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Hydrogen peroxide induces cell proliferation and apoptosis in pulp of rats after dental bleaching in vivo: Effects of the dental bleaching in pulp.
Archives of Oral Biology 2017 September
OBJECTIVE: This study provides an in vivo evaluation of the inflammatory response, levels of cell proliferation and apoptosis, and the presence of necrosis after dental bleaching with two concentrations of hydrogen peroxide (H2 O2 ).
DESIGN: Wistar rats were divided into Control (placebo gel), BLUE (20% H2 O2 , 1×50min), and MAXX (35% H2 O2 , 3×15min) groups. At 2 and 30days, the rats were killed (n=10). The jaws were processed for histology analysis and PCNA and Caspase-3-cleaved immunohistochemistry, and data were submitted to the Mann-Whitney or ANOVA test (P<0.05).
RESULTS: At 2days, the MAXX group showed necrosis and the BLUE group revealed moderate inflammation on the occlusal third of the crown (P<0.05). At 30days, tertiary dentin had formed and there was an absence of inflammation. The level of cell proliferation was higher in the middle third of the BLUE group (P<0.05), and cervical of MAXX at 2days (P<0.05), decreasing at 30days. The apoptosis was present at 2days, particularly in the cervical third of the crown in the bleached groups (P<0.05), with a decrease only at 30days in the BLUE group (P<0.05).
CONCLUSIONS: The concentration of H2 O2 influences effects on the pulp tissue, where a higher concentration of H2 O2 can cause necrosis in the pulp and a prolonged effect within the apoptotic process; lower concentrations of H2 O2 provide moderate inflammation, cell proliferation and apoptosis with a reduction of these processes over time.
DESIGN: Wistar rats were divided into Control (placebo gel), BLUE (20% H2 O2 , 1×50min), and MAXX (35% H2 O2 , 3×15min) groups. At 2 and 30days, the rats were killed (n=10). The jaws were processed for histology analysis and PCNA and Caspase-3-cleaved immunohistochemistry, and data were submitted to the Mann-Whitney or ANOVA test (P<0.05).
RESULTS: At 2days, the MAXX group showed necrosis and the BLUE group revealed moderate inflammation on the occlusal third of the crown (P<0.05). At 30days, tertiary dentin had formed and there was an absence of inflammation. The level of cell proliferation was higher in the middle third of the BLUE group (P<0.05), and cervical of MAXX at 2days (P<0.05), decreasing at 30days. The apoptosis was present at 2days, particularly in the cervical third of the crown in the bleached groups (P<0.05), with a decrease only at 30days in the BLUE group (P<0.05).
CONCLUSIONS: The concentration of H2 O2 influences effects on the pulp tissue, where a higher concentration of H2 O2 can cause necrosis in the pulp and a prolonged effect within the apoptotic process; lower concentrations of H2 O2 provide moderate inflammation, cell proliferation and apoptosis with a reduction of these processes over time.
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