Tumor necrosis factor alpha (TNFα), as a key pro-inflammatory cytokine, plays a central role in joint diseases. In recent years, numerous models of TNFα-induced cartilage inflammation have been developed. However, due to the significant differences between these models and the lack of consensus in their construction, it becomes difficult to compare the results of different studies. Therefore, we summarized and compared these models based on important parameters for model construction, such as cell source, cytokine concentration, stimulation time, mechanical stimulation, and more. We attempted to analyze the advantages and disadvantages of each model and provide a compilation of the analytical methods used in previous studies. Currently, TNFα chondrocyte inflammation models can be categorized into four main types: monolayer-based, construct-based, explant-based TNFα chondrocyte inflammation models, and miscellaneous TNFα chondrocyte inflammation models. The most commonly used models were the monolayer-based TNFα chondrocyte inflammation models (42.86% of cases), with 10 ng/mL TNFα being the most frequently used concentration. The most frequently used chondrocyte cell passage is passage 1 (50%). Human tissues were most frequently used in experiments (51.43%). Only five articles included models with mechanical stimulations. We observed variations in design conditions between different models. This systematic review provides the essential experimental characteristics of the available chondrocyte inflammation models with TNFα, and it provides a platform for better comparison between existing and new studies in this field. It is essential to perform further experiments to standardize each model and to find the most appropriate experimental parameters.
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http://dx.doi.org/10.3390/ijms251910805 | DOI Listing |
Sci 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 PDFArthrosc Sports Med Rehabil
December 2024
Department of Orthopedic Surgery, Sports Medicine & Shoulder Surgery, University of California, San Francisco, San Francisco, California, U.S.A.
Purpose: To evaluate the relationship between preoperative whole-joint imaging evaluation of the knee with patient-reported outcome (PRO) measures after cartilage restoration surgery (mosaicplasty, osteochondral allograft transplantation, matrix autologous chondrocyte implantation).
Methods: We retrospectively evaluated patients who underwent knee articular cartilage restoration at our institution from 2014 to 2020. The patients' knee magnetic resonance imaging (MRI) was evaluated with the Whole-Organ Magnetic Resonance Imaging Score (WORMS) and semiquantitative synovial inflammation imaging biomarkers of the preoperative MRI.
Nutrients
December 2024
Department of Biochemistry, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807378, Taiwan.
Background: Osteoarthritis (OA) is a chronic condition characterized by joint pain and disability, driven by excessive oxidative stress and inflammatory cytokine production in chondrocytes, resulting in cell death and cartilage matrix breakdown. Our previous study showed that in monosodium iodoacetate (MIA)-induced OA rats, oral administration of heat-killed subsp. 557 (LDL557) could significantly decrease OA progression.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Faculty of Pharmacy, "Carol Davila" University of Medicine and Pharmacy, Traian Vuia 6, 020956 Bucharest, Romania.
Osteoarthritis (OA) is a degenerative joint disease characterized by the breakdown of cartilage and the subsequent inflammation of joint tissues, leading to pain and reduced mobility. Despite advancements in symptomatic treatments, disease-modifying therapies for OA remain limited. This narrative review examines the dual role of autophagy in OA, emphasizing its protective functions during the early stages and its potential to contribute to cartilage degeneration in later stages.
View Article and Find Full Text PDFBiomolecules
December 2024
Department of Orthopaedic Surgery, Kanazawa Medical University, Daigaku 1-1, Uchinada-machi, Kahoku-gun 920-0293, Japan.
Inflammation and oxidative stress are crucial for osteoarthritis (OA) pathogenesis. Despite the potential of pharmacological pretreatment of chondrocytes in preventing OA, its efficacy in preventing the progression of cartilage damage and promoting its recovery has not been examined. In this study, an HO-induced human OA-like chondrocyte cell model was created using H1467 primary human chondrocytes to evaluate the efficacy of interleukin (IL)-6 and cyclooxygenase (COX)-2 inhibitors (tocilizumab and celecoxib, respectively) in the prevention and treatment of cartilage damage.
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