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首页> 外文期刊>Oxidative Medicine and Cellular Longevity >The Dual Effects of Reactive Oxygen Species on the Mandibular Alveolar Bone Formation in SOD1 Knockout Mice: Promotion or Inhibition
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The Dual Effects of Reactive Oxygen Species on the Mandibular Alveolar Bone Formation in SOD1 Knockout Mice: Promotion or Inhibition

机译：反应性氧物种对SOD1敲除小鼠下颌肺泡骨形成的双重影响：促进或抑制作用

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The status of reactive oxygen species (ROS) correlates closely with the normal development of the oral and maxillofacial tissues. Oxidative stress caused by ROS accumulation not only affects the development of enamel and dentin but also causes pathological changes in periodontal tissues (periodontal ligament and alveolar bone) that surround the root of the tooth. Although previous studies have shown that ROS accumulation plays a pathologic role in some oral and maxillofacial tissues, the effects of ROS on alveolar bone development remain unclear. In this study, we focused on mandibular alveolar bone development of mice deficient in superoxide dismutase1 (SOD1). Analyses were performed using microcomputerized tomography (micro-CT), TRAP staining, immunohistochemical (IHC) staining, and enzyme-linked immunosorbent assay (ELISA). We found for the first time that slightly higher ROS in mandibular alveolar bone of SOD1(-/-) mice at early ages (2-4 months) caused a distinct enlargement in bone size and increased bone volume fraction (BV/TV), trabecular thickness (Tb.Th), and expression of alkaline phosphatase (ALP), Runt-related transcription factor 2 (Runx2), and osteopontin (OPN). With ROS accumulation to oxidative stress level, increased trabecular bone separation (Tb.Sp) and decreased expression of ALP, Runx2, and OPN were found in SOD1(-/-) mice at 6 months. Additionally, dosing with N-acetylcysteine (NAC) effectively mitigated bone loss and normalized expression of ALP, Runx2, and OPN. These results indicate that redox imbalance caused by SOD1 deficiency has dual effects (promotion or inhibition) on mandibular alveolar bone development, which is closely related to the concentration of ROS and the stage of growth. We present a valuable model here for investigating the effects of ROS on mandibular alveolar bone formation and highlight important roles of ROS in regulating tissue development and pathological states, illustrating the complexity of the redox signal.
机译：反应性氧物质（ROS）的状态与口腔和颌面组织的正常发育密切相关。由ROS积累引起的氧化应激不仅影响牙釉质和牙本质的发育，而且还会导致围绕牙齿根的牙周组织（牙周韧带和肺泡骨）的病理变化。尽管之前的研究表明，ROS积累在一些口腔和颌面组织中发挥病原作用，但ROS对肺泡骨骼发育的影响仍不清楚。在这项研究中，我们专注于超氧化物歧化酶1（SOD1）缺乏小鼠的小鼠牙龈骨发育。使用微型计算机层析成像（微型CT），捕获染色，免疫组织化学（IHC）染色和酶联免疫检测（ELISA）进行分析。我们在早期（2-4个月）的SOD1（ - / - ）小鼠中颌骨肺泡骨中的第一次略高于略高的RO，导致骨骼大小和骨体积分数增加（BV / TV），小梁厚度（Tb.Th）和碱性磷酸酶（ALP），runt相关转录因子2（RONX2）和骨偶联蛋白（OPN）的表达。随着ROS积累到氧化应激水平，在SOD1（ - / - ）小鼠中，在6个月内发现增加的骨分离（TB.SP）和ALP，RONX2和OPN的表达降低。另外，用N-乙酰半胱氨酸（NAC）给药有效减轻骨质损失和ALP，RUNX2和OPN的标准化表达。这些结果表明，SOD1缺乏引起的氧化还原性失衡对下颌肺泡骨发育具有双重影响（促进或抑制），其与ROS浓度密切相关，并且生长阶段。我们在此提出了一种有价值的模型，用于研究ROS对下颌肺泡骨形成的影响，并突出ROS在调节组织发育和病理状态方面的重要作用，说明氧化还原信号的复杂性。

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