Objective:To evaluate the effect of zirconia surface grafted bioactive component chlorogenic acid (CGA) - chitosan (CS) complex on the promotion of osseointegration. Methods:CS wrap the CGA and graft it onto the surface of zirconia implants with PEI to build a biologically active coating. Using water contact angle measurement, X-ray photoelectron spectroscopy (XPS), scanning electron microscope (SEM), and other experiments to analyze the coating′s characterization. Pre-osteoblastic MC3T3-E1 cells with high osteogenic differentiation potential was used to evaluate the cell proliferation，adhesion promotion and osteoinduction effects of the coating. Results:PEI and CGA-CS complexes were successfully grafted on the surface of zirconia implants. The coating enhanced the hydrophilicity of zirconia surface, promoted the proliferation and adhesion of MC3T3-E1 cells, and promoted the expression of osteogenic related proteins such as Osteocalcin (Ocn) and Runt related transcription factor 2 (Runx2). Conclusions:The PEI coating grafted CGA-CS complexes can promote the osteogenesis on the surface of zirconia.

Objective:To observe the distribution of vascular endothelial progenitor cell (EPC) in the periodontal tissue remodeling area of orthodontic experimental rats and to investigate the effect of vascular endothelial cell factor (VEGF) on their chemotaxis and differentiation. Methods:Experimental rat tooth movement model was established, and rat peripheral blood EPC were isolated, cultured and identified. The proliferation and migration of EPC were observed by intervening VEGF in vitro. BrdU-labeled EPC were injected into model rats through the tail vein to observe the distribution of EPC in periodontal tissues, and the expression of VEGF. Results:Cell phenotype identification was completed by isolating and culturing rat EPC. VEGF can promote the proliferation ability of EPC in vitro and promote the chemotaxis and migration of EPC. After injection of BrdU-labeled EPC into model rats, the number of BrdU EPC positive periodontal tissues increased; the expression of VEGF on the tension side of the experimental group (tail vein injection of EPC cells) was higher than that of the control group (injection of saline). Conclusions:During orthodontic tooth movement, peripheral blood EPC can be chemotactic and accumulate in periodontal tissue, and participate in periodontal tissue remodeling under the regulation of VEGF.

Objective:?To explore the relationship between dental pulp fibroblast (DPF) lactate accumulation and inflammation in pulpitis. Methods:? SD rats were used to construct the pulpitis model. Hematoxylin-eosin was used to observe the inflammatory infiltration of pulpitis. The expression of inflammatory cytokines, IL-1β and TNF-α, as well as the key enzyme that catalyzes lactate production, lactate dehydrogenase A (LDHA), were visualized by immunohistochemical staining. Immunofluorescence staining was used to evaluate the colocalization of LDHA and the marker of dental pulp fibroblasts Vimentin. Human health and carious third molars were collected, then extracting normal and inflammatory pulp tissues to measure lactate content. DPF was cultured in vitro and LDHA inhibitor GSK2837808A was added. The cells were divided into control group, lipopolysaccharide (LPS) group, and LDHA inhibitor group. Lactate test kit was used to measure cellular lactate content. qRT-PCR was used to detect the mRNA expression of inflammatory cytokines IL-1β and TNF-α, and LDHA. Results:? Compared with the normal pulp of rats,the inflammatory infiltration increased during the modeling of pulpitis for 1d，3d, meanwhile the expression of LDHA and inflammatory cytokines IL-1β, TNF-α increased ,especially3d (P＜0.05),while decreased at 7 days, which has no significant difference as compared with that of the control group (P＞0.05). Vimentin and LDHAof DPF in inflammatory pulp tissue in rats could be seen co-localization. The content of lactate in human inflammatory pulp tissue was higher than that of healthy pulp (P＜0.05). By treating dental pulp fibroblasts with lactate dehydrogenase inhibitor GSK2837808A, lactate secretion decreased, and the expression of LDHA and inflammatory cytokines decreased (P＜0.05). Conclusions:?In the development of pulpitis, the production of lactate of DPF is related to the degree of inflammation, and the accumulation of lactate promoted the expression of inflammatory cytokines;and by inhibiting LDHA,human DPFlactate production and expression of inflammatory factors were reduced.

Objective: To detect the expression of membrane type 1 matrix metalloproteinase (MT1-MMP) in oral squamous cell carcinoma (OSCC) and its role on the proliferation and invasive ability of OSCC. Methods: RT-PCR was used to detect the expression of MT1-MMP and E-cadherin in OSCC and adjacent tissues; Small interfering RNA (siRNA) was used in targeted interference MT1-MMP gene in HSC3 cells. The experiment was divided into four groups: siControl group, siMT1-MMP group, siControl+transforming growth factor β1 (TGF-β1) group, siMT1-MMP+TGF-β1 group. CCK-8 method was used to detect cell proliferation of HSC3. Transwell assay was used to detect the invasive ability of cells. The expression of MT1-MMP, E-cadherin, TGF-β signaling pathway related proteins (CUTL1 and Wnt5a) was detected by Western blot. Results: Compared with the adjacent tissues, higher expression of MT1-MMP and lower expression of E-cadherin was exhibited in OSCC（P<0.05）; the cell proliferation of HSC3 cells did not change significantly after MT1-MMP interference（P＞0.05）; compared with siControl group and siMT1-MMP group, the HSC3 cell invasion number in siControl+TGF-β1 group and siMT1-MMP+TGF-β1 group was increased significantly; compared with siControl+TGF-β1 group, the HSC3 cell invasion number in siMT1-MMP+TGF-β1 group was decreased significantly（P<0.01）; compared with siControl group, protein expression of MT1-MMP, CUTL1 and Wnt5a increased significantly in siControl+TGF-β1 group, while the expression of E-cadherin decreased（P<0.01）; compared with siControl+TGF-β1 group, protein expression of MT1-MMP, CUTL1 and Wnt5a decreased partially in siMT1-MMP+TGF-β1 group, while the expression of E-cadherin increased significantly（P<0.05）. Conclusions: MT1-MMP interference may inhibit the invasion of OSCC through regulating the EMT process induced by TGF-β1.

