PDF(Pubmed)
Abstract：
Osteoarthritis (OA) is no longer regarded as a simple wear-and-tear problem of articular cartilage. Instead, OA is a whole joint disorder involving both cartilaginous and non-cartilaginous tissues such as subchondral bone and synovium. Among them, subchondral bone undergoes constant remodeling in response to the changes of mechanical environment. Current understanding of subchondral bone disturbance in OA is limited to its link with an altered local mechanical loading as a result of ligament or meniscus injury. Very recently, hypertension, the most common vascular morbidity, has been emerged as an independent risk factor of OA. It might suggest a plausible role of systemic hemodynamic mechanical stress in subchondral bone remodeling and the pathogenesis of OA. However, their relationship remains not fully understood. Based on our preliminary clinical observation on the association of hemodynamic parameters with subchondral bone mass and microstructure in late-stage knee OA patients, we formulate a vascular etiology hypothesis of OA from a mechanobiology perspective. Noteworthily, hemodynamic stress associated with subchondral bone mineral density; yet compressive mechanical loading does not. Furthermore, hemodynamic parameters positively correlated with subchondral plate-like trabecular bone volume but negatively associated with rod-like trabecular bone volume. In contrast, compressive mechanical loading tends to increase both plate-like and rod-like trabecular bone volume. Taken together, it warrants further investigations into the distinct role of hemodynamic or compressive stress in shaping subchondral bone in the pathophysiology of OA.
UNASSIGNED: This work provides a new insight, from the angle of biomechanics, into the emerging role of vascular pathologies, such as hypertension, in the pathogenesis of OA. It might open up a new avenue for the development of a mechanism-based discovery of novel diagnostics and therapeutics.
UNASSIGNED: This work provides a new insight, from the angle of biomechanics, into the emerging role of vascular pathologies, such as hypertension, in the pathogenesis of OA. It might open up a new avenue for the development of a mechanism-based discovery of novel diagnostics and therapeutics.
摘要：
骨关节炎（OA）不再被视为关节软骨的简单磨损问题。相反，OA是涉及软骨和非软骨组织如软骨下骨和滑膜的全关节病症。其中,软骨下骨随着力学环境的变化而不断重塑。目前对OA软骨下骨紊乱的理解仅限于其与韧带或半月板损伤引起的局部机械负荷改变的联系。最近,高血压,最常见的血管疾病，已成为OA的独立危险因素。这可能表明全身血流动力学机械应力在软骨下骨重塑和OA的发病机理中的作用。然而,他们的关系仍然没有完全理解。基于我们对晚期膝关节OA患者血流动力学参数与软骨下骨量和微结构的关系的初步临床观察，我们从机械生物学的角度提出了OA的血管病因学假说。值得注意的是,与软骨下骨矿物质密度相关的血流动力学应力；然而压缩机械载荷没有。此外，血流动力学参数与软骨下板状骨小梁体积呈正相关，但与棒状骨小梁体积呈负相关。相比之下,压缩机械载荷倾向于增加板状和棒状小梁骨体积。一起来看,值得进一步研究血液动力学或压应力在OA病理生理学中软骨下骨成形中的独特作用。
UNASSIGNED：这项工作提供了新的见解，从生物力学的角度来看，血管病变的新兴作用，比如高血压，在OA的发病机制中。它可能为开发基于机制的新型诊断和治疗方法开辟了一条新途径。
UNASSIGNED：这项工作提供了新的见解，从生物力学的角度来看，血管病变的新兴作用，比如高血压，在OA的发病机制中。它可能为开发基于机制的新型诊断和治疗方法开辟了一条新途径。
