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  1. Home
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Browsing by Subject "Knee joint"

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    Effect of SonoVue on the synovial membrane in rabbit knees
    (Wiley, 2011-09-01) Domenech, Ernesto; Bern Serna, Juan de Dios; Polo, Luis; Reus Pintado, Manuel; Berná Mestre, Juan de Dios; Canteras, Manuel; Dermatología, Estomatología, Radiología y Medicina Física
    Objectives: The purpose of this study was to evaluate the effect of intra-articular injection of SonoVue (sulfur hexafluoride with a phospholipid shell; Bracco SpA, Milan, Italy) on the synovial membrane in an animal model. Methods: Twenty-one New Zealand White rabbits (42 knees) were used in this study. We injected the knees with normal saline (saline group; n = 21) and SonoVue (SonoVue group; n = 21). A histologic examination of the knees was performed out at 3 and 12 hours and 3, 7, 15, 30, and 45 days after injection. Four histologic parameters (synovial hyperplasia, synovial stroma, vascular dilatation, and inflammatory infiltrates) were graded separately. Results: We found no significant differences in this study for synovial hyperplasia, vascular dilatation, or inflammatory infiltrates between the saline and SonoVue groups. A significant difference was only observed for synovial stroma (P < .05), and most of the histologic changes were mild in the saline group and moderate in the SonoVue group. The histologic changes observed in this study are considered transitory and reversible. Conclusions: The results suggest that intra-articular injection of SonoVue is a safe procedure.
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    Roles of TGF-beta 1 signaling in the development of osteoarthritis
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Fang, Jie; Xu, Lin; Li, Yefu; Zhao, Zhihe
    Osteoarthritis (OA) is a degenerative joint disorder characterized by the destruction of articular cartilage, subchondral bone and other joint tissues. Although multiple growth factors and cytokines have been shown to be involved in articular cartilage degeneration and subchondral bone destruction, which eventually leads to OA, the molecular mechanisms underlying the pathogenesis of OA are largely unknown. The canonical transforming growth factor beta 1 (TGFβ1) signaling functions as one of the key factors in cartilage and bone formation, remodeling, and maintenance. However, the effects of TGF-β1 signaling on the development of OA are unclear. Numerous studies provide evidence that TGF-β1 is required for the formation of articular cartilage at early stages of joint development. In contrast, other investigations indicate that TGF-β1 may, in fact, be a factor in joint destruction. Therefore, we, in this review article, discuss the “conflicting” roles of TGF-β1 signaling in the development of OA.

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