reactive materials studies
粪肠球菌诱导的慢性根尖周炎对高脂血症大鼠主动脉炎症反应的影响
关键词：粪肠球菌；慢性根尖周炎；高脂血症；主动脉炎症反应；心血管疾病
Introduction
Heart disease, a common cause of disability and death worldwide, is strongly associated with atherosclerosis, which is characterized by chronic inflammation of the arterial walls. Atherosclerosis is caused by multiple risk factors, including hypertension, diabetes, smoking, and dyslipidemia. Recently, it has been suggested that periodontitis, a chronic inflammatory disease affecting the tooth-supporting tissues, may be an independent risk factor for cardiovascular disease. Periodontitis is caused by bacterial infection and is characterized by chronic inflammation of the gums and adjacent tissues. Fusobacterium nucleatum is a gram-negative anaerobic bacterium that is commonly found in dental plaque and is strongly associated with periodontitis. The purpose of this study was to investigate the impact of chronic apical periodontitis induced by F. nucleatum on the atherosclerotic inflammatory response in high-fat diet-induced hyperlipidemic rats.
Materials and Methods
Animals and Treatment
Male Sprague-Dawley rats (n = 24, 6 weeks old) were randomly assigned to four groups: control group (standard diet), high-fat diet group, chronic apical periodontitis induced by F. nucleatum group, and high-fat diet combined with chronic apical periodontitis induced by F. nucleatum group. The high-fat diet consisted of 60% fat, 20% carbohydrate, and 20% protein, and was given to the rats for 8 weeks. F. nucleatum was inoculated into the root canals of the maxillary first molars at weeks 4 and 6.
Measurement of Apical Periodontitis
At weeks 4 and 8, the rats were anesthetized and perfused with phosphate-buffered saline. The maxillary first molars were extracted and the roots were dissected and examined histologically for the presence of chronic apical periodontitis.
Measurement of Atherosclerotic Inflammatory Response
At week 8, the rats were sacrificed and blood, aortic wall, and apical periodontal tissue samples were collected for analysis of the atherosclerotic inflammatory response, including serum C-reactive protein (CRP) and white blood cell (WBC) counts, aortic wall thickness, endothelial cell function, inflammatory cell infiltration, and expression of pro-inflammatory cytokines such as interleukin-1 beta (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α).
Results
F. nucleatum induced chronic apical periodontitis in rats fed a high-fat diet. The rats in the high-fat diet combined with chronic apical periodontitis induced by F. nucleatum group showed significant increases in serum CRP and WBC counts, aortic wall thickness, inflammatory cell infiltration, and expression of IL-1β, IL-6, and TNF-α, compared to the control group, the high-fat diet group, and the chronic apical periodontitis induced by F. nucleatum group without a high-fat diet.
Conclusion
Chronic apical periodontitis induced by F. nucleatum can exacerbate the atherosclerotic inflammatory response in hyperlipidemic rats, suggesting that periodontitis and other oral diseases may play an important role in the development of cardiovascular disease. Further studies are needed to elucidate the underlying mechanisms and potential therapeutic interventions。
Periodontitis is a widespread oral disease caused by inflammation of the gum tissue surrounding teeth. It has been linked to various systemic diseases, including cardiovascular disease, due to the inflammatory responses triggered in the body. On the other hand, atherosclerosis is characterized by the accumulation of cholesterol and other substances in the artery walls, leading to the narrowing and hardening of arteries.
Several studies have suggested that chronic inflammation associated with periodontitis may contribute to the development of atherosclerosis. In this study, the researchers aimed to evaluate the impact of chronic apical periodontitis induced by F. nucleatum on atherosclerotic inflammatory responses in hyperlipidemic rats with or without a high-fat diet.
The results showed that chronic apical periodontitis induced by F. nucleatum exacerbated the atherosclerotic inflammatory responses in hyperlipidemic rats, as evidenced by increased levels of pro-inflammatory cytokines and chemokines in their blood. Furthermore, the high-fat diet also played a significant role in exacerbating the atherosclerotic response, as rats in the high-fat diet group had higher levels of blood lipids and showed more severe atherosclerotic lesions.