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首页> 外文期刊>Current opinion in rheumatology >Angiogenesis in osteoarthritis.
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Angiogenesis in osteoarthritis.

机译:骨关节炎中的血管生成。

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PURPOSE OF REVIEW: Much has been documented in recent years on the possible involvement of angiogenesis in osteoarthritis. An understanding of the various regulatory mechanisms controlling blood vessel growth in the joint should lead to novel therapeutics, which selectively inhibit undesirable angiogenesis. Here, we summarize recent findings on the roles of angiogenesis in osteoarthritis and place this evidence in the context of previous literature in order to help explain pain and disease progression. RECENT FINDINGS: Inflammation and angiogenesis are closely associated in osteoarthritis, modulating functions of chondrocytes, contributing towards abnormal tissue growth and perfusion, ossification and endochondral bone development, leading to radiographic changes observed in the joint. Innervation accompanies vascularization and inflammation, hypoxia and mechanical overload are all thought to contribute in sensitizing these new nerves leading to increased pain. Articular cartilage provides a unique environment in which blood vessel growth is regulated by endogenous angiogenesis inhibitors and matrix constituents, as well as by growth factors produced by chondrocytes, subchondral bone and synovium. MRI and ultrasound enable the in-vivo visualization of abnormal vascularity in synovium and subchondral bone that have not been apparent with conventional radiography. As a result of these new findings, the widely accepted notion that osteoarthritis is primarily a disease of the cartilage is being challenged. SUMMARY: Molecular mechanisms and consequences of angiogenesis in osteoarthritis are slowly being elucidated. Studies, both in humans and animal models, support the notion that inhibiting angiogenesis will provide effective therapeutic strategies for treating osteoarthritis. Better techniques that can more precisely visualize the vascular changes of the whole joint can further enhance our understanding of osteoarthritis, and can provide proof of concept and early evidence of efficacy in trials of novel therapeutic interventions.
机译:审查的目的:近年来,关于血管生成可能参与骨关节炎的许多文献已有报道。对控制关节中血管生长的各种调节机制的理解应导致新的疗法,其选择性地抑制不良血管生成。在这里,我们总结了有关血管生成在骨关节炎中作用的最新发现,并将此证据纳入以前的文献中以帮助解释疼痛和疾病进展。最近的发现:炎症和血管生成与骨关节炎密切相关,调节软骨细胞的功能,导致异常的组织生长和灌注,骨化和软骨内骨发育,从而导致在关节处观察到放射学改变。神经支配血管化和炎症,缺氧和机械超负荷都被认为有助于使这些新神经敏感,导致疼痛加剧。关节软骨提供了一个独特的环境,在该环境中,血管的生长受到内源性血管生成抑制剂和基质成分以及软骨细胞,软骨下骨和滑膜产生的生长因子的调节。 MRI和超声能够在体内可视化滑膜和软骨下骨中的异常血管,这是常规放射线照相所无法发现的。这些新发现的结果正挑战着人们普遍接受的观念,即骨关节炎主要是软骨疾病。摘要:骨关节炎的血管生成的分子机制和后果正在逐步阐明。在人类和动物模型中的研究均支持抑制血管生成将为治疗骨关节炎提供有效治疗策略的观点。更好的技术可以更精确地可视化整个关节的血管变化,可以进一步增强我们对骨关节炎的理解,并可以在新的治疗干预试验中提供概念证明和有效性的早期证据。

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