Maintaining sufficient levels of adenosine, a biochemical involved in human cellular function, may prevent the onset of osteoarthritis, as reported by researchers at NYU Langone Medical Center working with rodent models. According to the authors, if similar results can be replicated in humans, adenosine replacement therapy could become an additional therapeutic tool in delaying osteoarthritis development and the need for joint replacement procedures. Adenosine is derived from adenosine triphosphate (ATP), the production of which is known to decrease with aging and inflammation. Senior investigator Bruce Cronstein, MD, commented, “Our study suggests that diminished ATP and adenosine production are likely contributing factors to the development of osteoarthritis in aging individuals.” The findings were published online last week in Nature Communications.
In the study, rats with damage to the anterior cruciate ligament (ACL), a condition known to induce osteoarthritis in humans, were administered adenosine packaged in lipid bubbles into the ACL injuries. The treated rodents did not develop osteoarthritis. The relationship appears to be driven by the role of adenosine in maintaining healthy chondrocytes, the cells that sustain cartilage. The population of these cells is adversely affected both by reduced adenosine levels and lower levels of the A2A adenosine receptor whose function is to pass on the adenosine signal. Rats with osteoarthritis were found to have higher levels of A2A receptors on their chondrocytes, which the team interprets as a “failed attempt” to compensate for loss of adenosine. Commenting on the potential of adenosine replacement therapy to forestall joint replacement surgeries, Dr. Cronstein noted, “Because joints may have to be replaced again and again, if we can put off the need for joint replacement until later in life, odds are that patients will only have to have this done once.”
Read more about the findings.
The journal article may be read here.
Posted on May 16, 2017