Department of Mechanical Engineering and Materials Science, Duke University, Durham, NC, USA.
Department of Orthopaedic Surgery, Duke University School of Medicine, DUMC Box 3093, Durham, NC, 27710, USA.
Curr Rheumatol Rep. 2023 Feb;25(2):35-46. doi: 10.1007/s11926-022-01093-3. Epub 2022 Dec 7.
Meniscus injury often leads to joint degeneration and post-traumatic osteoarthritis (PTOA) development. Therefore, the purpose of this review is to outline the current understanding of biomechanical and biological repercussions following meniscus injury and how these changes impact meniscus repair and PTOA development. Moreover, we identify key gaps in knowledge that must be further investigated to improve meniscus healing and prevent PTOA.
Following meniscus injury, both biomechanical and biological alterations frequently occur in multiple tissues in the joint. Biomechanically, meniscus tears compromise the ability of the meniscus to transfer load in the joint, making the cartilage more vulnerable to increased strain. Biologically, the post-injury environment is often characterized by an increase in pro-inflammatory cytokines, catabolic enzymes, and immune cells. These multi-faceted changes have a significant interplay and result in an environment that opposes tissue repair and contributes to PTOA development. Additionally, degenerative changes associated with OA may cause a feedback cycle, negatively impacting the healing capacity of the meniscus. Strides have been made towards understanding post-injury biological and biomechanical changes in the joint, their interplay, and how they affect healing and PTOA development. However, in order to improve clinical treatments to promote meniscus healing and prevent PTOA development, there is an urgent need to understand the physiologic changes in the joint following injury. In particular, work is needed on the in vivo characterization of the temporal biomechanical and biological changes that occur in patients following meniscus injury and how these changes contribute to PTOA development.
半月板损伤常导致关节退变和创伤后骨关节炎(PTOA)的发生。因此,本综述旨在概述半月板损伤后生物力学和生物学的反应,以及这些变化如何影响半月板修复和 PTOA 的发展。此外,我们确定了必须进一步研究的知识空白,以改善半月板愈合和预防 PTOA。
半月板损伤后,关节内的多个组织常发生生物力学和生物学改变。生物力学上,半月板撕裂会削弱半月板在关节中传递负荷的能力,使软骨更容易受到过度应变的影响。生物学上,损伤后的环境常伴有促炎细胞因子、分解代谢酶和免疫细胞的增加。这些多方面的变化相互作用,导致不利于组织修复的环境,从而促进 PTOA 的发展。此外,与 OA 相关的退行性变化可能会产生反馈循环,对半月板的愈合能力产生负面影响。目前已经在理解关节损伤后的生物力学和生物学变化、它们的相互作用以及它们如何影响愈合和 PTOA 的发展方面取得了进展。然而,为了改善促进半月板愈合和预防 PTOA 发展的临床治疗方法,迫切需要了解损伤后关节的生理变化。特别是需要对半月板损伤患者的生物力学和生物学的时间变化进行体内特征描述,以及这些变化如何导致 PTOA 的发展。