Cell-free methods for cartilage tissue repair have recently gained increased focus. One method to supply a chondrogenic cell source is to apply freshly harvested cartilage tissue to the defects area and to retain the tissue for cell outgrowth. The present study aims to investigate the cartilage repair response of autologous cartilage chips or chondrocytes in combination with a collagen membrane in a goat femoral condyle full thickness cartilage defect model. Fully 16 defects in 8 adult goats were used for the study. A total of 6 mm full-thickness cartilage defects in the femoral condyles were randomized to collagen membrane matrix scaffold with chondrocytes and minced cartilage placed under collagen membrane scaffold. Animals were followed for 4 months. No difference was found in O'Driscoll and Pinada histology scores, tissue filling (35%), or repair tissue stiffness between the two groups. This animal study demonstrated no difference in cartilage repair between the two different techniques. The general tissue regeneration was limited probably due to the early time point of investigation and the challenging mechanical environment.
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http://dx.doi.org/10.1080/03008200802325037 | DOI Listing |
J Orthop Surg Res
January 2025
Department of Joint Osteopathy, Liuzhou Worker's Hospital, Liuzhou, Guangxi Province, 545000, China.
Alcoholic osteonecrosis of the femoral head (AIONFH) is caused by long-term heavy drinking, which leads to abnormal alcohol and lipid metabolism, resulting in femoral head tissue damage, and then pathological necrosis of femoral head tissue. If not treated in time in clinical practice, it will seriously affect the quality of life of patients and even require hip replacement to treat alcoholic femoral head necrosis. This study will confirm whether M2 macrophage exosome (M2-Exo) miR-122 mediates alcohol-induced BMSCs osteogenic differentiation, ultimately leading to the inhibition of femoral head necrosis.
View Article and Find Full Text PDFJ Control Release
January 2025
School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China; Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, Sun Yat-sen University, Guangzhou 510006, China. Electronic address:
Osteoarthritis is the most prevalent form of arthritis, and a leading cause of pain and long-term disability. Dysregulation of redox homeostasis is a key feature in the pathological progression of osteoarthritis that amplifies the inflammatory response, aggravates synovitis and accelerates cartilage degradation. Herein, a hemin and chitosan-mediated antioxidant gel inducing ROS conversion (hc-MAGIC) was constructed to targeting oxidative stress for osteoarthritis treatment.
View Article and Find Full Text PDFAm J Sports Med
January 2025
Department of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Background: A larger joint line convergence angle (JLCA) increases the stress load on the medial compartment. Few reports, however, have discussed the effect of the JLCA on the cartilage status and clinical outcomes after opening-wedge high tibial osteotomy (OWHTO).
Purpose/hypothesis: To reveal the effect of the JLCA on clinical results after OWHTO.
Am J Sports Med
January 2025
Department of Orthopaedic Surgery/Sports Medicine Center, Southwest Hospital, Army Medical University, Chongqing, China.
Background: The challenge of achieving effective tendon-to-bone healing remains a significant concern in sports medicine, necessitating further exploration. Biomimetic electrospun nanomaterials present promising avenues for improving this critical healing process.
Purpose: To investigate the biological efficacy of a novel aligned-to-random PLGA/Col1-PLGA/nHA bilayer electrospun nanofiber membrane in facilitating tendon-to-bone healing.
J Cell Mol Med
February 2025
Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Osteoarthritis (OA) is a degenerative joint disease with a complex aetiology, which includes inflammation, cellular growth dysregulation and extracellular matrix (ECM) degradation. This study investigated the therapeutic potential of a small-molecule compound, 2-amino-4-(3,4,5-trimethoxyphenyl)-4H-benzo[h]chromene-3-carbonitrile (CN7:1h) in modulating these critical biochemical pathways in OA. Cellular models and rat models of OA were used to explore the impact of CN7:1h on the nuclear factor kappa light chain enhancer of activated B cells (NF-κB) and mechanistic target of rapamycin (mTOR) signalling pathways.
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