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Background: The gut microbiota plays a vital role in mental disorders, and the gut-brain axis has also been studied in the pathogenesis of depression. Furthermore, studies show the presence of the oral-gut microbiome axis. Oral microbiota dysbiosis is linked with mental disorders, suggesting that pathologic bacteria from the oral cavity may contribute to the development of mental disorders. However, whether independent oral microbiome that do not depend on gut microbes impacts the progression of depression, andthe presence and mechanism underlying about the microbiota-oral-brain axis in depression remains unclear. Here, saliva microbiota transplantation in germ-free mice used to study the impacts and mechanism of oral microbes on depression. 16S rRNA sequencing and liquid chromatography/mass spectrometry were performed on saliva, stool and serum to investigate alterations in microbiota and metabolites. Results: It was observed that differential shaping effect of oral and intestinal microbiota on depression. Moreover, germ-free mice transplanted with saliva from chronic restraint stress (CRS)-exposed mice displayed emotional impairment and oral microbial dysbiosis with significant differential abundance of bacterial species including the enrichment of Pseudomonas, Pasteurellaceae and Muribacter and depletion of Streptococcus. Metabolomic analysis showed the alternation of metabolites in the serum of CRS-exposed germ-free mice, especially Eicosapentaenoic Acid. Furthermore, ectopic colonization of oral microbiome induced by CRS in the intestine impaired gut barrier function, which is associated with increased blood-brain barrier permeability. Pseudomonas supplementation exacerbated depression-like behavior, while Eicosapentaenoic Acid treatment conferred protection against depression-like states in mice. Conclusions: These results suggest the external shaping process of gut microbiota by oral microbiome and indicate the great value of oral saliva samples in monitoring and assessing depression progression in clinical settings.

Diabetes microenvironment will accelerate the accumulation of Advanced glycation end products (AGEs), therefore, AGEs are a signature product in the study of the diabetes microenvironment. Adipose-derived stem cells (ASCs) have poor osteogenesis in the diabetes microenvironment, but the mechanism of the altered osteogenic potential of ASCs has not been elucidated. Bone tissue engineering by ASCs is widely used in the treatment of bone defects with diabetic osteoporosis. Therefore, this study investigated the effects of AGEs on osteogenic differentiation potential of ASCs and the underlying mechanisms. In the present study, we isolated and cultured ASCs in C57BL/6 mice, then treated ASCs with AGEs, the levels of autophagy and osteogenesis-related factors were decreased in the AGE-treated group. In order to verify autophagy and AGE-mediated changes in the osteogenic capacity of ASCs, we used 3-methyladenine, and rapamycin. After cotreatment with 3-methyladenine and AGEs, the levels of osteogenesis and autophagy were reduced more significantly, whereas rapamycin ameliorated the autophagy level and osteogenic differentiation potential of ASCs treated with AGEs. This study shows that AGEs can reduce the osteogenic differentiation potential of ASCs through autophagy, which may provide a reference for the treatment of bone defects with diabetes osteoporosis.

OBJECTIVES To study the accuracy of partially guided and fully guided templates applied to implant surgery of anterior teeth. MATERIALS AND METHODS Sixty patients who were scheduled to receive dental implant treatment in the anterior region were enrolled and randomly assigned to one of the following study groups (n = 20 each): routine implant-supported restoration treatment (control group, 30 implants), implant-supported restoration treatment using a partially guided template (test group 1, 36 implants), and implant-supported restoration treatment using a fully guided template (test group 2, 33 implants). The depth of implant was controlled for fully guided template. After implantation, planned implants and placed implants were superimposed using digital software, and the deviations (angular, coronal, apical, depth) were analyzed. Esthetic parameters were assessed at baseline, 6 months, and 1 year after the final restoration. Pink esthetic score (PES) and white esthetic score (WES) were respectively used to evaluate the soft tissue and restoration esthetic outcome. Each parameter of PES and WES is assessed with a 0-1-2 score with 2 being the best and 0 being the worst score. RESULTS There were significant differences in all of the deviation parameters between the control group, test group 1, and test group 2 (p

