Osteoarthritis is a degenerative bone disease that occurs commonly in the older demographic. Cartilage that usually lines the joints of our bones are under constant stress throughout our lives, and when we reach more advanced ages, this cartilage thins or dissolves completely. This creates an environment where bone on bone friction of the joints leads to debilitating bone pain and inflammation, with no effective cure for the condition. However, new research involving mouse studies have found that maintaining the supply of a certain molecule helps nourish cartilage, and in effect, prevent osteoarthritis development.
The molecule in question is called adenosine, and it has been found to play a role in making and sustaining cartilage in the body. More specifically, it is involved in maintaining a steady number of healthy chondrocytes that are involved in cartilage development. The molecule is derived from adenosine triphosphate (ATP), which is known for being the main energy component of cells. It is only now that researchers have linked decreases in adenosine to osteoarthritis despite knowing that diminished ATP production, and subsequently lower adenosine levels in chondrocytes, is a feature of both inflammation and aging.
Researchers started their experiment by maintaining an adenosine level in rats that reflected the level seen with osteoarthritis in humans, and amazingly enough, it prevented the disease from developing. If these results hold true in human studies, it could mean that adenosine replacement therapy can help delay the disease or even the need for joint replacement.
“We found that if adenosine levels decrease, or if the capacity to respond to adenosine diminishes, cartilage starts to degenerate. Our study suggests that diminished ATP and adenosine production are likely contributing factors to the development of osteoarthritis in aging individuals,” says study senior investigator Bruce Cronstein.
Looking a little deeper into why osteoarthritis develops led researchers to find that, not only is there a reduction in the number of cartilage producing cells, but there were also lower levels of adenosine receptors found on the surface of chondrocytes designed to receive and pass on adenosine’s signals. The researchers tested this theory by observing mice lacking this particular receptor, finding that those without out it did not move as easily compared to mice found to have the receptor. Further studies exploring this relationship led researchers to find that when giving excess adenosine, it prevented osteoarthritis in the animals tested.
This discovery may be implemented in future osteoarthritis therapies, the researchers hope. It would prevent or delay the need for joint replacement for millions of patients each year.