Department of Orthopaedics, Vanderbilt University Medical Center, Nashville, Tennessee, USA; Center for Bone Biology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
School of Medicine, Vanderbilt University, Nashville, Tennessee, USA.
J Thromb Haemost. 2023 Oct;21(10):2653-2665. doi: 10.1016/j.jtha.2023.08.002. Epub 2023 Aug 8.
The musculoskeletal system plays vital roles in the body, facilitating movement, protecting vital structures, and regulating hematopoiesis and mineral metabolism. Injuries to this system are common and can cause chronic pain, loss of range of motion, and disability. The acute phase response (APR) is a complex process necessary for surviving and repairing injured musculoskeletal tissue. To conceptualize the APR, it is useful to divide it into 2 distinct phases, survival and repair. During the survival-APR, a "damage matrix" primarily composed of fibrin, via thrombin activity, is produced to contain the zone of injury. Once containment is achieved, the APR transitions to the repair phase, where reparative inflammatory cells use plasmin to systematically remove the damage matrix and replace it with new permanent matrices produced by differentiated mesenchymal stem cells. The timing of thrombin and plasmin activation during their respective APR phases is crucial for appropriate regulation of the damage matrix. This review focuses on evidence indicating that inappropriate exuberant activation of plasmin during the survival-APR can result in an overactive APR, leading to an "immunocoagulopathy" that may cause "immunothrombosis" and death. Conversely, preclinical data suggest that too little plasmin activity during the repair-APR may contribute to failed tissue repair, such as a fracture nonunion, and chronic inflammatory degenerative diseases like osteoporosis. Future clinical studies are required to affirm these findings. Therefore, the temporal-spatial functions of plasmin in response to musculoskeletal injury and its pharmacologic manipulation are intriguing new targets for improving orthopedic care.
骨骼肌肉系统在体内起着至关重要的作用,它促进运动、保护重要结构,并调节造血和矿物质代谢。该系统的损伤很常见,可导致慢性疼痛、运动范围丧失和残疾。急性相反应(APR)是存活和修复受损骨骼肌肉组织所必需的复杂过程。为了理解 APR,可以将其分为两个不同的阶段,即存活和修复。在存活-APR 期间,主要由纤维蛋白组成的“损伤基质”通过凝血酶活性产生,以包含损伤区域。一旦达到包含,APR 就会过渡到修复阶段,修复性炎症细胞利用纤溶酶系统地去除损伤基质,并代之以分化的间充质干细胞产生的新永久性基质。在各自的 APR 阶段中凝血酶和纤溶酶激活的时机对于损伤基质的适当调节至关重要。本综述重点介绍了证据表明,在存活-APR 期间纤溶酶的过度激活会导致 APR 过度活跃,导致“免疫血栓形成”和死亡的“免疫凝血病”。相反,临床前数据表明,在修复-APR 期间纤溶酶活性过低可能导致组织修复失败,例如骨折不愈合,以及骨质疏松症等慢性炎症退行性疾病。需要进行未来的临床研究来证实这些发现。因此,纤溶酶对骨骼肌肉损伤的时空功能及其药理学操纵是改善骨科护理的有趣新靶点。