Abstract
Rheumatoid arthritis (RA) is one of the inflammatory joint diseases in a heterogeneous group of disorders that share features of destruction of the extracellular matrices of articular cartilage and bone. The underlying disturbance in immune regulation that is responsible for the localized joint pathology results in the release of inflammatory mediators in the synovial fluid and synovium that directly and indirectly influence cartilage homeostasis. Analysis of the breakdown products of the matrix components of joint cartilage in body fluids and quantitative imaging techniques have been used to assess the effects of the inflammatory joint disease on the local remodeling of joint structures. The role of the chondrocyte itself in cartilage destruction in the human rheumatoid joint has been difficult to address but has been inferred from studies in vitro and in animal models. This review covers current knowledge about the specific cellular and biochemical mechanisms that account for the disruption of the integrity of the cartilage matrix in RA.
Highlights
Rheumatoid arthritis (RA) is an inflammatory joint disease that most frequently affects the anatomical components of articular and juxta-articular tissues of diarthrodial joints
The glycosaminoglycan components of aggrecan and other cartilage matrix constituents are synthesized by chondrocytes under conditions of low turnover, and the matrix turnover may be more rapid in the immediate pericellular zones
Chondrocytes adapt to low oxygen tensions by upregulating hypoxia-inducible factor (HIF)-1α, which can stimulate the expression of glucose transporter proteins (GLUTs) [19] and angiogenic factors such as vascular endothelial growth factor (VEGF) [21,22], as well as ascorbate transport [23] and several genes associated with cartilage anabolism and chondrocyte differentiation, including Sox9 and type II collagen [24]
Summary
Rheumatoid arthritis (RA) is an inflammatory joint disease that most frequently affects the anatomical components of articular and juxta-articular tissues of diarthrodial joints. The synovium lines the joint cavity and is the site of production of synovial fluid, which provides the nutrition for the articular cartilage and lubricates the cartilage surfaces. In RA, the synovial lining of diarthrodial joints is the site of the initial inflammatory process [1,2] This lesion is characterized by proliferation of the synovial lining cells, increased vascularization, and infiltration of the tissue by inflammatory cells, including lymphocytes, plasma cells, and activated macrophages [3,4,5]. At the interface between the inflamed synovium and adjacent subchondral bone, there is evidence of local activation of bone resorption with destruction of the mineralized bone matrix, accompanied by cells expressing phenotypic features of osteoclasts, including calcitonin receptor mRNA, cathepsin K, and tartrate-resistant acid phosphatase (TRAP) [6,7]. This review will focus on the unique ways in which the chondrocyte responds to the inflammatory milieu and contributes to the disease process in the cartilage
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
