(1/173) The effect of triclosan toothpaste on enamel demineralization in a bacterial demineralization model.
Triclosan has been incorporated into toothpaste to enhance inhibitory effects on bacterial metabolism in dental plaque. Many studies have confirmed these effects by showing a reduction of accumulation of dental plaque, gingivitis and calculus. However, there is no evidence for triclosan having an inhibitory effect on the dental plaque-induced demineralization of the dental hard tissues. Therefore, the effect of 0.3% triclosan added to non-fluoride and fluoride toothpaste was tested in an in vitro model, in which bovine enamel specimens were to be demineralized by acids produced in overlaying Streptococcus mutans suspensions. In a first set of experiments the toothpastes were added to the S. mutans suspensions at 1:100, 1:1000 and 1:10,000 (w/v) dilutions. After 22 h incubation at 37 degrees C the suspensions were removed and assessed for calcium and lactate content, and pH. In this set of experiments, triclosan had no additive protective effect to the non-fluoride or fluoride toothpaste. In a second set of experiments, the enamel specimens were immersed daily for 3 min in 30% (w/v) slurries of the toothpastes before the 22 h incubation with the S. mutans suspensions. Under these conditions, triclosan showed an additional protective effect compared with non-fluoride toothpaste at a low concentration of S. mutans cells (0.07 mg cells dry weight per 600 microL suspension). It is concluded that the enamel surface may act as a reservoir for triclosan, which may protect the enamel surface against a mild acid attack. In combination with fluoride, however, as in toothpaste, triclosan has no additional protective effect against demineralization. (+info)
(2/173) Fluoride-releasing elastomerics--a prospective controlled clinical trial.
A prospective controlled clinical trial was undertaken to evaluate the effectiveness of stannous fluoride-releasing elastomeric modules (Fluor-I-Ties) and chain (Fluor-I-Chain) in the prevention of enamel decalcification during fixed appliance therapy. Forty-nine patients (782 teeth) were included in the experimental group, where the fluoride-releasing elastomerics were used. Forty-five patients (740 teeth) who received non fluoride-releasing elastomerics formed the control group. All patients had their elastomerics replaced at each visit. Enamel decalcification incidence and distribution were recorded using an index by direct clinical observation. In the control group enamel decalcification occurred in 73 per cent of patients and in 26 per cent of all teeth. In the experimental group the corresponding incidence was 63 and 16 per cent, respectively. The overall reduction in score per tooth produced by the fluoride-releasing elastomerics was 49 per cent, a highly significant difference (P < 0.001). A significant difference was seen in all but the occlusal enamel zones. The majority (over 50 per cent) of lesions occurred gingivally. The teeth most severely affected were the maxillary lateral incisors and mandibular second premolars. There was no difference in treatment duration between groups. (+info)
(3/173) Study of the fluoridated adhesive resin cement--fluoride release, fluoride uptake and acid resistance of tooth structures.
The objectives of this study, were to evaluate the fluoride release from fluoridate adhesive resin cement, fluoride uptake into surrounding tooth structures and the effect of their acid resistance. Several specimens were prepared using a plastic ring mould, from extracted human premolars, and prepared from enamel and dentin of the central area of the buccal surface of bovine teeth. The fluoride release rate of fluoridate adhesive resin cement (PN 200) per day was higher than other materials during the 7-day study period. Fluoride released and fluoride uptake by tooth structures was higher in the fluoridate adhesive resin cement. WDX analysis showed the fluoride concentration on dentin contact area was higher than that of enamel after 60 days of immersion in deionized water. The calcium release values were similar for enamel and dentin plates in the various test materials. The present findings indicated the important enhancement of tooth structure acid resistance by fluoridate material. (+info)
(4/173) Fluoride-releasing elastomeric modules reduce decalcification: a randomized controlled trial.
OBJECTIVE: To determine whether fluoride releasing elastomeric modules reduced the incidence of decalcification around orthodontic brackets during a complete course of orthodontic treatment. DESIGN: A randomised controlled, split mouth design. SETTING: The study was carried out in the orthodontic department of Newcastle-upon-Tyne Dental Hospital, UK. SUBJECT AND METHODS: 21 consecutive patients (126 teeth) undergoing fixed appliance therapy were studied. A split mouth technique was adopted to examine the upper labial segment, where one side (left or right) was randomly assigned to the experimental group, and the opposite side served as a control throughout their course of orthodontic treatment. INTERVENTIONS: The control teeth were ligated to the archwire using conventional modules. The experimental teeth were ligated to the archwire using Fluoride releasing elastomeric modules. OUTCOME MEASURES: Standardised photographs were taken of the upper labial segment before and after completion of orthodontic treatment, and the degree of decalcification assessed in each tooth quadrant, using a modification of the Enamel Defect Score. RESULTS: Decalcification was found to occur in both treatment groups, though to a significantly greater degree on the control side (p = 0.002). The fluoride module side showed significantly fewer serious decalcified lesions than the control (p = 0.013). No patients withdrew from the study. CONCLUSIONS: It would appear that the use of fluoride releasing elastomeric modules reduces the degree of decalcification experienced during orthodontic treatment. (+info)
(5/173) Dental enamel formation and its impact on clinical dentistry.
