Ultrastructural changes of knee articular cartilage in C57B1/6 mice were studied in the course of antigen-induced arthritis by means of scanning and transmission electron microscopy. First damages of the cartilage surface were seen one hour after arthritis induction. The earliest signs were the loss of the superficial electron-dense layer as well as a progressive loss of proteoglycans in the cartilaginous matrix on the surface. Breaks of collagen fibres were already detected at the first day of arthritis. The chondrocytes of the superficial cartilage layer showed an increase of the intracellular membraneous system in the early phase of arthritis. Thereafter chondrocytes on the surface became more and more necrotic. On the 7th day of arthritis acute alterations of cartilage had developed completely. Many lacunae of chondrocytes were opened and the cartilage surface showed deep structural defects with adhering cells, probably lymphocytes and macrophages. In the following time these destructive processes were demonstrated along with cellular proliferation as a sign of repair attempts in hyaline cartilage.
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http://dx.doi.org/10.1016/S0940-2993(96)80012-1 | DOI Listing |
J Orthop Surg Res
January 2025
Department of Hand-Foot Microsurgery, Shenzhen Nanshan People's Hospital, The 6th Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, China.
Background: Steroid-induced osteonecrosis of the femoral head (SIONFH) is a universal hip articular disease and is very hard to perceive at an early stage. The understanding of the pathogenesis of SIONFH is still limited, and the identification of efficient diagnostic biomarkers is insufficient. This research aims to recognize and validate the latent exosome-related molecular signature in SIONFH diagnosis by employing bioinformatics to investigate exosome-related mechanisms in SIONFH.
View Article and Find Full Text PDFActa Biomater
January 2025
Department of Biomedical Engineering, University of Connecticut, Storrs, CT, United States; School of Mechanical, Aerospace, and Manufacturing Engineering, University of Connecticut, Storrs, CT, United States. Electronic address:
In this study we investigate the mechanics of type II collagen fibrils, an essential structural component in many load-bearing tissues including cartilage. Although type II collagen plays a crucial role in maintaining tissue integrity, the stress-stretch and failure response of type II collagen fibrils in tension is not established in the current mechanics literature. To address this knowledge gap, we conducted tensile tests on isolated collagen networks from articular cartilage and established a validated constitutive model for type II collagen fibril.
View Article and Find Full Text PDFCell Genom
January 2025
Curriculum in Bioinformatics and Computational Biology, University of North Carolina, Chapel Hill, NC 27599, USA; Thurston Arthritis Research Center, University of North Carolina, Chapel Hill, NC 27599, USA; Curriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, NC 27599, USA; Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA; Department of Cell Biology and Physiology, University of North Carolina, Chapel Hill, NC 27599, USA. Electronic address:
Osteoarthritis (OA) poses a significant healthcare burden with limited treatment options. While genome-wide association studies (GWASs) have identified over 100 OA-associated loci, translating these findings into therapeutic targets remains challenging. To address this gap, we mapped gene expression, chromatin accessibility, and 3D chromatin structure in primary human articular chondrocytes in both resting and OA-mimicking conditions.
View Article and Find Full Text PDFFASEB J
January 2025
Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, Missouri, USA.
Osteoarthritis (OA) is characterized by articular cartilage degeneration, leading to pain and loss of joint function. Recent studies have demonstrated that omega-3 (ω3) polyunsaturated fatty acid (PUFA) supplementation can decrease injury-induced OA progression in mice fed a high-fat diet. Furthermore, PUFAs have been shown to influence the mechanical properties of chondrocyte membranes, suggesting that alterations in mechanosensitive ion channel signaling could contribute to the mechanism by which ω3 PUFAs decreased OA pathogenesis.
View Article and Find Full Text PDFCommun Biol
January 2025
Department of Orthopedics, Shengjing Hospital of China Medical University, Shenyang, China.
Osteoarthritis (OA) is a degenerative joint disease that affects the cartilage and surrounding tissues. The transcription factor Kruppel-like family factor 9 (KLF9) has been identified as a regulator of tumorigenesis. However, its role in OA is still not fully understood.
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