Ji-Ye He, Xin-Feng Zheng, Lei-Sheng Jiang
Department of Orthopaedic Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Handb Clin Neurol. 2013;117:161-71. doi: 10.1016/B978-0-444-53491-0.00014-6.
Bone remodeling is thought to be regulated by many factors including nutritional status, humoral factors, and biomechanical stress. However, the involvement of the autonomic nervous system, mainly the sympathetic nervous system (SNS), in the modulation of bone remodeling is beginning to receive more attention. Neural innervation of bone has been demonstrated. Both experimental and clinical evidence has indicated the involvement of autonomic nervous system regulation in bone metabolism. The sympathetic neural pathway is so far the only identified link between the potent leptin-dependent central control and bone cells. An intact autonomic nervous system contributes to the maintenance of healthy bone tissue. Conversely, disturbance of the autonomic nervous system could induce abnormal bone remodeling. In this chapter, we review current knowledge about the role of the autonomic nervous system in abnormal bone formation and its association with clinical diseases such as heterotopic ossification, ossification of the posterior longitudinal ligament, postmenopausal osteoporosis, adolescent idiopathic scoliosis, complex regional pain syndrome, Charcot neuro-osteoarthropathy, unloading-induced osteoporosis, central or peripheral nervous system damage, and depression-induced osteoporosis. Understanding the mechanism of sympathetic neural signaling in bone remodeling may shed light on a potential treatment avenue for the prevention or reversal of bone loss.
骨重塑被认为受多种因素调节，包括营养状况、体液因子和生物力学应力。然而，自主神经系统，主要是交感神经系统（SNS），在骨重塑调节中的作用开始受到更多关注。骨的神经支配已得到证实。实验和临床证据均表明自主神经系统调节参与骨代谢。到目前为止，交感神经通路是强大的瘦素依赖中枢控制与骨细胞之间唯一已确定的联系。完整的自主神经系统有助于维持健康的骨组织。相反，自主神经系统紊乱可诱发异常骨重塑。在本章中，我们综述了关于自主神经系统在异常骨形成中的作用及其与诸如异位骨化、后纵韧带骨化、绝经后骨质疏松症、青少年特发性脊柱侧凸、复杂性区域疼痛综合征、夏科神经骨关节病、失用性骨质疏松症、中枢或周围神经系统损伤以及抑郁性骨质疏松症等临床疾病的关联的现有知识。了解交感神经信号在骨重塑中的机制可能为预防或逆转骨质流失的潜在治疗途径提供线索。
