Cartilage chondroprotection and repair with pulsed electromagnetic fields: I-ONE therapy

Ruggero Cadossi, Stefania Setti () and Milena Fini
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Ruggero Cadossi: IGEA SpA, Clinical Biophysics
Stefania Setti: IGEA SpA, Clinical Biophysics
Milena Fini: Research Institute Codivilla-Putti, Rizzoli Orthopaedic Institute

Environment Systems and Decisions, 2011, vol. 31, issue 2, 149-154

Abstract: Abstract Articular cartilage is a complex tissue characterised by chondrocytes that are embedded within an organised dense extracellular matrix of collagen and proteoglycan. Under physiologic condition, articular metabolism is slow, but under pathological condition turnover can increase and the matrix undergoes faster mechanical failure and deterioration, resulting in cartilage degeneration. Moreover, modest damage of the articular cartilage, resulting from trauma or less invasive surgical procedure, produces an inflammatory reaction of the joint cartilage, which can cause irreversible degeneration through the increase in catabolic cytokines synthesis and the decrease in anabolic activity of chondrocytes. Pro-inflammatory cytokines increase the synthesis of matrix-degrading enzymes and limit the production of proteoglycans. It is known that physical stimuli modulate cartilage metabolism. In particular, pulsed electromagnetic fields (I-ONE therapy, Igea, Carpi, Italy) allow to treat homogenously the whole cartilage surface and thickness and the underlying subchondral bone. In vitro I-ONE therapy increases the binding between adenosine and A2A adenosine receptor on human neutrophils cell membrane, on bovine chondrocytes and on fibroblast-like synoviocytes. It has been shown that drugs with A2A adenosine receptor agonist activity prevent articular cartilage degeneration in animals. We hypothesised that the adenosine agonist effect of I-ONE therapy can also prevent cartilage degeneration. In a recent study, De Mattei et al. demonstrated how I-ONE therapy can strongly inhibit the release of PGE2 in bovine synovial fibroblasts exerting an anti-apoptotic effect on cells. Ex vitro, in bovine full thickness articular cartilage explants, I-ONE therapy induces the largest increase in proteoglycan synthesis and in IGF-1 synthesis, when cartilage is exposed to specific parameters of pulsed electromagnetic fields. These effective parameters were subsequently used in in vivo experiments. The effect of I-ONE therapy was investigated on Dunkin Hartley osteoarthritic knee by Mankin score and by histomorphometric and densitometric analysis; I-ONE therapy prevented cartilage degeneration and subchondral bone sclerosis. Osteochondral grafts were performed in the knees of sheep; I-ONE therapy favoured osteochondral grafts integration and prevented cyst-like resorption area formation, which can compromise the stability of graft and the success of the technique. To support the in vitro results, biochemical analyses of the synovial fluid were also performed in this animal model. The amount of inflammatory catabolic cytokines (IL-1β and TNF-α) in the synovial fluid of I-ONE treated animals was significantly lower than in control animals. On the contrary, TGF-β1 was significantly higher in stimulated animals than it was in controls. These results demonstrate not only the capability of I-ONE therapy to control the inflammatory reaction but also its capability to favour cartilage anabolic activity. These results provide the rational to design clinical studies to demonstrate the possibility to transfer the treatment to humans. Two randomised, prospective, double-blind clinical studies (Level I), one conducted to patients treated by arthroscopy with condroabrasion and/or perforations at the knee and the other after anterior cruciate ligament reconstruction, demonstrated that biophysical stimulation with I-ONE therapy leads to complete patient’s recovery in a significantly shorter time (P

Keywords: Chondroprotection; I-ONE therapy; Inflammation; Cartilage repair; Pulsed electromagnetic field (search for similar items in EconPapers)
Date: 2011
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DOI: 10.1007/s10669-011-9310-4

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