OBJECTIVE: To study the durability of the anti-demineralization effects of fluoride varnish after being applied to dental root surfaces. METHODS: Coronal and radicular dentin samples were prepared from extracted human teeth. Duraphat^® (DP) was applied to the dentine surfaces to form a protective film. The film-dentin interfaces were observed by scanning electron microscopy (SEM) and the fluoride element was analyzed with energy dispersive spectrometer (EDS). Thus, the differences between applying DP on crowns and roots were compared. Radicular dentin samples were prepared and randomly divi-ded into four groups: (1) Blank: DP was not applied, and demineralized in acetic acid (pH 4.5) for 4 days; (2) Blank+aging: DP was not applied, the samples were put into deionized water for 14 days at room temperature, and then demineralized in acetic acid (pH 4.5) for 4 days; (3) DP: DP was applied and demineralized in acetic acid (pH 4.5) for 4 days; (4) DP+aging: DP was applied, the samples were put into deionized water for 14 days at room temperature, and then demineralized in acetic acid (pH 4.5) for 4 days. Finally, SEM observation and EDS analysis of fluoride content were performed on film-dentin interfaces to evaluate the degree of demineralization, the morphology of DP film, and the penetration of fluorine. RESULTS: The immediate penetration depth of fluoride element from DP was deeper in the coronal dentin than that in radicular dentin. The samples in the blank and blank+aging groups demine-ralized significantly after acid etching. The DP group did not undergo demineralization, and the fluorine element penetrated to (76.00±8.94) μm below the interfaces. The structure of the protective film in the DP+aging group was damaged, but the underneath dentin did not undergo demineralization. The fluorine element still remained at a depth of (5.00±3.53) μm below the interfaces. CONCLUSION DP has an anti-demineralization effect on the root surface, and this effect can still be exerted for a period of time after losing the structure of protective film. It has the ability to prevent root caries and a certain durability.
Humans ; Tooth Root/drug effects* ; Fluorides, Topical/pharmacology* ; Tooth Demineralization/prevention & control* ; Dentin/drug effects* ; Fluorides ; In Vitro Techniques ; Cariostatic Agents/pharmacology*

OBJECTIVETo investigate the effects of fluoride on Fas expression, caspase-3 and caspase-8 activity and apoptosis in rat incisor cells.

METHODSForty male SD rats were divided into 4 groups randomly and provided with distilled water containing NaF at the doses of 0, 10, 50 and 100 mg/L respectively. Each group had 10 animals. Five animals were sacrificed at 60 and 90 days respectively. Fas expression was measured with immunohistochemistry, and colorimetric assay was used to examine caspase-3 and caspase-8 activity with enzyme-labelled meter. The apoptosis was detected by flow cytometry in mandibular incisor cells.

RESULTSNaF at the doses of 10, 50 and 100 mg/L for 60 d and 90 d caused Fas overexpression, promoted activity of caspase-3 and caspase-8, increased apoptosis rate in mandibular incisor cells. At 60 days, the value of Fas expression was 0.1819 ± 0.0025 for control, 0.2120 ± 0.0084 for 10 mg/L NaF group, 0.2283 ± 0.0183 for 50 mg/L NaF group, 0.2818 ± 0.0233 for 100 mg/L NaF group. At 90 days, the value of Fas expression was 0.2077 ± 0.0289 for control, 0.2216 ± 0.0105 for 10 mg/L NaF group, 0.2377 ± 0.0059 for 50 mg/L NaF group, 0.2775 ± 0.0088 for 100 mg/L NaF group. Statistics analysis yielded close relationship between the dose of NaF in water and the Fas expression, and also between the dose of NaF in water and caspase-3 activities, and the relative coefficient was 0.9728 (60 d, P < 0.01) and 0.9889 (90 d, P < 0.01) for Fas expression, 0.9533 (60 d, P < 0.01) and 0.9849 (90 d, P < 0.01) for caspase-3 activity respectively. Apoptosis rate and caspase-8 activity also had close relationship with the NaF doses, and the relative coefficient was 0.9733 (90 d, P < 0.01) for apoptosis, 0.9928 (90 d, P < 0.01) for caspase-8. At the doses of 10, 50 and 100 mg/L NaF for 60 d and 90 d, obvious relationship was found between Fas expression and caspase-3 activity, and the relative coefficient was 0.9619 (60 d, P < 0.01) and 0.9912 (90 d, P < 0.01). Obvious relationship between Fas expression and apoptosis, between Fas expression and caspase-8 activity was found in groups for 90 d, and the relative coefficient was 0.9841 (P < 0.01) for apoptosis, 0.9767 (P < 0.01) for caspase-8.

