Waad Kheder

This study was designed to investigate the impact of access cavity designs on fracture resistance of endodontically treated maxillary first premolars. The study sample consisted of 72 intact maxillary first premolars, randomly divided into six groups (n = 12). A standardized proximal cavity preparation was prepared for all samples using standard bur. Groups I: control group with only standard proximal cavity and no endodontic access, group II: Truss access cavity, group III: Separated access to buccal and palatal canals without removal of dentine in between, group IV: Access to buccal and palatal canals with removal of dentine in between, group V: Traditional access cavity, group VI: Mesio-occlusal-distal cavity (MOD). For groups I and VI, only composite restoration was used to restore the proximal cavity, while for groups II- V, the access was prepared and endodontic treatment was performed on all teeth, then composite restoration was placed. The root canals were instrumented using nickel-titanium files, irrigated with sodium hypochlorite, and filled with AH plus sealer and gutta-percha using warm vertical condensation. All samples were then placed in an acrylic mold and underwent thermal aging for 10,000 cycles between 5 and 55°C. The samples were fixed in a universal testing machine with the long axis of the roots positioned at 20° to a load applied at a crosshead speed of 1 mm/min using a stainless steel semi-spherical indenter (Ø = 3 mm) until fracture occurred to determine the fracture resistance force in Newton. The normality test (Shapiro-Wilk) showed that data are normally distributed. Group II exhibited the highest mean fracture resistance, and group VI was the least likely to resist the fracture. No statistically significant differences between tested groups (p-value = 0.237). The MOD group showed a more unfavorable mode of fracture compared to other groups. No significant difference in fracture resistance between conservative and traditional access cavities. The missing marginal ridges, such as in MOD cavities played an important role in decreasing the fracture resistance of endodontically treated teeth.

Titanium dental implants are one of the modalities to replace missing teeth. The release of titanium particles from the implant’s surface may modulate the immune cells, resulting in implant failure. However, little is known about the immune microenvironment that plays a role in peri-implant inflammation as a consequence of titanium particles. In this study, the peri-implant gingival tissues were collected from patients with failed implants, successful implants and no implants, and then a whole transcriptome analysis was performed. The gene set enrichment analysis confirmed that macrophage M1/M2 polarization and lymphocyte proliferation were differentially expressed between the study groups. The functional clustering and pathway analysis of the differentially expressed genes between the failed implants and successful implants versus no implants revealed that the immune response pathways were the most common in both comparisons, implying the critical role of infiltrating immune cells in the peri-implant tissues. The H&E and IHC staining confirmed the presence of titanium particles and immune cells in the tissue samples, with an increase in the infiltration of lymphocytes and macrophages in the failed implant samples. The in vitro validation showed a significant increase in the level of IL-1β, IL-8 and IL-18 expression by macrophages. Our findings showed evidence that titanium particles modulate lymphocyte and macrophage polarization in peri-implant gingival tissues, which can help in the understanding of the imbalance in osteoblast–osteoclast activity and failure of dental implant osseointegration.