Stem Cells

P181 - Chondroprotective effect of Durolane hyaluronic acid and conditioned medium of stem cells in an in vitro model of knee osteoarthritis



To investigate and compare the chondroprotective effect of therapies with non-animal stabilized hyaluronic acid (NASHA; Durolane) and mesenchymal stem cell conditioned culture medium (MSC-CM) in the treatment of knee OA in an in vitro model.

Methods and Materials

The joint tissue from the femoral condyles and the synovial capsule was recovered from seven patients undergoing total knee replacement. A cocultivation system was developed for the explants obtained from each patient. Four experimental groups were generated: control (basal medium), interleukin-1β (IL-1β; basal medium + IL-1β), NASHA (medium with NASHA + IL-1β) and MSC-CM (medium with MSC-CM + IL-1β). Total RNA was obtained from cartilage and synovium at 0, 48 and 72 hours to perform gene expression analysis. Glycosaminoglycans (GAG) and nitric oxide were quantified in the supernatant culture medium.


A decrease in the release of GAG was found in the explants enriched with NASHA and MSC-CM at 48 (p <0.05) and 72 h (p <0.01). Nitric oxide production was significantly lower only in the group treated with MSC-CM at 72 h (p <0.05). In cartilage, the expression of IL-1β was significantly reduced by MSC-CM at 72 h (p <0.05); both the NASHA and the MSC-CM significantly decreased the expression of ADAMTS5 and MMP13 at 72 h (p <0.05). In the synovial membrane, a decrease in the expression of IL-1β was found in the NASHA and MSC-CM groups. The expression of ADAMTS5 and MMP13 significantly decrease at 72 h (p <0.05) in the CMM group only. Both treatments increased the expression of TIMP-1 in cartilage and synovium (p <0.05).

il-1beta - cartilage.jpgil-1beta - synovial.jpg


Treatments with NASHA and MSC-CM may help to counteract the catabolism produced by the inflammatory state in knee OA. However, the mediators produced by the MSC promote a higher chondroprotective effect by inducing lower expression levels of inflammatory markers in our model.