School of Dentistry, Department of Periodontology, Recep Tayyip Erdogan University, Rize, 53100, TR, Turkey.
School of Medicine, Department of Radiation Oncology, Recep Tayyip Erdogan University, Rize, Turkey.
BMC Oral Health. 2024 Nov 29;24(1):1453. doi: 10.1186/s12903-024-05251-0.
The aim of this study was to investigate the preventive effects of amifostine and melatonin oxidatively, biochemically and histomorphometrically in rats with radiotherapy-induced experimental periodontitis.
40 female Sprague-Dawley rats were divided into 5 groups: Control, experimental periodontitis (Ep), Ep + radiotherapy (Ep + Rt), Ep + Rt + amifostine (Ep + Rt + Ami), Ep + Rt + melatonin (Ep + Rt + Mel). The day after induction of periodontitis by ligature, a single dose of 5 Gy radiotherapy was administered. On the same day, treatments with amifostine (200 mg/kg) for 3 days and melatonin (10 mg/kg) for 15 days were started. By after 23 days of experiment, periodontal bone loss was measured by histomorphometry. RANKL, OPG and Caspase-3 activities were analyzed immunohistochemically and inflammatory cytokine (IL-1β, IL-10, IL-6, TNF-α) levels and oxidative stress (TOS/TAS) were analyzed biochemically in tissue homogenates.
It was observed that there was a significant difference in many biochemical parameters and oxidative stress levels between the control group and Ep + Rt (p < 0.05). Alveolar bone destruction in the melatonin prophylaxis group was observed to be close to control (p > 0.05). Melatonin significantly improved biochemical, histochemical, apoptotic and bone loss levels in irradiated experimental periodontitis rats (p < 0.05). When comparing the two drug groups (Ep + Rt + Ami and Ep + Rt + Mel), no statistically significant difference was found at any parameter level (p > 0.05).
Both melatonin and amifostine can significantly limit RT-induced periodontal bone loss by suppressing inflammatory stress, apoptotic mechanisms, and RANKL-related osteoclastic activity. Given the limited side effects of melatonin, it may be an alternative to amifostine.
本研究旨在探讨氨磷汀和褪黑素在放射性治疗诱导的实验性牙周炎大鼠体内氧化、生化和组织形态计量学方面的预防作用。
将 40 只雌性 Sprague-Dawley 大鼠分为 5 组：对照组、实验性牙周炎组（Ep）、Ep+放射治疗组（Ep+Rt）、Ep+Rt+氨磷汀组（Ep+Rt+Ami）、Ep+Rt+褪黑素组（Ep+Rt+Mel）。在结扎诱导牙周炎的第二天，给予单次 5 Gy 放射治疗。同日，开始用氨磷汀（200mg/kg）治疗 3 天，褪黑素（10mg/kg）治疗 15 天。实验 23 天后，通过组织形态计量学测量牙周骨丢失。免疫组织化学分析 RANKL、OPG 和 Caspase-3 活性，组织匀浆分析炎症细胞因子（IL-1β、IL-10、IL-6、TNF-α）水平和氧化应激（TOS/TAS）。
与 Ep+Rt 组相比，对照组和 Ep+Rt 组的许多生化参数和氧化应激水平存在显著差异（p<0.05）。在放射治疗实验性牙周炎大鼠中，褪黑素预防组观察到牙槽骨破坏接近对照组（p>0.05）。褪黑素显著改善了放射性实验性牙周炎大鼠的生化、组织化学、凋亡和骨丢失水平（p<0.05）。比较两组药物（Ep+Rt+Ami 和 Ep+Rt+Mel），在任何参数水平均未发现统计学显著差异（p>0.05）。
氨磷汀和褪黑素均可通过抑制炎症应激、凋亡机制和 RANKL 相关破骨细胞活性，显著限制放射治疗引起的牙周骨丢失。鉴于褪黑素的副作用有限，它可能是氨磷汀的替代物。
