial cell transition to a mesenchymal phenotype with increased α smooth muscle actin expression and suppression of E-cadherin. Some of the GREM1 effects may be reversed with recombinant BMP7 or a pan-specific transforming growth factor ß (TGF-ß) antibody. Neovascularization was not inhibited with a TGF-ß antibody, suggesting a TGF-ß-independent angiogenic mechanism. Swiss/Jackson Laboratory (SJL) mice, which are resistant to TGF-ß-induced peritoneal fibrosis, responded in a similar fashion to AdGrem1 as did C57BL/6 mice with fibrosis, angiogenesis, and mesothelial-to-mesenchymal transition. GREM1 was associated with up-regulated TGF-ß expression in both SJL and C57BL/6 mice, but SJL mice demonstrated a defective TGF-ß-induced GREM1 expression. In summary, GREM1 induces fibrosis and angiogenesis in mouse peritoneum and is associated with increased solute transport in these PD patients.