Dentinal Microcracks Induced by Endodontic Procedures: Suggested Design for Experimental Studies Using Micro-Computed Tomography and Strain Gauges.

INTRODUCTION: The present study aimed to describe an in vitro study model to investigate root surface strain (RSS) and its correlation with the initiation/propagation of microcracks during different endodontic procedures. METHODS: Four lower human incisors extracted microcrack free were selected by micro-computed tomographic imaging. Two strain gauges were bonded to the root surface of each incisor. Then, the teeth were prepared to reproduce the periodontal ligament artificially. The gauges were attached to a data acquisition system. The RSS was recorded during the entire endodontic procedure, which consisted of accessing the endodontic cavity, cleaning, shaping preparation with an Mtwo rotary system (VDW, Munich, Germany), and filling with a standardized technique. Each incisor was submitted to a different retreatment protocol and supplementary cleaning method as follows: (1) Reciproc (RC, VDW) + Flatsonic (FS; Helse, Santa Rosa de Viterbo, Brazil), (2) RC + XP-endo Finisher (XPF; FKG Dentaire, La Chaux-de-Fonds, Switzerland), (3) Mtwo retreatment (MR) + FS, and (4) MR + XPF. Finally, the teeth were rescanned to establish the postoperative microcrack formation by 2 well-trained and blinded examiners. RESULTS: The maximum and minimum RSS values were -120 and 510 microstrains, respectively, for all of the files. RC showed the highest RSS values during endodontic retreatment compared with MR. FS demonstrated a higher variation between the minimum and maximum RSS than XPF. No microcracks were observed in the specimens. CONCLUSIONS: This preliminary study proposed an experimental model that would combine 2 methods to evaluate the effects of endodontic systems on dentin. Although strain gauges would provide data on the stresses created, the pre- and postoperative evaluation of micro-computed tomographic images would enable microcrack formation to be determined.

Effect of fluoride dentifrice and casein phosphopeptide-amorphous calcium phosphate cream with and without fluoride in preventing enamel demineralization in a pH cyclic study.

OBJECTIVE: Casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) complexes are anticariogenic and capable of remineralizing the early stages of enamel lesions. The use of fluoride prevents dental decay and the association of CPP-ACP with fluoride can increase remineralization. To evaluate the effect of CPP-ACP and CPP-ACPF creams associated with a fluoride dentifrice to prevent enamel demineralization in a pH cyclic model. MATERIAL AND METHODS: Previously selected by surface microhardness (SH) analysis, human enamel blocks (n = 56) were submitted to daily treatment with dentifrice in a pH-cycling model. The enamel blocks were divided into four groups; G1: Crest™ Cavity Protection - Procter & Gamble (1,100 ppmF of NaF); G2: Crest™ +MI Paste (MP) - Recaldent™ GC Corporation Tokyo, Japan); G3: Crest™ + MI Paste Plus (MPP) - Recaldent™ 900 ppm as NaF, GC Corporation Tokyo, Japan), and G4: control, saliva. Specimens were soaked alternatively in a demineralizing solution and in artificial saliva for 5 d. The fluoride dentifrice, with proportion of 1:3 (w/w), was applied three times for 60 s after the remineralization period. The undiluted MP and MPP creams were applied for 3 m/d. After cycling, SH was re-measured and cross section microhardness measurements were taken. RESULTS: The SH values observed for the groups G3 (257±70), G1 (205±70), and G2 (208±84) differed from the G4 group (98±110) (one-way ANOVA and Tukey's post hoc test). There were no differences between the groups G1xG2, G2xG3, and G1xG3 for demineralization inhibition. The percentage of volume mineral showed that, when applied with fluoride dentifrice, MPP was the most effective in preventing enamel demineralization at 50 µ from the outer enamel surface (Kruskal-Wallis and Mann Whitney p<0.05). CONCLUSION: Fluoride dentifrice associated with CPP-ACPF inhibited subsurface enamel demineralization.

Effect of fluoride dentifrice and casein phosphopeptide-amorphous calcium phosphate cream with and without fluoride in preventing enamel demineralization in a pH cyclic study

Abstract Casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) complexes are anticariogenic and capable of remineralizing the early stages of enamel lesions. The use of fluoride prevents dental decay and the association of CPP-ACP with fluoride can increase remineralization. Objective: To evaluate the effect of CPP-ACP and CPP-ACPF creams associated with a fluoride dentifrice to prevent enamel demineralization in a pH cyclic model. Material and Methods: Previously selected by surface microhardness (SH) analysis, human enamel blocks (n = 56) were submitted to daily treatment with dentifrice in a pH-cycling model. The enamel blocks were divided into four groups; G1: Crest™ Cavity Protection - Procter & Gamble (1,100 ppmF of NaF); G2: Crest™ +MI Paste (MP) - Recaldent™ GC Corporation Tokyo, Japan); G3: Crest™ + MI Paste Plus (MPP) - Recaldent™ 900 ppm as NaF, GC Corporation Tokyo, Japan), and G4: control, saliva. Specimens were soaked alternatively in a demineralizing solution and in artificial saliva for 5 d. The fluoride dentifrice, with proportion of 1:3 (w/w), was applied three times for 60 s after the remineralization period. The undiluted MP and MPP creams were applied for 3 m/d. After cycling, SH was re-measured and cross section microhardness measurements were taken. Results: The SH values observed for the groups G3 (257±70), G1 (205±70), and G2 (208±84) differed from the G4 group (98±110) (one-way ANOVA and Tukey's post hoc test). There were no differences between the groups G1xG2, G2xG3, and G1xG3 for demineralization inhibition. The percentage of volume mineral showed that, when applied with fluoride dentifrice, MPP was the most effective in preventing enamel demineralization at 50 µ from the outer enamel surface (Kruskal-Wallis and Mann Whitney p<0.05). Conclusion: Fluoride dentifrice associated with CPP-ACPF inhibited subsurface enamel demineralization.