Doctors used to think that osteoarthritis went hand in hand with aging; that all joints wear out like an old car. Over the years though, the medical community began to realize that not everyone got osteoarthritis (OA), and for those who do, not all joints are affected equally.
Joints are a living, biologically active tissue that changes over time; joints can also repair minor damage. After a serious injury, though, aging joints lose their ability to repair themselves and set off on a one-way trip to OA, damage that reaches every joint tissue including bone.
“One of the problems with osteoarthritis is that joints don’t do a good job at repairing damaged tissue and aging seems to play a role in that,” says Richard Loeser, MD, an arthritis researcher at Wake Forest University in Winston Salem, N.C.
Dr. Loeser and his colleagues are studying joint biology to figure out how aging makes joints more susceptible to disease. He also wants to know why cartilage doesn’t repair itself well after an injury.
Clues in Cartilage Damage
In one of Dr. Loeser’s projects, the team is studying oxidative damage to chondrocytes (cartilage cells). The damage comes from very small molecules that contain oxygen. These molecules, which are called reactive oxygen species, are formed as a byproduct of chemical reactions that occur when, for example cells metabolize nutrients. Oxidative byproducts can damage many tissues over time, in the joint, the brain, heart, and skin. That’s why many healthy foods and supplements are labeled as “anti-oxidants,” because they can potentially neutralize these harmful molecules.
Dr. Loeser’s group has figured out those reactive oxygen molecules in joint tissues increase with aging. Now they want to learn how chondrocytes react to such damaging molecules and craft a plan to foil any harm.
“Just using anti-oxidants to block reactive oxygen species hasn’t been very effective in the treatment of age related diseases so we need to know more specifically what reactive oxygen species are doing rather than trying to block them more generally,” says Dr. Loeser.
The answer can be found in the biology of joint tissue. Chondrocytes constantly need to churn out matrix, the sticky gel that gives cartilage bounce and keeps the joint healthy. Arthritis develops because chondrocytes can’t make enough matrix to keep pace with what’s broken down. Dr. Loeser’s research shows that lots of oxygen byproducts block the pathways that stimulate matrix synthesis.
“Right now we’re trying to determine the exact points in those pathways where matrix synthesis and degradation happens; that would represent new targets for therapy,” comments Dr. Loeser.
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