PDF(Pubmed)
Abstract：
Post-traumatic osteoarthritis (PTOA) develops secondary to a joint injury and accounts for 12 % of all osteoarthritis. These injuries, often of the lower extremity joints, occur due to trauma or accidents related to athletic or military activities. They primarily affect younger individuals although PTOA can occur across the spectrum of age. Pain and functional disability caused by PTOA confer a heavy economic toll on patients, in addition to detrimentally affecting their quality of life. Both high energy injuries that cause articular surface fracture with or without subchondral bone disruption and low-energy injuries involving joint dislocations or ligamentous injury cause PTOA, albeit through different mechanisms. Regardless, chondrocyte death, mitochondrial dysfunction, reactive oxygen species production, subchondral bone remodeling, inflammation and cytokine release in the cartilage and synovium play integral roles in the pathogenesis of PTOA. Evolving surgical methods are focused on stabilizing articular surface and joint structure congruity. However, to date there are no disease modifying medical therapies against PTOA. Increased recent understanding of the pathogenesis of the subchondral bone and synovial inflammation as well as that of chondrocyte mitochondrial dysfunction and apoptosis have led to the investigation of new therapeutics targeting these mechanisms to prevent or delay PTOA. This review discusses new advances in our understanding of cellular mechanisms underlying PTOA, and therapeutic approaches that are potentially effective in reducing the self-propagating cycle of subchondral bone alterations, inflammation, and cartilage degradation. Within this context, we focus therapeutic options involving anti-inflammatory and anti-apoptotic candidates that could prevent PTOA.
摘要：
创伤后骨关节炎（PTOA）继发于关节损伤，占所有骨关节炎的12％。这些伤口,通常是下肢关节，由于与运动或军事活动有关的创伤或事故而发生。它们主要影响年轻人，尽管PTOA可以在年龄范围内发生。PTOA引起的疼痛和功能障碍会给患者带来沉重的经济损失，除了不利地影响他们的生活质量。引起关节面骨折伴或不伴软骨下骨破坏的高能量损伤和涉及关节脱位或韧带损伤的低能量损伤均可引起PTOA。尽管通过不同的机制。无论如何,软骨细胞死亡，线粒体功能障碍，活性氧的产生，软骨下骨重建，软骨和滑膜中的炎症和细胞因子释放在PTOA的发病机理中起着不可或缺的作用。不断发展的手术方法集中在稳定关节表面和关节结构的一致性上。然而,迄今为止，还没有针对PTOA的疾病修饰医学疗法。最近对软骨下骨和滑膜炎症的发病机理以及软骨细胞线粒体功能障碍和凋亡的发病机理的了解增加，导致了针对这些机制以预防或延迟PTOA的新疗法的研究。这篇综述讨论了我们对PTOA背后的细胞机制的理解的新进展，和治疗方法可能有效地减少软骨下骨改变的自我传播周期，炎症,和软骨退化。在此背景下,我们关注的治疗方案包括可以预防PTOA的抗炎和抗凋亡候选药物.
