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PEMF osteoarthritic chondrocytes

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Clinical Interventions in Aging Dovepress open access to scientific and medical research
Open Access Full Text Article
Effects of regenerative radioelectric asymmetric conveyer treatment on human normal and osteoarthritic chondrocytes exposed to IL-1β. A biochemical and morphological study
Giulia Collodel1
Antonella Fioravanti2 Nicola Antonio Pascarelli2 Antonello Lamboglia2 Vania Fontani3
Margherita Maioli3–5
Sara Santaniello4,5 Gianfranco Pigliaru4,5 Alessandro Castagna3 Elena Moretti1
Francesca Iacoponi1 Salvatore Rinaldi3
Carlo Ventura3,5,6
1Department of Biomedical Sciences (Applied Biology), 2Department of Clinical Medicine and Immunological Sciences (Rheumatology Unit), University of Siena, Siena, Italy; 3Department of Regenerative Medicine, Rinaldi Fontani Institute, Florence, Italy; 4Department of Biomedical Sciences, University of Sassari, Sassari, Italy; 5Laboratory
of Molecular Biology and Stem Cell Engineering, National Institute of Biostructures and Biosystems, Bologna, Italy; 6Cardiovascular Department, S Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy
Correspondence: Salvatore Rinaldi Rinaldi Fontani Institute, Viale Belfiore 43, 50144 Florence, Italy Tel +39 055 290 307
Fax +39 055 290 399 Email
submit your manuscript | Dovepress
Purpose: Osteoarthritis (OA) is a degenerative disease characterized by a progressive loss of articular cartilage extracellular matrix and is due to functional impairments occurring in chondrocytes. In previous works, we highlighted that Regenerative Tissue Optimization (TO- RGN) treatment with radioelectric asymmetric conveyer (REAC) technology influenced the gene expression profiles controlling stem cell differentiation and the pluripotency of human skin-derived fibroblasts in vitro. Since interleukin-1 beta signaling has been implicated in the induction and progression of this disease (through metalloproteinase-3 synthesis and nitric oxide production), we investigated whether REAC TO-RGN might influence the biochemical and morphological changes induced by interleukin-1 beta in normal and OA chondrocytes. Methods: The induction of metalloproteinase-3 and proteoglycan synthesis was evaluated by a solid-phase enzyme-amplified sensitivity immunoassay, and nitric oxide production was evalu- ated with the Griess method. Ultrastructural features were observed by transmission electron microscopy.
Results: REAC TO-RGN treatment decreased nitric oxide and metalloproteinase-3 production in normal and OA chondrocytes, while inducing an increase in proteoglycan synthesis. OA chondrocytes were more affected by REAC TO-RGN treatment than were normal chondrocytes. Ultrastructural changes confirmed that REAC TO-RGN may counteract the negative effects of interleukin-1 beta incubation.
Conclusion: The results of this in vitro study suggest that REAC TO-RGN treatment may represent a new, promising approach for the management of OA.
Keywords: human chondrocytes ultrastructure, metalloproteinase, nitric oxide, proteoglycans, REAC TO-RGN treatment
Osteoarthritis (OA) is the most common articular disorder of hyaline cartilage and subchondral bone. The disease is responsible for substantial direct and indirect socio- economic costs.1,2 Chondrocytes are responsible for the synthesis and maintenance of extracellular matrix within articular cartilage, as they regulate the equilibrium between synthetic and degradative processes. Loss of homeostasis in favor of catabolic activities leads to the destruction of articular cartilage, and chondrocyte death has been postu- lated to be a crucial event in the pathogenesis of OA.3,4 Interleukin-1 beta (IL-1β) is a cytokine involved in the processes of cartilage degradation, also acting as a potent inhibitor of extracellular matrix synthesis. In response to IL-1β, chondrocytes secrete
Clinical Interventions in Aging 2013:8 309–316
© 2013 Collodel et al, publisher and licensee Dove Medical Press Ltd. This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

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