No abstract

No abstract

Objective To evaluate the clinical performance of brackets cured with a high-intensity, light-emitting diode (LED) with a shorter curing time. Materials and Methods Thirty-four patients and a total of 680 brackets were examined using a randomized split-mouth design. The maxillary right and mandibular left quadrants were cured for 6 seconds with a high-intensity LED light (3200 mW/cm2) and the maxillary left and mandibular right quadrants were cured for 20 seconds with a standard-intensity LED light (1200 mW/cm2). Alternating patients had the quadrants inverted for the curing protocol. The number and date of each first-time bracket failure was recorded from 199 to 585 days posttreatment. Results The bracket failure rate was 1.18% for both curing methods. The proportion of bracket failure was not significantly different between curing methods (P = 1.000), genders (P = 1.000), jaws (P = .725), sides (P = .725), or quadrants (P = .547). Posterior teeth exhibited a greater proportion of failures (2.21%) relative to anterior teeth (0.49%), although the difference was not statistically significant (P = .065). Conclusions No difference was found in bond failure rates between the two curing methods. Both methods showed bond failure rates low enough to be considered clinically sufficient. The high-intensity LED light used with a shorter curing time may be considered an advantage due to the reduced chair time.

Bladder urothelial carcinoma (BC) is a fatal invasive malignancy and the most common malignancy of the urinary system. In the current study, we investigated the function and mechanisms of Neuropilin-1 (NRP1), the co-receptor for vascular endothelial growth factor, in BC pathogenesis and progression. The expression of NRP1 was evaluated using data extracted from GEO and HPA databases and examined in BC cell lines. The effect on proliferation, apoptosis, angiogenesis, migration, and invasion of BC cells were validated after NRP1 knockdown. After identifying differentially expressed genes (DEGs) induced by NRP1 silencing, GO/KEGG and IPA® bioinformatics analyses were performed and specific predicted pathways and targets were confirmed in vitro. Additionally, the co-expressed genes and ceRNA network were predicted using data downloaded from CCLE and TCGA databases, respectively. High expression of NRP1 was observed in BC tissues and cells. NRP1 knockdown promoted apoptosis and suppressed proliferation, angiogenesis, migration, and invasion of BC cells. Additionally, after NRP1 silencing the activity of MAPK signaling and molecular mechanisms of cancer pathways were predicted by KEGG and IPA® pathway analysis and validated using western blot in BC cells. NRP1 knockdown also affected various biological functions, including antiviral response, immune response, cell cycle, proliferation and migration of cells, and neovascularisation. Furthermore, the main upstream molecule of the DEGs induced by NRP1 knockdown may be NUPR1, and NRP1 was also the downstream target of NUPR1 and essential for regulation of FOXP3 expression to activate neovascularisation. DCBLD2 was positively regulated by NRP1, and PPAR signaling was significantly associated with low NRP1 expression. We also found that NRP1 was a predicted target of miR-204, miR-143, miR-145, and miR-195 in BC development. Our data provide evidence for the biological function and molecular aetiology of NRP1 in BC and for the first time demonstrated an association between NRP1 and NUPR1, FOXP3, and DCBLD2. Specifically, downregulation of NRP1 contributes to BC progression, which is associated with activation of MAPK signaling and molecular mechanisms involved in cancer pathways. Therefore, NRP1 may serve as a target for new therapeutic strategies to treat BC and other cancers.

Objectives To analyze the biomechanical system of anterior retraction with clear aligner therapy (CAT) with and without an anterior mini-screw and elastics. Materials and Methods Models including a maxillary dentition (without first premolars), maxilla, periodontal ligaments (PDLs), attachments, and aligners were constructed and imported to finite element software. Three model groups were created: (1) control (CAT alone), (2) labial elastics (CAT with elastics between the anterior mini-screw and buttons on central incisors), and (3) linguoincisal elastics (CAT with elastics between the anterior mini-screw and precision cuts on the lingual sides of the aligner). Elastic forces (0–300 g, in 50 g increments) were applied. Results CAT alone caused lingual tipping and extrusion of the incisors. Labial elastics caused palatal root torquing and intrusion and mesial tipping of the central incisors, while linguoincisal elastics produced palatal root torquing and intrusion of both central and lateral incisors. Second premolars were intruded in all three groups, with less intrusion in the linguoincisal elastics group. For the control group, stress was concentrated on both labial and lingual root surfaces, alveolar ridge, and cervical and apical PDLs. Stress was more concentrated in the labial elastics group and less concentrated in the linguoincisal elastics group. Conclusions CAT produced lingual tipping and extrusion of incisors during anterior retraction. Anterior mini-screws and elastics can achieve incisor intrusion and palatal root torquing. Linguoincisal elastics are superior to labial elastics with a lower likelihood of buccal open bite. Root resorption and alveolar defects may occur in CAT, more likely for labial elastics and less likely for linguoincisal elastics.

Objective To provide a road map of buccal cortical bone thickness in interradicular locations where miniscrew implants are commonly placed. Materials and Methods Cone-beam computed tomography images from 100 study quadrants (50 maxillary and 50 mandibular) were studied. Cortical bone thickness was measured at the most mesial point, the midpoint, and the most distal point in interradicular areas from the canine to the first molar in both arches at 4 mm and 6 mm from the alveolar ridge. Indicator variables of whether the cortical bone thickness was thinner than 1 mm and thicker than 1.5 mm were constructed and analyzed in a general linear mixed model. Results Buccal cortical bone was significantly thinner at a point bisecting two teeth than the bone adjacent to the teeth (P < .0001). The site with the greatest percentage of measurements <1 mm (20%) was at the midpoint bisecting the mandibular canine and the first premolar. The site with the highest percentage of measurements >1.5 mm (50%) was in the mandible adjacent to the first molar (distal to the midpoint of the second premolar and first molar) at 6 mm from the alveolar crest. Conclusion Cortical bone thickness is significantly thinner centrally between two teeth than in the areas adjacent to the roots.

No abstract

No abstract