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.

中文翻译：

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大鼠心尖牙周炎与动脉粥样硬化的关系：脂质分布和组织学研究。

目的通过脂质分布和颈动脉内膜中药测量及根尖周周病变的组织学和组织学评价，探讨大鼠根尖周炎与动脉粥样硬化的关系。方法将40只雄性Wistar大鼠分为四组：对照组（C），根尖牙周炎（AP），动脉粥样硬化（AT）以及AP和AT（AP + AT）。动脉粥样硬化是由高脂饮食引起的，该饮食与颈动脉的外科手术结扎和超剂量的维生素D3有关。通过牙髓暴露于口腔环境诱导AP。在第45天和第75天，测量血清总胆固醇（TC），甘油三酸酯（TG），高密度脂蛋白胆固醇（HDL-C）和低密度脂蛋白胆固醇（LDL-C）的水平。收集上颌和下颌颌及颈动脉并进行处理以进行组织学分析。对非参数数据执行Kruskal-Wallis或Mann-Whitney检验，对参数数据执行Tukey或Student的t检验（P <0.05）。结果在非动脉粥样硬化动物中，根尖周炎的诱导显着增加了TG水平，从C组的63.1±11.4 mg dL-1到AP组的88.2±7.9 mg dL-1（P <0.05）。AP的诱导与动脉粥样硬化动物中TC和LDL-C水平升高的趋势有关（P> 0.05）；然而，它只会显着增加TG水平，从AT组的93.2±18.0 mg dL-1到AP + AT组的121.9±14.5 mg dL-1（P <0.05）。AP + AT组的动物为36。与AT组相比，颈动脉内膜的厚度增加了5％（P <0.05）。与AP组相比，AP + AT组的炎性浸润强度明显更大（P <0.05）。与AP组的151.4±49.1×104μm2相比，AP + AT组的牙槽骨损失明显更大，根尖周病变的大小为206.4±56.3×104μm2（P <0.05）。结论根尖周炎影响甘油三酸酯水平，甚至在没有动脉粥样硬化的情况下也增加甘油三酸酯水平，并且在存在动脉粥样硬化的情况下影响颈动脉内膜厚度的增加。动脉粥样硬化加剧了根尖周病变中的炎症反应并增加了骨吸收。与AP组相比，AP + AT组的炎性浸润强度明显更大（P <0.05）。与AP组的151.4±49.1×104μm2相比，AP + AT组的牙槽骨损失明显更大，根尖周病变的大小为206.4±56.3×104μm2（P <0.05）。结论根尖周炎影响甘油三酸酯水平，甚至在没有动脉粥样硬化的情况下也增加甘油三酸酯水平，并且在存在动脉粥样硬化的情况下影响颈动脉内膜厚度的增加。动脉粥样硬化加剧了根尖周病变中的炎症反应并增加了骨吸收。与AP组相比，AP + AT组的炎性浸润强度明显更大（P <0.05）。与AP组的151.4±49.1×104μm2相比，AP + AT组的牙槽骨损失明显更大，根尖周病变的大小为206.4±56.3×104μm2（P <0.05）。结论根尖周炎影响甘油三酸酯水平，甚至在没有动脉粥样硬化的情况下也增加甘油三酯水平，并且在存在动脉粥样硬化的情况下影响颈动脉内膜厚度的增加。动脉粥样硬化加剧了根尖周病变中的炎症反应并增加了骨吸收。根尖周病变的大小为206.4±56.3×104μm2，而AP组为151.4±49.1×104μm2（P <0.05）。结论根尖周炎影响甘油三酸酯水平，甚至在没有动脉粥样硬化的情况下也增加甘油三酸酯水平，并且在存在动脉粥样硬化的情况下影响颈动脉内膜厚度的增加。动脉粥样硬化加剧了根尖周病变中的炎症反应并增加了骨吸收。根尖周病变的大小为206.4±56.3×104μm2，而AP组为151.4±49.1×104μm2（P <0.05）。结论根尖周炎影响甘油三酸酯水平，甚至在没有动脉粥样硬化的情况下也增加甘油三酯水平，并且在存在动脉粥样硬化的情况下影响颈动脉内膜厚度的增加。动脉粥样硬化加剧了根尖周病变中的炎症反应并增加了骨吸收。