da Paz Aloysio Campos, Carod Artal Francisco J, Kalil Ricardo K
Sarah Network of Rehabilitation Hospitals, SMHS Q., 501 Conj A Brasilia, DF 70335-901, Brazil.
Med Hypotheses. 2007;68(1):67-73. doi: 10.1016/j.mehy.2006.06.035. Epub 2006 Aug 21.
Neurogenic heterotopic ossification is characterized by the formation of extra osseous bone in soft tissue surrounding peripheral joints in neurological patients. It occurs in 25% of spinal cord injury patients, and in 20% of these the pathologic process is severe enough to cause limitations in joint motion. Vascular and metabolic changes resulting from autonomic nervous system impairment may play a role in the etiology of heterotopic ossification. Repetitive vigorous passive manipulation of the joint to preserve range of motion, in the presence of reduced defense mechanisms, may also traumatize soft tissue, thereby initiating the pathological process. Nerve terminals within ligaments and capsules that allow for proprioception have a determinant role in triggering on and off muscle contraction, permitting acceleration and deceleration during gait. The Sarah Network of Rehabilitation Hospitals has treated over 20,000 patients with spinal cord and brain injury in the past 20 years. Based on the observation of heterotopic ossification development in some of these patients, and its tendency to relapse, this present article speculates whether, after an interruption in the neural pathways: (1) altered proprioception can forge a different relationship between tissues; and (2) chaotic new bone formation can occur. We postulate that heterotopic ossification in patients with injury to the central nervous system (CNS) may be related to a dysfunction of proprioception. With interruption of the neural tract of a given limb, ligaments lose control and coordination of their proprioceptive function and begin to react to direct stimulus in an independent, isolated and haphazard way. Free of CNS control and directly stimulated by such independent signals, mesenchymal osteoprogenitor cells located in soft tissues begin to occasion tissue maturation and differentiation into bone: heterotopic bone.
神经源性异位骨化的特征是在神经疾病患者外周关节周围的软组织中形成额外的骨组织。它发生在25%的脊髓损伤患者中,其中20%的患者病理过程严重到足以导致关节活动受限。自主神经系统损伤导致的血管和代谢变化可能在异位骨化的病因中起作用。在防御机制减弱的情况下,为保持关节活动范围而对关节进行反复剧烈的被动手法操作,也可能损伤软组织,从而引发病理过程。韧带和关节囊中负责本体感觉的神经末梢在触发肌肉收缩的开启和关闭方面具有决定性作用,从而在步态中实现加速和减速。在过去20年里,莎拉康复医院网络已经治疗了超过20000名脊髓和脑损伤患者。基于对其中一些患者异位骨化发展情况及其复发倾向的观察,本文推测在神经通路中断后:(1)改变的本体感觉是否会在组织之间形成不同的关系;(2)是否会发生混乱的新骨形成。我们假设中枢神经系统(CNS)损伤患者的异位骨化可能与本体感觉功能障碍有关。随着给定肢体神经束的中断,韧带失去对其本体感觉功能的控制和协调,并开始以独立、孤立和随意的方式对直接刺激做出反应。位于软组织中的间充质骨祖细胞在没有中枢神经系统控制且受到此类独立信号直接刺激的情况下,开始促使组织成熟并分化为骨:异位骨。