Apical periodontitis (AP) is a dental-driven condition caused by pathogens and their toxins infecting the inner portion of the tooth (i.e., dental pulp tissue), resulting in inflammation and apical bone resorption affecting 50% of the worldwide population, with more than 15 million root canals performed annually in the United States. Current treatment involves cleaning and decontaminating the infected tissue with chemo-mechanical approaches and materials introduced years ago, such as calcium hydroxide, zinc oxide–eugenol, or even formalin products. Here, we present, for the first time, a nanotherapeutics based on using synthetic high-density lipoprotein (sHDL) as an innovative and safe strategy to manage dental bone inflammation. sHDL application in concentrations ranging from 25 µg to 100 µg/mL decreases nuclear factor Kappa B (NF-κB) activation promoted by an inflammatory stimulus (lipopolysaccharide, LPS). Moreover, sHDL at 500 µg/mL concentration markedly decreases in vitro osteoclastogenesis (P < 0.001), and inhibits IL-1α (P = 0.027), TNF-α (P = 0.004), and IL-6 (P < 0.001) production in an inflammatory state. Notably, sHDL strongly dampens the Toll-Like Receptor signaling pathway facing LPS stimulation, mainly by downregulating at least 3-fold the pro-inflammatory genes, such as Il1b, Il1a, Il6, Ptgs2, and Tnf. In vivo, the lipoprotein nanoparticle applied after NaOCl reduced bone resorption volume to (1.3 ± 0.05) mm³ and attenuated the inflammatory reaction after treatment to (1 090 ± 184) cells compared to non-treated animals that had (2.9 ± 0.6) mm³ (P = 0.012 3) and (2 443 ± 931) cells (P = 0.004), thus highlighting its promising clinical potential as an alternative therapeutic for managing dental bone inflammation.

根尖周炎 (AP) 是一种由病原体及其毒素感染牙齿内部（即牙髓组织）引起的牙齿疾病，导致炎症和根尖骨吸收，影响全球 50% 的人口，其中更多美国每年进行超过 1500 万例根管治疗。目前的治疗方法包括使用多年前引入的化学机械方法和材料来清洁和净化受感染的组织，例如氢氧化钙、氧化锌-丁子香酚，甚至福尔马林产品。在这里，我们首次提出一种基于使用合成高密度脂蛋白（sHDL）的纳米疗法作为控制牙骨炎症的创新且安全的策略。浓度范围为 25 µg 至 100 µg/mL 的 sHDL 应用可降低炎症刺激（脂多糖，LPS）促进的核因子 Kappa B (NF-κB) 激活。此外，500 µg/mL 浓度的 sHDL 显着降低体外破骨细胞生成 ( P < 0.001)，并抑制 IL-1α ( P = 0.027)、TNF-α ( P = 0.004) 和 IL-6 ( P < 0.001) 产生处于炎症状态。值得注意的是，sHDL 强烈抑制面临 LPS 刺激的 Toll 样受体信号通路，主要是通过下调至少 3 倍的促炎基因，如Il1b 、 Il1a 、 Il6 、 Ptgs2和Tnf 。在体内，与未经治疗的动物（2.9±0.6）mm相比，NaOCl后应用的脂蛋白纳米颗粒将骨吸收体积减少至（1.3±0.05）mm ³ ，并且在治疗后将炎症反应减弱至（1 090±184）个细胞。 ³ （ P = 0。012 3) 和 (2 443 ± 931) 细胞 ( P = 0.004)，从而突出了其作为治疗牙骨炎症的替代疗法的有前景的临床潜力。