Edd Shannon N, Giori Nicholas J, Andriacchi Thomas P
Mechanical Engineering, Stanford University, Stanford, CA, United States; VA Palo Alto, Palo Alto, CA, United States.
VA Palo Alto, Palo Alto, CA, United States; Department of Orthopaedic Surgery, Stanford University Medical Center, Stanford, CA, United States.
J Biomech. 2015 Jun 1;48(8):1420-6. doi: 10.1016/j.jbiomech.2015.02.035. Epub 2015 Feb 26.
Meniscal damage and meniscectomy lead to subsequent osteoarthritis (OA) of the knee joint through multiple and diverse mechanisms, yet the interaction of these mechanisms remains unknown. Therefore, the aim of this review is to suggest the multi-scale, multi-faceted components involved between meniscal injury or meniscectomy and the initiation of OA. There is evidence of structural, mechanical, and biological changes after meniscal damage, all of which can be greatly affected by the presence of local or systemic inflammation. Meniscal damage or resection causes changes in knee mechanics during walking, resulting in altered cartilage loading. Because cartilage is mechanically sensitive, these loading changes can initiate a catabolic effect, culminating in tissue degeneration. The evidence suggests that the addition of elevated inflammation at the time of meniscal damage or meniscectomy results in an accelerated progression toward cartilage degradation. Initial cartilage degradation produces inflammation and pain in conjunction with structural changes to the joint, thus perpetuating the cycle of altered cartilage loading and subsequent degradation. Furthermore, the inflammation secondary to obesity and aging introduces an increased risk of developing OA following meniscal injury. Therefore, an overall route between meniscal damage or resection and OA is presented here in a manner that considers two distinct pathways; these pathways reflect the absence or presence of conditions that cause elevated inflammation.
半月板损伤和半月板切除术通过多种不同机制导致随后的膝关节骨关节炎（OA），但这些机制之间的相互作用仍不清楚。因此，本综述的目的是指出半月板损伤或半月板切除与OA发病之间涉及的多尺度、多方面的因素。有证据表明半月板损伤后会出现结构、力学和生物学变化，所有这些变化都会受到局部或全身炎症的显著影响。半月板损伤或切除会导致行走过程中膝关节力学发生改变，从而导致软骨负荷改变。由于软骨对力学敏感，这些负荷变化会引发分解代谢效应，最终导致组织退变。证据表明，在半月板损伤或半月板切除时炎症加剧会导致软骨降解加速。最初的软骨降解会伴随关节结构变化产生炎症和疼痛，从而使软骨负荷改变和随后的降解循环持续下去。此外，肥胖和衰老引发的炎症会增加半月板损伤后发生OA的风险。因此，本文以考虑两种不同途径的方式呈现半月板损伤或切除与OA之间的总体路径；这些途径反映了是否存在导致炎症加剧的情况。
