Researcher(s)
- Akanksha Katoch, Economics, University of Delaware
Faculty Mentor(s)
- Xin Lucas Lu, Mechanical Engineering, University of Delaware
Abstract
Introduction: Osteoarthritis (OA) is a whole-joint disease characterized by the breakdown of articular cartilage and changes in surrounding joint tissues, including the synovium. Current treatments are limited to symptom management rather than slowing or preventing cartilage degeneration. Glycosaminoglycans (GAGs) and collagen are major components of the cartilage extracellular matrix, and their synthesis is important for maintaining cartilage. The synovium can release inflammatory cytokines and other soluble factors that may negatively affect cartilage and contribute to OA progression. This study investigated how human OA synovium and factors released by the synovium affect GAG and collagen synthesis in human OA cartilage.
Methods: Human OA cartilage and synovial tissue were obtained from surgical waste following total knee replacement surgeries. Cartilage explants were cultured for four days either alone or in direct co-cultured with synovial tissue to evaluate GAG synthesis, or with synovium-conditioned medium to evaluate collagen synthesis. GAG and collagen synthesis were measured using a click chemistry-based technique. Metformin (10 or 100 μM) was also evaluated in the co-culture model to determine whether it could alter the effect of synovium on GAG synthesis.
Results: Direct co-culture with synovial tissue significantly decreased GAG synthesis compared with cartilage cultured alone. Synovium-conditioned medium significantly decreased collagen synthesis, suggesting that factors released by the synovium can affect cartilage matrix synthesis. Metformin treatment did not significantly affect GAG synthesis in the co-culture model.
Significance: These findings suggest that human OA synovium can negatively affect cartilage matrix synthesis and that soluble factors released by the synovium may contribute to this response. Understanding how the synovium affects cartilage may help identify mechanisms involved in OA and potential targets for future treatments.