David Burris, Ph.D., an assistant professor in the Mechanical Engineering Department at the University of Delaware, has found some answers to the question, “Why doesn’t cartilage deflate over the course of days, months or years?”
Working from the idea that the cartilage was able to reabsorb the fluid that leaks out when we’re stationary, Dr. Burris hypothesized that the reabsorption process was driven by hydrodynamic pressurization. As indicated in the October 12, 2015 news release, the researchers “placed oversized cartilage samples against a glass flat to ensure the presence of the necessary wedge. They found that at slow sliding speeds cartilage thinning and an increase in friction occurred over time, but as the sliding speed increased toward typical walking speeds, the effect was reversed.”
Dr. Burris told OTW, “From biphasic modeling, we know that cartilage loses fluid during loading over time, but in vivo measurements show that although this is true in static conditions, articulation actually drives fluid back into the tissue. The community has not understood this mechanism and given the importance of the fluid in the tissue for mechanical and biological function, we felt this was an absolutely critical scientific question to answer. To date the only hypotheses have been that migration limits time in contact and articulation exposes the contact to the bath, which enable it to imbibe fluid to recover. We were shocked to find the same recovery mechanism others observe in the natural joint in a contact that did not involve migration and bath exposure. The results suggest that hydrodynamic pressure develops during articulation, but instead of creating fluid films as described in biomechanics textbooks, these external pressures combat the exudation process associated with interstitial pressurization. We believe this ‘tribological rehydration’ mechanism is critical for sustaining joint function and health and can be leveraged to provide unprecedented control in cartilage studies while maintaining physiological fluid pressures.”
Asked what orthopedic surgeons should know about this work, Dr. Burris commented, “First, the results contradict the conventional wisdom that articulation causes wear. The mechanism we propose based on our results suggest that the mechanical intensity felt by the solid is far less when active than when inactive. It suggests that obesity, inactivity, and low amplitude oscillations are more damaging mechanically than normal activity. In other words, we expect recommendations of 10, 000 steps per day to also benefit joint health (in addition to cardiovascular, etc.).”
“Second, most textbooks focus on lubrication during articulation and suggest that fluid films are responsible for exceptionally low friction and wear. The problem with this mental model is that it fails to address how our joints deal with static conditions in which there are no fluid films. This is critical since our joints are static ~95% of the time. Our research suggests that the joint excels because it is designed specifically to address inactivity. Cartilage acts as a buffer to the inevitable ‘crash landing’ when motion stops. The extremely slow exudation process ensures negligible losses of lubrication over ~1 hour of inactivity. When activity resumes, this buffer is quickly refilled to prepare cartilage for the next crash landing. Joint replacement devices do not possess such a buffer and therefore experience the full brunt of the crash landing, poor lubrication, surface damage, wear, and the biological consequences thereof. If we want reliable joint replacement devices, we must stop striving to create fluid films during articulation at all cost and start focusing on mitigating stresses and damage during long periods of static loading; we need to leverage the interstitial lubrication that nature exploits so effectively.”
