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软骨基质硬度的改变作为骨关节炎的指标和调节物。

Alteration in cartilage matrix stiffness as an indicator and modulator of osteoarthritis.

机构信息

Qingdao University Affiliated Qingdao Women and Children's Hospital, Department of Stomatology Medical Center, Qingdao University, Qingdao, Shandong, CN, China.

The Affiliated Hospital of Qingdao University, Department of Stomatology Medical Center, Qingdao University, Qingdao, Shandong, CN, China.

出版信息

Biosci Rep. 2024 Jan 31;44(1). doi: 10.1042/BSR20231730.

DOI:10.1042/BSR20231730
PMID:38014522
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10794814/
Abstract

Osteoarthritis (OA) is characterized by cartilage degeneration and destruction, leading to joint ankylosis and disability. The major challenge in diagnosing OA at early stage is not only lack of clinical symptoms but also the insufficient histological and immunohistochemical signs. Alteration in cartilage stiffness during OA progression, especially at OA initiation, has been confirmed by growing evidences. Moreover, the stiffness of cartilage extracellular matrix (ECM), pericellular matrix (PCM) and chondrocytes during OA development are dynamically changed in unique and distinct fashions, revealing possibly inconsistent conclusions when detecting cartilage matrix stiffness at different locations and scales. In addition, it will be discussed regarding the mechanisms through which OA-related cartilage degenerations exhibit stiffened or softened matrix, highlighting some critical events that generally incurred to cartilage stiffness alteration, as well as some typical molecules that participated in constituting the mechanical properties of cartilage. Finally, in vitro culturing chondrocytes in various stiffness-tunable scaffolds provided a reliable method to explore the matrix stiffness-dependent modulation of chondrocyte metabolism, which offers valuable information on optimizing implant scaffolds to maximally promote cartilage repair and regeneration during OA. Overall, this review systematically and comprehensively elucidated the current progresses in the relationship between cartilage stiffness alteration and OA progression. We hope that deeper attention and understanding in this researching field will not only develop more innovative methods in OA early detection and diagnose but also provide promising ideas in OA therapy and prognosis.

摘要

骨关节炎(OA)的特征是软骨退化和破坏,导致关节强直和残疾。在早期诊断 OA 的主要挑战不仅是缺乏临床症状,而且组织学和免疫组织化学迹象也不足。越来越多的证据证实,OA 进展过程中软骨硬度的改变,尤其是在 OA 起始时,已经得到证实。此外,OA 发展过程中软骨细胞外基质(ECM)、细胞周基质(PCM)和软骨细胞的硬度呈动态变化,以独特而不同的方式发生变化,在不同位置和尺度检测软骨基质硬度时可能会得出不一致的结论。此外,还将讨论 OA 相关软骨退变表现出变硬或变软基质的机制,强调一些通常导致软骨硬度改变的关键事件,以及一些参与构成软骨力学特性的典型分子。最后,在各种可调节硬度的支架中体外培养软骨细胞,为探索基质硬度对软骨细胞代谢的调节提供了一种可靠的方法,为优化植入物支架以最大限度地促进 OA 期间软骨修复和再生提供了有价值的信息。总的来说,本综述系统而全面地阐述了软骨硬度改变与 OA 进展之间的关系的最新进展。我们希望,在这一研究领域引起更深入的关注和理解,不仅能开发出更具创新性的 OA 早期检测和诊断方法,而且能为 OA 的治疗和预后提供有希望的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d4/10794814/abd276021cb0/bsr-44-bsr20231730-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d4/10794814/227414b27cee/bsr-44-bsr20231730-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d4/10794814/abd276021cb0/bsr-44-bsr20231730-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d4/10794814/227414b27cee/bsr-44-bsr20231730-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23d4/10794814/abd276021cb0/bsr-44-bsr20231730-g2.jpg

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The effect of allyl isothiocyanate on chondrocyte phenotype is matrix stiffness-dependent: Possible involvement of TRPA1 activation.异硫氰酸烯丙酯对软骨细胞表型的影响取决于基质硬度:TRPA1激活可能参与其中。
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Micro-computed Tomography-Based Collagen Orientation and Anisotropy Analysis of Rabbit Articular Cartilage.
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BMC Musculoskelet Disord. 2024 Dec 23;25(1):1060. doi: 10.1186/s12891-024-08178-3.
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Bioactive Compounds in Osteoarthritis: Molecular Mechanisms and Therapeutic Roles.骨关节炎中的生物活性化合物:分子机制和治疗作用。
Int J Mol Sci. 2024 Oct 30;25(21):11656. doi: 10.3390/ijms252111656.
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Cartilage responses to inflammatory stimuli and adipose stem/stromal cell-derived conditioned medium: Results from an ex vivo model.软骨对炎症刺激和脂肪干细胞/基质细胞衍生的条件培养基的反应:体外模型的结果
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