ABSTRACT
OBJECTIVE: examination of the influence of chemical composition changes on the ability of sealers to withstand a pull-out test. MATERIALS AND METHODS: Fifty distal or palatal canals of extracted teeth were prepared by Dc Taper files. The teeth were divided into five groups: AH Plus, BJM RCS, Total Fill BC,AH Plus Bioceramic and a group with Gutta Percha with no sealer added. Ten days after obturation, each cone was subjected to the "pull-out test" with the Shimadzo Universal Testing Machine until it was torn or removed from the canal. A force to Stroke graph was generated and the maximum vertex of this graph was recorded. The number of times the cone was torn or removed was recorded. RESULTS: The amount of force needed to remove or rupture the cone was significantly higher in all sealer groups compared to the AH Plus Bioceramic group. The force needed for the AH Plus group was double that needed for the AH Plus Bioceramic group 4 (1.87 ± 0.53 N vs 0.93 ± 0.48 N, respectively, P < 0.001). All of the cones (n = 10) in the AH Plus Bio Ceramic Sealer group were removed in their entirety (P = 0.01 compared to each of the other groups). CONCLUSIONS: The addition of macromolecules to epoxy sealer does not change the material's ability to withstand the pull-out test. Decreasing the amount of tri- and di-calcium silicate compounds combined with increasing amounts of zirconium oxide in a Bioceramic sealer significantly decreased the material's ability to withstand the pull-out test.
ABSTRACT
BACKGROUND: Neurons of adult mammalian CNS are prevented from regenerating injured axons due to formation of a non-permissive environment. The retinal ganglion cells (RGC), which are part of the CNS, share this characteristic. In sharp contrast, the RGC of lower vertebrates, such as fish, are capable of re-growing injured optic nerve axons, and achieve, through a complex multi-factorial process, functional vision after injury. Semaphorin-3A (sema-3A), a member of the class 3 semaphorins known for its repellent and apoptotic activities, has previously been shown to play a key role in the formation of a non-permissive environment after CNS injury in mammalians. METHODS: The expression of sema-3A and its effect on regenerative processes in injured gold fish retina and optic nerve were investigated in this study. Unilateral optic nerve axotomy or crush was induced in goldfish. 2 microl sema-3A was injected intraviterally 48 hours post injury. Neuronal viability was measured using the lipophilic neurotracer dye 4-Di-10-Asp. Axonal regeneration was initiated using the anterograde dye dextran. Retinas and optic nerves were collected at intervals of 2, 3, 7, 14 and 28 days after the procedure. Using Western blot and immunohistochemical analysis, the expression levels of semaphorin-3A, axonal regeneration, the removal of myelin debris and macrophage invasion were studied. RESULTS: We found a decrease in sema-3A levels in the retina at an early stage after optic nerve injury, but no change in sema-3A levels in the injured optic nerve. Intravitreal injection of sema-3A to goldfish eye, shortly after optic nerve injury, led to destructive effects on several pathways of the regenerative processes, including the survival of retinal ganglion cells, axonal growth, and clearance of myelin debris from the lesion site by macrophages. CONCLUSIONS: Exogenous administration of sema-3A in fish indirectly interferes with the regeneration process of the optic nerve. The findings corroborate our previous findings in mammals, and further validate sema-3A as a key factor in the generation of a non-permissive environment after transection of the optic nerve.
