Department of Orthopedics, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
Int J Mol Sci. 2024 May 28;25(11):5903. doi: 10.3390/ijms25115903.
Post-traumatic osteoarthritis of the ankle (PTOA) is frequently observed following a debilitating consequence of intra-articular ankle fractures. Numerous risk factors contribute to the pathogenesis of PTOA, including articular incongruity, joint malalignment, and concomitant soft tissue damage. Despite attempts to restore joint anatomy and manage soft tissues to avoid long-term complications after intra-articular ankle fractures, the incidence of PTOA remains markedly elevated. Inflammatory processes triggered by intra-articular ankle fractures have emerged as potential instigators that expedite the progression of PTOA. Injury to the articular cartilage and subchondral bone may lead to the release of inflammatory mediators, which can contribute to cartilage degradation and bone resorption. This study provides a narrative review on the current knowledge concerning the association between inflammation and the development of PTOA following intra-articular ankle fractures. We also discuss novel therapeutic agents that target inflammatory pathways to impede the progression of post-traumatic osteoarthritis after intra-articular ankle fractures. These medication and interventions were summarized within this review article.
创伤性踝关节炎（PTOA）是关节内踝骨折后常见的一种致残后果。许多危险因素导致 PTOA 的发病机制，包括关节不平整、关节对线不良和伴随的软组织损伤。尽管尝试恢复关节解剖结构并管理软组织以避免关节内踝骨折后的长期并发症，但 PTOA 的发生率仍然明显升高。关节内踝骨折引发的炎症过程已成为加速 PTOA 进展的潜在触发因素。关节软骨和软骨下骨的损伤可能导致炎症介质的释放，这可能导致软骨降解和骨吸收。本研究就关节内踝骨折后炎症与 PTOA 发展之间的关系提供了一篇综述。我们还讨论了针对炎症途径的新型治疗药物，以阻止关节内踝骨折后创伤性骨关节炎的进展。这些药物和干预措施在本文中进行了总结。
