Osteoarthritis is a devastating and extremely common disease. It can be caused by aging, heredity and injury from trauma or disease. About 46 million people in the U.S. (and more than half of all people older than 75) have some form of arthritis, which costs this country about $128 billion a year in treatments, rehabilitation, and lost productivity, according to the U.S. Centers for Disease Control.
Osteoarthritis is a devastating and extremely common disease. It can be caused by aging, heredity and injury from trauma or disease. About 46 million people in the U.S. (and more than half of all people older than 75) have some form of arthritis, which costs this country about $128 billion a year in treatments, rehabilitation, and lost productivity, according to the U.S. Centers for Disease Control.
There is no successful treatment for osteoarthritis, but an intriguing talk we saw at TedMed 2011 made a connection between this disease and telomeres, the “caps” on the end of chromosomes that play a strong role in aging.
As part of Popper and Co.’s efforts to bring you the latest in health care innovation, strategy and business development, we are highlighting new research that shows that telomere shortening associated with aging can not only be influenced by stress and psychological states of mind, but also may accelerate the development of osteoarthritis.
A recent paper reported that in cartilage cells (chondrocytes) of patients with osteoarthritis, telomere lengths were shortened much more than patients without the disease. In this study, a Danish research team used a newly developed universal single telomere length assay that measures telomere lengths. The team found that telomeres were much shorter in cells that were nearer to the damaged areas of the joint. In addition, higher numbers of shortened telomeres were found in more severe cases.
This study is remarkable because it is one of the first studies of telomeres in human patients, and because it made use of a new assay technology that could more precisely measure telomere length and relate it to disease progression. Other papers have made connections between osteoarthritis, oxidative stress and telomere length.
All of this points to new therapeutic possibilities for osteoarthritis. Could reversing telomere shortening halt osteoarthritis? Or is it already too late when you see telomere shortening? How could we control oxidative stress on chondrocytes to prevent or slow the progression of osteoarthritis? Do you see this as having therapeutic promise for the life sciences industry? Let us know what you think.