Objective:?To study the effect of ferrocenyl retinoic acid nanoparticles (FCRA Nps) on ferroptosis induced by oral squamous cell carcinoma cells (OSCC). Methods:?Human OSCC cells CAL27 were cultured, and the effect of FCRA Nps on the proliferation of CAL27 cells was determined by CCK-8 method; the effects of FCRA Nps on the contents of glutathione (GSH) and reactive oxygen species (ROS) in CAL27 cells were observed by fluorescence microscope; Mitochondrial red fluorescent probe was used to specifically label the biologically active mitochondria in cells, Hoechst 33342 staining solution was used to label the nucleus, and the effect of FCRA Nps on the morphology of mitochondria and nucleus in CAL27 cells was observed under a fluorescence microscope. Results:?Compared with the control group, FCRA NPs had an inhibitory effect on the proliferation of CAL27 cells; the effect of FCRA NPs reduced the content of GSH and increased the content of ROS in CAL27 cells (P<0.01); compared with the control group, the mitochondrial volume of the FCRA NPs group became smaller, the nucleus did not change significantly. Conclusions:?FCRA Nps can induce ferroptosis in OSCC cells.

Objective: To explore the effect of the inhibitor GsMTx4 of Piezo1 protein channel on periodontal tissue reconstruction at the pressure side during orthodontic tooth movement in rats through RANKL/OPG pathway. Methods: The orthodontic model was established in 75 healthy male SD rats. The rats were randomly divided into control group, force group and force+GsMTx4 group. The mesial movement distance of the first molars was measured. HE staining was used to observe the pathological changes of periodontal tissue in the pressure side of the proximal root of the mandibular first molars. Immunohistochemical staining was used to observe the expression and localization of nuclear factor-κB receptor activator ligand (RANKL) and OPG in the periodontal tissue at pressure side. The change of the ratio of RANKL to osteoprotegerin (OPG) and the number of osteoclasts in periodontal tissues at the pressure side through tartrate-resistant acid phosphatase staining were observed. Results:With the extension of force time, the tooth movement distance gradually increased, and tooth movement distance in force group was higher than that in force+GsMTx4 group (P<0.05). RANKL, the ratio of RANKL/OPG and the number of osteoclasts in force group and force+GsMTx4 group showed a trend of increasing first and then decreasing, and OPG showed a gradual increasing trend. Compared with force group, the values in force+GsMTx4 group were all decreased (P<0.05). Conclusions: GsMTx4 can reduce the expression of RANKL and OPG proteins in the periodontal tissue at the pressure side during orthodontic tooth movement in rats, and inhibit osteoclasts differentiation, thereby reducing bone resorption activity and inhibiting tooth movement.

Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases in the elderly population. However, the etiology and pathogenesis of AD are complicated and remain elucidated. Increasing reports suggest that periodontal microorganisms may play a role in the initiation and progress of AD. Thus, this article will review the association and potential mechanisms between periodontal microorganisms and AD, and explain the significance of management targeting periodontal microorganisms in the treatment of AD.

Tooth development is an organogenetic process in which epithelial-mesenchymal interactions and differentiation are precisely regulated by a complex cascade network of signaling molecules. In this paper, from the perspective of the changes in the fate of dental germ epithelial and mesenchymal cells in different stages of tooth morphogenesis, the research progress of morphological regulation during tooth development in recent years is reviewed, in order to improve the understanding of organ development and morphogenesis, and provide ideas and references for precise regulation of the regenerated tooth morphology during tooth regeneration.

The function of bone marrow mesenchymal stem cells is the biological basis of bone injury repair. Mitochondria, as the energy factory and signal transmission center of BMSCs, play a role in bone injury repair by regulating the function of BMSCs. The damage of mitochondrial structure and function not only leads to abnormal energy metabolism of BMSCs, but also can release pro-injury signal molecules, resulting in abnormal proliferation and differentiation of BMSCs, thus affecting bone repair. In this paper, the research progress of the role of mitochondrial structure and function in bone injury repair and mitochondrial quality control mechanism in recent years is reviewed, in order to provide reference and theoretical guidance for the clinical treatment of bone injury repair.

Bmal1 is the core gene of biological clock genes, which dominates the expression and translation of other biological clock genes through negative feedback regulation. The development of dental hard tissue is a series of complex physiological processes, including the formation and mineralization of enamel, dentin and cementum matrix. Bmal1 gene, as the core gene of biological rhythm, has an important effect on the development of dental hard tissue. This paper reviews the research progress of the effect of Bmal1 gene on the growth and development of dental hard tissue.

Streptococcus mutans is the principal cariogenic bacteria in oral microecology, and intraspecific and interspecific information exchange is particularly important for the development of Streptococcus mutans. The release and uptake of pheromones regulate a series of information exchange, forming a complex quorum sensing system. In this paper, we will review the research progress on quorum sensing systems, which have been paid more attention in recent years, so as to provide some basis for the understanding and prevention of dental caries.