Dens invaginatus is a malformation with varying anatomical features, posing challenges to treatment. Early and accurate diagnosis plays a significant role in selecting the appropriate treatment. The diagnosis of teeth with a complex root canal system including dens invaginatus has made progress with the application of three-dimensional imaging techniques in endodontics. Advanced treatment options provide hope for teeth that could not be saved before. This review discusses diagnostic methods and treatment options for teeth with dens invaginatus, and provides guidelines for the management of dens invaginatus cases in clinic. Current as well as traditional diagnostic techniques are summarized. Treatment options including state-of-the-art alternatives are presented for coronal dens invaginatus and radicular dens invaginatus.

Periodontitis is a prevalent and chronic inflammatory disease that is interrelated with systemic health. Periodontitis can be promoted by tumor necrosis factor α (TNF-α). Cementum, a vital part of the periodontium, is a bone-like mineralized tissue that is produced by cementoblasts. Our laboratory previously revealed that TNF-α inhibits cementoblast differentiation and mineralization. However, how TNF-α modulates cementoblast differentiation and mineralization remains largely unknown. MicroRNA-155 (miR-155) is induced and regulates TNF-α-inhibited osteogenic differentiation. In this study, we found that miR-155-3p was increased during TNF-α-stimulated OCCM-30 cells and involved in cementoblast differentiation and mineralization. Overexpression of miR-155-3p suppressed cementoblast mineralization. Bioinformatics analysis revealed that potassium channel tetramerization domain containing 1 ( Kctd1) is a candidate target gene of miR-155-3p. Moreover, miR-155-3p overexpression suppressed KCTD1 levels. Meanwhile, its knockdown increased KCTD1 expression. Transfection with miR-155-3p also inhibited the luciferase activity of 3'-untranslated regions in the Kctd1 wild type but not the mutant. These data indicated that Kctd1 is a direct and novel target of miR-155-3p. The Wnt signaling pathway inhibits cementoblast differentiation, and we further demonstrated that miR-155-3p partially modulates cementoblast differentiation through the canonical Wnt signaling pathway. In addition to the gain/loss function assay of miR-155-3p, the luciferase activity assay of canonical Wnt signaling was performed. The assays revealed that miR-155-3p increased β-catenin-mediated transcriptional activation. Overall, our data clarified that miR-155-3p mediated TNF-α-inhibited cementoblast differentiation by targeting Kctd1, at least partially through canonical Wnt signaling pathway. These findings reveal the expanded function of miRNAs in cementoblast differentiation and mineralization.

Aim To investigate the role of GATA‐binding protein 4 (GATA4) in the inflammatory response induced by DNA double‐strand breaks (DSBs) in human dental pulp cells (hDPCs). Methodology Lipopolysaccharide (LPS) was used for stimulating inflammation in dental pulp tissue in vivo and hDPCs in vitro. Expression levels of GATA4 and γ‐H2A.X (a marker for DSBs) were detected at different stages of pulpitis in a rat model and human pulp tissues by immunohistochemistry. Real‐time quantitative polymerase chain reaction and Western blot were performed to assess expression of GATA4 and γ‐H2A.X and the activation of nuclear factor κB (NF‐κB) in hDPCs stimulated by LPS. The comet assay was used for detecting the extent of DSBs in hDPCs. Immunocytochemistry and Western blot were utilized to evaluate expression of γ‐H2A.X and GATA4 and activation of NF‐κB in hDPCs pre‐treated with inhibitors of DNA damage response or transfected with GATA4 small interfering RNA before the treatment of LPS. Data were analysed statistically using one‐way anova or Kruskal–Wallis tests. Results The expression of GATA4 and activation of DNA damage response and NF‐κB in inflamed pulp tissue and LPS‐treated hDPCs were identified. Significantly decreased expression of GATA4 and significantly decreased inflammatory processes in hDPCs were demonstrated via suppression of DNA damage response (P < 0.05). In GATA4‐knockdown cells, the expression of γ‐H2A.X did not change, but nuclear translocation of p65 was significantly suppressed (P < 0.05) upon induction by LPS. Conclusions Lipopolysaccharide‐induced DSBs activated the NF‐κB signalling pathway in hDPCs, and GATA4 acts as a positive moderator of the progress. The involvement of GATA4 in this pathology may serve as a therapeutic target in pulpitis.

Porphyromonas gingivalis is responsible for the destruction of cementum in patients with periodontitis and periapical periodontitis. However, research about the effects of P. gingivalis on cementoblast mineralization and the underlying mechanism is still lacking. Casein kinase 2 interacting protein 1 (Ckip-1) is a scaffold protein that interacts with various proteins and signals to regulate different cell functions, such as cell morphology, apoptosis, and differentiation. In this study, we verified the suppressive effects of P. gingivalis and lipopolysaccharide (Pg-LPS) on OCCM-30 mineralization. We also showed that Ckip-1 gradually decreased during OCCM-30 mineralization but increased with the aggravation of Pg-induced inflammation. However, it remained unchanged when cells were stimulated with Pg-LPS, regardless of the concentration and incubation time. Then, more cellular cementum and enhanced Osterix expression were observed in Ckip-1 knockout mice when compared with the wild-type mice. Meanwhile, Ckip-1 silencing significantly enhanced cementoblast mineralization with or without P. gingivalis–associated inflammation. The trend was opposite when Ckip-1 was overexpressed. Finally, we found that the p38, Akt, and Wnt pathways were activated, while the Erk1/2 pathway was inhibited when Ckip-1 was silenced. The opposite results were also observed in the Ckip-1 overexpression group. Furthermore, we proved that cell mineralization was weakened when p38, Akt inhibitors were applied and strengthened when the Erk1/2 pathway was inhibited. In summary, Ckip-1 is upregulated under P. gingivalis–induced inflammation and negatively regulates cementoblast mineralization partially through mitogen-activated protein kinases and Akt signaling pathways, which may contribute to the restoration of cementum destroyed by P. gingivalis.

Ammonium toxicity in plants is considered a global phenomenon, but the primary mechanisms remain poorly characterized. Here, we showed that although the addition of potassium (K+) or nitrate (NO3-) partially alleviated the inhibition of rice root growth caused by ammonium toxicity, the coexistence of K+ and NO3- clearly improved the alleviation via a synergistic mechanism. The synergism led to significantly improved alleviation effects on root biomass, length, surface area, number and meristem cell number. The aberrant auxin distribution in root tips, rhizosphere acidification level and abnormal cell morphology in the root cap and elongation zone caused by ammonium toxicity could be recovered by this synergism. RNA sequencing and the weighted gene correlation network analysis (WGCNA) revealed that the mechanism of this synergism involves cellulose synthesis, auxin and gibberellin metabolism regulation at the transcription level.