G Bisson Daniel, Lama Polly, Abduljabbar Fahad, Rosenzweig Derek H, Saran Neil, Ouellet Jean A, Haglund Lisbet
Orthopaedic Research Laboratory Shriners Hospital for Children Montreal Quebec Canada.
Department of Orthopedic Surgery McGill University Montreal Quebec Canada.
JOR Spine. 2018 May 24;1(2):e1016. doi: 10.1002/jsp2.1016. eCollection 2018 Jun.
Adolescent idiopathic scoliosis (AIS) is a poorly understood deformity of the thoracolumbar spine which affects the intervertebral discs (IVDs) and the articular facet joints. The knowledge concerning facet joints in this context is very limited, although facet joint degeneration is a known contributor of back pain. In this study, a comprehensive investigation was performed to characterize the facet joint chondrocytes and extracellular matrix within the scoliotic spine. Surgically removed articular facet joint tissues were collected from patients undergoing spinal corrective surgery for AIS deformities, while non-scoliotic articular facet joint tissues were obtained from cadaveric organ donors. Alterations in cartilage tissue structure were evaluated histologically with safranin-O fast green and a modified OARSI grading scale. Pro-inflammatory cytokines, matrix-degrading proteases, and fragmented matrix molecules associated with cartilage degradation were analyzed by immunohistochemistry and western blotting. Safranin-O fast green staining revealed that young scoliotic facet joints show clear signs of degeneration with substantial proteoglycan loss, similar to osteoarthritis (OA). The proteoglycan levels were significantly lower than in healthy asymptomatic non-scoliotic control individuals. In comparison to controls, scoliotic articular facets showed increased cell density, increased expression of the proliferation marker Ki-67, and higher expression of MMP-3, MMP-13, and IL-1β. Expression and fragmentation of the small leucine-rich proteins (SLRPs) chondroadherin, decorin, biglycan, lumican, and fibromodulin were analyzed with western blot. Chondroadherin and decorin were fragmented in cartilage from patients with a curve greater than 70°, whereas biglycan and fibromodulin did not show curve-related fragmentation. AIS facet joint cartilage shows hallmarks of OA including proteoglycan loss, overexpression of pro-inflammatory mediators, increased synthesis of matrix-degrading proteases and fragmentation of SLRPs. As with patients with age-related OA, the premature joint degeneration seen in scoliotic patients is likely to contribute to the pain perceived in some individuals.
青少年特发性脊柱侧凸（AIS）是一种对其了解较少的胸腰椎畸形，它会影响椎间盘（IVD）和关节突关节。尽管关节突关节退变是背痛的一个已知原因，但在这种情况下关于关节突关节的知识非常有限。在本研究中，进行了一项全面调查，以表征脊柱侧凸脊柱内的关节突关节软骨细胞和细胞外基质。从接受AIS畸形脊柱矫正手术的患者身上收集手术切除的关节突关节组织，而从尸体器官捐赠者身上获取非脊柱侧凸关节突关节组织。用番红O固绿染色和改良的OARSI分级量表对软骨组织结构的改变进行组织学评估。通过免疫组织化学和蛋白质印迹法分析与软骨降解相关的促炎细胞因子、基质降解蛋白酶和破碎的基质分子。番红O固绿染色显示，年轻的脊柱侧凸关节突关节显示出明显的退变迹象，蛋白聚糖大量丢失，类似于骨关节炎（OA）。蛋白聚糖水平显著低于健康无症状的非脊柱侧凸对照个体。与对照组相比，脊柱侧凸关节突显示细胞密度增加、增殖标志物Ki-67的表达增加以及MMP-3、MMP-13和IL-1β的表达更高。用蛋白质印迹法分析富含亮氨酸的小蛋白（SLRP）软骨粘连蛋白、核心蛋白聚糖、双糖链蛋白聚糖、纤连蛋白聚糖和纤维调节蛋白的表达和片段化。曲线大于70°的患者软骨中的软骨粘连蛋白和核心蛋白聚糖发生了片段化，而双糖链蛋白聚糖和纤维调节蛋白未显示与曲线相关的片段化。AIS关节突关节软骨显示出OA的特征，包括蛋白聚糖丢失、促炎介质的过度表达、基质降解蛋白酶的合成增加以及SLRP的片段化。与年龄相关性OA患者一样，脊柱侧凸患者中出现的关节过早退变可能会导致一些个体感觉到疼痛。
