This is a 33-year-old former NBA player, had intermittent pain, two intra-articular CSIs previously, multiple symbiotic injections, pain sitting, coaching, can't defend his players on the court, and mild pain with sprinting. His x-rays are as follows. MRI is here, so you can see some subchondral bone marrow edema. It might scare us a little bit. Labral tear, otherwise relatively good chondral preservation. CT scan is here, showing a large volumetric cam deformity, otherwise normal acetabulum. This is what we get when we get in. This was a not-so-lovely experience. Coming in, you see a large chondral flap, and then you lift it up. Effectively, that's a third to two-thirds of his acetabular cartilage that peels off. This was my first lovely experience into wondering what to do with the cartilage, because I didn't see that coming, and I didn't know what to do with it. I said, I don't know what to do with it, so I didn't do anything, and then decided maybe that wasn't the right answer. At that point, we started to try to figure this out. Ultimately, this is the playing field. Effectively, 98% of athletes had acetabular cartilage lesions when scoped. We've seen some wonderful talks previously about this and the potential impacts of those chondral injuries to players and to their health when they're later on down the road. My questions were, can we identify these lesions preoperatively? If so, can we potentially plan for it? Can we decide what lesions require treatment? All of this is a giant black box in the hip right now. Have you seen back criteria that were discussed in previous talks earlier, as well as the impact of tonus grading? Tonus is effectively a sledgehammer. We should ideally be a little more precise in terms of what types of cartilage lesions are problematic. Lastly, can we identify the optimal treatment for these lesions? Do they have them? Can we see it? What to do with it, and how do we treat it? This was the thought process. You've also heard about potential labral impaction on this, meaning if you take out the labrum, it has a bad impact, and if you don't take it out, it has potentially a better impact. But what about the midterm? Do you repair it? Do you not repair it? Taking out a labrum we know is not necessarily a good idea, but do we really need to repair a small little wave sign? I don't think we know the answer. In terms of evaluating these preoperatively, it's still really tough. The answer, there are a lot of research diagnostic algorithms using T1 row, degemeric, 3D dual echo steady state, or DES can also potentially show early promise. This is what we're doing in our labs right now. These are some identified images to try to elucidate and identify these issues. So then we ask the question, does it really matter, and can we identify the size of the lesions, where they specifically exist, and whether those locations and size impact potential degeneration? We know in the knee, for instance, that if you have a centimeter or less chondral lesion, you probably don't need to do anything about it. Is that true in the hip? We don't know. Is a trochlear lesion different than a medial femoral chondral lesion? We all know that to be true in the knee. Is that true in the hip? We don't know. So these are some of the methods that we've used to try to really identify whether or not cartilage defects in the hip have impacts. These are in some of our studies in journal biomechanics, looking at the addition of a defect and noting that the differential, that the defect change distribution of contact stresses on the articular surface and the location of the defect change articular contact stress. In this case, we actually identify that what you think might happen is actually not what happens. So the knee is very different than the hip. We thought if you put a hole in the hip cartilage, it'll make the cartilage area around the outside or on the outside of that hole see more stress. It actually does the opposite. So in a knee, because of the differential curvature of the tibial plateau and femoral condyle, you actually have point loading. The opposite occurs in the hip. It's a very conformed joint. So if you put a hole in the socket of the hip, what you see is actually unloading of the hole. Instead, it produces, and you can see in those two pictures on the left and the right, it focuses the loading elsewhere in the acetabulum, not around where the defect is, but in other areas. So this may be a potential explanation as to why you get joint degeneration. This next subsequent question is, well, if you fill the hole, does it help? The answer is probably, how do you fill it? So you saw some pictures earlier about microfracture. Some of the questions about microfracture, does it really work in the knee? Maybe not so well. In the hip, maybe. In this case, based on this systematic review, the answer was no. It really isn't, while it's easy, it's not necessarily indicated. What about this, though? Another study by Mark Philippon and his group suggested they had really good positive outcomes on microfracture. So I think the question's still out there. And again, location and size may play a role here. We don't know the answer. Lastly, can we save it? There's articular cartilage. You saw the flap there. Can we just take it out, chew it up, and put it back in? Some studies would say that this really is not a good technique. What if you glue it down? Would that work? Some people, Ricky Villar's group, has suggested you can just glue this down. It has some decent outcomes. That being said, Mark Saffron's group and others have looked at this cartilage from the flap and said, you know, it really doesn't have good chondral viability. We should throw it out and do something better. Then again, Vonder Reit's group and others have shown that it actually has decent cartilage viability. So the question is still out there. What do we really do? What about ACT? My question here is, why would you want to do this? It's really, really hard. I'm not technically good enough to pull this off, so there has to be a better way of doing this. That being said, there have been studies doing it, and if you can pull this off, it's two-stage surgery, but it may have good outcomes. Bulk allograft transplants, another option, surgical hip dislocations. This is a patient of mine that I did with one of my open surgical colleagues. These are really difficult outcomes. We really don't have good long-term outcomes, but it's probably a reasonable salvage procedure for someone who's had microfracture. So what do we do in this case? I came back on him after doing the initial injury and decided we could do something better. So after figuring this out and trying to come up with a better option, we came back in and decided to use the femoral head neck cartilage that you normally sacrifice by taking it away with a burr when you're doing your osteochondroplasty. Why throw it away? We could actually use it. And so effectively what we did was what we called an AMEC procedure, which is effectively taking the cartilage from the femoral head using a capture device on the suction of the shaver and then transplanting it back into his acetabulum. Again, this is normally cartilage we'd be throwing away. We then do the CAM osteochondroplasty, which you all know very well how to do, of course. But after that, we'll then take the cartilage from the femoral head, which we'd normally sacrifice, and transplant it into the acetabular defect. I threw away the cartilage defect from the acetabulum because my conclusion on the literature is there's not enough evidence to suggest that that's good enough, but the CAM cartilage may be appropriate. So this is effectively transplanting the patient's own femoral head neck cartilage back into his acetabulum and then sealing it with fiber and glue. And this is his effective post-op. So my biggest question is, am I making this up or is there any data behind it? At that point, we started to look into it. The answer is yes. Chondral viability of the femoral head neck junction cartilage is excellent. It's about 50% cartilage via the chondrocyte viability, which then increases with the inappropriate milieu. In our case, in vitro, we also looked at it in vivo. It can get up at five to nine days of culture to 99% chondrocyte viability with that cartilage at the head neck junction. So it is very reasonable to transplant that. So my conclusion on all of this, this is my experience. At this point, most chondral lesions greater than one centimeter, I use Amec or AutoCard. Smaller partial thickness lesions, I debride them. Huge lesions, consider other options. It's probably not there yet for those. And remember, microfracture does burn a bridge. Just like ACT and MACI, if you transplant cartilage on top of a microfractured acetabulum or femur, it's probably not going to have any better outcome than it does in the femur or in the knee. So consider bulk transplant in those circumstances. Thank you.

hip pain

cartilage defects

subchondral bone marrow edema

labral tear

cartilage lesions