Varady Nathan H, Rodeo Scott A
Department of Sports Medicine, Hospital for Special Surgery, New York, NY, USA.
Connect Tissue Res. 2025 Apr 14:1-6. doi: 10.1080/03008207.2025.2487916.
Post-traumatic osteoarthritis (PTOA) is a common and debilitating problem following meniscal injury, which may lead to pain, loss of function, and early joint failure. Over the past 25 years, clinical, laboratory, and translational studies have greatly improved our understanding of PTOA pathogenesis and prevention. Clinical studies have established the benefit of meniscal preservation in preventing PTOA, leading to a significant increase in meniscus repair. Similarly, improved understanding of the biomechanical importance of the meniscal root attachment has increased focus on the detection and treatment of meniscal root injuries. Laboratory studies have demonstrated a preliminary mechanistic pathway of PTOA development following meniscal injury, whereby injury and altered joint loading stimulate a pro-inflammatory response that leads to both articular cartilage breakdown and impaired meniscal healing. In vitro evidence suggests that mechanical loading of the meniscus may ameliorate this catabolic response, with implications for treatment and rehabilitation protocols. Numerous animal models have emerged, allowing for in vivo assessment of PTOA initiation and offering a platform to test potential therapeutic targets. Despite these advances, meniscal repair remains imperfect and is not always possible, and investigations translating laboratory findings to the human setting have been limited. Future directions include further characterizing the immune and cellular responses to meniscal injury, investigating therapies to target the pro-inflammatory cascade and enhance meniscal healing, and developing new models to better distinguish PTOA pathogenesis in human subjects. Continued laboratory, translational, and clinical research efforts are required to identify treatment strategies to reduce the burden of PTOA after meniscal injury.
创伤后骨关节炎(PTOA)是半月板损伤后常见且使人衰弱的问题,可能导致疼痛、功能丧失和早期关节功能衰竭。在过去25年中,临床、实验室和转化研究极大地增进了我们对PTOA发病机制和预防的理解。临床研究已证实保留半月板对预防PTOA有益,这导致半月板修复显著增加。同样,对半月板根部附着生物力学重要性的深入理解使人们更加关注半月板根部损伤的检测和治疗。实验室研究已证明半月板损伤后PTOA发展的初步机制途径,即损伤和改变的关节负荷刺激促炎反应,导致关节软骨破坏和半月板愈合受损。体外证据表明,半月板的机械负荷可能改善这种分解代谢反应,这对治疗和康复方案具有启示意义。众多动物模型已出现,可用于在体内评估PTOA的起始,并提供一个测试潜在治疗靶点的平台。尽管取得了这些进展,但半月板修复仍然不完善,并非总是可行,而且将实验室研究结果转化到人体的研究一直有限。未来的方向包括进一步明确对半月板损伤的免疫和细胞反应,研究针对促炎级联反应并促进半月板愈合的疗法,以及开发新模型以更好地区分人类受试者的PTOA发病机制。需要持续的实验室、转化和临床研究努力来确定治疗策略,以减轻半月板损伤后PTOA的负担。