METHODOLOGY: Three sodium-fluoride(NaF) concentration(0.01%w/v,0.1%w/v and 0.5%w/v respectively)and two poly-γ-glutamic acid(PGGA)concentration(1%w/v and 2%w/v respectively)were prepared in 0.1 M acetic acid(pH4.0)and deionized distilled water.For de/re-mineralisation study, tooth samples (18 teeth varnished, leaving a 2 mm2 window on the mid-buccal surfaces) were immersed in respective acidified NaF and PGGA solutions. The Ca2+ release/uptake was monitored with ISE over 72-hr with increasing pH every 24-h from 4.0 to 6.0.These teeth were later subjected to cross-sectional microhardness to determine integrated mineral recovery of enamel on increasing pH of respective acidified solution.In order to determine mechanism of PGGA,two concentrations of PGGA in deionized-water-solutions were used for tooth samples immersion followed by overnight drying then later subjected to Fourier Transform Infra-Red(FT-IR) analysis.The FT-IR analysis was also carried out on PGGA powder.For control,the experiment was repeated using hydroxyapatite(HAp)pellets.The density of PGGA solutions(1%and2%)was also measured to determine their dynamic viscosities.
RESULTS: The ISE and microhardness testing revealed statistically significant (ρ ≤ 0.05) dissolution inhibition and remineralisation potential for tooth sample treated with acidified 2%PGGA. From the FT-IR spectra, it was observed that the profiles of the enamel and HAp surfaces treated with 1%-and 2%-PGGA solutions were similar to those of PGGA powder.It was found that the viscosity of PGGA increases with increasing concentration.
CONCLUSION: The study implies that 2% PGGA is more effective than NaF as forms a coating layer to protect from demineralisation and promote remineralisation of the tooth surface.
OBJECTIVE: This study aimed to determine the potential of ascorbic acid alone in inducing differentially expressed osteoblast-related proteins in dental stem cells via the liquid chromatography-mass spectrometry/ mass spectrometry (LC-MS/MS) approach.
METHODS: The cells were isolated from deciduous (SHED) and permanent teeth (DPSC) and induced with 10 μg/mL of ascorbic acid. Bone mineralisation and osteoblast gene expression were determined using von Kossa staining and reverse transcriptase-polymerase chain reaction. The label-free protein samples were harvested on days 7 and 21, followed by protein identification and quantification using LC-MS/MS. Based on the similar protein expressed throughout treatment and controls for SHED and DPSC, overall biological processes followed by osteoblast-related protein abundance were determined using the PANTHER database. STRING database was performed to determine differentially expressed proteins as candidates for SHED and DPSC during osteoblast development.
RESULTS: Both cells indicated brownish mineral stain and expression of osteoblast-related genes on day 21. Overall, a total of 700 proteins were similar among all treatments on days 7 and 21, with 482 proteins appearing in the PANTHER database. Osteoblast-related protein abundance indicated 31 and 14 proteins related to SHED and DPSC, respectively. Further analysis by the STRING database identified only 22 and 11 proteins from the respective group. Differential expressed analysis of similar proteins from these two groups revealed ACTN4 and ACTN1 as proteins involved in both SHED and DPSC. In addition, three (PSMD11/RPN11, PLS3, and CLIC1) and one (SYNCRIP) protein were differentially expressed specifically for SHED and DPSC, respectively.
CONCLUSION: Proteome differential expression showed that ascorbic acid alone could induce osteoblastrelated proteins in SHED and DPSC and generate specific differentially expressed protein markers.
MATERIALS AND METHODS: This parallel, single-blinded, randomised controlled trial (RCT) consisted of 22 periodontitis patients who had molar with advanced furcation involvement (FI). All patients followed the same inclusion criteria and were treated following the same protocol, except for radiographic evaluation (CBCT vs. periapical). This study proposed and evaluated five parameters that represent the extent and severity of furcation defects in molars teeth, including CEJ-BD (clinical attachment loss), BL-H (depth), BL-V (height), RT (root trunk), and FW (width).
RESULTS: There were no statistically significant differences between CBCT and intrasurgical linear measurements for any clinical parameter (p > 0.05). However, there were statistically significant differences in BL-V measurements (p
Materials and Methods: GCF of 160 individuals (4-15 years of age) was collected by the extracrevicular method. They were categorized into four groups (40 per each group). Group I: subjects with primary dentition (4-5 years of age), Group II: 40 subjects in early transition period (6-8 years), Group III: 40 individuals in the late transition period (9-11 years), and Group IV: 40 individuals with permanent dentition (12-15 years). MIP-lα and MIP-1β levels were determined in the samples of GCF by ELISA method. Data were analyzed by software SPSS Version 20 (IBM SPSS Statistics for Windows, IBM Corp., Armonk, NY: USA).
Results: MIP-1α and MIP-1β were detected in all samples. The highest mean MIP-1α and MIP-1β concentrations in GCF were detected in the early transition period, while the lowest concentrations were seen in primary dentition group. The chemokine levels were higher in girls than in boys in Group III. There was a substantial rise of MIP-1α and MIP-1β levels during eruption.
Conclusions: Since levels of MIP-1α and MIP-1β in GCF are positively associated with tooth eruption, they may perhaps be deemed as novel biomarkers in the eruption process.