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首页> 外文期刊>Cartilage >Increased Substance P Immunoreactivity in Ipsilateral Knee Cartilage of Rats Exposed to Lumbar Spine Injury
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Increased Substance P Immunoreactivity in Ipsilateral Knee Cartilage of Rats Exposed to Lumbar Spine Injury

机译：暴露于腰椎脊柱损伤的大鼠同侧膝关节软骨中的P含量增加免疫反应性

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摘要

Augmented expression of substance P (SP) in the cartilaginous tissue has been shown to promote degenerative changes in the cartilaginous matrix of distal contralateral articular joints via neurogenic inflammation post monoarthritis-induction contributing to the symmetrical spread of osteoarthritis (OA). However, no studies have explored whether similar changes are also present within neurosegmentally linked ipsilateral heterologous cartilage. Objective The present study aimed to investigate whether experimentally induced lumbar facet-joint OA lead to degenerative changes and enhanced SP expression within the ipsilateral neurosegmentally linked tibiofemoral cartilage. Methods Adult male Sprague-Dawley rats were assigned to left side L5-L6 facet mechanical compression injury (surgery) ( n = 6), L5-L6 facet exposure with no compression (sham) ( n = 5), or na?ve (no surgery) ( n = 4) groups. The morphology of the tibiofemoral articular cartilage was assessed using a modified Mankin scoring system. Immunohistochemistry was used to examine the density of chondrocytes stained positive for SP (cells/cm~(2)) in the ipsilateral tibiofemoral cartilage at 28 days postintervention. Results Tibiofemoral cartilage in the surgery group showed consistent loss of superficial zone chondrocytes, mild roughening of the articular surface and occasional chondrocyte clusters as well as a greater density of SP mainly in the superficial cartilage zone compared with sham and na?ve groups, although they also had a basic SP-expression. Conclusion Our results support the hypothesis that neurogenic mechanisms may mediate the spread of SP to neurosegmentally linked heterologous joints affecting the distal cartilage homeostasis. These findings contribute additional insight into the potential role of neurogenic inflammation with implications in the pathophysiology of chronic inflammatory joint disease and OA.
机译：已经证明了软骨组织中物质p（sp）的增强表达，通过神经源性炎症术后脑膜炎（OA）对称扩散促进远端对侧关节关节的软骨末端关节关节的硬质炎症术中的退行性变化。然而，没有研究探索了神经定义链接的同侧异源软骨中是否存在类似的变化。目的本研究旨在调查实验诱导的腰部关节OA是否导致再生物变化和同侧神经定义连接的胫骨软骨内的增强SP表达。方法将成年雄性Sprague-Dawley大鼠分配给左侧L5-L6面部机械压缩损伤（手术）（n = 6），L5-L6小平面暴露，没有压缩（假）（n = 5），或na？ve（没有手术）（n = 4）组。使用改进的人国金属分量系统评估了胫骨型关节软骨的形态。使用免疫组织化学在28天的术后28天在同侧胫酮软骨中染色的软骨细胞染色阳性的阳性密度。结果手术组的胫脂冶金软骨表现出浅损伤的浅表区软骨细胞，轻度粗糙化的关节表面和偶尔的软骨细胞簇，以及与假和Na've群体相比的浅表软骨区的更大密度。也有一个基本的sp表达。结论我们的研究结果支持神经源机制可能介导SP的扩散到影响远端软骨稳态的神经定义连接的异源关节的假设。这些发现有助于额外洞察神经源性炎症的潜在作用与慢性炎症关节疾病和OA的病理生理学的影响。

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