Changchun University of Chinese Medicine, Changchun, 130021, Jilin, China.
Orthopedic Center, Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, 130021, Jilin, China.
J Orthop Surg Res. 2024 Sep 9;19(1):550. doi: 10.1186/s13018-024-05055-6.
Osteoarthritis (OA) is a chronic joint disease characterized by the degeneration, destruction, and excessive ossification of articular cartilage. The prevalence of OA is rising annually, concomitant with the aging global population and increasing rates of obesity. This condition imposes a substantial and escalating burden on individual health, healthcare systems, and broader social and economic frameworks. The etiology of OA is multifaceted and not fully understood. Current research suggests that the death of chondrocytes, encompassing mechanisms such as cellular apoptosis, pyroptosis, autophagy, ferroptosis and cuproptosis, contributes to both the initiation and progression of the disease. These cell death pathways not only diminish the population of chondrocytes but also exacerbate joint damage through the induction of inflammation and other deleterious processes. This paper delineates the morphological characteristics associated with various modes of cell death and summarizes current research results on the molecular mechanisms of different cell death patterns in OA. The objective is to review the advancements in understanding chondrocyte cell death in OA, thereby offering novel insights for potential clinical interventions.
骨关节炎（OA）是一种慢性关节疾病，其特征为关节软骨的退化、破坏和过度骨化。随着全球人口老龄化和肥胖率的上升，OA 的患病率每年都在上升。这种疾病给个人健康、医疗保健系统以及更广泛的社会和经济框架带来了巨大且不断增加的负担。OA 的病因是多方面的，目前还不完全清楚。目前的研究表明，软骨细胞的死亡，包括细胞凋亡、细胞焦亡、自噬、铁死亡和铜死亡等机制，既导致了疾病的发生，也导致了疾病的进展。这些细胞死亡途径不仅减少了软骨细胞的数量，而且通过引发炎症和其他有害过程加剧了关节损伤。本文描述了与各种细胞死亡方式相关的形态学特征，并总结了 OA 中不同细胞死亡模式的分子机制的现有研究结果。目的是综述对 OA 中软骨细胞死亡的认识进展，从而为潜在的临床干预提供新的见解。
