This study evaluated the cytotoxicity and biocompatibility of a new bioceramic endodontic sealer (i.e., Sealer Plus BC) in comparison with those of MTA Fillapex and AH Plus. L929 fibroblasts were cultured and Alamar Blue was used to evaluate cell viability of diluted extracts (1:50, 1:100, and 1:200) from each sealer at 24 h. Polyethylene tubes that were filled with material or empty (as a control) were implanted in the subcutaneous tissue of rats. The rats were killed after 7 and 30 d (n = 8), and the tubes were removed for histological analysis. Parametric data was analyzed using a one-way ANOVA test, and nonparametric data was analyzed via the Kruskal-Wallis test followed by the Dunn test (p < 0.05). A reduction in cell viability was observed in the extracts that were more diluted for Sealer Plus BC when compared to that of Control and AH Plus (p < 0.05). However, the 1:50 dilution of the Sealer Plus BC was similar to that of the Control (p > 0.05). Conversely, more diluted extracts of MTA Fillapex (1:200) and AH Plus (1:100 and 1:200) were similar to the Control (p > 0.05). Histological analysis performed at 7 d did not indicate any significant difference between tissue response for all materials, and the fibrous capsule was thick (p > 0.05). At 30 d, Sealer Plus BC was similar to the Control (p > 0.05) and MTA Fillapex and AH Plus exhibited greater inflammation than the Control (p < 0.05). The fibrous capsule was thin for the Control and for most specimens of Sealer Plus BC and AH Plus. Thus, Sealer Plus BC is biocompatible when compared to MTA Fillapex and AH Plus, and it is less cytotoxic when less-diluted extracts are used.

Aim To investigate the relationship between apical periodontitis and atherosclerosis in rats by lipid profile and carotid artery intima tunic measurement, and histological and histometric evaluation of periapical lesions. Methodology Forty male Wistar rats were allocated into four groups: control (C), with apical periodontitis (AP), with atherosclerosis (AT) and with AP and AT (AP + AT). Atherosclerosis was induced using a high‐lipid diet associated with a surgical ligature in the carotid artery and a super dosage of vitamin D3. AP was induced via pulp exposure to the oral environment. At 45 and 75 days, serum levels of total cholesterol (TC), triglycerides (TG), high‐density lipoprotein cholesterol (HDL‐C) and low‐density lipoprotein cholesterol (LDL‐C) were measured. The maxillary and mandibular jaws and carotid artery were collected and processed for histological analysis. The Kruskal–Wallis or Mann–Whitney test was performed for nonparametric data, and the Tukey’s or Student’s t‐test was performed for parametric data (P < 0.05). Results In nonatherosclerotic animals, the induction of apical periodontitis increased TG levels significantly, from 63.1 ± 11.4 mg dL−1 in group C to 88.2 ± 7.9 mg dL−1 in the AP group (P < 0.05). The induction of AP was associated with a trend for higher TC and LDL‐C levels in atherosclerotic animals (P > 0.05); however, it only significantly increased TG levels, from 93.2 ± 18.0 mg dL−1 in AT group to 121.9 ± 14.5 mg dL−1 in the AP + AT group (P < 0.05). Animals in the AP + AT group had a 36.5% increase in the thickness of the carotid intima tunic when compared with the AT group (P < 0.05). The intensity of the inflammatory infiltrate was significantly larger in the AP + AT group when compared with AP group (P < 0.05). The AP + AT group exhibited significantly greater alveolar bone loss, with a periapical lesion size of 206.4 ± 56.3 × 104 μm2, compared with 151.4 ± 49.1 × 104 μm2 in the AP group (P < 0.05). Conclusion Apical periodontitis influenced triglyceride levels, increasing them even in the absence of atherosclerosis, and influenced the increase in the thickness of the carotid artery intima tunic in the presence of atherosclerosis. Atherosclerosis intensified the inflammatory reaction and increased bone resorption in periapical lesions.

Aim To investigate the effects of liver fibrosis (LF) on the pro-inflammatory mediators and periapical bone resorption of apical periodontitis (AP) in rats. Methodology Forty male Wistar rats were distributed into four groups: Ccontrol, APrats with AP, LFrats with LF, AP + LFrats with AP and LF. LF was induced by carbon tetrachloride administration for 8 weeks and surgical bile duct ligation for 4 weeks; AP was induced in the teeth of rats by dental pulp exposure to the oral environment for 30 days. Jaws and livers were removed after euthanasia. Haematoxylin and Eosin (H&E) and Picrosirius Red (PSR) staining were used to confirm fibrosis in the livers. The jaws were analysed using H&E staining, immunohistochemical assays of interleukin (IL)-1b, IL-6 and tumour necrosis factor-alpha (TNF-a). Student's t-test and Mann-Whitney's U-test were used for statistical analysis (P < 0.05). Results Inflammatory infiltrate was moderate in the AP group and severe in the AP + LF group (P < 0.05). Periapical bone resorption was significantly larger in the AP + LF group compared with the AP group (P < 0.05). IL-1b, IL-6 and TNF-a levels were significantly higher in AP + LF group when compared to the AP group (P < 0.05). Conclusion More intense inflammatory infiltrate, greater amounts of pro-inflammatory cytokines and increased periapical bone resorption were observed in the presence of liver fibrosis in rats with exposed pulps.

Omega-3 polyunsaturated fatty acids (ω-3 PUFAs) have been reported to exert important roles in the inflammatory response (Vardar et al., 2004). The major ω-3 PUFAs are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), both being able of competitively inhibiting the production of arachidonic acid metabolites via the cyclooxygenase and lipoxygenase pathways, thus reducing the pro-inflammatory arachidonic mediators (Calder, 2006). DHA has demonstrated anti-inflammatory effects by interference with interleukin-1 signaling pathways leading to cyclooxygenase-2 induction in endothelial cells (Massaro et al., 2006). In addition, EPA lowers the level of arachidonic acid available for metabolism and competes against arachidonic acid for metabolism to form metabolites of leukotrienes and prostaglandins, decreasing the inflammatory response (Mukaro et al., 2008).As a consequence of possessing anti-inflammatory properties, ω-3 PUFAs has been accepted as an adjunct therapy in the treatment

The systematic review tried to answer the following question: Does the melatonin administered systemically or topically ameliorate patients involved with oral health conditions or dental procedures? The systematic review has been registered in the PROSPERO (2021CRD42021095959). Eligibility criteria included only randomized controlled clinical trials (RCTs) with at least 10 participants that compared patients that received melatonin as a treatment before and/or after their oral intervention topically or systemically, with control patients. A search was performed in PubMed/MEDLINE, Web of Science, Cochrane Library, and Academic Google databases for articles up to February 2021. The Cochrane risk‐of‐bias tool for randomized clinical trials was used and revealed that the studies included presented low risk of bias for the majority of criteria assessed. It was selected 25 articles, of which only six did not demonstrate positive effects and three presented null effects with the use of melatonin. Melatonin has improved the inflammatory response in periodontal disease, dental surgeries, and mucositis of head and neck oncologic irradiated patients. In addition, it showed anxiolytic potential in patients that were submitted to dental procedures. In conclusion, melatonin favored the treatment of oral changes when used topically and systemically.