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T Cell Cytokines as Immunomodulators of Arthritis Disease Pathology
Published in Thomas F. Kresina, Monoclonal Antibodies, Cytokines, and Arthritis, 2020
Thomas F. Kresina, Donna J. Spannaus-Martin
Peritendinitis and periostitis are also noted (9). In chronic arthritis, analysis of serial sections of involved joints reveals proliferation of synoviocytes and fibroblasts resulting in synovial hypertrophy and fibrosis. Replacement of cartilage and subchondral bone is observed starting at the margin. Also observed at this disease stage is the fibrous tissue replacement of synovium and cartilage to the extent of forming adhesions between the joints (8).
Osteoarthritis
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
David Musnick, Richard D. Batson
There can be a progressive decrease in collagen and proteoglycans in a joint. There can also be an increase in the rate of apoptosis of chondrocytes in a joint. With a decrease in the collagen and proteoglycan content, fissuring can occur. If there is enough cartilage loss in a surface the subchondral bone can be exposed. More loss is likely in weight-bearing surfaces than in non-weight-bearing surfaces.
Basic Science of Osteoarthritis
Published in Manoj Ramachandran, Tom Nunn, Basic Orthopaedic Sciences, 2018
Increased bone remodelling occurs due to a combination of mechanical loading, micro-fractures and soluble mediators. This is associated with increased vascularity and cellular metabolism. Modification of the trabecular architecture, thickening of the subchondral cortical plate and mineralization lead to subchondral sclerosis and eburnation. The increase in stiffness reduces the protective shock absorbing capacity of the subchondral bone, predisposing the overlying cartilage to damage from repetitive loading. The remodelling process becomes increasingly abnormal and disordered. The weakened bone undergoes attrition and collapse under compression.
Fibroblast-like Synoviocytes-derived Exosomal PCGEM1 Accelerates IL-1β-induced Apoptosis and Cartilage Matrix Degradation by miR-142-5p/RUNX2 in Chondrocytes
Published in Immunological Investigations, 2022
Guangxuan Zeng, Gang Deng, Shiliang Xiao, Fei Li
Osteoarthritis (OA) is a degenerative joint disease that causes major pain and disability in middle-aged and elderly people (Gossan et al. 2015; Primorac and Molnar 2020). It is characterized by pathological changes on articular cartilage and subchondral bone, and the clinical symptoms are pain and motor dysfunction (Batshon et al. 2020; Reynard and Barter 2020; Vincent 2020). Under normal conditions, the fibroblast-like synoviocytes (FLSs) that make up the synovial tissue can provide nutrition for the articular cartilage and protect the joint structure and surrounding skeletal muscle tissue (Karouzakis et al. 2009). Chondrocytes, unique cells in articular cartilage, maintain cartilage homeostasis by synthesizing and breaking down cartilage extracellular matrix (ECM) (Olivotto et al. 2013). Studies have shown that FLSs participate in the degradation of OA cartilage by producing inflammation and decomposition factors (Pan et al. 2017; Song et al. 2019). Also, it is reported that chondrocyte apoptosis is related to the pathogenesis of OA (Hwang and Kim 2015). At present, there is still no effective method to prevent and resist OA. Therefore, exploring the relationship between chondrocytes and FLSs is essential to clarify the pathogenesis of OA.
Targeted treatment for osteoarthritis: drugs and delivery system
Published in Drug Delivery, 2021
Liwei Mao, Wei Wu, Miao Wang, Jianmin Guo, Hui Li, Shihua Zhang, Jiake Xu, Jun Zou
OA is the most common degenerative disease of the whole joint, progressively affecting the articular cartilage, synovium, subchondral bone, and periarticular tissues like ligaments, capsule, and periarticular muscles (Glyn-Jones et al., 2015; Martel-Pelletier et al., 2016; Sharma, 2021). The main pathological manifestations are degeneration of articular cartilage, thinning of subchondral bone, osteophyte formation around the joint, meniscal alterations, synovial fluid inflammation, ligament injury, and joint capsule hypertrophy (Hügle & Geurts, 2017; Roseti et al., 2019). Cardinal symptoms include pain, swelling or even deformity of the joints, stiffness (especially severe and transient morning stiffness), popping or crepitus during joint motion, and mobility disorder (Fu et al., 2018; Bacon et al., 2020; He et al., 2020). Traditionally, OA is regarded as a passive degenerative disease or injury caused by long-term wear and tear. However, new insights suggest that OA is actually an active dynamic process arising from imbalance of joint damage and repair. Initially, erosion begins on the surface of the cartilage and gradually deepens into the calcified cartilage area. During this process, chondrocytes attempt to repair the damage by enhancing proliferation and differentiation, but the accompanying inflammatory response inhibits chondrocyte function. Then the subchondral bone proliferates pathologically and erodes the cartilage layer. The endochondral pathologic enhancement of osteogenesis results in the formation of osteophytes around the joint margins (Figure 2).
Factors associated with osteophyte formation in patients with rheumatoid arthritis undergoing total knee arthroplasty
Published in Modern Rheumatology, 2020
Nobuyuki Asai, Shuji Asai, Nobunori Takahashi, Naoki Ishiguro, Toshihisa Kojima
New medications including biologics and aggressive treatment strategies have enabled patients with rheumatoid arthritis (RA) to prevent irreversible joint destruction, and sometimes even to repair damaged joints. In the process of repairing damaged joints, subchondral bone sclerosis and osteophyte formation might be detected radiographically. These findings, referred to as secondary osteoarthritis (OA) changes [1], are included in the definition of structural remodeling of large joints according to the ‘assessment of rheumatoid arthritis by scoring of large joint destruction and healing in radiographic imaging’ (ARASHI) score [2], and have been suggested to contribute to the stability of large joints. Improvements in periarticular bone quality such as secondary OA changes may lead to a reduction in premature prosthesis loosening in patients with RA undergoing total joint arthroplasty. Previous studies have demonstrated that age, disease duration, and bone erosion are associated with osteophyte formation in the hands of patients with RA [3,4]. However, little has been reported on this aspect in large joints. Accordingly, this study aimed to determine factors associated with osteophyte formation in patients with RA undergoing total knee arthroplasty (TKA).