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To evaluate in vitro root caries formation in human permanent teeth and to determine the effects of commercially available dentifrices containing different amounts of fluoride, while employing a well-tested artificial caries system using an acidified gel.Root surfaces from caries-free human permanent teeth (n = 10) underwent debridement and fluoride-free prophylaxis. The tooth roots were sectioned into six portions, and acid-resistant varnish was placed with two sound root surface windows exposed on each tooth portion. Each portion from a single tooth was assigned to a treatment group: (1) No treatment control; (2) Denticious 5000 dentifrice (5,000 ppm F + xylitol); (3) PreviDent 5000 (5,000 ppm F); (4) AIM dentifrice (1,500 ppm F); (5) Listerine dentifrice (1,300 ppm F); and (6) Crest Regular Paste (1,500 ppm F). Tooth portions were treated with fresh dentifrice twice daily for 180 seconds, followed by fresh synthetic saliva rinsing over a 7-day period. Controls were exposed twice daily to fresh synthetic saliva rinsing over a 7-day period. In vitro root caries were created using an acidified gel (pH 4.25, 21 days). Longitudinal sections (three sections/tooth portion, 30 sections/group; 60 lesions/group) were evaluated for mean lesion depths (water imbibition, polarized light). Statistical analyses were performed using ANOVA and Duncan's Multiple Range test.Mean lesion depths were 389 +/- 43 microm for No treatment - control, 223 +/- 33 microm for Denticious 5000 dentifrice, 242 +/- 42 microm for Prevident 5000, 337 +/- 29 microm for AIM dentifrice, 297 +/- 37 microm for Listerine dentifrice, and 282 +/- 34 microm for Crest Regular Paste dentifrice. All treatment groups had mean depths significantly less than the No treatment - control group (P0.05). Denticious 5000 and PreviDent 5000 had significantly reduced mean depth compared with the other dentifrice treatment groups (P0.05).

To evaluate a remineralizing fluid for its influence on in vitro caries formation and progression.Caries-free teeth (n = 12) were sectioned into 3 segments. Each segment was assigned to a treatment group: (1) remineralizing fluid for 2 minutes; (2) 1.23% acidulated phosphate fluoride (APF) gel for 1 minute; (3) no-treatment control. Following treatment, the tooth segments were rinsed in distilled/deionized water and exposed to synthetic saliva for 24 hours. In vitro caries were formed and longitudinal sections obtained. The tooth segments were treated again and rinsed as above, before undergoing in vitro caries progression. Longitudinal sections were evaluated for lesion depth (ANOVA, Duncan multiple range analysis).Following lesion formation, mean lesion depths were 173 +/- 19 microm for no-treatment control; 97 +/- 11 microm for APF gel; and 52 +/- 12 microm for remineralizing fluid. After lesion progression, mean lesion depths were 236 +/- 23 microm for no-treatment control; 184 +/- 26 microm for APF gel; and 112 +/- 17 microm for remineralizing fluid. Mean lesion depths for the remineralizing fluid and APF gel groups for the lesion formation and progression periods were significantly less than those for the control group (P.05). After lesion formation and progression, the APF group had significantly greater mean lesion depths than did the remineralizing fluid group (P.05).A remineralizing fluid containing calcium, phosphate, and fluoride in a carbopol base enhanced resistance against in vitro caries formation and progression when compared with APF treatment.