Background The osteogenic differentiation ability of adipose-derived stem cells (ASCs) is attenuated in type 2 diabetic osteoporosis (Dop) mice. Several studies suggest autophagy and Notch signaling pathway play vital roles in cell proliferation, differentiation, and osteogenesis. However, the mechanisms of autophagy and Notch signaling in the osteogenic differentiation of Dop ASCs were unclear. Thus, it is meaningful to reveal potential correlations between autophagy, Notch signaling, and osteogenesis, and explore involved molecular mechanisms in Dop ASCs. Materials and methods The diabetic osteoporosis C57BL/6 mouse model, which was confirmed by micro-CT and HE & Masson staining, was established through high-sugar and high-fat diet and streptozotocin injection. ASCs were obtained from the inguinal subcutaneous fat of Dop mice. The multi-differentiation potential of ASCs was evaluated by staining with Alizarin Red (osteogenesis), Oil Red O (adipogenesis), and Alcian blue (chondrogenesis). Cell viability was assessed by Cell Counting Kit-8 assay. Torin1, an inhibitor of mTOR, was used to stimulate the autophagy signaling pathway. DAPT, a γ-secretase inhibitor, was used to suppress Notch signaling pathway activity. Gene and protein expression of autophagy, Notch signaling pathway, and osteogenic factors were detected by real-time quantitative PCR, western blot, and immunofluorescence microscopy. Results Our findings showed autophagy and osteogenic differentiation ability of Dop ASCs exhibited downward trends that were both rescued by Torin1. Notch signaling was suppressed in Dop ASCs, but upregulated when autophagy was activated. After activation of autophagy, DAPT treatment led to decreased Notch signaling pathway activation and attenuated osteogenic differentiation ability in Dop ASCs. Conclusions Downregulated autophagy suppressed Notch signaling, leading to a reduced osteogenic differentiation capacity of Dop ASCs, and Torin1 can rescue this process by activating autophagy. Our findings contribute to understanding the mechanism underlying impairment of the osteogenic differentiation ability of Dop ASCs.

Objective: Although it has been demonstrated that adipose-derived stem cells (ASCs) from osteoporosis mice (OP-ASCs) exhibit impaired osteogenic differentiation potential, the molecular mechanism has not yet been elucidated. We found that Fzd6 was decreased in OP-ASCs compared with ASCs. This study investigates the effects and underlying mechanisms of Fzd6 in the osteogenic potential of OP-ASCs. Methods: Fzd6 expression in ASCs and OP-ASCs was measured by PCR gene chip. Fzd6 overexpression and silencing lentiviruses were used to evaluate the role of Fzd6 in the osteogenic differentiation of OP-ASCs. Real-time PCR (qPCR) and western blotting (WB) was performed to detect the expression of Fzd6 and bone-related molecules, including runt-related transcription factor 2 (Runx2) and osteopontin (Opn). Alizarin red staining and Alkaline phosphatase (ALP) staining was performed following osteogenic induction. Microscopic CT (Micro-CT), hematoxylin and eosin staining (H&E) staining, and Masson staining were used to assess the role of Fzd6 in osteogenic differentiation of osteoporosis (OP) mice in vivo.Results: Expression of Fzd6 was decreased significantly in OP-ASCs. Fzd6 silencing down-regulated the osteogenic ability of OP-ASCs in vitro. Overexpression of Fzd6 rescued the impaired osteogenic capacity in OP-ASCs in vitro. We obtained similar results in vivo.Conclusions: Fzd6 plays an important role in regulating the osteogenic ability of OP-ASCs both in vivo and in vitro. Overexpression of Fzd6 associated with the Wnt signaling pathway promotes the osteogenic ability of OP-ASCs, which provides new insights for the prevention and treatment of OP.