Aims and Objectives: Endodontic treatment is directed to eliminate microbial challenges from the root canal system and to create a complete seal. The aim of this study was to assess the apical sealing ability of resin-based Epiphany-Resilon root canal filling system and to compare it with the sealing abilities of different combinations of AH Plus, gutta-percha, Epiphany, and Resilon. Materials and Methods: One hundred extracted human maxillary incisor roots were treated endodontically. The samples were divided into groups A, B, C, and D, with each group containing 25 samples. Group A: Canals obturated with gutta-percha and AH Plus sealer; Group B: Canals obturated with Resilon and Epiphany; Group C: Canals obturated with gutta-percha and Epiphany; Group D: Control group canals obturated with gutta-percha without a sealer. The sealing ability of each of the obturation techniques was tested using the dye penetration method followed by the clearing method using alcohol. Stereo microscope was used to measure the extent of dye penetration. Statistical data analysis was performed using analysis of variance and Tukey tests. Results: Microleakage was found in all the four groups. Apical extent of mean microleakage was maximum for gutta-percha, followed by Gutta-percha + AH-plus and Gutta-percha + Epiphany, and the least with Resilon + Epiphany. Statistically significant difference (P < 0.01) was seen in the apical leakage. Conclusion: All the samples tested showed microleakage. The “Epiphany soft resin endodontic obturation system” showed a superior result compared to other obturation materials.
CD47 is a self-marker expressed on the surface of RBCs and work to prevent the process of phagocytosis. SIRPα is the ligand of CD47 that is expressed on the surface of phagocytic cells, such as macrophages, to control the removal of dead/diseased cells. This study aimed to examine the expression of CD47 on RBCs and SIRPα on PBMC cells in SCD patients and the apoptosis of SCD RBCs. We also measured the levels of pro-inflammatory cytokines in SCD patients and correlated it with the cell surface marker expression of CD47 and SIRPα to determine whether CD47 and/or SIRPα played a role in promoting the pro-inflammatory phenotype in SCD. Whole blood samples were drawn from SCD patients, and healthy control and PBMC were isolated and stained with SIRPα. Change in CD47, apoptosis by annexin V marker, and pro-inflammatory cytokines were measured and correlation among these variants was determined. The expression of CD47 was significantly decreased and the apoptosis was increased in RBCs of SCD patients. A higher level of pro-inflammatory cytokines, IL-6 and IL-1β, was found in SCD patients and IL-1β was found to be inversely correlated with SIRPα expression. Our data showed that CD47 of erythrocytes of SCD samples is reduced and that the apoptosis is increased in those patients. Based on the role of CD47, we suggest that increased apoptosis in SCD would be impacted by the reduced level of CD47. An inverse relationship was found between SIRPα marker on PBMC and the increased production of pro-inflammatory cytokines in SCD.