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.

Aim Natural substances such as omega‐3 have been used in the medical field due to their numerous properties and, in particular, modulating effect on the systemic and local inflammatory processes. Thus, this study evaluated the influence of omega‐3 supplementation on the subcutaneous tissue response of endodontic sealers in Wistar Rats. Methodology Polyethylene tubes were implanted in the subcutaneous tissue of 48 animals (one empty for control and three filled with Sealapex, AH Plus or Endofill). The animals were treated with omega‐3 (TO) or water (TW). Treatments started 15 days before implantation until euthanasia. After 5, 15 and 30 days (n = 8), animals were euthanized and polyethylene tubes and surrounding tissue were removed and processed for histological analysis. The inflammatory reaction was analysed by Haematoxylin and Eosin stain and immunolabelling for IL‐6 and TNF‐α. The collagen maturity was analysed by picrosirius red stain and calcium deposition by von Kossa stain and polarized light. Results were statistically analysed (p < .05). Results Amongst TW sealer groups, Endofill evoked a more intense inflammatory infiltrate compared with AH Plus and control in the 30‐day period (p = .009). However, in TO sealer groups, there was no difference amongst the sealers and control in all periods (p > .05). Comparing each sealer as a function of the supplementation with water or omega‐3, there are differences for Endofill (p = .001) and Sealapex (p = .005) in the 30‐day period, presenting lower inflammatory infiltrate in the animals treated with omega‐3. A higher percentage of immature fibres was observed at 15 and 30 days in the TO group, compared with the TW group (p < .05). The deposition of calcium particles was observed only by Sealapex in all periods, despite the supplementation procedure. Conclusions Omega‐3 supplementation influence the tissue reactions of endodontic sealers, modulating inflammation, the immunolabelling of IL‐6 and TNF‐α, the repair process and it does not interfere with calcium deposition.

Aim The aim of the study was to evaluate the effect of systemic curcumin administration on the severity of apical periodontitis (AP). Methodology Forty male Wistar rats weighing 250–280 g each, age 2.5 months, were distributed into four groups (n = 10): control untreated rats (C), control rats treated with curcumin (CUR), rats with pulp exposure‐induced apical periodontitis (AP) and rats with pulp exposure‐induced apical periodontitis treated with curcumin (AP‐CUR). Curcumin treatment was administered orally once daily for 15 days before pulp exposure and continued for 30 days after pulp exposure. The rats were sacrificed at 30 days, and the jaws were collected and reconstructed in a programme specific for micro‐CT. The jaws were processed for analysis of the inflammatory process using haematoxylin and eosin staining and immunohistochemical assays for interleukin tumour necrosis factor alpha (TNF‐α), interleukin (Il)‐6 and Il‐1β. Tartrate‐resistant acid phosphatase (TRAP) and osteocalcin (OCN) staining were used to analyse the resorptive process on the bone surface of periapical area. Kruskal–Wallis with Dunn's test was performed for nonparametric data and anova with Tukey's test for parametric data, p < .05. Results Micro‐CT revealed no statistically significant differences in bone resorption between the AP and AP‐CUR groups (p > .05). The levels of inflammatory cell infiltration and immunoreactivity for the proinflammatory cytokines TNF‐α, Il‐6 and Il‐1β were significantly higher in the periapical lesions of the AP group than in the AP‐CUR group (p < .05). The number of TRAP‐positive multinucleated cells was higher in the AP group than in the AP‐CUR group (p < .05). In OCN‐positive cells, no differences were observed between the AP and AP‐CUR groups (p > .05). Conclusions Oral supplementation with curcumin had a significant effect on the AP severity in rats, suggesting an anti‐inflammatory effect of curcumin on AP development.