Kobayashi Shigeru, Meir Adam, Kokubo Yasuo, Uchida Kenzo, Takeno Kenichi, Miyazaki Tsuyoshi, Yayama Takafumi, Kubota Masafumi, Nomura Eiki, Mwaka Erisa, Baba Hisatoshi
Department of Orthopaedics and Rehabilitation Medicine, The University of Fukui, Shimoaizuki 23, Matsuoka, Fukui, Japan.
Spine (Phila Pa 1976). 2009 Apr 1;34(7):655-62. doi: 10.1097/BRS.0b013e31819c9d5b.
The mechanisms responsible for the spontaneous regression of lumbar disc herniation (LDH) were studied by examining herniated tissue collected at operation from patients with LDH.
The aim of the present study was to investigate the role of neovascularization and macrophages in hernias when spontaneous regression of LDH occurred.
Spontaneous regression of LDHs has already been demonstrated by diagnostic imaging with tools such as magnetic resonance imaging. However, there have been few studies on the mechanisms of spontaneous regression based on pathologic examination of herniated tissue. In particular, there has been no detailed work on the role of macrophages, which are thought to be closely associated with spontaneous regression.
The magnetic resonance imaging and operative findings of 73 patients who underwent surgery were investigated, and specimens collected during surgery were examined by light and transmission electron microscopy.
Capillaries that invade the hernia and macrophages derived from monocytes migrating out of these capillaries are considered to be important factors in the regression of the herniated disc. Macrophages contain lysosomes filled with collagen-degrading enzymes that break down substances after phagocytosis, whereas primary lysosomes are secreted by these cells and break down intercellular substances such as collagen. Both of these mechanisms are closely involved in the regression of herniation.
The inflammatory response that occurs around hernia tissue in the epidural space is believed to play an important role in herniated disc resorption, although it may also have a harmful effect on the adjacent nerve root. Therefore, control of the inflammatory reaction is an important challenge when treating patients with disc herniation.
通过检查从腰椎间盘突出症(LDH)患者手术中收集的突出组织,研究腰椎间盘突出症自发消退的机制。
本研究的目的是探讨新生血管形成和巨噬细胞在LDH自发消退时在疝中的作用。
LDH的自发消退已通过磁共振成像等诊断成像工具得到证实。然而,基于突出组织病理检查的自发消退机制的研究很少。特别是,对于被认为与自发消退密切相关的巨噬细胞的作用,尚无详细研究。
调查了73例接受手术患者的磁共振成像和手术结果,并对手术中收集的标本进行了光镜和透射电镜检查。
侵入疝的毛细血管和从这些毛细血管迁出的单核细胞衍生的巨噬细胞被认为是椎间盘突出消退的重要因素。巨噬细胞含有充满胶原降解酶的溶酶体,这些酶在吞噬后分解物质,而初级溶酶体由这些细胞分泌并分解细胞间物质如胶原。这两种机制都与突出的消退密切相关。
硬膜外间隙疝组织周围发生的炎症反应被认为在椎间盘突出吸收中起重要作用,尽管它也可能对相邻神经根产生有害影响。因此,在治疗椎间盘突出症患者时,控制炎症反应是一项重要挑战。