软骨退变与大鼠化学诱导性关节痛加重相关：一项初步研究。
Cartilage degeneration is associated with augmented chemically-induced joint pain in rats: a pilot study.
机构信息
Department of Orthopaedic Surgery, Asahikawa Medical College, Midorigaoka-Higashi 2-1-1-1, Hokkaido, Asahikawa 178-8510, Japan.
出版信息
Clin Orthop Relat Res. 2010 May;468(5):1423-7. doi: 10.1007/s11999-009-1193-z. Epub 2009 Dec 15.
BACKGROUND
Osteoarthritis arising from cartilage degeneration is the most common cause of joint pain. However, the relationship between joint pain and cartilage degeneration is not well understood.
QUESTIONS/PURPOSES: We asked whether the inflammatory mediators participate in the joint pain in the presence of cartilage degeneration.
METHODS
We observed electromyographic responses of hindlimb flexors to four inflammatory mediators (bradykinin, ATP, acetylcholine, and serotonin) injected in normal rat knees and in those with monosodium iodoacetate (MIA)-induced arthritis.
RESULTS
Joint cartilage of all the rats with MIA-induced arthritis histologically showed severe degeneration. We observed greater magnitude and longer duration responses in the MIA-induced arthritis than normal joints with all four mediators.
CONCLUSIONS
The data suggested nociceptors in osteoarthritic joints are more sensitive to inflammatory mediators than in normal joints. Such nociceptive sensitization to inflammatory mediators may participate in the joint pain in osteoarthritis.
背景
由软骨退化引起的骨关节炎是最常见的关节疼痛原因。然而，关节疼痛与软骨退化之间的关系尚不清楚。
问题/目的：我们想知道在软骨退化的情况下，炎症介质是否参与关节疼痛。
方法
我们观察了向正常大鼠膝关节和碘乙酸单钠（MIA）诱导关节炎大鼠膝关节注射四种炎症介质（缓激肽、ATP、乙酰胆碱和 5-羟色胺）后后肢屈肌的肌电图反应。
结果
所有 MIA 诱导关节炎大鼠的关节软骨组织学上均显示严重退化。与正常关节相比，所有四种介质在 MIA 诱导关节炎大鼠中引起的反应幅度更大、持续时间更长。
结论
数据表明，骨关节炎关节中的伤害感受器对炎症介质比正常关节更敏感。这种对炎症介质的伤害感受敏化可能参与骨关节炎的关节疼痛。
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