Bonding performance of glass ionomer cement to carious dentin treated with different surface treatment protocols using silver diamine fluoride.

This study investigated the influence of silver diamine fluoride (SDF) on the shear bond strength (SBS) to artificial carious dentin and GIC restorations with various SDF application protocols. Artificial caries were prepared on human dentin discs using bacteria model. These samples were randomly allocated to five groups (n = 10/group) according to the following treatment: (1) control group (CD): no treatment (2) CSR: dentin conditioner, SDF, and rinsing (3) CS: dentin conditioner and SDF (4) SRC: SDF, rinsing and dentin conditioner, and (5) SC: SDF and dentin conditioner. The treated-dentin surface was bonded with GIC and subjected to SBS test. Mean SBS was analyzed using one-way ANOVA. Surface morphology and elemental contents after surface treatment were examined (n = 3/group) by scanning electron microscopy with energy-dispersive X-ray spectroscopy (SEM/EDX). There was no significant difference in the mean SBS among CD (2.45 ± 0.99 MPa), CSR (1.76 ± 0.65 MPa), and SRC (2.64 ± 0.95 MPa). Meanwhile, the mean SBS of CS (0.35 ± 0.21 MPa) was significantly lower than the control and SRC group. SEM/EDX demonstrated deeper silver penetration in CSR and CS groups when compared to SRC and SC groups. SDF-modified GIC restorations resulted in significantly lower bond strength in CS and SC groups. The findings suggested treating the carious dentin surface with CSR and SRC protocol. SDF-treated carious dentin should be rinsed off prior to restore with GIC.

Correlation of plasma osteopontin and osteocalcin with lower renal function in dental patients with carotid artery calcification and tooth loss.

OBJECTIVES: To investigate plasma osteopontin (OPN) and osteocalcin (OCN) levels in dental patients with carotid artery calcification (CAC) and determine the correlations between these proteins and renal function and tooth loss. METHODS: The health parameters and number of teeth of 99 participants were recorded. Panoramic radiographs were taken for CAC evaluation, and OPN and OCN levels were measured. RESULTS: None of the participants had overt kidney disease, and 14 (14.14%) had CAC. The age, sex, and health profiles of patients with CAC were not different from those without CAC. The OPN and OCN levels in participants with CAC were higher than in those without (p = 0.026 and p = 0.025, respectively). The OPN levels were correlated with the estimated glomerular filtration rate (eGFR) (p = 0.021) and tooth loss (p = 0.027). The OCN levels were correlated with the eGFR (p = 0.002), tooth loss (p = 0.023), blood urea nitrogen (p = 0.040), and creatinine levels (p = 0.031). The median tooth loss in individuals with an eGFR <60 mL/min/1.73 m2 was higher than that of individuals with an eGFR ≥60 mL/min/1.73 m2 (p = 0.033). In individuals with CAC, tooth loss correlated more strongly with the eGFR, and the correlation between OPN and OCN levels was more apparent. CONCLUSION: Dental patients with CAC and increased tooth loss have a greater tendency for decreased renal function, which may be associated with OPN and OCN; thus, these patients should be referred for investigation.

High glucose-induced oxidative stress impairs proliferation and migration of human gingival fibroblasts.

