Effects of dimethyl sulfoxide pretreatment on the bonding properties of fluorotic dentin of different severity: An in vitro study.

STATEMENT OF PROBLEM: Bonding to fluorotic dentin is weaker than to sound dentin, but methods to improve bonding have not been well addressed. PURPOSE: The purpose of this in vitro study was to investigate the effects of dimethyl sulfoxide (DMSO) pretreatment on the bond strength and resin-dentin surface of fluorotic dentin of different severity. MATERIAL AND METHODS: Phosphoric acid-etched dentin specimens exhibiting mild fluorosis (ML-F), moderate fluorosis (MD-F), and severe fluorosis (SE-F) were randomly bonded with Single Bond 2 (SB2) pretreated with 50% DMSO (experimental groups) or deionized water (control groups). The bonded teeth were sectioned for microshear bond strength (µSBS) testing immediately or after aging, for micromorphology observation of the bonding interface under a scanning electron microscope, and for resin tags and microleakage evaluation under a confocal laser scanning microscope. The degree of conversion of the adhesive resin was calculated by Fourier transform infrared spectroscopy. According to varying bonding steps, the mineralized dentin powders of ML-F, MD-F, and SE-F were randomly divided into 4 subgroups (blank, PA, PA+SB2, and PA+DMSO+SB2) and incubated in artificial saliva to examine the level of enzymatic degradation product of type I collagen. Data were analyzed by using ANOVA and the Tukey test (α=.05). RESULTS: Dental fluorosis and thermocycling had negative effects on µSBS (P<.001), while DMSO pretreatment preserved or even improved µSBS (P<.001). DMSO had no influence on the degree of conversion (P=.618). Significant effects were found for bonding steps (P<.001), but not that of dental fluorosis (P=.131) on the enzymatic degradation product of type I collagen. Images showed sparser and more expanded collagen fibril meshwork, deeper resin penetration, and less microleakage in the experimental groups. CONCLUSIONS: DMSO pretreatment provided increased and durable dentin bonding to fluorotic dentin probably by dispersing collagen fibrils into a sparser network and inhibiting the degradation of type I collagen.

Effect of 45S5 bioactive glass on the microshear bond strength of dental fluorosis.

The aim of this in vitro study was to estimate the effect of the species concentration of 45S5 bioactive glass (BAG) used as pretreatment on the microshear bond strength (MSBS) of dental fluorosis (DF). Based on the Thylstrup and Fejerskov index, 80 teeth were randomly divided equally into four groups: TFI 0, sound dentin; TFI 1-3, mild fluorosis; TFI 4-5, moderate fluorosis; and TFI 6-9, severe fluorosis. Each group was randomized into five subgroups. After preparing the dentin hypersensitivity model of DF, the dentin was pretreated as follows, Subgroup 1: deionized water (Control group); Subgroup 2: 1% BAG; Subgroup 3: 5% BAG; Subgroup 4: 10% BAG, and Subgroup 5: 20% BAG. Stochastically one specimen was selected from each subgroup for scanning electron microscope and energy dispersive spectrometer analysis. After being made of resin-tooth bonding samples, the remains were in water bath at 37 °C for 24 hr. Subsequently, samples from each subgroup were randomly selected to test MSBS without aging, or after a thermocycle of 5,000 and 10,000 times, respectively. The fracture modes were analyzed. Compared with the group of 1% BAG and Control, the exposure area of tubules in 5%, 10%, and 20% BAG group had significant difference (p < .05). MSBS results indicated that there were significant differences between 10% BAG with other groups. The 20% BAG group showed the lowest MSBS among all groups. Pretreatment of 10% BAG solution may be conductive to enhance the bond strength of DF, while 20% BAG solution adversely.

Effectiveness of sodium hypochlorite treatment on the bonding of four adhesive systems to fluorotic enamel.

