Combating Wear and Tear on Our Collagen – University of Utah – Mar-2017
This article explains much of what causes our pain from EDS. With our defective collagen, even small stresses can cause “sub-failure damage” which accumulates until the tissue fails completely.
University of Utah bioengineers detect early signs of damage in connective tissues such as ligaments, tendons and cartilage
By the time someone realizes they damaged a ligament, tendon or cartilage from too much exercise or other types of physical activity, it’s too late. The tissue is stretched and torn and the person is writhing in pain.
Damage to collagen, the main building block of all human tissue, can occur much earlier at a molecular level from too much physical stress, alerting doctors and scientists that a patient is on the path to major tissue damage and pain.
This could be especially helpful for some who want to know earlier if they are developing diseases such as arthritis or for athletes who want to know if repeated stress on their bodies is taking a toll.
“The scientific value of this is high because collagen is everywhere,” Yu says. “When we are talking about this mechanical damage, we’re talking about cartilage and tendons and even heart valves that move all the time. There are so many tissues which involve collagen that can go bad mechanically. This issue is important for understanding many injuries and diseases.”
The team’s research, funded by the National Institutes of Health, was published this week in the latest issue of Nature Communications.
Before, scientists thought collagen — which are strands of protein braided into a ropelike structure that give tissue its strength and stiffness — would just stretch or slide by each other during repeated stress. They never knew if they actually got damaged. As a result, patients who put repeated stress on their body would not know if they were on the road to something worse from tough physical activity.
But now the team discovered that the collagen molecule does in fact get unraveled at a molecular level before complete failure of the tissue occurs.
On the left, fluorescent photographs of collagen strands show increasing levels of damage revealed in tendons that are progressively stretched (from top to bottom: 7.5%, 10.5%, 13.5% elongation). The fluorescent signals match the computer simulation on the right of the damage to the collagen molecule under tension.
This type of minor damage, called “subfailure damage,” is associated with common injuries to connective tissues such as ligament and meniscus tears and various types of tendinitis such as tennis elbow and rotator cuff tendinopathy.
“Accumulation of subfailure damage can go on for a long time with no catastrophic failure, but repeated damage results in inflammation,” says Weiss, “So this vicious cycle continues, the inflammation breaks down the tissue, making it more susceptible to damage, which then can result in a massive tear.”
“A fundamental understanding of the loads and strain that cause molecular damage has eluded us until now,” says Weiss. “Our findings can translate into recommendations for athletes on how to train or what rehabilitation protocols people who are injured can use.”
This news release and photos may be downloaded from: http://unews.utah.edu