The Orthopaedic Research Laboratory, Montreal General Hospital, McGill University, 1650 Cedar Avenue, Room C10.148.2, Montreal, QC, H3G 1A4,
Eur Cell Mater. 2021 Mar 19;41:355-369. doi: 10.22203/eCM.v041a23.
Intervertebral disc (IVD) degeneration is characterised by catabolic and inflammatory processes that contribute largely to tissue degradation and chronic back pain. The disc cells are responsible for the pathological production of pro-inflammatory cytokines and catabolic enzymes leading to degeneration. However, this phenotypical change is poorly understood. Growing evidence in animal and human studies implicates Toll-like receptors (TLR) and their activation through danger-associated alarmins, found increasingly in degenerating IVDs. TLR signalling results in the release of pro-inflammatory cytokines and proteolytic enzymes that can directly cause IVD degeneration and back pain. This review aims to summarise the current literature on TLR activation in IVD degeneration and discuss potential treatment modalities to alleviate the inflammatory phenotype of disc cells in order to arrest IVD degeneration and back pain.
椎间盘（IVD）退变的特征是分解代谢和炎症过程，这些过程在很大程度上导致组织退化和慢性背痛。椎间盘细胞负责病理性产生促炎细胞因子和分解代谢酶，导致退变。然而，这种表型变化还不太清楚。越来越多的动物和人体研究证据表明，Toll 样受体（TLR）及其通过危险相关警报素的激活，在退变的 IVD 中被发现。TLR 信号导致促炎细胞因子和蛋白水解酶的释放，这些物质可直接导致 IVD 退变和背痛。本综述旨在总结 TLR 在 IVD 退变中的激活的最新文献，并讨论潜在的治疗方法，以减轻椎间盘细胞的炎症表型，从而阻止 IVD 退变和背痛。
