Department of Orthopaedics, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.
Chin Med J (Engl). 2011 Aug;124(16):2480-4.
Cervical spondylotic myelopathy (CSM), in part, results from degeneration of the posterior longitudinal ligament (PLL), which mechanically compresses the spinal cord. Much research was done on the ossification of PLL, but not concerning the non-ossifying degeneration of cervical PLL. The degeneration of cervical PLL may be related to inflammation. The aim of this study was to elucidate the pathological features of the PLL and the role of cyclooxygenase 2 (COX-2) in the degeneration of the PLL in CSM.
A total of 23 PLL specimens were collected during surgery from patients with CSM for the histological and immunohistochemical (type II collagen and Ki-67) study. For the control group 14 cervical PLL autopsy specimens were investigated in the same manner. mRNA expression of COX-2 was quantitatively measured by real-time reverse transcription-polymerase chain reaction (RT-PCR) from 18 PLL specimens of patients with CSM and 18 PLL specimens of autopsy cases. Immunohistochemistry was used to evaluate the cellular location of COX-2 in PLL.
A distinct amount of fibrotic area, chondrometaplastic tissue and calcification were found in the PLL of the patient group, compared with the control group. Type II collagen was apparent around chondrometaplastic cells. Ki-67 positive reaction was less than 5%. A COX-2 positive reaction was found in 9 of the patient specimens (39.1%) in which the COX-2 was released from vascular endothelial cells in the PLL. However, such reactions were not found in the control group. Real-time PCR showed that the mRNA expression level of COX-2 in the patient group was significantly higher than that in the control group (P < 0.01).
Chondrometaplastic tissue producing type II collagen was identified as the most predominant pathological feature in the degenerative PLL. The higher expression of COX-2 might be related to degeneration of the PLL in CSM.
颈椎脊髓病（CSM）部分源于后纵韧带（PLL）的退变，其机械压迫脊髓。大量研究针对 PLL 的骨化，但不涉及颈椎 PLL 的非骨化退变。颈椎 PLL 的退变可能与炎症有关。本研究旨在阐明 PLL 的病理特征以及环氧化酶 2（COX-2）在 CSM 中 PLL 退变中的作用。
共收集 23 例 CSM 患者手术中的 PLL 标本进行组织学和免疫组织化学（Ⅱ型胶原和 Ki-67）研究。对照组 14 例颈椎 PLL 尸检标本以同样的方式进行研究。通过实时逆转录-聚合酶链反应（RT-PCR）定量测量 18 例 CSM 患者 PLL 和 18 例尸检 PLL 标本中 COX-2 的 mRNA 表达。免疫组化用于评估 COX-2 在 PLL 中的细胞定位。
与对照组相比，患者组的 PLL 中存在大量纤维性区域、软骨化生组织和钙化。软骨化生细胞周围有明显的Ⅱ型胶原。Ki-67 阳性反应小于 5%。在 9 例患者标本中发现 COX-2 阳性反应（39.1%），其中 COX-2 从 PLL 中的血管内皮细胞释放。然而，对照组中未发现这种反应。实时 PCR 显示患者组 COX-2 的 mRNA 表达水平明显高于对照组（P < 0.01）。
产生Ⅱ型胶原的软骨化生组织被认为是退变 PLL 中最主要的病理特征。COX-2 的高表达可能与 CSM 中 PLL 的退变有关。
