Anti-inflammatory effect of luteoloside against methylglyoxal induced human dental pulp cells.

PURPOSE: The aim of this study was to investigate whether luteoloside, a flavonoid, could protect human dental pulp cells (HDPCs) against inflammation and oxidative stress induced by methylglyoxal (MGO), one of the advanced glycated end products (AGE) substances. METHODS: HDPCs were stimulated with MGO and treated with luteoloside. MTT assay was used to determine cell viability. Protein expression was measured via western blotting. Reactive oxygen species (ROS) were measured with a Muse Cell Analyzer. Alkaline phosphatase activity (ALP) and Alizarin red staining were used for mineralization assay. RESULTS: Luteoloside down-regulated the expression of inflammatory molecules such as ICAM-1, VCAM-1, TNF-α, IL-1ß, MMP-2, MMP-9, and COX-2 in MGO-induced HDPCs without showing any cytotoxicity. It attenuated ROS formation and enhanced osteogenic differentiation such as ALP activity and Alizarin red staining in MGO-induced HDPCs. Overall, luteoloside showed protective actions against inflammation and oxidative stress in HDPCs induced by MGO through its anti-inflammatory, anti-oxidative, and osteogenic activities by down-regulating p-JNK in the MAPK pathway. CONCLUSION: These results suggest that luteoloside might be a potential adjunctive therapeutic agent for treating pulpal pathological conditions in patients with diabetes mellitus.

Photovoltaic and thermal properties of electrolytes based on electrospun poly(vinylidene fluoride-hexafluoro propylene)/poly(methyl methacrylate) nanofibers for dye-sensitized solar cells.

We prepared electrospun polymer nanofibers by electrospnning method and investigated about their applications to dye-sensitized solar cells (DSSCs). Electrospun polymer nanofibers applied to the polymer matrix in electrolyte for DSSCs. To improve the stiffness of polymer nanofiber, poly(vinylidene fluoride-hexafluoro propylene)/Poly(methyl methacrylate) (PVDF-HFP/PMMA) blend nanofibers were prepared and examined. In the electrospun PVDF-HFP/PMMA (1:1) blend nanofibers, the best results of VOC, JSC, FF, and efficiency of the DSSC devices showed 0.71 V, 12.8 mA/cm2, 0.61, and 5.56% under AM 1.5 illumination.

Gallic acid improves glucose tolerance and triglyceride concentration in diet-induced obesity mice.

Gallic acid, a phenolic phytochemical, has been shown to exert a variety of effects, including anti-oxidative, anti- carcinogenic, anti-allergic, and anti-inflammatory effects. In this study, we attempted to determine whether gallic acid affects metabolic syndrome such as obesity and diabetes. Diet-induced obesity mice were treated intraperitoneally once per day with gallic acid (10 mg/kg/day). After 2 weeks of treatment, the mice were sacrificed to collect the blood for metabolic parameter assessments, and the adipose tissues and liver to weigh and analyze. The triglyceride concentrations were significantly improved in the gallic acid group relative to those measured in the control group. And most importantly, the blood glucose concentrations in the gallic acid group were significantly improved. In the epididymal white adipose tissue of the gallic acid group, adipocyte size was reduced, PPARγ expression was induced, and the Akt signaling pathway was activated. Our results demonstrate that gallic acid improves glucose tolerance and lipid metabolism in the obesity mice, thereby showing evidence of anti-hyperglycemic activity. The findings of an upregulation of PPARγ expression and Akt activation also contribute to our current understanding of the mechanisms underlying the effects of gallic acid on glucose metabolism.

Non-Coding RNAs as Potential Targets for Diagnosis and Treatment of Oral Lichen Planus: A Narrative Review.

Oral lichen planus (OLP) is a chronic inflammatory disease that is characterized by the infiltration of T cells into the oral mucosa, causing the apoptosis of basal keratinocytes. OLP is a multifactorial disease of unknown etiology and is not solely caused by the malfunction of a single key gene but rather by various intracellular and extracellular factors. Non-coding RNAs play a critical role in immunological homeostasis and inflammatory response and are found in all cell types and bodily fluids, and their expression is closely regulated to preserve normal physiologies. The dysregulation of non-coding RNAs may be highly implicated in the onset and progression of diverse inflammatory disorders, including OLP. This narrative review summarizes the role of non-coding RNAs in molecular and cellular changes in the oral epithelium during OLP pathogenesis.