The nature of tooth enamel is of inherent interest to dental professionals. The current-day clinical practice of dentistry involves the prevention of enamel demineralization, the promotion of enamel remineralization, the restoration of cavitated enamel where demineralization has become irreversible, the vital bleaching of dental enamel that has become discolored, and the diagnosis and treatment of developmental enamel malformations, which can be caused by environmental or genetic factors. On a daily basis, dental health providers make diagnostic and treatment decisions that are influenced by their understanding of tooth formation. A systemic condition during tooth development, such as high fever, can produce a pattern of enamel defects in the dentition. Knowing the timing of tooth development permits estimates about the timing of the disturbance. The process of enamel maturation continues following tooth eruption, so that erupted teeth can become less susceptible to decay over time. Mutations in the genes encoding enamel proteins lead to amelogenesis imperfecta, a collection of inherited diseases having enamel malformations as the predominant phenotype. Defects in the amelogenin gene cause X-linked amelogenesis imperfecta, and genes encoding other enamel proteins are candidates for autosomal forms. Here we review our current understanding of dental enamel formation, and relate this information to clinical circumstances where this understanding may be particularly relevant. (+info)
(6/173) Varnish or polymeric coating for the prevention of demineralization? An ex vivo study.
OBJECTIVE: The ability of an experimental coating, Odyssey, to prevent demineralisation ex vivo was compared with that of a fluoride varnish, Duraphat and a chlorhexidine-containing varnish, Cervitec. DESIGN: an ex vivo single-blind study. SETTING: Hard tissue research laboratory. MATERIALS AND METHODS: thirty bovine enamel blocks 0.5 cm x 1.5 cm were divided into 6 groups of 5 specimens. The enamel blocks were then allocated to one of 6 surface treatments. INTERVENTIONS: (1) surface left unprepared (control), (2) Duraphat application, (3) Cervitec application, (4) experimental polymer coating, (5) enamel conditioned with 10% citric acid and coated with the experimental polymer coating Odyssey (O + C), (6) enamel etched for 30 sec with 37% phosphoric acid and coated with the experimental coating (O + E). All specimens were cycled for 7 days through a daily procedure of demineralisation for 4 hours and remineralisation for 20 hours, and exposed to an equivalent of 2 months toothbrushing. A single operator blinded to the treatment allocation of each specimen carried artificial lesion depth assessment out using computer-assisted transverse microradiography. RESULTS: The control group had the greatest mean lesion depth (97.16 + 29.8 microm) with the Duraphat group exhibiting the lowest mean lesion depth (24.53 + 15.44 microm). The Duraphat, Odyssey, O + C and O + E groups all had significantly less lesion depth when compared with no surface preparation (p < 0.05 for all comparisons). There were no significant differences between any of the Odyssey groups. CONCLUSIONS: The efficacy of Duraphat application in preventing demineralisation ex vivo has been demonstrated in the present study, but clinical trials are required to assess its usefulness in orthodontic practice. (+info)
(7/173) A resin veneer for enamel protection during orthodontic treatment.
The aims of this study were to test the tensile bond strength of a recently developed veneer. Sound premolar teeth (120) extracted for orthodontic purposes were divided into two experimental and two control groups. In one experimental group (V1) 4-META/MMA-TBB resin (4META) was used on the surface veneer prepared with micro particle filled resin (MFR) as an adhesive for bracketing and in the second group (V2) 4META was applied on the surface veneer with the trial resin. For the controls, in group R 4META was used on the enamel surface without veneer and in group G light-cured glass ionomer cement was applied. The 30 samples in each group were divided into three groups of 10 samples and thermal cycled (TC) at 3000, 10,000 or left uncycled. Tensile testing was carried out using an Instron machine. After tensile testing the bond failures in the experimental groups were recorded using a stereomicroscope. Statistical analysis was performed using ANOVA. In group V2 the resin veneer was able to maintain sufficient bond force to enamel during clinical use. The bond strength of group V1 was significantly higher than that of groups R (P < 0.05) and G (P < 0.01) at TC 0, but for both TC 3000 and 10,000, the bond strength of group V1 was lower than groups R and G, respectively. There were significant differences between groups V1 and R (P < 0.01) for TC 3000, and between groups V1 and R and G (P < 0.01) at TC 10,000. The bond strength of group V2 was almost equal to that of group R at TC 0. At TC 3000, group V2 showed significantly lower bond strength than group R (P < 0.05), but no significant difference was found compared with group G. At TC 10,000, there were no significant differences between groups V2, R or G. When comparing groups V1 and V2, the bond strength of group V1 was significantly higher than that of group V2 (P < 0.01) at TC 0, but the bond strength of group V1 was significantly lower than that of group V2 for both TC 3000 (P < 0.05) and TC 10,000 (P < 0.01). Comparison between groups R and G, showed that the bond strength of group R was significantly higher than that of group G for both TC 0 (P < 0.01) and TC 3000 (P < 0.01), but no significant difference was found for TC 10,000. In group V2, nine samples showed adhesive failure between the veneer surface and bracket adhesive before thermal cycling. There were significant differences between the MFR and both trial resin and glass ionomer cement (P < 0.01) when examining thermal expansion. No significant difference was found between the trial resin and glass ionomer cement. It is suggested that application of a resin veneer prior to bracket bonding is suitable for clinical application to protect the teeth and to prevent decalcification and caries. (+info)
(8/173) Effect of experimental fluoride-releasing tooth separator on acid resistance of human enamel in vitro.
This study aimed to investigate the fluoride-releasing ability of an experimental tooth separator consisting of polyurethane elastomer with tin fluoride and its effect on the acid resistance of human enamel. The tooth separator was set around an enamel slab and stored in de-ionized water for 10 days. The daily concentration of fluoride in the de-ionized water was measured. Then the enamel surface was artificially decalcified by a lactic acid buffer solution (pH 4.5) for 96 hours. The mineral density at the surface layer of the enamel was measured to evaluate the acid resistance. The fluoride release increased with the amount of fluoride in the separator, but decreased with the immersion time. Both the enamel area contacting with the separator and its surrounding area showed lower mineral loss and lesion depth compared with the controls (P < 0.05). It is suggested that the experimental tooth separator would release enough fluoride and improve the acid resistance of the enamel surface layer. (+info)