A two-year retrospective study on traumatic dental injury in the primary dentition.

The aim of this study was to analyze the causes, clinical characteristics, social factors, and current status of treatment of traumatic dental injury (TDI) in the primary dentition. A retrospective analysis was performed on 144 children (213 teeth) with TDI in the primary dentition from our hospital between December 2017 and June 2020. Data were analyzed using the chi-square test and the Mann-Withney-Wilcoxon test. Boys accounted for 68.1% (98/144) and girls for 31.9% (46/144) of all 144 children with TDI in the primary dentition, with a boy-girl ratio of 2.13:1. The primary age of TDI in deciduous teeth was 2 to 4 years old, accounting for 59% of all cases. Collision with others and fall were the 2 main causes of trauma to the deciduous teeth, making up 52.1% and 44.4% of all causes, respectively. Crown fracture injury was the most common type of TDI in the primary dentition, accounting for 37% of all cases (53/144). Of the 144 cases, 17.4% (25/144) was accompanied by soft tissue laceration, while 22.2% (32/144) by swelling or contusion of tissue. Maxillary teeth (92.4%) were more vulnerable to injury than mandibular teeth (7.5%), with maxillary incisor being the most vulnerable 1 (91.5%). The percentage of children arrived at the hospital for treatment 24 hours after the injury was the highest (57.0%, 82/144). After the hospital visit, 74.3% of children received treatment for the dental trauma. In terms of the treatment modalities, extraction of the traumatized teeth (27.1%) and pulpectomy + resin filling (or preformed crown) restoration were predominant. Approximately 28.5% (41/144) of cases were reviewed within 2 years, with the proportion of children with pulpitis or periapical infection being the highest (29.3%, 12/41). Age, gender, collision, and fall are the factors linked to a higher risk of TDI in the primary dentition in children under the age of 7. Resin filling (or preformed crown) restoration and pulpectomy are effective in preserving the affected tooth and controlling infection. However, the preservation of the affected tooth and the prevention of infection may be hampered by late visits and low follow-up rates.

MiR-20a promotes osteogenic differentiation in bone marrow-derived mesenchymal stem/stromal cells and bone repair of the maxillary sinus defect model in rabbits.

Introduction: This study aimed to determine whether miR-20 promoted osteogenic differentiation in bone marrow-derived mesenchymal stem/stromal cells (BMSCs) and accelerated bone formation in the maxillary sinus bone defect model in rabbits. Methods: BMSCs were transfected with miR-20a or anti-miR-20a for 12 h, followed by detection of RUNX2, Sp7 mRNA, bone morphogenetic protein 2 (BMP2), and RUNX2 protein expression. Alkaline phosphatase (ALP) activity and Alizarin Red S staining were used to detect calcified nodule deposition. In the rabbit maxillary sinus bone defect model, miR-20a loaded with AAV and BMP2 protein were mixed with Bio-Oss bone powder for filling the bone defect. At 4 weeks and 8 weeks, bone density was detected by cone beam computed tomography (CBCT), and new bone, osteoblasts, and collagen type 1 were evaluated by hematoxylin and eosin (HE) staining and immunohistochemical (IHC) staining. Results: Overexpression of miR-20a enhanced the mRNA and protein levels of BMP2, RUNX2, and SP7, the activity of ALP, and the levels of matrix mineralization, whereas the levels and activity of the aforementioned factors were decreased by anti-miR-20a treatment of BMSCs. Furthermore, miR-20a significantly increased the bone density, the number of osteoblasts, and the secretion of collagen type 1 in bone defects compared with Bio-Oss bone powder in the rabbit maxillary sinus bone defect model. Conclusion: Overall, miR-20a can induce osteogenic differentiation in BMSCs and accelerate bone formation of maxillary sinus defects in rabbits.

MicroRNA-134 Promotes the Development of Atherosclerosis Via the ANGPTL4/LPL Pathway in Apolipoprotein E Knockout Mice.

AIMS: Atherosclerosis is the most common cause of cardiovascular disease, such as myocardial infarction and stroke. Previous study revealed that microRNA (miR)-134 promotes lipid accumulation and proinflammatory cytokine secretion through angiopoietin-like 4 (ANGPTL4)/lipid lipoprotein (LPL) signaling in THP-1 macrophages. METHODS: ApoE KO male mice on a C57BL/6 background were fed a high-fat/high-cholesterol Western diet, from 8 to 16 weeks of age. Mice were divided into four groups, and received a tail vein injection of miR-134 agomir, miR-134 antagomir, or one of the corresponding controls, respectively, once every 2 weeks after starting the Western diet. After 8 weeks we measured aortic atherosclerosis, LPL Activity, mRNA and protein levels of ANGPTL4 and LPL, LPL/ low-density lipoprotein receptor related protein 1 Complex Formation, proinflammatory cytokine secretion and lipid levels. RESULTS: Despite this finding, the influence of miR-134 on atherosclerosis in vivo remains to be determined. Using the well-characterized mouse atherosclerosis model of apolipoprotein E knockout, we found that systemic delivery of miR-134 agomir markedly enhanced the atherosclerotic lesion size, together with a significant increase in proinflammatory cytokine secretion and peritoneal macrophages lipid contents. Moreover, overexpression of miR-134 decreased ANGPTL4 expression but increased LPL expression and activity in both aortic tissues and peritoneal macrophages, which was accompanied by increased formation of LPL/low-density lipoprotein receptor-related protein 1 complexes in peritoneal macrophages. However, an opposite effect was observed in response to miR-134 antagomir. CONCLUSIONS: These findings suggest that miR-134 accelerates atherogenesis by promoting lipid accumulation and proinflammatory cytokine secretion via the ANGPTL4/LPL pathway. Therefore, targeting miR-134 may offer a promising strategy for the prevention and treatment of atherosclerotic cardiovascular disease.