Concentration‐dependent effect of bleaching agents on the immunolabelling of interleukin‐6, interleukin‐17 and CD5‐positive cells in the dental pulp

Aim To evaluate lymphocyte‐like cell activation (CD5‐positive cells) and the expression of interleukin (IL)‐6 and IL‐17 in the pulp after tooth bleaching with two concentrations of hydrogen peroxide (H 2 O 2 ). Methodology The right and left maxillary molars from 40 rats were treated randomly with bleaching gel with 20% H 2 O 2 (BLUE group, 1 application of 50 min), 35% H 2 O 2 (MAXX group, three applications of 15 min), or placebo gel (control). After 2 and 30 days, the rats were killed ( n  = 10), and the jaws were processed for histological and immunohistochemistry analysis of the pulp tissue. The scores of inflammation and immunolabelling (IL‐6/IL‐17) were submitted to Mann–Whitney and Kruskal–Wallis followed Dunn tests, respectively; anova tests were used for comparisons of number of CD5‐positive cells and pulp chamber area values ( P  <   0.05). Results At 2 days, 60% of specimens of the BLUE group were associated with moderate inflammation in pulp horns, and in the MAXX group with necrosis ( P  <   0.05). At 30 days, the pulp was organized, and tertiary dentine was formed. The MAXX group had superior immunolabelling of IL‐17 at 2 days differing significantly from other groups ( P  <   0.05). At 2 days, 90% of the specimens of the BLUE group had moderate immunolabelling of IL‐6, and 50% of the MAXX group had severe immunolabelling, both significantly different from the control ( P  <   0.05). There was no significant difference between the groups at 30 days ( P  >   0.05). CD5‐positive cells were present at 2 and 30 days, particularly in the bleached groups ( P  <   0.05), without significant difference between time periods ( P  >   0.05). Conclusions IL‐6 and IL‐17 participated in inflammation in the pulp tissue of rats after tooth bleaching, particularly at 2 days. The immunolabelling was greater with increasing H 2 O 2 concentration. This process was accompanied by the prolonged activation of CD5‐positive cells.