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Abstract：
Background and objectives: Bisphosphonates represent selective inhibitors of excess osteoblastic bone resorption that characterizes all osteopathies, targeting osteoclasts and their precursors. Their long-term administration in postmenopausal women suffering from osteoporosis has resulted in neural adverse effects. The current study focuses on the research of possible alterations in the femoral nerve, caused by bisphosphonates. We hypothesized that bisphosphonates, taken orally (per os), may produce degenerative changes to the femoral nerve, affecting lower-limb posture and walking neuronal commands. Materials and Methods: In order to support our hypothesis, femoral nerve specimens were extracted from ten female 12-month-old Wistar rats given 0.05 milligrams (mg) per kilogram (kg) of body weight (b.w.) per week alendronate per os for 13 weeks and from ten female 12-month-old Wistar rats given normal saline that were used as a control group. Specimens were studied using immunohistochemistry for selected antibodies NeuN (Neuronal Nuclear Protein), a protein located within mature, postmitotic neural nucleus, and cytosol and Sox10 (Sex-determining Region Y (SRY) - High-Motility Group (HMG) - box 10). The latter marker is fundamental for myelination of peripheral nerves. Obtained slides were examined under a light microscope. Results: Samples extracted from rats given alendronate were more Sox10 positive compared to samples of the control group, where the marker\'s expression was not so intense. Both groups were equally NeuN positive. Our results are in agreement with previous studies conducted under a transmission electron microscope. Conclusions: The suggested pathophysiological mechanism linked to histological alterations described above is possibly related to toxic drug effects on Schwann and neuronal cells. Our hypothesis enhances the existing scientific evidence of degenerative changes present on femoral nerve following bisphosphonates administration, indicating a possible relationship between alendronate use and neuronal function.
摘要：
背景和目的：双膦酸盐代表了所有骨病特征的过度成骨细胞骨吸收的选择性抑制剂。靶向破骨细胞及其前体。它们在患有骨质疏松症的绝经后妇女中的长期给药导致神经不良反应。目前的研究重点是股神经可能改变的研究，由双膦酸盐引起。我们假设双膦酸盐，口服(按操作系统)，可能会导致股神经的退行性变化，影响下肢姿势和行走神经元命令。材料和方法：为了支持我们的假设，股神经标本从10只12个月大的雌性Wistar大鼠中提取，给予阿仑膦酸钠每公斤（kg）体重（b.w.）每周0.05毫克（mg），持续13周，并从10只给予生理盐水的12个月大的雌性Wistar大鼠中提取，作为对照组。使用免疫组织化学对选定的抗体NeuN（神经元核蛋白）进行了样本研究，一种位于成熟体内的蛋白质，有丝分裂后神经核，和胞质溶胶和Sox10(性别决定区Y(SRY)-高运动性组(HMG)-方框10)。后一种标记是周围神经髓鞘形成的基础。在光学显微镜下检查获得的载玻片。结果：从给予阿仑膦酸钠的大鼠中提取的样品与对照组的样品相比，Sox10阳性更高，标记的表达不是那么强烈。两组均为NeuN阳性。我们的结果与先前在透射电子显微镜下进行的研究一致。结论：与上述组织学改变相关的病理生理机制可能与药物对雪旺氏和神经元细胞的毒性作用有关。我们的假设增强了双膦酸盐给药后股神经退行性变化的现有科学证据，表明阿仑膦酸钠的使用与神经元功能之间可能存在关系。
