Platelet-rich plasma (PRP) is a fairly new treatment tool for a variety of musculoskeletal problems. Platelets taken from the person’s own blood are injected into the damaged or injured area. Special growth factors always present in platelets are released and stimulate tissue healing.
In this study, scientists from the Netherlands take a look at the mechanism behind this healing process and see if it could be used for osteoarthritic joints. The study was conducted in a laboratory setting. They used human chondrocytes (joint cartilage cells) from older donor adults.
By working at the cellular level of investigation, they were able to see two things: 1) the cascade of events that occurs when a cartilage cell is exposed to platelet-rich plasma (PRP) and 2) the effect PRP has on joint cartilage cells.
The authors admit this is what happens in a sterile lab and may not mimic exactly what happens in the human body. But it is a place to start with the hope of finding better ways to stop the arthritic degenerative process in our joints as we age.
Here are a few things we already know about the inflammatory cycle that results in osteoarthritic changes in human joints. There are inflammatory factors that start the destructive process in the joints. For example, interleukin (IL)-1 beta is probably one of the most powerful of these inflammatory factors. It is part of a group of cells called cytokines.
This particular cytokine inhibits (stops or prevents) the formation of new, healthy cells. At the same time, IL-1 beta produces proteases. Proteases are enzymes that break down proteins. In the case of osteoarthritis, proteases contribute to the destructive process.
That sounds fairly simple and straightforward but the truth is that IL-1 beta has quite a few different ways to act in the body. These different pathways are called signaling cascades. A signaling cascade is exactly like a line of dominoes. When the first tile is pushed, it sets off a sequence of events that don’t stop until the last domino is down. It’s the same thing with a signaling cascade. When the first signal starts, every step in the reaction or process takes place until the final one.
One of the signaling cascades that has been identified in osteoarthritic destruction is the activation of a protein called Nuclear Factor kappa B or NFkB. This protein moves into the cell nucleus (center) and starts signaling (talking) with various regulatory genes. These regulatory genes decide when cells die (a process called apoptosis), when inflammatory cells are activated, and when other immune responses are initiated. NFkB actually regulates at least 150 genes, some of which are directly involved with inflammation and immune function.
Now, how does platelet-rich plasma (PRP) figure in here? PRP counteracts the effects of IL-1 beta on genes that are responsible for the building up of collagen and breakdown of cartilage cells. In this laboratory study, they took a look at the effect of PRP in this setting. They found that PRP actually reduced several different effects of the IL-1 beta. In particular, PRP was able to counteract the effects of NFkB on genes responsible for chondrocyte (cartilage cell) destruction.
How does this study help the average person with joint osteoarthritis? It doesn’t quite yet. But it is an important step in understanding the processes by which joint destruction occurs. If scientists can identify specific mechanisms at the cellular level that lead to chondrocyte destruction AND turn those signals off (either by interrupting the domino cascade once it starts or stopping the first domino from tipping), then we may have some clinical applications.
This study shows that PRP has antiinflammatory abilities. Although there are many different pathways leading to joint destruction, at least one has to do with gene expression that either builds up or tears down the matrix (cells that group together) forming joint cartilage. At least in a petri dish in the lab, IL-1 beta can be stopped by PRP. The end result is protection of the chondrocytes in the same dish.
The authors of this study say this is just one step of many needed to fully investigate the use of PRP for joint osteoarthritis. With so much variation in chondrocytes from person to person, with so many potential signaling pathways, and many different ways to prepare the platelet-rich plasma, there is a need for further concentrated study in this area. The authors conclude if an effective, self-induced, low-cost treatment can be found from these studies, then it will be time and money well spent.