Lotz Jeffrey C, Ulrich Jill A
Orthopaedic Bioengineering Laboratory, Department of Orthopaedic Surgery, University of California at San Francisco, Box 0514, 533 Parnassus Avenue, University Hall U-454, San Francisco, CA 94110, USA.
J Bone Joint Surg Am. 2006 Apr;88 Suppl 2:76-82. doi: 10.2106/JBJS.E.01448.
Animal models provide important clues to the pathomechanisms of human intervertebral disc degeneration. Previous reviews on this topic have highlighted the fact that loss of nuclear volume (and, consequently, pressure) is a common trigger for tissue-remodeling and anatomic change consistent with degeneration in humans. Unfortunately, a large gap still exists in the medical knowledge base that serves to distinguish symptomatic from asymptomatic degeneration. Because disc degeneration per se is not a basis for clinical intervention, identification of specific features underlying discogenic pain is of the utmost importance to advance the current level of care and identify novel therapeutic targets. This article presents animal-model evidence that pathologic, or painful, degeneration is characterized by ineffective injury-healing of peripheral tissue. Because the disc is only vascularized at the vertebral end plate and the outer part of the anulus, these are the likely sites for focal damage, inflammation, neoinnervation, and nociceptor sensitization. Consequently, while nuclear insufficiency is likely the root of degenerative change, the end plate and peripheral part of the anulus are more likely the source of patient discomfort.
动物模型为人类椎间盘退变的发病机制提供了重要线索。此前关于该主题的综述强调，髓核体积减小（以及随之而来的压力降低）是组织重塑和与人类退变相符的解剖学变化的常见触发因素。不幸的是，在区分有症状退变和无症状退变的医学知识库中，仍然存在很大差距。由于椎间盘退变本身并非临床干预的依据，识别椎间盘源性疼痛的特定特征对于提高当前的治疗水平和确定新的治疗靶点至关重要。本文提供了动物模型证据，表明病理性或疼痛性退变的特征是外周组织损伤愈合无效。由于椎间盘仅在椎体终板和纤维环外部有血管供应，这些部位可能是局灶性损伤、炎症、神经新生和伤害感受器敏化的发生部位。因此，虽然髓核功能不全可能是退变改变的根源，但终板和纤维环外周部分更可能是患者不适的来源。