The study evaluated the effect of sodium hypochlorite (NaOCl) treatment on fluorotic enamel bonding of four adhesive systems. They were Single Bond 2 (SB2), Prime&Bond NT (PBN), Clearfil SE Bond (CSB), and Single Bond Universal (SBU). One hundred eighteen extracted moderate fluorotic molars were divided into eight groups according to NaOCl pretreatment and four adhesive systems. The microshear bond strength (µSBS), etching pattern, and penetration depth (PD) were observed. The statistical method was two-way ANOVA and least significant difference (LSD) test (α=0.05). The application of NaOCl significantly increased the µSBS of PBN and SBU (p<0.05). The enamel-etching pattern of CSB and SBU was deeper under SEM. A noticeable increase of PD was in SB2 and SBU after the application of NaOCl (p<0.05). Pretreatment of 5.25% NaOCl for the 60 s can increase µSBS of PBN and SBU, PD of SB2 and SBU, and improve enamel-etching pattern of CSB and SBU to fluorotic enamel.

Targeting the Nod-like receptor protein 3 Inflammasome with inhibitor MCC950 rescues lipopolysaccharide-induced inhibition of osteogenesis in Human periodontal ligament cells.

OBJECTIVE: We aim to investigate whether lipopolysaccharide-stimulated activition of Nod-like receptor protein 3 (NLRP3) Inflammasome inhibits osteogenesis in Human periodontal ligament cells (HPDLCs). Futhermore, to study whether MCC950 (a inhibitor of NLRP3 Inflammasome) rescues lipopolysaccharide-induced inhibition of osteogenesis in HPDLCs as well as the underlying mechanisms. METHODS: HPDLCs were isolated from periodontal ligament of healthy orthodontic teeth from teenagers, and cells surface marker protein were detected by flow cytometry. Cells viability were determined by Cell Counting kit 8 assay. Enzyme-linked immunosorbent assay was used to analyze the secretion of proinflammatory factors. Western blot and real-time quantitative polymerase chain reaction (RT-qPCR) were measured assessing the expression of NLRP3 and Caspase-1. RT-qPCR, Alizarin red staining and Alkaline phosphatase staining were tested to determine the osteogenic differentiation capacity of HPDLCs. RESULTS: It was found that lipopolysaccharide in the range of concentrations from 10 to 100 µg/ml significantly inhibited HPDLCs viability at 24 h and significantly improved proinflammatory cytokine expressions at 8 h and 24 h. MCC950 reversed lipopolysaccharide-stimulated proinflammatory cytokine expressions including interleukin-1ß and interleukin-18, but not tumor necrosis factor-α. In addition, MCC950 rescued the lipopolysaccharide-inhibited osteogenic gene (Alkaline phosphatase, Runt-related transcription factor 2, and Osteocalcin). Moreover, MCC950 downregulated lipopolysaccharide-induced relative protein of NLRP3 Inflammasome signaling pathway, such as NLRP3 and Caspase-1. CONCLUSION: MCC950 rescues lipopolysaccharide-induced inhibition of osteogenesis in HPDLCs via blocking NLRP3 Inflammasome signaling pathway, and it may be used as a promising therapeutic agent for periodontitis or periondontal regenerative related disease.

The effects of 45S5 bioactive glass and Er:YAG Laser on the microtensile bond strength of fluorosed teeth.

This vitro study aimed to evaluate the effects of 45S5 bioactive glass (BAG) and Er:YAG laser as desensitization treatments on the microtensile bond strength (MTBS) of fluorosed teeth. The 120 noncarious fluorosis were to obtain superficial dentin, being classified into four groups according to the Thylstrup and Fejerskov Index (TFI). Specimens from each group were randomly divided into five subgroups. After fluorosed teeth hypersensitivity models were established, the following pretreatments were applied on dentine surface: Subgroup 1: deionized water (Control); Subgroup 2: BAG; Subgroup 3: Er:YAG laser; Subgroup 4: BAG + Er:YAG laser, and Subgroup 5: Er:YAG laser + BAG. One sample was randomly selected from each subgroup for scanning electron microscope (SEM). The remaining samples were bonded with composite resin by Adper Single Bond 2 adhesive. Then water bath at 37°C for 24 hr. After 5,000 thermocycling, MTBS was tested and fracture mode was analyzed. The difference of MTBS between BAG group and Control group was found statistically significant (p < .05) in fluorosis. The Er:YAG laser + BAG group showed lowest MTBS values in fluorosis. In conclusion, the pretreatment of BAG might be beneficial to the adhesive of fluorosed teeth. Er:YAG laser desensitization alone or using BAG first and then Er:YAG laser desensitization might not affect the adhesive of fluorosed teeth, while Er:YAG laser desensitization followed by the pretreatment of BAG would be not conducive to the adhesive of fluorosed teeth.