Allograft adipose matrix increases interleukin-10 and transforming growth factor-β1 concentrations in impinged fat pads of the knee

Journal of Cartilage & Joint Preservation · Published 2025-05-09 · DOI 10.1016/j.jcjp.2025.100246

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Abstract

Introduction: Fat pads of the knee both help the patella smoothly track during knee flexion and protect the patella through release of anti-inflammatory, anabolic cytokines, growth factors, and stem cells. When impingement of fat pads occurs, proinflammatory molecules are released, worsening osteoarthritis. Treatments that help restore fat pad volume may delay OA progression. Allograft adipose matrix (AAM) is an acellular, inert matrix that retains collagens and various growth factors promoting cellular infiltration and volume restoration of native adipose tissue that could potentially be used in treatment of fat pad impingement. Objectives: We sought to determine the effects AAM on gene expression and protein concentrations in osteoarthritic tissues and cells. Methods: The cartilage and fat pads were collected from 20 patients undergoing total knee arthroplasty. The tissues were used to create explants or digested to isolate the chondrocytes and adipocytes for cell culture. Explants and cells were then cultured in media containing AAM. After 48 hours, expression and concentrations of extracellular matrix genes, metalloproteinase (MMP) genes, adipokine genes, inflammatory cytokines, and growth factors were measured. Results: IL-10 concentrations were increased in fat pad explants. Concentrations of TGF-β1 were increased in fat pad/cartilage explant cocultures. TGF-β1 concentrations were decreased in adipocyte/chondrocyte cocultures. ECM, MMP, and adipokine gene expression was unaltered, but tissue inhibitor of metalloproteinases-2 (TIMP-2) expression was significantly downregulated. MMP-3 and -13 concentrations were also unaffected. Conclusions: AAM increases in vitro concentrations of IL-10 and TGF-β1 in osteoarthritic adipocytes and chondrocytes isolated from the knee joint.

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Publication details

Year
2025

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