Browsing by Subject "Cartilage explants"

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    The matrix synthesis and anti-inflammatory effect of autologous leukocyte-poor platelet rich plasma in human cartilage explants
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Simental Mendía, Mario; Vilchez Cavazos, Félix; García Garza, Rubén; Lara Arias, Jorge; Montes de Oca Luna, Roberto; Said Fernández, Salvador; Martínez Rodríguez, Herminia G.
    Objective. To determine the effects of autologous leukocyte-poor platelet-rich plasma (LPPRP) on the expression of markers involved in cartilageextracellular matrix production and inflammation in cartilage explants bearing osteoarthritis. Materials and Methods. Cartilage explants and LP-PRP were obtained from 10 patients who underwent total knee arthroplasty. The explants were cultured in spinner flasks for 28 days in the presence of interleukin (IL)-1β and/or LP-PRP. The gene expression of catabolic (MMP13, ADAMTS5, and IL1β) and anabolic factors (COL2A1, ACAN, and SOX9) was quantified. A histological assessment was performed according to a modified Mankin score, and quantification of type II and I collagen deposition. Results. The gene expression of catabolic factors and the Mankin score were lower in LP-PRP- and LP-PRP/IL1β- than in IL-1β-treated explants, suggesting less matrix degradation in explants cultured in the presence of LP-PRP. Higher expression of genes involved in cartilage matrix restoration was observed in LP-PRP and LP-PRP/IL-1β- when compared to IL-1β-treated explants. The explants treated with LP-PRP and LPPRP/IL-1β exhibited a higher deposition of type II collagen as well as a lower deposition of type I collagen and also better surface integrity and a significant increase in the number of chondrocytes. Conclusion. LPPRP treatment favored restoration in early osteoarthritic cartilage and reduced the pro-inflammatory effect of IL1β. LP-PRP is a promising therapy for early osteoarthritis, as it promotes extracellular matrix repair, reduces inflammation, and slows cartilage degeneration.