Abstract
Animal experimental studies indicate that pulsed low-intensity ultrasound might enhance cartilage repair in early stages of osteoarthritis (OA) and to improve healing of osteochondral defects. The purpose of this in vitro study was to determine systematically whether and to what extent pulsed low-intensity ultrasound
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influences the synthesis and release of PGs,
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modulates chondrocyte viability within human osteoarthritic cartilage explants, and
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is affected by the degree of OA alterations.
Full-thickness cartilage explants of the lateral compartment of the proximal tibia were taken from OA patients undergoing knee replacement surgery. Explants with mild or moderate OA alterations were cultured in a CO2-incubator at 37°C, 5% CO2 and 95% relative humidity. After 2 days, explants were subjected to ultrasound applied in a pulsed-wave form (1: 4) on the following 3 days. The ultrasound application apparatus was specifically designed and constructed to function within an explant culture system under sterile conditions. The effect of the ultrasound parameters intensity (2, 30, 120, 250 mW/cm2), duration (20, 3 × 30 minutes/day) and frequency (0.5, 1.2, 4.7 MHz) on PG synthesis and release were measured. PG synthesis was determined by the incorporation of 35SO4 during the final 22 h of the experiments whereas the content of PGs were quantitated with the DMMB-assay. The viability of chondrocytes was assessed microscopically using fluorescein diacetate and propidium iodide. Results were compared to untreated explants from the same joint. Each experimental condition was repeated five times using explants always obtained frrom 6 different patients (N=6).
Neither the degree of OA alterations of explants, nor the various ultrasound parameters tested displayed any significant effect on the synthesis and release of PGs as well as on the viability of explants.
This work was supported by the Deutsche Arthrose-Hilfe e.V.
Correspondence should be addressed to EORS Secretariat Mag. Gerlinde M. Jahn, c/o Vienna Medical Academy, Alserstrasse 4, 1090 Vienna, Austria. Fax: +43-1-4078274. Email: eors@medacad.org
