前交叉韧带损伤后形成骨性关节炎机制研究进展—基于生物学方向OACSTPCD
Recent research progress from biological perspective on the mechanism of formation of osteoarthritis after anterior cruciate ligament injury
前交叉韧带(ACL)主要是通过限制胫骨关节处胫骨力和旋转力的前平移从而起到稳定膝关节的作用,若此韧带损伤,则会引起关节的疼痛、活动受限、膝关节不稳定等.据相关研究表示,前交叉韧带损伤后引起创伤性骨性关节炎(PTOA)的发病率高达87%,尽管有许多研究表明ACL损伤患者易患PTOA,但目前确切的机制尚不清楚.这可能与该韧带损伤后引起的生物学因素、结构因素、机械因素等有关.先前的研究表明,ACL损伤后关节腔内炎症介质升高,可致使软骨细胞坏死以及软骨基质的降解.这些潜在的生化介质有助于PTOA形成,进行早期干预可以减少未来PTOA的发生.近年来,许多学者致力于研究ACL损伤后形成骨性关节炎与潜在的重要因子和信号通路有关,并探讨其分子机制,使该领域获得了巨大的发展.本文主要从生物学方向去研究及探讨前交叉韧带损伤后形成骨性关节炎的机制.
The anterior cruciate ligament(ACL)mainly plays a role in stabilizing the knee joint by limiting the forward translation of tibial force and rotational force at the tibial joint,and if this ligament is damaged,it will cause joint pain,limited mo-bility,and knee instability etc.According to related studies,the incidence of post-traumatic osteoarthritis(PTOA)after ACL inju-ry is as high as 87%,although many studies have shown that patients with ACL injury are susceptible to PTOA,but the exact mechanism is currently unknown.This may be related to biological,structural,and mechanical factors caused by the ligament inju-ry.Previous studies have shown that elevated inflammatory mediators in the joint cavity following ACL injury can lead to chondro-cytes necrosis and degradation of the cartilage matrix.These potential biochemical mediators contribute to PTOA formation,and early intervention can reduce future episodes of PTOA.In recent years,many scholars have devoted themselves to studying the po-tential important factors and signaling pathways involved in the formation of osteoarthritis after ACL injury,and exploring its mo-lecular mechanism,which has led to great progress in this field.This paper mainly studies and discusses the mechanism of osteoar-thritis formation after ACL injury from the biological perspective.
周塏;杜秀藩;王广积
海南医学院附属海南医院 海南省人民医院 运动医学科, 海南 海口 570311
临床医学
前交叉韧带损伤生物学骨性关节炎
Anterior cruciate ligament injuryBiologyOsteoarthritis
《海南医学院学报》 2024 (004)
315-320 / 6
This study was supported by Research Foundation of Hainan Medical University(HYPY2020014);National Natural Science Foundation of China(2021MSXM10)海南医学院科研培育基金项目(HYPY2020014);国家自然科学基金培育530工程面上项目(2021MSXM10)
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