I’ve been posting a lot lately about all my athletic endeavors, and realized that I have been not incorporating updates about my academic life. Truth be told, the last month has left me feeling as if my research was just kind of hanging out on the back burner and my athleticism was taking over.
Luckily, I’m back in the lab, doing histology, acquiring samples, and even attempting to engineer some new drug delivery methods. Even though my research is in the field of engineering, it’s definitely driven by biology and fundamental molecular pathways of inflammation. I won’t get too far into that. What I will get into is the impact that my research will (hopefully) have on the general public. What am I referring to? Osteoarthritis, of course.
Recently, a fellow blogger friend of mine, a principle scientist at the University of Washington, posted this treat on his blog. I felt like he posted it just for me! Now, maybe he did, maybe he didn’t, but holy cripes, was I excited. It just piles on the motivation for me to get my publications wrapped up and shipped out! And then I was slightly disappointed (why wasn’t my collabo’s work featured in NYTs!? Are our university marketing departments slacking?!), but I’m still excited.
The NYT’s article is referring to a manuscript by Dr Chu’s group that was just published in the American Journal of Sports Medicine in December of this year. In the study, the authors look at chondrocyte death in cartilage after blunt impaction to the bovine articular cartilage explants. The translational research from in vitro cow studies to real-life human injuries still needs to be made, by my collaborators and I have published several papers related to impaction-induced arthritis in a closed-joint traumatic model in the last year and a half [1,2,3]. We’ve even identified potential treatments! That’s exciting news.
So what’s the story? Basically, impaction-induced arthritis is fairly common, and can develop after a car accident (where the knee hits the dashboard) or a sports injury. Although the incident of injury is a specific time point that can be linked to joint degradation, the exact mechanism by which arthritis accelerates is what stimulates curiosity. You see, secondary osteoarthritis (OA) develops much faster than primary (age related) OA. Along with trauma, it can also be caused by obesity, genetic disorders, or joint malalignment. Instead of taking a lifetime to develop, it can be seen radiologically (ie. x-ray) within the first few years, especially following traumatic injury such as anterior cruciate ligament (ACL) rupture. In fact, histological changes to the cartilage* have been found within a year following injury . How does trauma accelerate cartilage degradation so much? What factors are involved, and how can we slow it down and prevent it? There are so many factors that are not well understood. Take for example ACL repair. If a soccer player tears their ACL, they will probably have it fixed because it is well understood that abnormal loading in the knee will lead to arthritic changes to the cartilage. Why, then, ten years later, does that soccer player still get OA? The answers are not yet known.
Powered by Sidelines
*Before I get too far in, though, I should probably explain the anatomy of the knee a bit. The long bones of the leg are covered at the ends with something called cartilage (I’m sure most of you have heard of this, yeah?). The picture to the right is a pig’s knee, the tibial plateau to be exact. Imagine looking at your shank from the top-down. That’s what it would look like if your femur and ligaments (ACL, pcl, mcl, lcl) were no longer intact and your shank was removed from your body (and my hands, with the blue gloves, were holding it). Cartilage, outlined in the red hash line to the right, actually covers the entire tibial plateau, even under those yellow-outlined rubbery looking tissues (which are the menisci).