The new method of manufacturing NiTi instruments by twisting coupled with heat treatment might contribute to the increased phase transformation temperatures and superior flexibility.
The purpose of this study was to test nickel titanium (NiTi) instrument performance under different surrounding temperatures. Twenty-four superelastic NiTi instruments with a conical shape comprising a 0.30-mm-diameter tip and 0.06 taper were equally divided into 3 groups according to the temperature employed. Using a specially designed cyclic fatigue testing apparatus, each instrument was deflected to give a curvature 10 mm in radius and a 30° angle. This position was kept as the instrument was immersed in a continuous flow of water under a temperature of 10, 37, or 50 °C for 20 s to calculate the deflecting load (DL). In the same position, the instrument was then allowed to rotate at 300 rpm to fracture, and the working time was converted to the number of cycles to fracture (NCF). The statistical significance was set at p = 0.05. The mean DL (in N) and NCF (in cycles) of the groups at 10, 37, and 50 °C were 10.16 ± 1.36 and 135.50 ± 31.48, 13.50 ± 0.92 and 89.20 ± 16.44, and 14.70 ± 1.21 and 65.50 ± 15.90, respectively. The group at 10 °C had significantly the lowest DL that favorably resulted in the highest NCF. Within the limitations of this study, the surrounding temperature influences the cyclic fatigue resistance and DL of the superelastic NiTi instruments. Lower temperatures are found to favorably decrease the DL and extend the lifetime of the superelastic NiTi instrument. Further NiTi instrument failure studies should be performed under simulated body temperature.
The nano-indentation technique can be applied to determine the performance and the failure mechanism of NiTi instruments. The fatigue process revealed a significant decrease in the hardness and elastic modulus of the NiTi instrument. As indicated by the low hardness, the fatigue process did not result in work hardening but rather work softening.
Apical periodontitis (AP) is an acute or chronic inflammatory disease caused by complex interactions between infected root canal and host immune system. It results in the induction of inflammatory mediators such as chemokines and cytokines leading to periapical tissue destruction. To understand the molecular pathogenesis of AP, we have investigated inflammatory-related genes that regulate AP development. We found here that macrophage-derived CXCL9, which acts through CXCR3, is recruited by progressed AP. The inhibition of CXCL9 by a CXCR3 antagonist reduced the lesion size in a mouse AP model with decreasing IL-1β, IL-6 and TNFα expression. The treatment of peritoneal macrophages with CXCL9 and LPS induced the transmigration and upregulation of osteoclastogenic cytokines such as IL-1β, IL-6 and matrix metalloprotease 2, a marker of activated macrophages. This suggests that the CXCL9-CXCR3 axis plays a crucial role in the development of AP, mediated by the migration and activation of macrophages for periapical tissue destruction. Our data thus show that CXCL9 regulates the functions of macrophages which contribute to AP pathogenesis, and that blocking CXCL9 suppresses AP progression. Knowledge of the principal factors involved in the progression of AP, and the identification of related inflammatory markers, may help to establish new therapeutic strategies.
The treatment of vertical bone defects caused by severe periodontal disease requires the regeneration of periodontal tissue. Although various bone substitutes have been clinically applied to vertical bone defect correction, the evaluation of these materials in periodontal tissue remains incomplete. The purpose of this study was to examine the bone regeneration abilities of various bone substitutes including Cytrans, Cerasorb, Neobone and Bio-Oss in a 3-wall bone defect animal model. All of these bone substitutes showed a similar healing ability to periodontal ligament and cementum. However, Cytrans showed the fastest bone healing ability compared with the other materials at 4 weeks post-transplantation. In addition, the recruitment of osteoclasts and endothelial cells was observed in Cytrans grafts at 4 weeks, but only detected at 8 weeks in the other materials. These results suggest that Cytrans promotes faster bone healing by inducing bone remodeling and angiogenesis.
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