Targeting the Origins of Inflammation in Post-Traumatic Osteoarthritis

创伤后骨关节炎（PTOA）的特征是由各种关节损伤引起的进行性关节软骨侵蚀，严重程度从非接触性前交叉韧带撕裂（ACLT）到关节内骨折（IAF）不等。即使在IAF的情况下，对软骨和软骨细胞的直接损害通常仅占关节表面的百分之几。然而，这种局部病变可以随着时间的推移而扩大;这是一种与介质从受损软骨中释放相关的现象。然而，软骨侵蚀也发生在远离最初受损的软骨，表明滑液中携带的分解代谢因子引发未受损软骨的退化。因此，以预防创伤诱导的炎症为中心的干预具有减少创伤诱导的软骨损失的巨大潜力。关节软骨的机械损伤导致损伤部位的软骨细胞死亡和基质变性，并且随着时间的推移，导致邻近软骨的软骨细胞死亡和基质变性。发出组织损伤信号的基质碎片和细胞碎片（统称为

Post-traumatic osteoarthritis (PTOA) is characterized by progressive articular cartilage erosion initiated by a variety of joint injuries ranging in severity from non-contact anterior cruciate ligament tears (ACLT) to intra-articular fracture (IAF). Even in the case of IAF, the immediate damage to cartilage and chondrocytes typically amounts to only a few percent of the joint surface. Yet, such localized lesions can expand over time; a phenomenon associated with release of mediators from injured cartilage. However, cartilage erosion also occurs away from originally damaged cartilage, indicating that catabolic factors carried in synovial fluid initiate degeneration in undamaged cartilage. Thus, an intervention centered on preventing trauma-induced inflammation holds great potential for reducing trauma-induced cartilage loss. Mechanical injuries to articular cartilage cause the death of chondrocytes and matrix degeneration in injury sites and, over time, in adjacent cartilage. Matrix fragments and cell debris signaling tissue damage (known collectively as