MCL Injuries: Why Kevin Durant Will Be Back

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Kevin Durant reportedly just tore his medial collateral ligament. In the old days he would have been put in a cast and told to wait six weeks for healing—which would have occurred with stiff scar tissue. Here is why, with today’s techniques, he can be fully back to action sooner than you might think. 

The medial collateral ligament (MCL) extends from the thigh bone to the shin bone on the inside of the knee. It stops the joint from opening like a book, yet permits enough freedom for the joint to both bend and extend fully. How? 

The ligament has two major components: a set of deep fibers and a shallower band. These tissues are made up of cross-linked collagen. This collagen has the ability to stretch slightly without breaking, fold without ripping off the bone, and rotate as the knee itself bends and rotates through its full range of motion.   

This fibrous collagen structure, however, is not inert. The fibers are interspersed with cells that have mechanoreceptors: pressure gauges and chemical sensors.  When the cells are stimulated by the compression or stretching associated with various movements, they send signals to the brain and release growth factors.  Thus, the dynamic cellular and fibrous structure of the MCL updates itself with every slight motion of the knee. 

When the MCL is stretched by a misplaced foot—or by another player crashing into it—a physiologic general alarm is issued, unleashing a cascade of responses.   

If the stretch is slight, no tearing of fibers occurs. Still, pain is sensed by the overstimulation of the cells and by the nerve endings in the tissue. A call for a small amount of growth factors goes out. Cells release recruiting factors, blood vessels leak a little fluid, and a tiny amount of swelling occurs. The swollen area is filled with enzymes that remodel any injured fibers and with anabolic factors that (if necessary) stimulate repair of the stretched fibers. 

If the stretch is moderate, but not complete, a greater call to action is released. There is more pain and responsive swelling, and a more robust collagen formation and a stronger healing response are initiated. 

If the stretch is so extreme that the ligament ruptures, a blood clot forms at the broken ends of the vessels and tissues. The joint remains unstable until natural healing forms new fibers across the gap or a surgeon sews the ends together. 

Fortunately, the medial collateral ligament has a great blood supply. Unlike the anterior cruciate ligament (ACL) in the middle of the knee, the MCL can usually heal on its own. Today, given the availability of stem cells from various sources, we can accelerate the healing by injecting these cells and their potent growth factors to the injured tissues. These work by recruiting more cells, by stimulating cells to lie down new collagen, and by reducing scarring and inflammation.  Amniotic tissues have two to fifty times the growth factors found in normal circulating blood and are currently the most powerful tool we have to return torn tissues to their healed status.   

Even more exciting, recent data suggests that the addition of amniotic tissue to torn ligaments may drive them to heal with the normal concentration of small and large diameter fibers. This is a big improvement over the usual stiff scar tissue, which has only large diameter fibers. 

These healing MCL bands can then be exposed to careful motion that stimulates, but does not further stretch, the tissue. This, along with soft tissue manipulation by qualified physical therapists, stimulates the mechanoreceptors on the cells to lay down additional collagen—which promotes faster, stronger healing. 

So, for Kevin Durant’s knee—and for yours, if it’s injured—there are now phenomenally potent tools to drive healing to a full, faster than ever recovery. You just have to use them.

Posted by Kevin R. Stone, M.D on March 12th, 2017
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Kevin R. Stone · Jonathan R. Pelsis · Scott T. Surrette · Ann W. Walgenbach · Thomas J. Turek 

Stone, K.R., Pelsis J.R., Adelson W.S., Walgenbach, A.W. 2010.