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Bone Regeneration Effect of Cassia occidentalis Linn. Extract and Its Isolated Compounds
Published in Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay, Phytochemistry of Plants of Genus Cassia, 2021
Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay
NFκB is the major inflammatory molecule that not only supports osteoclastogenesis and bone resorption but also causes joint destruction in RA and OA. In a mouse model of collagen-induced RA, the so-called CIA model, emodin (10 mg/kg, i.p.) in a therapeutic mode (administered 25 days after collagen-II challenge) decreased the arthritis disease score, suppressed synovial inflammation and joint destruction. In the joints of CIA mice, the enhancement of NFκB signaling revealed by decreased cytoplasmic levels of inhibitor κB (IκB) and increased nuclear levels of p65 and p50 in the nuclear fraction was reversed by emodin treatment. Consequently, the CIA-induced elevations in inflammatory cytokines including TNFα, IL1β, RANKL and IL17 in the joints were decreased by emodin, as well as the serum levels of TNFα and IL1β. Furthermore, the matrix-degrading matrix metalloproteinases-1,3 (MMP1 and MMP3) levels that were increased in the joints of CIA mice were significantly suppressed by emodin treatment (Hwang, 2013).
Introduction and Review of Biological Background
Published in Luke R. Bucci, Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
Just under the fibrous joint capsule, the dense irregular connective tissue that surrounds most joint structures, the synovium, is found. The synovium is divided into two layers — the subintima and intima. There is no basement membrane in synovium. The subintima is highly vascular, loose connective tissue and contains nerves and lymphatics. The intima is one to four cells thick and faces the inside of the joint cavity. Two major cell types are present in the subintima. Type A cells are macrophage-like, and Type B cells are fibroblast-like. However, these cells have overlapping functions, which has led some investigators to identify Type C cells (intermediate synovial cells). Both synthetic and phagocytic properties are possessed by synoviocytes. In vitro, synovial cells secrete hyaluronan, proteoglycans, collagens (Types I, III), collagenases, neutral metalloproteinases, activators of collagenases and proteases, fibronectin, laminin, and many other unidentified matrix constituents. Importantly, synoviocytes also can be induced to secrete interleukin-1 (IL-1), prostaglandin E2, and possibly other cytokines and lymphokines.33,63–65 Thus, synoviocytes are extremely important in regulating the degradation of cartilage, and, thus, joint function.
Biology of Joints
Published in Verna Wright, Eric L. Radin, Mechanics of Human Joints, 2020
The synovium itself is an extremely thin tissue. Its depth varies from one site to another but usually is about 25 μm deep in histological sections. When the tissue is fixed under a modest intraarticular pressure of 25 cmH20, the synovium thins significantly (25). Presumably, similar thinning and thickening take place when positioning of the joint does or does not impose tensile stresses.
Reduction of systemic exposure and side effects by intra-articular injection of anti-inflammatory agents for osteoarthritis: what is the safer strategy?
Published in Journal of Drug Targeting, 2023
Zuoxu Xie, Lu Wang, Jie Chen, Zicong Zheng, Songpol Srinual, Annie Guo, Rongjin Sun, Ming Hu
OA was once considered a non-immunological or non-inflammatory related disease because the pathophysiological findings were focussed on only mechanical effects such as degeneration and remodelling of the cartilage and bone [13]. However, recent research proposed low-grade chronic inflammation as a driving factor for disease progression [14]. The macroscopic and microscopic examination showed a correlation between synovitis and disease progression in more than 50% of OA patients [15]. Synovium was affected primarily after inflammation occurs. Not only synovial hyperplasia was found in the first step of the disease, but the overexpression of inflammatory mediators such as COX-2, tumour necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) were also found in OA associated tissues [16]. Inhibition of these inflammatory mediators and cytokines has shown promise in slowing down the progression of OA. The conventional pathways such as the reduction of arachidonic acid production through the inhibition of cyclooxygenase enzymes have been considered the drug development target for OA treatment. Selective COX-2 inhibitors, celecoxib, and etoricoxib have been widely used for OA even though concerns over its severe cardiovascular adverse effects persist [17].
Intra-articular drug delivery systems for osteoarthritis therapy: shifting from sustained release to enhancing penetration into cartilage
Published in Drug Delivery, 2022
Huirong Huang, Zijian Lou, Shimin Zheng, Jianing Wu, Qing Yao, Ruijie Chen, Longfa Kou, Daosen Chen
The articular capsule is a cystic structure composed of fibrous connective tissue that closes the articular cavity. It is divided into inner and outer layers, whereby the outer layer is collagen fibril dense connective tissue, which is continuous with the periosteum for maintenance of the joint stability. On the other hand, the inner layer, which is also called synovium, is loose and has a smooth surface. It protrudes to the joint cavity to form synovial folds or villi and has lymphatic vessels inside it. There are two types of synovial cells covering the synovial. One is the macrophage-like cell, which contains more lysosomes and has phagocytosis ability and the other is the fibroblast, which contains rougher endoplasmic reticulum and secretes hyaluronic acid as well as mucopolysaccharide, which lubricates the joints.
Long non-coding RNA MEG3 and its genetic variant rs941576 are associated with rheumatoid arthritis pathogenesis in Egyptian patients
Published in Archives of Physiology and Biochemistry, 2022
Alaa S. Wahba, Maha E. Ibrahim, Noha M. Mesbah, Samy M. Saleh, Dina M. Abo-elmatty, Eman T. Mehanna
The interaction between these causative factors triggers protein citrullination and production of autoantibodies (preclinical RA). Clinical synovitis is initiated due to inflammatory cells infiltration into the synovium (early RA) (Arend and Firestein 2012). Progression to established RA occurs as fibroblast-like synoviocytes (FLSs) secrete cytokines, growth factors and enzymes (matrix metalloproteinases (MMPs) and collagenase), promoting synovial hyperplasia and cartilage destruction (Guo et al.2018). Synovial hyperplasia results from cellular proliferation, influx of cells from the circulation and reduced apoptosis through B-cell lymphoma-2 (Bcl-2) family proteins dysregulation (Li and Wan 2013), leading to inadequate oxygenation and local hypoxia (Chimenti et al.2015). The main factor mediating the response to hypoxic stress is hypoxia inducible factor (HIF)-1, which transactivates a series of genes such as vascular endothelial growth factor (VEGF) that participates in angiogenesis (Hu et al.2014).