Tooth bleaching increased IL-6 and TNF-α in the pulp tissue regardless of diabetes mellitus; however, diabetic rats had higher TNF-α levels for longer periods. Tooth bleaching influenced the increase in IL-17 in the early periods in normoglycaemic rats.

Bleaching gel containing hydrogen peroxide (H2O2) cause damages in pulp tissue. This study investigated the action of a topical anti-inflammatory, the Otosporin®, in rats’ bleached teeth with the null hypothesis of which the Otosporin® is no able to minimize the pulp inflammation that bleaching gel generates. The rat’s molars were divided into groups: BLE: bleached (35% H2O2 concentration /single application of 30 min); BLE-O: bleached followed by Otosporin® (10 min); and control: placebo gel. In the second day after dental bleaching, the rats were killed, and the jaws were processed for hematoxylin-eosin and immunohistochemistry analysis for tumor necrosis factor alpha (TNF-α), interleukin (IL)-6 and IL-17. The data collected were subjected to Kruskal-Wallis and Dunn statistical tests with at a 5% level of significance (p<0.05). The BLE group had moderate to strong inflammation in the occlusal third of the coronary pulp, with necrotic areas; and BLE-O, mild inflammation (p<0.05). There was a significant difference in the occlusal and middle thirds of the coronary pulp between the BLE with BLE-O and control groups (p<0.05). There was no difference in the cervical third (p>0.05). The BLE group had a high immunoexpression of TNF-α than BLE-O and control groups (p<0.05), with moderate and mild immunoexpression, respectively. Regarding IL-6 and IL-17, the BLE group had higher immunoexpression than control (p<0.05); the BLE-O was similar to the control (p>0.05). The topical anti-inflammatory Otosporin® can reduce pulp inflammation after dental bleaching in the rat teeth.

Aim To analyse the influence of H2O2 on pulp repair through osteocalcin and osteopontin immunolabelling and in cellular defence by using the antireactive oxygen species (ROS) antibody. Methodology The maxillary molars of 50 rats were treated with 35% H2O2 (Ble groups) or placebo gel (control groups). At 0 h and 2, 7, 15 and 30 days (n = 10 hemimaxillae), the rats were killed and pulp tissue was evaluated using inflammation and immunolabelling scores (osteocalcin/osteopontin); ROS‐positive cells were counted. Paired t‐test and Wilcoxon signed‐rank test were used (P < 0.05). Results The Ble group had necrosis in the coronal pulp at 0 h and in the occlusal third of the coronal pulp at 2 days; at 7, 15 and 30 days, no inflammation was noted similar to the controls (P > 0.05). Osteocalcin was absent in the Ble at 0 h, moderate at 2 days and increased thereafter, differing from the controls at all two periods (P < 0.05). Osteopontin was higher principally at 7 and 15 days in Ble groups, but differing with control groups from 2 days after bleaching (P < 0.05). The Ble group had more ROS‐positive cells in the pulp at 7 and 15 days (P < 0.05). Tertiary dentine was observed at 7 days, increasing thereafter (P < 0.05). Conclusions Post‐bleaching pulp repair was associated with increased osteocalcin over time. Osteopontin also participated in this process, and anti‐ROS was involved in cellular defence against H2O2.

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Aim To investigate hydrogen peroxide (H2O2)‐induced responsiveness in pulp cells using heme oxygenase‐1 (HO‐1) immunolabelling, Jun‐D immunolabelling to study the effects of H2O2 on odontoblastic differentiation and CD90+/CD73+/CD105+/CD45‐ cell counting for in vivo identification of mesenchymal stem cells in the pulp. Methodology The maxillary molars of 50 rats were treated with a bleaching gel (35% H2O2, 1 × 30 min) or placebo gel (control groups). At 2, 3, 7, 15 and 30 days after the treatment (n = 10), inflammation in pulp tissue was analysed by haematoxylin–eosin staining, HO‐1‐ and Jun‐D‐immunolabelled cells were counted in each third of the pulp chamber, and the number of CD90+/CD73+/CD105+/CD45‐ cells was quantified by immunofluorescence. The results were assessed using the Paired t‐test or Wilcoxon signed‐rank test (P < 0.05). Results Significant H2O2‐induced inflammation was noted at 2 and 3 days (P < 0.05), with tertiary dentine formation occurring from 7 days. The bleached specimens had greater HO‐1 immunolabelling in the middle and cervical thirds of the coronal pulp at 2 and 3 days, in all thirds at 7 days, and in the occlusal third at 15 days (P < 0.05), and significant nuclear Jun‐D immunolabelling in the cervical third at 2 and 3 days and in the occlusal and middle thirds at 7 days (P < 0.05). Bleached and control groups had low numbers of CD90+/CD73+/CD105+/CD45‐ cells in the pulp at all periods (P > 0.05). Conclusions Pulp cells responded to oxidative stress by expressing HO‐1 during the post‐bleaching inflammation phase until the beginning of the repair phase. Jun‐D expression occurred during the reduction of inflammation and the beginning of tertiary dentine production. The presence of oxidative stress did not influence the number of CD90+/CD73+/CD105+/CD45‐ cells identified in vivo in the dental pulp.