Objective: To evaluate the effectiveness of interventions on accelerating orthodontic tooth movement. Materials and Methods: We searched the databases of PubMed, Embase, Science Citation Index, CENTRAL, and SIGLE from January 1990 to August 2011 for randomized or quasirandomized controlled trials that assessed the effectiveness of interventions on accelerating orthodontic tooth movement. The processes of study search, selection, and quality assessment were conducted independently in duplicate by two review authors. Original outcome data, if possible, underwent statistical pooling by using Review Manager 5. Results: Through a predefined search strategy, we finally included nine eligible studies. Among them, five interventions were studied (ie, low-level laser therapy, corticotomy, electrical current, pulsed electromagnetic fields, and dentoalveolar or periodontal distraction). Six outcomes were evaluated in these studies (ie, accumulative moved distance or movement rate, time required to move tooth to its destination, anchorage loss, periodontal health, pulp vitality, and root resorption). Conclusion: Among the five interventions, corticotomy is effective and safe to accelerate orthodontic tooth movement, low-level laser therapy was unable to accelerate orthodontic tooth movement, current evidence does not reveal whether electrical current and pulsed electromagnetic fields are effective in accelerating orthodontic tooth movement, and dentoalveolar or periodontal distraction is promising in accelerating orthodontic tooth movement but lacks convincing evidence. (Angle Orthod. 2013;83:164-171.)

Trillium tschonoskii Maxim (TTM), a traditional Chinese medicine, has been demonstrated to have a potent anti-tumor effect. Recently, polyphyllin VI (PPVI), a main saponin isolated from TTM, was reported by us to significantly suppress the proliferation of non-small cell lung cancer (NSCLC) via the induction of apoptosis and autophagy in vitro and in vivo. In this study, we further found that the NLRP3 inflammasome was activated in PPVI administrated A549-bearing athymic nude mice. As is known to us, pyroptosis is an inflammatory form of caspase-1-dependent programmed cell death that plays an important role in cancer. By using A549 and H1299 cells, the in vitro effect and action mechanism by which PPVI induces activation of the NLRP3 inflammasome in NSCLC were investigated. The anti-proliferative effect of PPVI in A549 and H1299 cells was firstly measured and validated by MTT assay. The activation of the NLRP3 inflammasome was detected by using Hoechst33324/PI staining, flow cytometry analysis and real-time live cell imaging methods. We found that PPVI significantly increased the percentage of cells with PI signal in A549 and H1299, and the dynamic change in cell morphology and the process of cell death of A549 cells indicated that PPVI induced an apoptosis-to-pyroptosis switch, and, ultimately, lytic cell death. In addition, belnacasan (VX-765), an inhibitor of caspase-1, could remarkably decrease the pyroptotic cell death of PPVI-treated A549 and H1299 cells. Moreover, by detecting the expression of NLRP3, ASC, caspase-1, IL-1β, IL-18 and GSDMD in A549 and h1299 cells using Western blotting, immunofluorescence imaging and flow cytometric analysis, measuring the caspase-1 activity using colorimetric assay, and quantifying the cytokines level of IL-1β and IL-18 using ELISA, the NLRP3 inflammasome was found to be activated in a dose manner, while VX-765 and necrosulfonamide (NSA), an inhibitor of GSDMD, could inhibit PPVI-induced activation of the NLRP3 inflammasome. Furthermore, the mechanism study found that PPVI could activate the NF-κB signaling pathway via increasing reactive oxygen Cancers 2020, 12, 193 2 of 27 species (ROS) levels in A549 and H1299 cells, and N-acetyl-L-cysteine (NAC), a scavenger of ROS, remarkably inhibited the cell death, and the activation of NF-κB and the NLRP3 inflammasome in PPVI-treated A549 and H1299 cells. Taken together, these data suggested that PPVI-induced, caspase-1-mediated pyroptosis via the induction of the ROS/NF-κB/NLRP3/GSDMD signal axis in NSCLC, which further clarified the mechanism of PPVI in the inhibition of NSCLC, and thereby provided a possibility for PPVI to serve as a novel therapeutic agent for NSCLC in the future.

