Background/Aims Indirect pulp capping, pulpotomy, and apexification are three common endodontic treatments for immature traumatized incisors. They all affect tooth root development to some extent. The aim of this retrospective study was to compare the influence of these treatments on root development of immature permanent incisors following dental trauma. Materials and Methods Twenty‐one indirect pulp capping, 48 pulpotomy, and 58 apexification cases with a mean age of 8.4 ± 1.0 years and median follow up of 12 months were included. NIH ImageJ with TurboReg plug‐in was used to correct angular differences between the pre‐operative and recall periapical radiographs, and to calculate variations of root length, dentin wall thickness, and apical closure. Kruskal‐Wallis ANOVA followed by pairwise comparisons was applied to compare the radiographic variations. The type of apical closure was assessed qualitatively and analyzed using Fisher's exact test. Results The apexification group had a lower trend toward apical closure than the other two groups (P < .05). It also showed thinner dentin wall thickness compared with the pulpotomy group (P = .001). There was no significant difference between pulpotomy and indirect pulp capping in the trend to apical closure (P > .05) or dentin wall thickness (P = .775). There was no significant difference in the variation of root length among the three groups (P = .06). There was a moderate correlation between the treatment and the type of apical closure (Cramer's V Coefficient = .375). Pulpotomy tended to form a normal apical constriction rather than a calcific barrier while apexification showed the opposite inclination. Indirect pulp capping had no specific inclination toward any type of apical closure. Conclusions Apexification resulted in an abnormal root development mostly by affecting the dentin wall thickness and apical closure. Pulpotomy was beneficial for normal root development of immature traumatized teeth.
Recent studies have demonstrated that acquisition of cancer stem-like properties plays an essential role in promoting epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) resistance in non-small cell lung cancer (NSCLC); however, how to regulate cancer stem-like properties and EGFR-TKI resistance is largely unclear. In this study, we discovered that increased iroquois-class homeodomain protein 4 (IRX4) was related to gefitinib resistance in NSCLC cells. Knockdown of IRX4 inhibited cell proliferation, sphere formation, and the expression of CD133, ALDH1A1, NANOG, Sox2 and Notch1, and the transcriptional activity of NANOG promoter. IRX4 overexpression increased the protein level of NANOG and CD133 in PC-9 cells. Combination of knocking-down IRX4 with gefitinib increased cell apoptosis and decreased cell viability and the expression of p-EGFR and NANOG in PC-9/GR cells. IRX4 knockdown in a PC-9/GR xenograft tumor model inhibited tumor progression and the expression of NANOG and CD133 more effectively than single treatment alone. Knockdown of NANOG inhibited the expression of CD133 and restored gefitinib cytotoxicity, and NANOG overexpression-induced cancer stem-like properties and gefitinib resistance could be obviously reversed by knocking-down IRX4. Further, we found that 1,25-dihydroxyvitamin D3 (1,25(OH) 2 D 3) reduced obviously the expression of IRX4 and NANOG by inhibiting the activation of TGF-β1/Smad3 signaling pathway; moreover, combination of 1,25(OH) 2 D 3 and gefitinib decreased cell viability and proliferation or tumor progression and the expression of IRX4 and NANOG compared with single treatment alone both in PC-9/GR cells and in a PC-9/GR xenograft tumor model. These results reveal that inhibition of IRX4-mediated cancer stem-like properties by regulating 1,25(OH) 2 D 3 signaling may increase gefitinib cytotoxicity. Combination therapy of gefitinib and 1,25 (OH) 2 D 3 by targeting IRX4 and NANOG, could provide a promising strategy to improve gefitinib cytotoxicity.
Tubulointerstitial fibrosis is one of the most common pathological features of diabetic nephropathy. Autophagy, an intracellular mechanism to remove damaged or dysfunctional cell parts and maintain metabolic homeostasis, is inhibited in diabetic neuropathy. Icariin is a traditional Chinese medicine extract known for nourishing the kidney and reinforcing Yang. In this study, we investigated the effects and mechanism of Icariin on renal function, autophagy, and fibrosis in type 2 diabetic nephropathic rats and in high-glucose-incubated human renal tubular epithelial cells and rat renal fibroblasts (in vitro). Icariin improved diabetes, renal function, restored autophagy, and alleviated fibrosis in type 2 diabetic neuropathic rats and in vitro. After we applied autophagy-related gene 5-small interfering RNA, we found that fibrosis improvement by Icariin was related to autophagy restoration. By detecting serum sex hormone levels, and using dihydrotestosterone, siRNA for androgen receptor, and the androgen receptor antagonist Apalutamide (ARN-509), we found that Icariin had an androgen-like effect and restored autophagy and reduced fibrosis by regulating the androgen receptor. In addition, miR-192-5p levels were increased under high glucose but reduced after dihydrotestosterone and Icariin treatment. Furthermore, dihydrotestosterone and Icariin inhibited miR-192-5p overexpression-induced fibrosis production and autophagy limitation. Glucagon-like peptide-1 receptor (GLP-1R) was downregulated by high glucose and overexpression of miR-192-5p and could be restored by dihydrotestosterone and Icariin. By using ARN-509, we found that Icariin increased GLP-1R expression by regulating the androgen receptor. GLP-1R-siRNA transfection weakened the effects of Icariin on autophagy and fibrosis. These findings indicate that Icariin alleviates tubulointerstitial fibrosis by restoring autophagy through the miR-192-5p/GLP-1R pathway and is a novel therapeutic option for diabetic fibrosis.
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