Anti­tumor properties of FoxO1 in YD­9 oral squamous cell carcinoma cells.

Oral squamous cell carcinoma (OSCC) is a tumor with a poor prognosis and a high recurrence rate. Despite its high annual incidence worldwide, appropriate therapeutic strategies have not yet been developed. Consequently, the 5­year survival rate for OSCC is low when advanced stages or recurrence is diagnosed. Forkhead transcriptional factor O1 (FoxO1) is a key mediator for maintaining cellular homeostasis. FoxO1 can function as a tumor suppressor as well as an oncogene depending on the cancer type. Therefore, the precise molecular functions of FoxO1 need to be validated, considering intracellular factors and the extracellular environment. To the best of our knowledge, however, the roles of FoxO1 in OSCC have not yet been defined. The present study examined FoxO1 levels under pathological conditions (oral lichen planus and oral cancer) and selected an appropriate OSCC cell line (YD­9). Crispr/Cas9 was used to generate FoxO1­deficient YD­9 cells in which the protein levels of phospho ERK and phospho STAT3 were upregulated, promoting cancer proliferation and migration. In addition, FoxO1 reduction increased the levels of the cell proliferation markers phospho H3 (Ser10) and PCNA. FoxO1 loss significantly reduced cellular ROS levels and apoptosis in YD­9 cells. Collectively, the present study demonstrated that FoxO1 exerted an anti­tumor effect by suppressing proliferation and migration/invasion but promoting oxidative stress­linked cell death in YD­9 OSCC cells.

Cerium oxide nanozymes confer a cytoprotective and bio-friendly surface micro-environment to methacrylate based oro-facial prostheses.

Poly-(methyl methacrylate) (PMMA) is the preferred biomaterial for orofacial prostheses used for the rehabilitation of naso-palatal defects. However, conventional PMMA has limitations determined by the complexity of the local microbiota and the friability of oral mucosa adjacent to these defects. Our purpose was to develop a new type of PMMA, i-PMMA, with good biocompatibility and better biological effects such as higher resistance to microbial adhesion of multiple species and enhanced antioxidant effect. The addition of cerium oxide nanoparticles to PMMA using a mesoporous nano-silica carrier and polybetaine conditioning, resulted in an increased release of cerium ions and enzyme mimetic activity, without tangible loss of mechanical properties. Ex vivo experiments confirmed these observations. In stressed human gingival fibroblasts, i-PMMA reduced the levels of reactive oxygen species and increased the expression of homeostasis-related proteins (PPARg, ATG5, LCI/III). Furthermore, i-PMMA increased the levels of expression of superoxide dismutase and mitogen-activated protein kinases (ERK and Akt), and cellular migration. Lastly, we demonstrated the biosafety of i-PMMA using two in vivo models: skin sensitization assay and oral mucosa irritation test, respectively. Therefore, i-PMMA offers a cytoprotective interface that prevents microbial adhesion and attenuates oxidative stress, thus supporting physiological recovery of the oral mucosa.

The geographic origin of Helicobacter pylori influences the association of the homB gene with gastric cancer.

We found that South Korean Helicobacter pylori isolates predominantly carry homB at locus B and that there is no association between the homB allele and the cagA allele or the development of gastric cancer within this population. Uniquely, several East Asian strains carried multiple copies of the hom genes.

Oral Microbiome Research on Oral Lichen Planus: Current Findings and Perspectives.

Oral lichen planus (OLP) is a chronic inflammatory disease of the oral mucosa with an unknown etiology. The role of oral microbes in the development of OLP has gained researchers' interest. In this review, we summarized the findings of studies focused on the relationship between OLP and oral microbiome, which includes the composition of oral microbiota, molecules produced by oral microbiota or the host, and the oral environment of the host. According to the studies, the oral microbial community in OLP patients undergoes dysbiosis, and the microbial dysbiosis in OLP patients is more prominent in the buccal mucosa than in the saliva. However, no same microorganisms have been suggested to be associated with OLP in multiple investigations, implying that the functional aspects of the oral microbiota are more important in OLP development than the composition of the oral microbiota. According to studies on host factors that make up the oral environment, signal pathways involved in cellular processes, such as keratinization, inflammation, and T cell responses are triggered in OLP. Studies on the functional aspects of the oral microbiota, as well as interactions between the host and the oral microbiota, are still lacking, and more research is required.