To examine, in vitro, the caries-like lesion formation in enamel adjacent to fluoride-releasing orthodontic bonding agents using polarized light microscopic techniques.40 human extracted permanent third molars with sound enamel smooth surfaces were divided into two treatment groups: Light Bond group, a fluoride-releasing filled resin orthodontic bonding agent (n=20); and Pro Seal group, an orthodontic bonding agent with glass-ionomer (n=20). Prior to bonding agent placement on the buccal surfaces, acid-resistant varnish was applied to the molar teeth leaving a 2 mm (occlusal-cervical direction) by 5 mm (mesial-distal direction) exposed sound enamel window on the buccal surfaces of each molar tooth. The exposed window had the assigned orthodontic bonding agent applied, according to the manufacturer's instructions. With each specimen, a 1 mm (occlusal-cervical direction) by 5 mm (mesiodistal direction) sound enamel window was exposed by selectively removing the acid-resistant varnish on the opposing lingual or palatal surface with each molar tooth, and serving as a matched internal control with each molar. The molar teeth were then sectioned into buccal and lingual/palatal tooth halves. Acid-resistant varnish was applied to the cut surfaces. Each group underwent synthetic saliva rinsing for 2 weeks prior to in vitro caries formation using a modified ten Cate solution over a 2-week lesion initiation period. Longitudinal sections (three per treatment and control groups) were taken for polarized light study. The remaining tooth portions were exposed to synthetic saliva rinsing for 1 week and then exposed to the in vitro caries solution for an additional 1-week period to allow for lesion progression within the exposed enamel windows (progression 1 period). Longitudinal sections (three per treatment and control groups) were taken at the end of lesion progression 1 for polarized light study. After lesion progression 1, the remaining tooth portions were exposed to synthetic saliva rinsing for 1 week and then exposed to the in vitro caries solution for 1 week to allow for additional lesion progression within the exposed enamel windows (progression 2 period). Longitudinal sections (three per treatment and control groups) were taken at the end of lesion progression 2 for polarized light study. All longitudinal sections from the treatment and control groups at all three time periods (lesion initiation, progression 1 and progression 2) were imbibed with water and examined with polarized light microscopy to determine lesion depths and evaluate the enamel-resin interface. Mean (SD) lesion depths were determined and compared (ANOVA, t-test).Following lesion initiation, lesion progression 1 and lesion progression 2 periods, both treatment groups exhibited significant reductions in mean lesion depth when compared with the matched no treatment control group (P0.05). The Pro Seal group exhibited statistically significant reductions in mean lesion depths when compared with those for the Light Bond group at lesion initiation, lesion progression 1 and lesion progression 2 periods (P0.05, ANOVA, t-test). Both orthodontic bonding agents showed intact and intimate enamel-bonding agent interfaces with no lesion formation within the underlying bonded enamel. Caries-like lesions were only present in the exposed enamel windows adjacent to the orthodontic bonding agents.

To evaluate argon laser irradiation (AL), light-emitting diode exposure (LED), and acidulated phosphate fluoride treatment (APF) in vitro effects on caries-like enamel caries formation.Sound teeth (n = 18) were divided into four tooth quarters and coated with an acid-resistant varnish, leaving an enamel window exposed per tooth quarter. The tooth quarters were assigned to: (1) no treatment (control, mesiobuccal); (2) 1.23% APF (4 minutes, distolingual); (3) LED (Ultradent Ultra-Lume LED2 20 seconds, mesiolingual); and (4) AL (HGM Model 8, 11.5 J/cm2, 231 mW, 5mm beam size, 10 seconds, distobuccal). Following caries-like lesion formation (modified ten Cate solution), longitudinal sections (three per tooth quarter, 54 lesions per group) were obtained and evaluated for mean lesion depths (water imbibition, polarized light microscopy, ANOVA, DMR).Mean lesion depths were: 198 +/- 21 microm for controls; 186 +/- 17 microm for LED; 117 +/- 19 microm for AL; and 104 +/- 23 microm for APF. Lesion depths were statistically significantly decreased for AL (41%) and APF (47%) groups (P0.05), compared with controls. A slight lesion depth reduction for LED (6%) was present compared with controls; however this was not statistically significantly different (P0.05).

To evaluate the effects of a fluoride-releasing resin designed for amalgam bonding on secondary caries formation in primary teeth restored with amalgams.Primary teeth with caries-free buccal and lingual surfaces were selected and underwent a fluoride-free prophylaxis. Cavity preparations were performed in the buccal and lingual smooth surfaces of 20 primary teeth. A fluoride-releasing dimethacrylate resin bonding agent (Alloybond) was placed prior to amalgam restoration (Dispersalloy) of the cavity preparations in 10 teeth. Amalgam restorations placed in 10 teeth following copal cavity varnish (Copalite) served as controls. The teeth were thermocycled in synthetic saliva (500 cycles, 5 degrees-50 degrees C), and then coated with an acid-resistant coating, leaving a 1mm rim of sound enamel surrounding the restorations. Artificial secondary caries were created (2.2 mM calcium, 2.2 mM phosphate, 50 mM acetic acid, 0.5 ppm fluoride, pH 3.90). Following lesion formation, longitudinal sections (five per tooth) were prepared for polarized light evaluation. Mean depths for the primary surface lesions were determined using a computer-interfaced digitized tablet. Cavity wall lesion frequencies were also evaluated. Comparisons were made between groups (ANOVA, DMR).Primary surface lesion depth was reduced significantly (P0.05) with Alloybond-amalgams (135 +/- 14 microm) when compared with Copalite-amalgams (184 +/- 21 microm). Cavity wall lesion frequency was decreased (P0.05) significantly with Alloybond-amalgams (57%) compared with Copalite-amalgams (89%). The beneficial effect of the fluoride-releasing amalgam bonding agent was not limited to the cavosurface enamel. The caries susceptibility of enamel surfaces adjacent to amalgams with the fluoride-releasing bonding agent was decreased considerably. The incorporation of the amalgam-bonding resin with fluoride-releasing capabilities provided greater protection against a constant cariogenic attack over that for a conventional amalgam restoration.