Low back pain (LBP), as a leading cause of disability, is a common musculoskeletal disorder that results in major social and economic burdens. Recent research has identified inflammation and related signaling pathways as important factors in the onset and progression of disc degeneration, a significant contributor to LBP. Inflammatory mediators also play an indispensable role in discogenic LBP. The suppression of LBP is a primary goal of clinical practice but has not received enough attention in disc research studies. Here, an overview of the advances in inflammation-related pain in disc degeneration is provided, with a discussion on the role of inflammation in IVD degeneration and pain induction. Puncture models, mechanical models, and spontaneous models as the main animal models to study painful disc degeneration are discussed, and the underlying signaling pathways are summarized. Furthermore, potential drug candidates, either under laboratory investigation or undergoing clinical trials, to suppress discogenic LBP by eliminating inflammation are explored. We hope to attract more research interest to address inflammation and pain in IDD and contribute to promoting more translational research.

腰痛 (LBP) 是导致残疾的主要原因，是一种常见的肌肉骨骼疾病，会导致重大的社会和经济负担。最近的研究已经确定炎症和相关信号通路是椎间盘退变发生和进展的重要因素，椎间盘退变是 LBP 的重要贡献者。炎症介质在椎间盘源性 LBP 中也起着不可或缺的作用。抑制 LBP 是临床实践的主要目标，但在椎间盘研究中并未受到足够的重视。本文概述了椎间盘退变中炎症相关疼痛的进展，并讨论了炎症在 IVD 退变和疼痛诱导中的作用。讨论了穿刺模型、机械模型和自发模型作为研究疼痛性椎间盘退变的主要动物模型，并总结了潜在的信号通路。此外，探索了通过消除炎症来抑制椎间盘源性 LBP 的潜在候选药物，无论是在实验室研究中还是在进行临床试验。我们希望吸引更多的研究兴趣来解决 IDD 中的炎症和疼痛问题，并为促进更多的转化研究做出贡献。