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http://dx.doi.org/10.1016/j.annpat.2009.07.050 | DOI Listing |
JBJS Case Connect
October 2024
Department of Orthopaedic Surgery, The University of Tokyo Hospital, Bunkyo-ku, Tokyo, Japan.
Case: An 18-year-old woman presented with shoulder pain that had persisted for a year. The magnetic resonance imaging showed a solitary lesion in the subacromial bursa (SAB). Arthroscopy revealed an ovoid mass connected to the bursal wall with thin synovial tissue that was excised en bloc arthroscopically.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Orthopedic Surgery, 920th Hospital of Joint Logistics Support Force of PLA, Kunming, China.
Osteoarthritis (OA) is a degenerative bone disease characterized by the destruction of joint cartilage and synovial inflammation, involving intricate immune regulation processes. Disulfidptosis, a novel form of programmed cell death, has recently been identified; however, the effects and roles of disulfidptosis-related genes (DR-DEGs) in OA remain unclear. We obtained six OA datasets from the GEO database, using four as training sets and two as validation sets.
View Article and Find Full Text PDFInflamm Res
January 2025
Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, School of Pharmacy, Anhui Medical University, Hefei, 230032, Anhui Province, China.
Objective: Fibroblast-like synoviocytes (FLS) are key players in rheumatoid arthritis (RA) by resisting apoptosis via increased autophagy. Elevated synovial aquaporin 1 (AQP1) affects RA FLS behaviors, but its relationship with FLS autophagy is unclear. We aim to clarify that silencing AQP1 inhibits autophagy to exert its anti-RA effects.
View Article and Find Full Text PDFJ Transl Med
January 2025
Center of Interventional Medicine for Precision and Advanced Cellular Therapy, IMPACT, Santiago, Chile.
Objective: The inflammatory responses from synovial fibroblasts and macrophages and the mitochondrial dysfunction in chondrocytes lead to oxidative stress, disrupt extracellular matrix (ECM) homeostasis, and accelerate the deterioration process of articular cartilage in osteoarthritis (OA). In recent years, it has been proposed that mesenchymal stromal cells (MSC) transfer their functional mitochondria to damaged cells in response to cellular stress, becoming one of the mechanisms underpinning their therapeutic effects. Therefore, we hypothesize that a novel cell-free treatment for OA could involve direct mitochondria transplantation, restoring both cellular and mitochondrial homeostasis.
View Article and Find Full Text PDFAm J Sports Med
January 2025
Musculoskeletal Institute, Atrium Health Carolinas Medical Center; Orthopaedic Surgery, Wake Forest University School of Medicine; and OrthoCarolina, Charlotte, North Carolina, USA.
Background: Loss of motion and arthrofibrosis after anterior cruciate ligament (ACL) reconstruction (ACLR) can be devastating complications for athletes. The cellular and molecular pathogenesis of arthrofibrosis is poorly understood, limiting prevention and treatment options. Synovial inflammation may contribute to post-ACLR arthrofibrosis.
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