CONCLUSIONSFluoride could induce Fas overexpression and mediate caspase activation and apoptosis at the doses of 10, 50 and 100 mg/L for 60 d and 90 d in rat mandibular incisor cells.

Animals ; Apoptosis ; drug effects ; Cariostatic Agents ; administration & dosage ; pharmacology ; Caspase 3 ; metabolism ; Caspase 8 ; metabolism ; Dose-Response Relationship, Drug ; Incisor ; cytology ; metabolism ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Sodium Fluoride ; administration & dosage ; pharmacology ; fas Receptor ; metabolism

OBJECTIVETo study the combined effect of fluoride and arsenate on the expression of SD rat osteoblastic osteoclast differentiation factor (ODF) mRNA and osteoprotegerin (OPG) mRNA.

METHODSOsteoblasts were obtained by enzymatic isolation from newborn SD rats. A factorial experiment was performed. Osteoblasts were exposed to NaF (0.5 mmolF/L, 4 molF/L) and Na3AsH2 (12.5 micromolAs/L and 200 micromolAs/L) separately or F plus As and cultured for 48 h. The gene expression of osteoblastic ODF and OPG was observed by RT-PCR.

RESULTSThe expression of ODF mRNA increased in F0.5, F4 groups compared with control group and two groups of F0.5As200, F4As200 compared with As200 group, and decreased significantly in groups of F4Asl2.5, F0.5As200, and F4AS200. The expression of OPG mRNA decreased in groups of F4, As200, F4As12.5, F0.5AS200, and F4AS200.

CONCLUSIONThe joint effect of fluoride and arsenate on the gene expression of ODF is antagonistic, while the combined effect on the gene expression of OPG is synergistic. F4, F4As12.5, and F0.5As200 promote bone resorption of rat osteoclasts, whereas F0.5As12.5 inhibits osteolytic effect of rat osteoclasts.

Animals ; Animals, Newborn ; Arsenates ; pharmacology ; Bone and Bones ; drug effects ; Cariostatic Agents ; pharmacology ; Fluorides ; pharmacology ; Gene Expression ; drug effects ; Hazardous Substances ; pharmacology ; Osteoblasts ; cytology ; drug effects ; Osteoprotegerin ; biosynthesis ; genetics ; RANK Ligand ; biosynthesis ; genetics ; Rats

OBJECTIVETo evaluate the in vitro cario-static effect of Galla chinesis with biofilm model.

METHODSA four-organism bacterial consortium was cultured in a biofilm model on hydroxyapatite (HA) discs in a continuous culture system and exposed to repeated solution pulsing. There were three groups with different solution pulsed in the model: negative control group was pulsed with distilled water, positive control group was pulsed with 100 mmol/L sucrose solution and experimental group was pulsed with 100 mmol/L sucrose solution containing 4.0 g/L Galla chinensis. During the experiment, the dynamic changes of pH were recorded. After 6 pulses, surface structure of the biofilm was observed with a scanning electron microscope and the population on the biofilm was enumerated.

RESULTSGalla chinesis significantly inhibited the adherence of Actinomyces naelundii to HA disc compared with the control group and facilitated the removal of acid products. It was also found that the extra-cellular polysaccharide was reduced with the pulsing of Galla chinesis.

CONCLUSIONGalla chinesis in the biofilm model can partially reduce the cario-genic response of sucrose solution.

Actinomyces ; drug effects ; physiology ; Bacterial Adhesion ; drug effects ; Biofilms ; growth & development ; Cariostatic Agents ; pharmacology ; Dental Caries ; microbiology ; Drugs, Chinese Herbal ; pharmacology ; Durapatite ; Humans ; Models, Biological ; Streptococcus mutans ; drug effects ; physiology ; Streptococcus sanguis ; drug effects ; physiology ; Sucrose ; pharmacology