Background: Only few studies have investigated the effect of topical application of tranexamic acid (TXA) on "minimally" invasive joint surgical procedures in which articular cartilage is preserved; for this reason, actually many surgeons avoid the use of topical TXA even if the disadvantage related to a blood loss can occur. The aim of this study was to evaluate the cytotoxicity, on human chondrocytes, of TXA at different concentrations and times of exposure and the mechanisms of cell death.
Methods: Experiments were carried out on isolated human chondrocytes harvested from eight patients who underwent total knee replacement. Cell viability was determined using XTT assay and was assessed at 0, 24 and 48 h intervals after a 10-min-long treatment, followed by thorough washes, or at 24 and 48 h of treatment at TXA concentrations of 20, 50, 70 and 100 mg/ml. Cell cycle alterations and occurrence of cell death for apoptosis or necrosis were assessed by cytofluorimetry. Data were analyzed using Proc Mixed Procedure; LSMEANS was used to compare multiple group means with Tukey's honestly significant difference test.
Results: A significant correlation between the controlled for factors (type of treatment, time and concentration) was found in the performed experiment. No significant effect on cell viability was observed when the TXA exposure was limited to 10 min, while for increased exposure, 24 and 48 h, a remarkable reduction was found; cell death occurred by apoptosis and was already appreciable after 24 h, reaching a statistical significance after the 48-h-long treatment.
Conclusion: A prolonged exposure to TXA may cause cartilage damage, thus its topical application can be expanded also to clinical scenarios that include retention of native cartilage chondrocytes, only if it is limited to few minutes and used at concentrations of 70 mg/ml or less.
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http://dx.doi.org/10.1186/s40001-019-0373-x | DOI Listing |
Int J Rheum Dis
January 2025
Department of Orthopaedics, Shaanxi Rehbilitation Hospital, Xi'an, Shaanxi, China.
Background: Osteoarthritis (OA) is one of the most common bone disorders and has a serious impact on the quality of life of patients. LncRNA-HCP5 (HCP5) is downregulated in OA tissues. However, the latent function and regulatory mechanisms of HCP5 in OA are unclear.
View Article and Find Full Text PDFInt J Rheum Dis
January 2025
Hubei Provincial Key Laboratory of Occurrence and Intervention of Rheumatic Disease, Minda Hospital of Hubei Minzu University, Enshi, China.
Osteoarthritis is a systemic disease that primarily damages articular cartilage and also affects the synovium, ligaments, and bone tissues. The key mechanisms involved are chondrocyte death and degradation of the extracellular matrix. This study aims to identify differentially expressed genes (DEGs) associated with ferroptosis and investigate their roles in the development of osteoarthritis.
View Article and Find Full Text PDFACS Biomater Sci Eng
January 2025
Chair and Department of Biochemistry and Biotechnology, Medical University of Lublin, Chodzki 1 Street, 20-093 Lublin, Poland.
The aim of this work is to provide a comprehensive set of biological tests to assess the biomedical potential of novel osteochondral scaffolds with methods proposed to comply with the 3Rs principle, focusing here on a biphasic Curdlan-based osteochondral scaffold as a promising model biomaterial. experiments include the evaluation of cytotoxicity, mutagenicity, and genotoxicity referring to ISO standards, the assessment of the viability and proliferation of human chondrocytes and osteoblasts, and the estimation of inflammation after direct contact of biomaterials with human macrophages. experiments include assessments of the response of the surrounding osteochondral tissue after incubation with the implanted biomaterial.
View Article and Find Full Text PDFDev Biol
January 2025
The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, 3052, Australia; Department of Medical Biology, The University of Melbourne, Parkville, Victoria, 3052, Australia. Electronic address:
The MYST family histone acetyltransferase gene, KAT6B (MYST4, MORF, QKF) is mutated in two distinct human congenital disorders characterised by intellectual disability, facial dysmorphogenesis and skeletal abnormalities; Say-Barber-Biesecker-Young-Simpson variant of Ohdo syndrome and Genitopatellar syndrome. Despite its requirement in normal skeletal development, the cellular and transcriptional effects of KAT6B in skeletogenesis have not been thoroughly studied. Here, we show that germline deletion of the Kat6b gene in mice causes premature ossification in vivo, resulting in shortened craniofacial elements and increased bone density, as well as shortened tibias with an expanded pre-hypertrophic layer, as compared to wild type controls.
View Article and Find Full Text PDFInt J Nanomedicine
January 2025
School of Pharmacy, Changzhou University, Changzhou, People's Republic of China.
Introduction: Osteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage degeneration. Chondrocyte inflammation, apoptosis, and extracellular matrix degradation accelerated OA progression. MicroRNA (miRNA) has the potential to be a therapeutic method for osteoarthritis.
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