Surgeons often talk about repairing or reconstructing a torn anterior cruciate ligament (ACL), but those terms can be misleading. Fixing an ACL isn't like replacing a punctured car tire. The healing requires biological and biomechanical processes that we can influence but not control.
For this reason, I believe that orthobiologic interventions, such as platelet-rich plasma (PRP), will play an increasingly important role in treating these injuries.
Whether we take the torn edges of the ACL and sew them back together, or replace the damaged ligament with a graft, we are creating a scaffold. Stem and other cells gradually inhabit the tissue, regenerating collagen, blood vessels, and other components of a living tendon.
But along with the anabolic regeneration of the ligament, catabolic processes are taking place in the joint. They may help explain why 20% of people with ACL injuries suffer reinjury within 2 years.[1]
In this catabolic process, matrix metalloproteases and cytokines also cause degradation of cartilage. Long-term, between 60% and 90% of people with ACL injuries develop osteoarthritis of the knee, compared with 12% of the overall US population.[2]
That's why the ACL injury is not just a surgical problem, or biomechanical problem; it's a problem of facilitating homeostasis.
