Peng Baogan, Hao Jianhua, Hou Shuxun, Wu Wenwen, Jiang Duyin, Fu Xiaobing, Yang Yi
Department of Orthopaedics, 304th hospital, Beijing, China.
Spine (Phila Pa 1976). 2006 Mar 1;31(5):560-6. doi: 10.1097/01.brs.0000201324.45537.46.
We collected the specimens of lumbar intervertebral disc (i.e., the symptomatic degenerative disc) from patients with discogenic low back pain to study the histopathologic features and growth factor expressions.
To study the pathogenesis of disc degeneration, meanwhile discriminating between common disc degeneration (aging disc) (i.e., black asymptomatic disc, not clinically relevant) and painful disc degeneration (i.e., symptomatic disc, clinically relevant).
The pathogenesis of intervertebral disc degeneration is poorly understood, mainly because of the difficulty to establish the experimental model with good reproducibility. Recently, the popularity of spinal fusion leads to more opportunities to obtain disc specimens, which could be applied to explore the pathogenesis of disc degeneration with modern biologic techniques.
There were 21 specimens of lumbar intervertebral discs from 15 patients with discogenic low back pain during posterior lumbar interbody fusion, 16 aging discs from patients without low back pain, and 10 normal discs as control collected for the study of their histopathologic features, as well as the expressions of basic fibroblast growth factor (bFGF) and its receptor (Flg), transforming growth factor-beta1 (TGF-beta1) and its receptor (TGF-betaRI) by immunohistochemistry. The distribution of macrophages and mast cells was also noted. Proliferating cell nuclear antigen was assessed to evaluate proliferating activities of disc cells.
The distinct histologic characteristic of the disc from the patient with discogenic low back pain was the ingrowth of vascularized granulation tissue along torn fissures, extending from the external layer of the anulus fibrosus into the nucleus pulposus. The immunohistochemical staining showed that there were strong expressions of bFGF and TGF-beta1 and their receptors, as well as a strong expression of proliferating cell nuclear antigen in the zones of granulation tissue in the painful discs. However, there were only weak expressions in the nongranulation tissue zones in the painful discs and aging discs, and no expression in the control discs. In addition, abundant macrophages and mast cells were found in the granulation tissue zones of painful discs but absent in the nongranulation tissue zones of painful discs or aging discs and the normal control discs.
The findings indicated that degeneration of the painful disc might originate from the injury and subsequent repair of anulus fibrosus. Growth factors, such as bFGF and TGF-beta1, macrophages and mast cells might play a key role in the repair of the injured anulus fibrosus and subsequent disc degeneration.
我们收集了椎间盘源性下腰痛患者的腰椎间盘标本（即有症状的退变椎间盘），以研究其组织病理学特征和生长因子表达。
研究椎间盘退变的发病机制，同时区分普通椎间盘退变（老化椎间盘）（即无症状的黑色椎间盘，临床不相关）和疼痛性椎间盘退变（即有症状的椎间盘，临床相关）。
椎间盘退变的发病机制尚不清楚，主要是因为难以建立具有良好重复性的实验模型。最近，脊柱融合术的普及为获取椎间盘标本提供了更多机会，可应用现代生物学技术来探索椎间盘退变的发病机制。
在腰椎椎间融合术中，收集了15例椎间盘源性下腰痛患者的21个腰椎间盘标本、16例无下腰痛患者的老化椎间盘以及10个正常椎间盘作为对照，用于研究其组织病理学特征，以及通过免疫组织化学研究碱性成纤维细胞生长因子（bFGF）及其受体（Flg）、转化生长因子-β1（TGF-β1）及其受体（TGF-βRI）的表达。还记录了巨噬细胞和肥大细胞的分布情况。评估增殖细胞核抗原以评估椎间盘细胞的增殖活性。
椎间盘源性下腰痛患者的椎间盘明显的组织学特征是血管化肉芽组织沿撕裂裂隙向内生长，从纤维环外层延伸至髓核。免疫组织化学染色显示，疼痛性椎间盘的肉芽组织区域中bFGF和TGF-β1及其受体表达强烈，增殖细胞核抗原表达也强烈。然而，疼痛性椎间盘和老化椎间盘的非肉芽组织区域仅表达较弱，对照盘中无表达。此外，在疼痛性椎间盘的肉芽组织区域发现大量巨噬细胞和肥大细胞，但在疼痛性椎间盘或老化椎间盘的非肉芽组织区域以及正常对照盘中未发现。
研究结果表明，疼痛性椎间盘退变可能源于纤维环的损伤及随后的修复。生长因子，如bFGF和TGF-β1、巨噬细胞和肥大细胞可能在受损纤维环的修复及随后的椎间盘退变中起关键作用。