Insulin growth factor binding protein-3 enhances dental implant osseointegration against methylglyoxal-induced bone deterioration in a rat model.

PURPOSE: The aim of this study was to determine the effect of insulin growth factor binding protein-3 (IGFBP-3) on the inhibition of glucose oxidative stress and promotion of bone formation near the implant site in a rat model of methylglyoxal (MGO)-induced bone loss. METHODS: An in vitro study was performed in MC3T3 E1 cells treated with chitosan gold nanoparticles (Ch-GNPs) conjugated with IGFBP-3 cDNA followed by MGO. An in vivo study was conducted in a rat model induced by MGO administration after the insertion of a dental implant coated with IGFBP-3. RESULTS: MGO treatment downregulated molecules involved in osteogenic differentiation and bone formation in MC3T3 E1 cells and influenced the bone mineral density and bone volume of the femur and alveolar bone. In contrast, IGFBP-3 inhibited oxidative stress and inflammation and enhanced osteogenesis in MGO-treated MC3T3 E1 cells. In addition, IGFBP-3 promoted bone formation by reducing inflammatory proteins in MGO-administered rats. The application of Ch-GNPs conjugated with IGFBP-3 as a coating of titanium implants enhanced osteogenesis and the osseointegration of dental implants. CONCLUSIONS: This study demonstrated that IGFBP-3 could be applied as a therapeutic component in dental implants to promote the osseointegration of dental implants in patients with diabetes, which affects MGO levels.

Nasal obstruction promotes alveolar bone destruction in the juvenile rat model.

BACKGROUND/PURPOSE: Nasal obstruction leads to oral breathing and consequently hypoxia. The purpose of this study was to determine the influence of hypoxia on inflammatory response and the effect on alveolar bone development in a rat model in which mouth breathing was induced by nasal obstruction. MATERIALS AND METHODS: Unilateral nasal obstruction was performed by injecting a Merocel sponge into the nasal cavity of 8-week-old Sprague Dawley (SD) rats. After 3 and 6 weeks of nasal obstruction, rats were sacrificed, the organs were weighed, and the changes in mandibular bone quality were examined by micro-computed tomography (µ-CT). The stereomicroscope was used for the morphological analysis of alveolar bone loss in response to nasal obstruction. Hematoxylin and Eosin (H&E) and immunohistochemical staining were employed to examine inflammation and bone remodeling induced by hypoxia. RESULTS: Nasal obstruction led to a delay in overall growth and organ development. The bone mineral density (BMD) and bone volume/total volume (BV/TV) of the mandible were reduced due to nasal obstruction, and the loss of the alveolar bone was confirmed morphologically. Our nasal obstruction method was observed to be successful in inducing hypoxia along with an increase in hypoxia-inducible factor 1-alpha (HIF-α). Oral hypoxia induced by nasal obstruction increased inflammatory response, and increased expression of receptor activator of nuclear factor kappa-Β ligand (RANKL) led to bone destruction. CONCLUSION: This study demonstrated that nasal obstruction induced mouth breathing led to hypoxia in a rat model. Under hypoxic conditions, an increase in osteoclast differentiation induced by activation of the inflammatory pathway causes destructive changes in the alveolar bone.

Helicobacter pylori-mediated gastric pathogenesis is attenuated by treatment of 2-deoxyglucose and metformin.

Helicobacter pylori infection causes chronic inflammation in the stomach, which is linked to the development of gastric cancer. The anti-inflammatory and anticancer effects of a glycolysis inhibitor 2-deoxyglucose (2DG) and an antidiabetic medication metformin (Met) have gotten attention. Using a Mongolian gerbil animal model, we investigated H. pylori-mediated gastric pathogenesis and how this pathogenesis is influenced by 2DG and Met. Five-week-old male gerbils were infected with H. pylori strain 7.13. After 2 weeks of infection, gerbils were fed 2DG-containing food (0.03% w/w), Met-containing water (0.5% w/v), or both (Combi) for 2 (short-term) or 10 weeks (long-term). Gastric pathogenesis and host response to H. pylori infection were examined by macroscopic and histopathologic analysis of gerbils' stomach. As a result, indicators of gastric pathogenesis by H. pylori infection including infiltration of polymorphonuclear neutrophils and lymphocytes, intestinal metaplasia, atrophy, and proliferation of gastric epithelial cells were attenuated by short-term administration of 2DG, Met, or Combi. When the infection was sustained for long-term, gastric pathogenesis in drug-treated gerbils was equivalent to that in untreated gerbils, with the exception that the infiltration of neutrophil was reduced by 2DG. Colonization of H. pylori in stomach was unaffected by both short- and long-term treatments. Our findings demonstrate that the progression of gastric pathogenesis induced by H. pylori infection can be attenuated by the short-term individual or combinational treatment of 2DG and Met, implying that 2DG or Met could be considered as a treatment option for gastric diseases in the early stages of infection.

