The role of changes in extracellular matrix of cartilage in the presence of inflammation on the pathology of osteoarthritis.

The role of changes in extracellular matrix of cartilage in the presence of inflammation on the pathology of osteoarthritis.
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DOI:
10.1155/2013/284873
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发表时间:
2013
影响因子:
--
通讯作者:
Nam J
Nam J
中科院分区:
生物学3区
文献类型:
--
作者:
Maldonado M;Nam J

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骨关节炎(OA)是一种退行性疾病,影响关节周围的各种组织,如关节软骨、软骨下骨、滑膜和韧带。目前没有治疗方法可以完全预防疾病的开始或进展,部分原因是对疾病病理机制的理解不足。软骨是受OA影响的主要组织,软骨细胞是组织中唯一的细胞成分,积极参与退化过程。多种因素影响OA的发展和进展,包括在疾病进展期间持续的炎症和由于软骨磨损或创伤引起的生物力学条件的改变。在OA的进展过程中,软骨细胞在炎症条件下主动重塑软骨的细胞外基质(ECM)。ECM的这种改变反过来又改变了软骨细胞的生物力学环境,这进一步推动了炎症存在下疾病的进展。ECM组成和结构的变化也通过抑制间充质干细胞的软骨分化来阻止间充质干细胞参与修复过程。本文综述了炎症诱导的ECM重塑如何干扰细胞活动,以防止在OA的病理软骨的自我再生。
Osteoarthritis (OA) is a degenerative disease that affects various tissues surrounding joints such as articular cartilage, subchondral bone, synovial membrane, and ligaments. No therapy is currently available to completely prevent the initiation or progression of the disease partly due to poor understanding of the mechanisms of the disease pathology. Cartilage is the main tissue afflicted by OA, and chondrocytes, the sole cellular component in the tissue, actively participate in the degeneration process. Multiple factors affect the development and progression of OA including inflammation that is sustained during the progression of the disease and alteration in biomechanical conditions due to wear and tear or trauma in cartilage. During the progression of OA, extracellular matrix (ECM) of cartilage is actively remodeled by chondrocytes under inflammatory conditions. This alteration of ECM, in turn, changes the biomechanical environment of chondrocytes, which further drives the progression of the disease in the presence of inflammation. The changes in ECM composition and structure also prevent participation of mesenchymal stem cells in the repair process by inhibiting their chondrogenic differentiation. This review focuses on how inflammation-induced ECM remodeling disturbs cellular activities to prevent self-regeneration of cartilage in the pathology of OA.
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