Bioceramic materials possess desirable biological properties, highlighting their non-reactivity and osteoconductivity. Their use has been extended in vital pulp treatment. The purpose of this study was to evaluate and compare the effects of beta-tricalcium phosphate (β-TCP), hydroxyapatite (HA), and collagen (C) scaffold with mineral trioxide aggregate (MTA) on the vital pulp of rat molars. Thirty-two molars of Sprague–Dawley rats underwent direct pulp capping with β-TCP/HA/C (n = 16) and MTA (n = 16). After 30 days, the following parameters were evaluated in the tested samples: the degree of pulp inflammation and pulp vitality, the presence of reparative dentin, the homogeneity of the odontoblastic layer, and the presence of pulp fibrosis. No statistically significant differences were observed between HA/β-TCP/C and MTA in terms of the degree of inflammation (p = 0.124). Significant differences were found in reparative dentin formation between the treatment groups (p = 0.0005). Dentin bridge formation was observed in the MTA-treated group. The local action of HA/β-TCP/C is similar to that of MTA when used as an agent for pulp vital treatment in terms of absence of inflammation and maintenance of pulp vitality, although there are significant differences between both materials regarding the formation of dentin bridges.

Melatonin plays an essential role in the regulation of bone growth. The actions that melatonin exerts on odontoblasts may be similar to its action on osteoblasts. This research aimed to evaluate the pulp response to melatonin used for direct pulp capping to evaluate the antioxidant effect of melatonin administered orally and its influence on dental pulp. Direct pulp capping was performed on the upper molars of Sprague Dawley rats using melatonin or Mineral Trioxide Aggregate (MTA). The study groups were: MTA; Melatonin; MTA + Melatonin administered orally; and Melatonin + Melatonin administered orally. In the latter two groups, the animals drank water dosed with melatonin ad libitum (10 mg/100 mL). After 30 days, the animals were sacrificed, and 5 ml of blood, the kidneys, and the liver were extracted in order to evaluate oxidative stress using thiobarbituric acid reactive substances testing (TBARS). Fragments of the maxilla containing the study molars were prepared for histological evaluation. The degree of pulp inflammation and pulp necrosis, the presence of reparative dentin and dentin bridging the pulp chamber, the presence and regularity of the odontoblastic layer, and the presence of pulp fibrosis were evaluated. No significant differences were found between the four study groups for any of the studied histological variables. The oral administration of melatonin did not modify the local effects of MTA or melatonin on dental pulp, or reduce basal-level oxidative stress. The effect of melatonin on pulp is similar to that of MTA and may be used as an agent for direct pulp capping.

44 Chronic infusion of subpressor doses of Ang II causes blood pressure to increase progressively over several days. The mechanisms underlying this response are unknown but may involve Ang II-induced generation of additional vasoconstrictor processes. In this study, we tested whether endothelin and/or oxidative stress are implicated in the slow pressor responses to Ang II. We infused either vehicle (group 1; n=6) or Ang II (group 2; n=5) intravenously at 5 ng/kg/min via osmotic pumps for 15 days into Sprague Dawley rats. In addition to the Ang II infusion, groups 3 and 4 (n=6 each) received 30 mg/kg/day of either losartan (an angiotensin AT 1 receptor blocker) or bosentan (a blocker of both endothelin receptors, ET A and ET B ) in their drinking water. We measured systolic blood pressure (SBP) during the infusion, and the levels of circulating Ang II and isoprostanes (a marker of oxidative stress) at the conclusion of the experiments. Rats infused with vehicle had no change in SBP (from 138±13 to 138±2 mmHg) and normal levels of Ang II (34.5±9 pg/ml) and isoprostanes (111±10 pg/ml). Ang II infusion increased SBP from 133±10 to 158±8 mmHg, as well as circulating levels of Ang II (144±65 pg/ml) and isoprostanes (156±19 pg/ml). Losartan treatment abolished Ang II induced increases in SBP (SBP went from 137±5 to 120±4 mmHg), and isoprostanes (115±15 pg/ml), without altering Ang II levels (101±30 pg/ml). Bosentan also blocked Ang II-induced increases in SBP (from 135±4 to 139±3) but did not alter the increased isoprostane levels (146±14 pg/ml). Surprisingly, bosentan blunted the increase in Ang II levels (51±10 pg/ml). In conclusion, low dose Ang II-induced increases in SBP and oxidant stress depend on the AT 1 receptor. Endothelin receptor blockade also reduces SBP, but it does so independently of reducing oxidative stress (as measured by isoprostanes).