Host immune response mediates changes in cagA copy number and virulence potential of Helicobacter pylori.

Helicobacter pylori is the major risk factor for gastric cancer. H. pylori harboring the type IV secretion system (T4SS) and its effector CagA encoded on the cag pathogenicity Island (cagPAI) increases the risk. H. pylori PMSS1 has a multi-cagA genotype, modulating cagA copy number dynamically from zero to four copies. To examine the effect of the immune response on cagA copy number change, we utilized a mouse model with different immune status. PMSS1 recovered from Rag1-/- mice, lacking functional T or B cells, retained more cagA copies. PMSS1 recovered from Il10-/- mice, showing intense inflammation, had fewer cagA copies compared to those recovered from wild-type mice. Moreover, cagA copy number of PMSS1 recovered from wild-type and Il10-/- mice was positively correlated with the capacity to induce IL-8 secretion at four weeks of infection. Since recombination in cagY influences T4SS function, including CagA translocation and IL-8 induction, we constructed a multiple linear regression model to predict H. pylori-induced IL-8 expression based on cagA copy number and cagY recombination status; H. pylori induces more IL-8 secretion when the strain has more cagA copies and intact cagY. This study shows that H. pylori PMSS1 in mice with less intense immune response possess higher cagA copy number than those infected in mice with more intense immune response and thus the multi-cagA genotype, along with cagY recombination, functions as an immune-sensitive regulator of H. pylori virulence.

Polymorphisms in the intermediate region of VacA impact Helicobacter pylori-induced disease development.

Helicobacter pylori is the etiological agent of diseases such as gastritis, gastric and duodenal ulcers, and two types of gastric cancers. While some insight has been gained into the etiology of these diverse manifestations, by and large, the reason that some individuals develop more severe disease remains elusive. Recent studies have focused on the roles of H. pylori toxins CagA and VacA on the disease process and have suggested that both toxins are intimately involved. Moreover, CagA and VacA are polymorphic within different H. pylori strains, and particular polymorphisms seem to show a correlation with the development of particular disease states. Among VacA polymorphisms, the intermediate region has recently been proposed to play a major role in disease outcome. In this article, we describe a detailed sequence analysis of the polymorphic intermediate region of vacA from strains obtained from a large South Korean population. We show that polymorphisms found at amino acid position 196 are associated with more severe disease manifestations. Additionally, polymorphisms found at amino acid position 231 are linked to disease in strains that carry the non-EPIYA-ABD allele of CagA. Collectively, these data help explain the impact of the VacA intermediate region on disease and lead to the hypothesis that there are allele-driven interactions between VacA and CagA.

Mussel adhesive protein blended with gelatin loaded into nanotube titanium dental implants enhances osseointegration.

The purpose of this study was to investigate whether mussel adhesive protein (MAP) blended with gelatin loaded into nanotube titanium (Ti) dental implants enhances osseointegration and supports bone formation. Cell viability, crystal violet staining, Western blot analysis, alizarin red S staining, alkaline phosphatase (ALP) activity, micro-computed tomography (µ-CT), hematoxylin and eosin (H&E), and immunohistochemistry (IHC) staining were employed to test the biocompatibility of MAP blended with gelatin (MAP/Gel). MC3T3 E1 cells were used for in vitro and Sprague-Dawley rats for in vivo models in this study. MC3T3 E1 cells cultured in MAP/Gel loaded into nanotube Ti surface demonstrated activation of FAK-PI3K-MAPKs-Wnt/ß-catenin signaling pathway and enhanced osteogenic differentiation. µ-CT, H&E, and IHC staining confirmed that MAP/Gel dental implants promoted bone regeneration around the nanotube Ti implants by upregulation of Runx-2, BMP-2/7, Osterix, and OPG in rat mandible model. MAP/Gel supports osseointegration of dental implant after implantation. It is hypothesized that MAP/Gel loaded into nanotube Ti dental implants may be applicable as a potential treatment for bone formation and proper integration of dental implants with alveolar bone. Graphical abstract.

