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The Effect of Electrical Fields on Gene and Protein Expression in Human Osteoarthritic Cartilage Explants

¹ McKay Laboratory of Orthopaedic Surgery Research, University of Pennsylvania School of Medicine, 424 Stemmler Hall, Philadelphia, PA 19104-6081. E-mail address for C.T. Brighton: ctb{at}mail.med.upenn.edu
Investigation performed at the McKay Laboratory of Orthopaedic Surgery Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Disclosure: In support of their research for or preparation of this work, one or more of the authors received, in any one year, outside funding or grants in excess of $10,000 from BioniCare Medical Technologies. In addition, one or more of the authors or a member of his or her immediate family received, in any one year, payments or other benefits in excess of $10,000 or a commitment or agreement to provide such benefits from a commercial entity (BioniCare Medical Technologies).

Methods: Full-thickness articular cartilage explants from osteoarthritic adult human knee joints were cultured in the absence or presence of interleukin-1β (IL-1β) and in the absence or presence of a specifically defined capacitively coupled electrical signal for seven or fourteen days. Total collagen and proteoglycan production were assessed by means of hydroxyproline and hexosamine analyses, respectively. Quantitative real-time polymerase chain reaction assays were used to measure mRNA expression levels of aggrecan, type-II collagen, collagenase-1 (MMP-1), collagenase-3 (MMP-13), stromelysin-1 (MMP-3), aggrecanase-1 (ADAM-TS4), and aggrecanase-2 (ADAM-TS5).

Results: Electrical stimulation of cultured explants for seven or fourteen days resulted in significant increases (p < 0.007) in proteoglycan and collagen production and a highly significant upregulation (p 0.005) of aggrecan and type-II collagen mRNA expression. This occurred even in the presence of IL-1β. In the absence of IL-1β, the expression of metalloproteinases was at barely detectable levels in these explants. Treatment with IL-1β led to the significant upregulation of metalloproteinase expression (p < 0.03), but simultaneous administration of the capacitively coupled electrical signal dramatically inhibited this stimulation.

Conclusions: The data show that, even in the presence of IL-1β, a specific, defined capacitively coupled electrical signal can result in significant upregulation of cartilage matrix protein expression and production while simultaneously significantly attenuating the upregulation of metalloproteinase expression. These results support the contention that delivery of a specific, defined electrical field to articular cartilage could result in matrix preservation.

Clinical Relevance: Osteoarthritis ultimately results in the progressive destruction of articular cartilage through mechanisms involving metalloproteinase activity. The use of electrical stimulation to both increase matrix production and diminish matrix destruction has the promising potential to treat osteoarthritic patients in a noninvasive manner.

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