The combination of arginine and fluoride-containing bioactive glass acted synergistically in inhibiting enamel demineralization in permanent teeth.

OBJECTIVES: To evaluate the in-vitro efficacy of inhibiting enamel demineralization using arginine in combination with fluoride-containing bioactive glass (FBG). METHODS: In this study, the healthy enamel blocks were first demineralized in acetic acid for 24 h, then soaked in anti-demineralization treatment solutions containing either arginine or FBG or both for 96 h.The specimens treated in acetic acid were applied as the control group. The pH, calcium and phosphorus ion concentrations of the solutions were measured before and after treatment. Changes in enamel mineral weight, microhardness, and composition were also analyzed. RESULTS: The present of arginine facilitated fluorine release from treatment solutions with the presence of FBG. Both arginine and FBG significantly increased the pH of treatment solutions and prevented the further mineral weight loss compared to the control group. All anti-demineralization treatment groups showed significant increases in microhardness, but there was no statistical difference among the treatment groups. The SEM analysis showed enamel restoration in the arginine and FBG groups upon treatment, while the combined groups showing a superior anti-demineralization efficacy. 19F NMR showed the formation of fluorapatite in samples treated with solutions containing FBG. CONCLUSIONS: Both arginine and FBG could inhibit enamel demineralization to some extent, and their combination demonstrated an enhanced anti-demineralization efficacy. The low-concentration combination group exhibited anti-demineralization effects comparable to those of high-concentration ones. CLINICAL SIGNIFICANCE: This study introduces a new approach for caries prevention by combining the application of arginine and FBG. The release of fluorine promoted by the presented arginine along with calcium and phosphorus ions from FBG facilitated FAP formation. Additionally, the increment of pH resulting from arginine and FBG degradation further prevents enamel demineralization.

Identification and functional study of a novel variant of PAX9 causing tooth agenesis.

OBJECTIVES: To search for pathogenic gene of a family with non-syndromic tooth agenesis, and explore the possible pathogenesis. MATERIALS AND METHODS: A Chinese family with non-syndromic tooth agenesis was recruited and screened for the pathogenic variants by whole exome sequencing technology and co-segregation analysis. The subcellular localization of wild-type and mutant protein was detected by immunofluorescence assay. Cycloheximide chase assay was performed to examine the difference in degradation rate between mutant protein and wild-type one. Dual-luciferase reporter assays were conducted to explore the alterations of mutant protein in the regulation of downstream target genes. RESULTS: A novel missense variant of PAX9 (c.296C>A:p.A99D) was found in this family. Bioinformatics software showed ß-return and the random coil were shortened in the p.A99D. The variant did not affect the subcellular localization of PAX9, but the degradation rate of p.A99D was accelerated (p < 0.05). p.A99D inhibited the activation of downstream target gene BMP4 (p < 0.05). CONCLUSIONS: This novel variant expands the pathogenic gene spectrum. The variant impaired the protein structure, accelerated the degradation of protein, and inhibited the activation of the downstream target gene BMP4, an upstream molecule in the TGF-ß/BMP pathway, which may contribute to tooth agenesis in this family.

[Effect of periodontal initial therapy on the amount of SFRP1 in gingival crevicular fluid in patients with periodontitis].

PURPOSE: To detect the change of secreted frizzled-related protein-1（SFRP1） in gingival crevicular fluid during periodontal initial treatment and explore the relationship between SFRP1 and the activity of chronic periodontitis. METHODS: Twenty-two patients with moderate to severe periodontitis were selected, and 5 healthy volunteers were enrolled into the study as control group. The bleeding index(BI),periodontal probing depth(PD)and clinical attachment loss(CAL) were recorded at 1 week after supragingival scaling, one month after subgingival scaling. Gingival crevicular fluid (GCF) was collected at 1 week after supragingival scaling, one week after subgingival scaling, one month after subgingival scaling. The level of SFRP1 in GCF samples was detected by ELISA. SPSS19.0 software package was used for data processing. RESULTS: The amount of SFRP1 in GCF of moderate to severe periodontitis group was (40.80±4.85) pg, and that of normal control was (33.42±2.24) pg at 1 week after supragingival scaling. The amount of SFRP1 in GCF was significantly higher in moderate to severe periodontitis compared to normal control group (P<0.05). In moderate to severe periodontitis group, the amount of SFRP1 in GCF significantly increased at l week after subgingival scaling (45.99±5.23) pg compared to 1 week after supragingival scaling and 1 month after subgingival scaling (36.92±4.00) pg (P<0.05); There was significant decrease in the amount of SFRP1 in GCF at 1 month after subgingival scaling,compared to 1 week after supragingival scaling and l week after subgingival scaling (P<0.05). CONCLUSIONS: The BI, PD in the periodontitis groups were significantly improved at 1 month after initial therapy,and the amount of SFRP1 in GCF changed with different periodontal inflammation state．

[Exploring the relationship between secreted frizzled-related protein 1 and chronic periodontitis].

OBJECTIVE: This study detects the expression of secreted frizzled-related protein 1 (SFRP1) in healthy patients and patients with chronic periodontitis (CP) and explores the relationship between SFRP1 and the occurrence and development of CP. METHODS: First, 28 patients forming the CP group were further divided into mild, moderate, and severe CP subgroups according to clinical attachment loss (CAL) data. Ten healthy volunteers were recruited in the control group. Gingival crevicular fluid (GCF) was collected from all of the patients, and the concentration of SFRP1 in the GCF samples was detected using enzyme-linked immunosorbent assay. Next, gingival lesions were obtained from 22 patients in the CP group and healthy gingival tissues were obtained from the 10 healthy patients in the control group. Immunohistochemical analysis for SFRP1 was used to analyze the correlation between the expression of SFRP1 and the severity of CP based on staining intensities. RESULTS: The concentration of SFRP1 in GCF samples taken from of the CP group (281.07 ng x L(-1) +/- 33.37 ng x L(-1)) was significantly higher than that in samples taken from the control group (245.30 ng x L(-1) +/- 35.69 ng x L(-1)) (P < 0.05). A significant positive correlation was observed between the concentration of SFRP1 in GCF and CAL (r = 0.651, P < 0.001). Furthermore, the SFRP1 scores in the CP groups (4.500 +/- 0.913) were significantly higher than those in the control group (2.800 +/- 1.135) (P < 0.001). SFRP1 scores did not vary significantly among the CP subgroups (P > 0.05). CONCLUSION: SFRP1 expression in the CP groups was significantly higher than that in the control group. Thus, SFRP1 may play a significant role in the development of CP.