Delayed gingival wound healing is widely observed in periodontal patients with diabetes. However, the molecular mechanisms of the impaired function of gingival fibroblasts in diabetes remain unclear. The purpose of this study was to investigate changes in the properties of human gingival fibroblasts (HGFs) under high-glucose conditions. Primary HGFs were isolated from healthy gingiva and cultured with 5.5, 25, 50, and 75 mM glucose for 72 h. In vitro wound healing, 5-ethynyl-2'-deoxyuridine (EdU), and water-soluble tetrazolium salt (WST-8) assays were performed to examine cell migration and proliferation. Lactase dehydrogenase (LDH) levels were measured to determine cytotoxicity. The mRNA expression levels of oxidative stress markers were quantified by real-time PCR. Intracellular reactive oxygen species (ROS) were also measured in live cells. The antioxidant N-acetyl-l-cysteine (NAC, 1 mM) was added to evaluate the involvement of ROS in the glucose effect on HGFs. As a result, the in vitro wound healing assay showed that high glucose levels significantly reduced fibroblast migration and proliferation at 6, 12, 24, 36, and 48 h. The numbers of cells positive for EdU staining were decreased, as was cell viability, at 50 and 75 mM glucose. A significant increase in LDH was proportional to the glucose concentration. The mRNA levels of heme oxygenase-1 and superoxide dismutase-1 and ROS levels were significantly increased in HGFs after 72 h of exposure to 50 mM glucose concentration. The addition of NAC diminished the inhibitory effect of high glucose in the in vitro wound healing assay. The results of the present study show that high glucose impairs the proliferation and migration of HGFs. Fibroblast dysfunction may therefore be caused by high glucose-induced oxidative stress and may explain the delayed gingival wound healing in diabetic patients.

Lgr4 Expression in Osteoblastic Cells Is Suppressed by Hydrogen Peroxide Treatment.

LGR4 is expressed in bone and has been shown to be involved in bone metabolism. Oxidative stress is one of the key issues in pathophysiology of osteoporosis. However, the link between Lgr4 and oxidative stress has not been known. Therefore, effects of hydrogen peroxide on Lgr4 expression in osteoblasts were examined. Hydrogen peroxide treatment suppressed the levels of Lgr4 mRNA expression in an osteoblastic cell line, MC3T3-E1. The suppressive effects were not obvious at 0.1 mM, while 1 mM hydrogen peroxide suppressed Lgr4 expression by more than 50%. Hydrogen peroxide treatment suppressed Lgr4 expression within 12 h and this suppression lasted at least up to 48 h. Hydrogen peroxide suppression of Lgr4 expression was still observed in the presence of a transcription inhibitor but was no longer observed in the presence of a protein synthesis inhibitor. Although Lgr4 expression in osteoblasts is enhanced by BMP2 treatment as reported before, hydrogen peroxide treatment suppressed Lgr4 even in the presence of BMP2. Finally, hydrogen peroxide suppressed Lgr4 expression in primary cultures of osteoblasts similarly to MC3T3-E1 cells. These date indicate that hydrogen peroxide suppresses Lgr4 expression in osteoblastic cells. J. Cell. Physiol. 232: 1761-1766, 2017. © 2016 Wiley Periodicals, Inc.

BMP-2 Enhances Lgr4 Gene Expression in Osteoblastic Cells.

Osteoporosis is one of the most prevalent diseases and the number of patients suffering from this disease is soaring due to the increase in the aged population in the world. The severity of bone loss in osteoporosis is based on the levels of impairment in the balance between bone formation and bone resorption, two arms of the bone metabolism, and bone remodeling. However, determination of bone formation levels is under many layers of control that are as yet fully defined. Bone morphogenetic protein (BMP) plays a key role in regulation of bone formation while its downstream targets are still incompletely understood. Lgr4 gene encodes an orphan receptor and has been identified as a genetic determinant for bone mass in osteoporotic patients. Here, we examine the effects of BMP on the expression of Lgr4 in osteoblastic cells. Lgr4 gene is expressed in an osteoblastic cell line, MC3T3E1 in a time dependent manner during the culture. BMP treatment enhances Lgr4 mRNA expression at least in part via transcriptional event. When Lgr4 mRNA is knocked down, the levels of BMP-induced increase in alkaline phosphatase (Alp) activity and Alp mRNA are suppressed. BMP enhancement of Lgr4 gene expression is suppressed by FGF and reversed by dexamethasone. BMP also enhances Lgr4 expression in primary cultures of calvarial osteoblasts. These data indicate that Lgr4 gene is regulated by BMP and is required for BMP effects on osteoblastic differentiation. J. Cell. Physiol. 231: 887-895, 2016. © 2015 Wiley Periodicals, Inc.