Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, 100 High Street, Buffalo, NY, 14203-1126, USA.
Neuromolecular Med. 2018 Mar;20(1):37-53. doi: 10.1007/s12017-018-8481-2. Epub 2018 Feb 10.
The high prevalence of osteoporosis, observed in multiple sclerosis (MS) patients, has been attributed to reduced mobility and or the use of disease-modifying drugs. However, MS-impaired cardiovascular autonomic nervous system (ANS) function has the potential of reducing bone mass density (BMD) by altering the expression and/or function of the neuronal, systemic, and local mediators of bone remodeling. This review describes the complex regulation of bone homeostasis with a focus on MS, providing evidence that ANS dysfunction and low BMD are intertwined with MS inflammatory and neurodegenerative processes, and with other MS-related morbidities, including depression, fatigue, and migraine. Strategies for improving ANS function could reduce the prevalence of MS osteoporosis and slow the rate of MS progression, with a significant positive impact on patients' quality of life.
多发性硬化症 (MS) 患者中普遍存在的骨质疏松症，归因于活动减少和/或使用疾病修正药物。然而，MS 损害的心血管自主神经系统 (ANS) 功能有可能通过改变骨重塑的神经元、全身和局部介质的表达和/或功能来降低骨密度 (BMD)。本综述描述了骨稳态的复杂调节，重点介绍了 MS，提供的证据表明，ANS 功能障碍和低 BMD 与 MS 炎症和神经退行性过程以及其他与 MS 相关的疾病（包括抑郁、疲劳和偏头痛）交织在一起。改善 ANS 功能的策略可以降低 MS 骨质疏松症的发生率并减缓 MS 进展的速度，对患者的生活质量产生显著的积极影响。
