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• W2802145527 abstract "Purpose: Osteoarthritis (OA) is the most common form of arthritis and the leading cause of disability among elderly. It is a multicomponent chronic disease characterized by articular cartilage degeneration, but also affecting surrounding joint tissue and of particular interest is the ligament. Ligaments, made up of dense connective tissue with an extensive extracellular matrix, are responsible in stabilizing the joint and guiding motion. Trauma to the ligament has been closely linked to OA in humans, and is also seen in OA animal models (Pond-Nuki model in dogs, and destabilization of the medial meniscus (DMM) in mice). The goal of this study was to understand the pathology of these changes in the ligaments during disease progression in murine spontaneous and posttraumatic OA. Methods: Histological sections were taken from mouse knee joints of three different OA models: STR/ort mice, C57Bl/6 mice following DMM surgery, and CBA mice following non-invasive knee trauma. Samples were imaged for microCT analyses, processed for histology and stained with Toluidine Blue for pathophysiological changes. Immunohistochemistry (IHC) was performed on the non-invasive knee trauma model at 4 and 14 weeks post-trauma and STR/ort mice at three different stages: grade 1–2, 3–4, and 5–6 (OARSI grading system); markers included cartilage matrix (collagen type II, aggrecan, and sox9) and chondrocyte hypertrophy (runx2). Mechanical testing of the viscoelastic properties of wild type murine cruciate ligaments was optimized using an Instron dual column universal testing system. Results: Toluidine Blue staining showed changes in the ligaments that were consistent with endochondral ossification, including increased extracellular matrix (ECM) staining, loss of fiber alignment, and cell hypertrophy near attachment sites. MicroCT of the joint space revealed an increase in mineralized tissue volume with increasing severity of OA grades in STR/ort mice, in response to DMM surgery and to non-invasive trauma compared to age-matched controls. IHC demonstrated modification particularly in collagen type II and sox9 expression in the ligament attachment site that were associated with OA progression. In the trauma model, results included collagen type II deposition in the matrix of the mid-ligament region along with sox9 expression. Additionally in the tibial attachment site, sox9 was strongly expressed along with runx2. Meanwhile in the STR/ort models, collagen type II deposition was found only in the tibial attachment site of the ligaments. Hyperplasia and cell hypertrophy in the attachment sites correlated to expression of sox9 and runx2 in both OA mouse models. Lastly, initial mechanical testing of the ligaments showed the expected viscoelastic behaviour. Conclusions: Overall, ligament pathology is affected during OA progression, and pathology changes are consistent with chondrogenesis and potentially endochondral ossification. The full extent of these changes in the ligament matrix along with the consequences to ligament function and OA remains to be determined. Further analysis of the ligament matrix needs to be characterized to determine the extent of matrix changes and the progression." @default.
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• W2802145527 date "2018-04-01" @default.
• W2802145527 modified "2023-10-11" @default.
• W2802145527 title "Murine cruciate ligament pathology during osteoarthritis development" @default.
• W2802145527 doi "https://doi.org/10.1016/j.joca.2018.02.778" @default.
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