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Updated: Jun 12, 2026

Three-Dimensional Cell Culture of Adipose-Derived Stem Cells in a Hydrogel with Photobiomodulation Augmentation
Published on: April 5, 2024
Photobiomodulation outperforms ultrasound in reducing IL-1 β -driven chondrocyte inflammation
Sofia Oliveira1, Débora Ferreira, Ligia R Rodrigues
1CMEMS-UMinho, University of Minho, 4800-058 Guimarães, Portugal.
None:
Therapeutic ultrasound (US) and photobiomodulation (PBM) are promising treatment modalities for restoring articular cartilage. Owing to their different mechanisms of action, individual or combined stimulation may elicit different bioeffects on chondrocytes. This study aimed to evaluate the potential of US and PBM, applied alone or combined, in augmenting chondrocytes' responses toward cartilage matrix synthesis and reverting their catabolic activities, with or without interleukin-1β (IL-1β) incubation. Human chondrocytes were cultured under basal or proinflammatory conditions (1 ng/ml IL-1β) and stimulated daily for 6 days with US, PBM, US followed by PBM, and PBM followed by US. Chondrocyte activity, along with protein and mRNA expression of cartilage synthesis- and degradation-related markers, was analyzed. IL-1β incubation did not significantly affect chondrocytes' metabolic activity or sulfated glycosaminoglycans (GAGs) production. Both US and PBM, alone or combined, increased the protein and mRNA of collagen type II (COL II) and aggrecan (ACAN) under basal and proinflammatory conditions. PBM had a stimulatory effect on GAG synthesis. While PBM did not influence the expression of cartilage destruction markers, US potentiated the chondrocytes' response to inflammation by increasing metalloproteinases and IL-1β mRNA levels. The sequential combination of US and PBM induced distinct bioeffects depending on the application order, but these were not superior to the effects of individual treatments. As this study used chondrocytes from a single donor, generalizability may be limited. While both US and PBM stimulated matrix synthesis, PBM showed a comparatively greater ability to mitigate chondrocyte degradation and may be of interest for cartilage repair strategies.