Orthodontic pain is an inflammatory pain that is initiated by orthodontic force-induced vascular occlusion followed by a cascade of inflammatory responses, including vascular changes, the recruitment of inflammatory and immune cells, and the release of neurogenic and pro-inflammatory mediators. Ultimately, endogenous analgesic mechanisms check the inflammatory response and the sensation of pain subsides. The orthodontic pain signal, once received by periodontal sensory endings, reaches the sensory cortex for pain perception through three-order neurons: the trigeminal neuron at the trigeminal ganglia, the trigeminal nucleus caudalis at the medulla oblongata and the ventroposterior nucleus at the thalamus. Many brain areas participate in the emotion, cognition and memory of orthodontic pain, including the insular cortex, amygdala, hippocampus, locus coeruleus and hypothalamus. A built-in analgesic neural pathway—periaqueductal grey and dorsal raphe—has an important role in alleviating orthodontic pain. Currently, several treatment modalities have been applied for the relief of orthodontic pain, including pharmacological, mechanical and behavioural approaches and low-level laser therapy. The effectiveness of nonsteroidal anti-inflammatory drugs for pain relief has been validated, but its effects on tooth movement are controversial. However, more studies are needed to verify the effectiveness of other modalities. Furthermore, gene therapy is a novel, viable and promising modality for alleviating orthodontic pain in the future.

The objective of this systematic review was to compare the outcomes between coronectomy and total removal for third molar extractions with high risk of nerve injury and to help practitioners make prudent decisions on whether and how third molars should be removed. PubMed, Embase, Web of Science, CENTRAL, and SIGLE were searched from January 1990 to October 2011 for randomized or non-randomized controlled trials. Four studies met our inclusion criteria. The pooled risk ratio (coronectomy vs. total removal) was 0.11 (95% CI = 0.03-0.36), 1.03 (95% CI = 0.54-1.98), 0.55 (95% CI = 0.28-1.05), and 1.14 (95% CI = 0.57-2.30) for inferior alveolar nerve injury, post-operative infection, dry socket, and pain at 1 wk after surgery, respectively. A relatively high rate of failed coronectomy in one study (38.3%, compared with 2.3%-9.4% in others) may be attributed to a higher proportion of narrowing roots and vertical impactions. Although root migration rate was high (13.2%-85.29%), the migration distances were short (3.06 ± 1.67 mm), and the directions were away from the nerves. Moreover, the rates of re-operation and root exposure were low. Therefore, coronectomy appears superior to total removal for reducing inferior alveolar nerve damage and could be used in clinical practice for third molar extractions with high risk of nerve injury.

The role of epigenetic regulation in immunity is emerging, especially for RNA N6‐methyladenosine (m6A) modification. However, little is known about the role of m6A in the regulation of the immune microenvironment of periodontitis. Thus, we aim to investigate the impact of m6A modification in periodontitis immune microenvironment. The RNA modification patterns mediated by 23 m6A‐regulators were systematically evaluated in 310 periodontitis samples. The impact of m6A modification on immune microenvironment characteristics was explored, including infiltrating immunocytes, immune reaction gene‐sets and HLAs (human leukocyte antigen) gene. m6A phenotype‐related immune genes were also identified. 17 m6A regulators were dysregulated and a 15‐m6A regulator signature can well distinguish periodontitis and control samples. ALKBH5 and FMR1 are closely related to infiltrating monocyte abundance. ELAVL1 and CBLL1 are significant regulators in immune reaction of TNF_Family_Members_Receptors and Cytokine. The expression of HLA‐B and HLA‐DOA is affected by ALKBH5 and LRPPRC. 3 distinct RNA modification patterns mediated by 23 m6A regulators were identified. They differ from immunocyte abundance, immune reaction and HLA gene. 1631 m6A phenotype‐related genes and 70 m6A‐mediated immune genes were identified, and the biological functions of these were explored. Our finding demonstrated the m6A modification plays a crucial role in the diversity and complexity of the immune microenvironment of periodontitis.