Background: Articular cartilage is closely related to epiphyseal growth plate cartilage with one major discriminant: while epiphyseal growth plate cartilage is transformed into bone by endochondral ossification, epiphyseal growth plate cartilage remains stable in a healthy situation. In contrast in diseases like osteoarthritis articular cartilage acquires characteristics of epiphyseal growth plate cartilage. The underlying molecular pathophysiology is largely unknown.
Objective and hypotheses: It is our aim to elucidate the molecular mechanisms responsible for the transformation of an healthy articular chondrocyte into a diseased epiphyseal growth plate like chondrocyte. Understanding these mechanisms may lead to highly needed biomarkers to assess joint homeostasis as well as protocols for the derivation of articular chondrocytes from mesenchymal stromal cells (MSCs) to engineer articular cartilage for therapeutic purposes.
Method: In our studies we combine state of the art molecular and cellular biological techniques with advanced chemistry to develop methods for assessing joint homeostasis and injectable MSC based strategies to repair the damaged articular cartilage surface in osteoarthritis.
Results: We have identified WNT and BMP signalling as driving forces in transformation of a healthy articular chondrocyte into a diseased chondrocyte with potential to serve as biomarkers. In addition we have developed strategies to derive stable articular cartilage like chondrocytes from MSCs in vitro.
Conclusion: Increased understanding of the molecular pathways that differentiate the two types of hyaline cartilage, i.e. articular cartilage versus growth plate cartilage has provided new cues that can help in assessing osteoarthritis much earlier in the disease process which can be exploited to develop highly needed causal treatment.