Abstract：
BACKGROUND: Oxidative stress has a critical effect on both persistent pain states and periodontal disease. Voltage-gated sodium NaV1.7 (SCN9A), and transient receptor potential ankyrin 1 (TRPA1) are pain genes. The goal of this study was to investigate oxidative stress markers, periodontal status, SCN9A, and TRPA1 channel expression in periodontal tissues of rats with paclitaxel-induced neuropathic pain-like behavior (NPLB).
RESULTS: Totally 16 male Sprague Dawley rats were used: control (n = 8) and paclitaxel-induced pain (PTX) (n = 8). The alveolar bone loss and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels were analyzed histometrically and immunohistochemically. Gingival superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities (spectrophotometric assay) were measured. The relative TRPA1 and SCN9A genes expression levels were evaluated using quantitative real-time PCR (qPCR) in the tissues of gingiva and brain. The PTX group had significantly higher alveolar bone loss and 8-OHdG compared to the control. The PTX group had significantly lower gingival SOD, GPx and CAT activity than the control groups. The PTX group had significantly higher relative gene expression of SCN9A (p = 0.0002) and TRPA1 (p = 0.0002) than the control in gingival tissues. Increased nociceptive susceptibility may affect the increase in oxidative stress and periodontal destruction.
CONCLUSIONS: Chronic pain conditions may increase TRPA1 and SCN9A gene expression in the periodontium. The data of the current study may help develop novel approaches both to maintain periodontal health and alleviate pain in patients suffering from orofacial pain.
RESULTS: Totally 16 male Sprague Dawley rats were used: control (n = 8) and paclitaxel-induced pain (PTX) (n = 8). The alveolar bone loss and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels were analyzed histometrically and immunohistochemically. Gingival superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities (spectrophotometric assay) were measured. The relative TRPA1 and SCN9A genes expression levels were evaluated using quantitative real-time PCR (qPCR) in the tissues of gingiva and brain. The PTX group had significantly higher alveolar bone loss and 8-OHdG compared to the control. The PTX group had significantly lower gingival SOD, GPx and CAT activity than the control groups. The PTX group had significantly higher relative gene expression of SCN9A (p = 0.0002) and TRPA1 (p = 0.0002) than the control in gingival tissues. Increased nociceptive susceptibility may affect the increase in oxidative stress and periodontal destruction.
CONCLUSIONS: Chronic pain conditions may increase TRPA1 and SCN9A gene expression in the periodontium. The data of the current study may help develop novel approaches both to maintain periodontal health and alleviate pain in patients suffering from orofacial pain.
摘要：
背景：氧化应激对持续性疼痛状态和牙周病都有重要影响。电压门控钠NaV1.7(SCN9A),瞬时受体电位锚蛋白1（TRPA1）是疼痛基因。这项研究的目的是研究氧化应激标志物，牙周状况，SCN9A,和TRPA1通道在紫杉醇诱导的神经病理性疼痛样行为（NPLB）大鼠牙周组织中的表达。
结果：使用16只雄性SD大鼠：对照组（n=8）和紫杉醇诱导的疼痛（PTX）（n=8）。通过组织学和免疫组织化学分析了牙槽骨丢失和8-羟基-2-脱氧鸟苷（8-OHdG）水平。牙龈超氧化物歧化酶(SOD),过氧化氢酶(CAT),并测定谷胱甘肽过氧化物酶（GPx）活性（分光光度法）。使用定量实时PCR(qPCR)在牙龈和脑组织中评估TRPA1和SCN9A基因的相对表达水平。与对照组相比，PTX组的牙槽骨丢失和8-OHdG明显更高。PTX组牙龈SOD明显降低，GPx和CAT活性高于对照组。在牙龈组织中，PTX组的SCN9A（p=0.0002）和TRPA1（p=0.0002）的相对基因表达明显高于对照组。增加的伤害性敏感性可能会影响氧化应激和牙周破坏的增加。
结论：慢性疼痛可能会增加牙周组织中TRPA1和SCN9A基因的表达。当前研究的数据可能有助于开发新的方法，以维持牙周健康并减轻患有口面疼痛的患者的疼痛。
结果：使用16只雄性SD大鼠：对照组（n=8）和紫杉醇诱导的疼痛（PTX）（n=8）。通过组织学和免疫组织化学分析了牙槽骨丢失和8-羟基-2-脱氧鸟苷（8-OHdG）水平。牙龈超氧化物歧化酶(SOD),过氧化氢酶(CAT),并测定谷胱甘肽过氧化物酶（GPx）活性（分光光度法）。使用定量实时PCR(qPCR)在牙龈和脑组织中评估TRPA1和SCN9A基因的相对表达水平。与对照组相比，PTX组的牙槽骨丢失和8-OHdG明显更高。PTX组牙龈SOD明显降低，GPx和CAT活性高于对照组。在牙龈组织中，PTX组的SCN9A（p=0.0002）和TRPA1（p=0.0002）的相对基因表达明显高于对照组。增加的伤害性敏感性可能会影响氧化应激和牙周破坏的增加。
结论：慢性疼痛可能会增加牙周组织中TRPA1和SCN9A基因的表达。当前研究的数据可能有助于开发新的方法，以维持牙周健康并减轻患有口面疼痛的患者的疼痛。
