Wang Jia-Zeng, Fang Xiu-Tong, Lv E, Yu Fang, Wang Zhen-Wei, Song Hong-Xing
Department of Orthopaedics, Beijing Shijitan Hospital, Capital Medical University Beijing 100038, China ; Shandong Medical College Linyi 276000, Shandong, China.
Department of Orthopaedics, Beijing Shijitan Hospital, Capital Medical University Beijing 100038, China.
Int J Clin Exp Med. 2015 Feb 15;8(2):2233-9. eCollection 2015.
This study aimed to elucidate the pathogenesis of posterior longitudinal ligament (PLL) hypertrophy.
Cervical PLL specimens were collected from CSM patients during surgery (n = 30) and during routine autopsy (n = 14), and processed for histological examination (HE staining and Masson's Trichrome staining) and IHC (CD3, CD68, CD31, TGF-β1 and collagen II). In addition, the mRNA expression of collagen I was detected in cervical PLL specimens from 16 CSM patients (n = 16) and from routine autopsy (n = 16) by RT-PCR.
Obvious fibrosis, cartilage metaplasia and calcification were found in the cervical PLL of CSM patients. In the degenerated PLL, CD68(+) macrophages were frequently identified, CD3(+) T lymphocytes were occasionally found, and many newly generated small vessels were also present. In the degenerated PLL, of the number of TGF-β1 positive cells increased markedly when compared with control group. IHC indicated TGF-β1 was secreted by macrophages. RT-PCR showed a significantly lower mRNA expression of collagen I in the PLL of CSM patients as compared to control group.
Macrophages are the major type of inflammatory cells involved in the cervical PLL degeneration, and TGF-β1 is related to the cervical PLL degeneration. TGF-β1 is mainly secreted by macrophages. Anti-inflammation may serve as an alternative non-surgical treatment and prophylactic strategy for PLL degeneration.
本研究旨在阐明后纵韧带(PLL)肥厚的发病机制。
在手术过程中从脊髓型颈椎病(CSM)患者中收集颈椎PLL标本(n = 30),并在常规尸检时收集(n = 14),进行组织学检查(苏木精-伊红染色和Masson三色染色)以及免疫组化(CD3、CD68、CD31、转化生长因子-β1(TGF-β1)和胶原蛋白II)。此外,通过逆转录-聚合酶链反应(RT-PCR)检测16例CSM患者(n = 16)和常规尸检(n = 16)的颈椎PLL标本中I型胶原蛋白的mRNA表达。
在CSM患者的颈椎PLL中发现明显的纤维化、软骨化生和钙化。在退变的PLL中,经常鉴定出CD68(+)巨噬细胞,偶尔发现CD3(+)T淋巴细胞,并且还存在许多新生成的小血管。在退变的PLL中,与对照组相比,TGF-β1阳性细胞数量明显增加。免疫组化表明TGF-β1由巨噬细胞分泌。RT-PCR显示,与对照组相比,CSM患者PLL中I型胶原蛋白的mRNA表达明显降低。
巨噬细胞是参与颈椎PLL退变的主要炎症细胞类型,TGF-β1与颈椎PLL退变有关。TGF-β1主要由巨噬细胞分泌。抗炎可能是PLL退变的一种替代性非手术治疗和预防策略。