Epidemiological link between gastric disease and polymorphisms in VacA and CagA.

Gastritis, peptic ulcer disease, and gastric cancer are a few of the diverse disease manifestations that have been shown to be associated with infection by Helicobacter pylori. Why some individuals develop more severe forms of disease remains largely unknown. In this study, 225 South Korean strains were genotyped for vacA and then analyzed to determine if particular genotypes varied across disease state, sex, or cagA allele. Of these strains, 206 strains carried an s1/i1/m1 allele, 11 strains carried an s1/i1/m2 allele, and 8 strains carried an s1/i2/m2 allele. By using Fisher's exact test, a statistical association between variations in the cagA and vacA alleles was identified (P = 0.0007), and by using log linear modeling, this variation was shown to affect the severity of disease outcome (P = 0.027). Additionally, we present evidence that variation within the middle region of VacA contributes significantly to the distribution of vacA alleles across gender (P = 0.008) as well as the association with disease outcome (P = 0.011). In this South Korean population, the majority of H. pylori strains carry the vacA s1/i1/m1 allele and the CagA EPIYA-ABD allele. These facts may contribute to the high incidence of gastric maladies, including gastric cancer.

Wogonin inhibits osteoclast formation induced by lipopolysaccharide.

To evaluate the inhibitory activity of wogonin against lipopolysaccharide (LPS)-induced bone resorption, we investigated the effect of wogonin on osteoclastogenesis induced by LPS. Wogonin inhibited LPS-induced osteoclastogenesis in co-cultures of mouse calvaria-derived osteoblasts and bone marrow-derived pre-osteoclasts. Wogonin also suppressed osteoclastogenesis in LPS-injected mouse calvaria. In osteoblasts, the upregulation of receptor activator of nuclear factor-kappaB (RANKL) expression and the downregulation of osteoprotegerin (OPG) expression by LPS were inhibited by wogonin. Wogonin and NS-398, a COX-2 inhibitor, suppressed LPS-stimulated PGE(2) production in osteoblasts. NS-398 inhibited the effect of LPS on RANKL and OPG expression in osteoblasts. These results suggest that wogonin acts as an inhibitor of LPS-induced osteoclastogenesis through downregulation of RANKL and upregulation of OPG expression via blockage of PGE(2) production. Based on these results, wogonin has potential for use as a therapeutic agent in bacteria-induced bone resorption.

Polymorphism in the CagA EPIYA motif impacts development of gastric cancer.

Helicobacter pylori causes diseases ranging from gastritis to peptic ulcer disease to gastric cancer. Geographically, areas with high incidences of H. pylori infection often overlap with areas with high incidences of gastric cancer, which remains one of the leading causes of cancer-related deaths worldwide. Strains of H. pylori that carry the virulence factor cytotoxin-associated gene A (cagA) are much more likely to be associated with the development of gastric cancer. Moreover, particular C-terminal polymorphisms in CagA vary by geography and have been suggested to influence disease development. We conducted a large-scale molecular epidemiologic analysis of South Korean strains and herein report a statistical link between the East Asian CagA EPIYA-ABD genotype and the development of gastric cancer. Characterization of a subset of the Korean isolates showed that all strains from cancer patients expressed and delivered phosphorylatable CagA to host cells, whereas the presence of the cagA gene did not strictly correlate to expression and delivery of CagA in all noncancer strains.

Bioactive resin-based composite with surface pre-reacted glass-ionomer filler and zwitterionic material to prevent the formation of multi-species biofilm.

