Most of us think that bones are inert; that they just sit in our skeleton, holding our bodies up.
But new research from RCSI’s Department of Anatomy and Regenerative Medicine shows that bones have much more personality than that, and that when they are injured, they can even be a negative influence on the cartilage in our joints.
The study, published in the International Journal of Molecular Science, opens up a new understanding of how bone tissue communicates with cartilage, a protective cushioning layer in the joints where bones meet. The researchers discovered that signals from bone cells may have a role in the development of painful and debilitating conditions such as osteoarthritis following injury.
This conversation between bone and cartilage is of particular interest following an injury such as ligament injury in the knee joint (such as ACL rupture, which is common in athletes). This trauma - even if it is successfully treated surgically - can still lead to osteoarthritis. By understanding how the bone reacts to such an injury, new therapies can be developed to slow down or even prevent osteoarthritis from developing.
To examine the communication between bone and cartilage cells, the researchers built a bioreactor system in the lab that allowed them to carefully examine these specific interactions. Using bone and cartilage cells, they exposed the isolated cells to the kinds of mechanical conditions that mimic either the healthy skeletal condition or the scenario that occurs during an injury.
To simulate the injury the researchers varied the way fluid flowed over the bone cells, because in the body fluid-based shear stress is a cue that can ‘tell’ bone cells about their environment, and any damage that may have occurred.
By examining what the cells produced in response to these fluid stresses, the researchers worked out that bone cells called osteoblasts can send out biochemical signals that can negatively affect nearby cartilage cells called chondrocytes.
When the bone cells were under ‘normal’ stress, their signals encouraged the cartilage cells to remain healthy. However at high levels of shear stress, such as might be experienced in response to injury, the signals sent from the bone cells damaged the chondrocytes.
The research team will now build on this understand to delve deeper into the role of what they call bone-cartilage crosstalk in osteoarthritis, particularly after a traumatic injury in a joint.
The research was carried out at RCSI, Trinity College Dublin and AMBER, the SFI Research Centre for Advanced Materials and BioEngineering Research. It was funded through the RCSI StaR programme and the Science Foundation Ireland Career Development Award (CDA) programme.
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