OBJECTIVE: This study evaluated the synergetic effect between surface pre-reacted glass-ionomer (SPRG) filler and 2-methacryloyloxyethyl phosphorylcholine (MPC), for inhibiting multi-species biofilm formation, while maintaining or even improving the original beneficial features of SPRG-filled resin-based composite (RBC). METHODS: MPC (1.5-10wt%) was incorporated into commercial SPRG-filled RBC. Then, the inherent properties of RBC, and ion release and acid-neutralising properties associated with SPRG were investigated. Further, protein adsorptions and bacterial adhesion and viability on the SPRG-filled RBC surfaces were studied using four kinds of oral bacteria; Streptococcus mutans, Actinomyces naeslundii, Veillonella parvula, and Porphyromonas gingivalis. Finally, the thickness and biomass of the human saliva-derived biofilm model cultured on test and control samples were analysed. RESULTS: Addition of MPC content resulted in decreased flexural strength and wettability of SPRG-filled RBC. SPRG-filled RBC released significantly higher amounts of multiple ions as contents of MPC increased. Meanwhile, SPRG-filled RBC with 5-wt% MPC significantly improved acid-neutralising properties than those of other test and control samples (P<0.001). SPRG-filled RBC with 3wt% MPC significantly reduced the amount of adsorbed bovine serum albumin and proteins from the brain heart infusion medium as compared to the control (P<0.01). A similar trend was observed in the attachment of four types of bacteria and multi-species biofilm (P<0.01). SIGNIFICANCE: Despite limitation in terms of deteriorations of some physical properties, addition of 3% MPC to SPRG-filled RBC leads to inhibition of the attachment of multi-species bacteria on its surface, as well as inhibition of biofilm growth. Moreover, the original important bioactive features of SPRG-filled RBC such as ion release and acid neutralisations are either maintained or improved upon adding MPC.

Evolutionary mechanism leading to the multi-cagA genotype in Helicobacter pylori.

Infection with CagA+ Helicobacter pylori strains is linked to an increased risk for gastric diseases, including gastric cancer. Recent evidence indicates that dynamic expansion and contraction of cagA copy number may serve as a novel mechanism to enhance disease development. Herein, comparative genomic analysis divided hpEurope into two groups: hpEurope/type-A and type-B. Only hpEurope/type-B displayed the multi-cagA genotype. Further analysis showed that cagPAI appears to have been independently introduced into two different H. pylori types, termed pre-type-A and pre-type-B, which consequently evolved to cagPAI type-A and type-B, respectively; importantly, all multi-cagA genotype strains displayed cagPAI type-B. Two direct cagA-flanking repeats of a genetic element termed CHA-ud were essential for the multi-cagA genotype in strain PMSS1 (hpEurope/type-B and cagPAI type-B). Furthermore, introduction of this genetic element into strain G27 (hpEurope/type-A and cagPAI type-A) was sufficient to generate the multi-cagA genotype. The critical steps in the evolution of the multi-cagA genotype involved creation of CHA-ud at cagA upstream in cagPAI type-B strains followed by its duplication to cagA downstream. En masse, elucidation of the mechanism by which H. pylori evolved to carry multiple copies of cagA helps to provide a better understanding of how this ancient pathogen interacts with its host.

Novel anti-biofouling light-curable fluoride varnish containing 2-methacryloyloxyethyl phosphorylcholine to prevent enamel demineralization.

We evaluated the efficacy of light-curable fluoride varnish (LCFV) that contains 2-methacryloyloxyethyl phosphorylcholine (MPC) in terms of anti-biofouling properties and prevention of tooth enamel demineralization. MPC was mixed with and incorporated into LCFV at 0 (control), 1.5, 3.0, 5.0, 10.0, 20.0, and 40.0 weight percentage (wt%). Addition of high wt% of MPC resulted in increased film thickness and decreased the degree of conversion, indicating loss of the advantageous properties of LCFV. Addition of 1.5, 3, or 5 wt% MPC significantly reduced the amount of bovine serum albumin adsorbed from a solution and proteins adsorbed from brain heart infusion medium compared to the control (P < 0.001). A similar pattern was observed for bacterial adhesion: significantly less Streptococcus mutans cells adhered on the surface of LCFV with 1.5, 3, or 5 wt% MPC (P < 0.001) than on the control, and similar results were obtained for Actinomyces naeslundii and Streptococcus sanguinis adherence to LCFV with 3 wt% MPC. Finally, bacterial adhesion, surface microhardness loss, and the depth of demineralization were substantially lower on bovine tooth enamel surface coated with LCFV containing 3 wt% of MPC than in the control treatment (0 wt% MPC). Therefore, this novel LCFV containing a low concentration of MPC (e.g., 3 wt%) would be effective in anti-biofouling while maintaining the important advantageous features of light-curable fluoride in preventing demineralization.