Christian Laderman, who will be offering our algorithm And thank you for having me talk about my favorite topic, So, when is a defect symptomatic? There can be non-activity related. If that's the case, you have to worry, because you have to figure out if this is OA, or whether this is actually a chondrodefect that's symptomatic. And you also have to look a little bit at activity. If you have the typical high-performance person, less, maybe more, with regards to chondrodefect. If you have the player who basically immediately increased his activity over the last three months, because he had January 1st coming by and wanted to run a marathon, you need to manage expectations. And then if you have the moderate activity, active lifestyle guy, that's probably the person where you get the biggest bang for the buck. There's mechanical issues. Be careful if there is other symptoms, such as weakness, numbness, tingling, poorly located pain, etc. Those are all warning signs that this may not actually just be a symptomatic defect. So now there's algorithms, obviously, and this is what I'm supposed to talk about. And we published a recent paper a couple of years ago, which goes over all of these algorithms and all the different techniques that are out there. So if that's what you're after, we're done here, we're done with the talk. But, there's always a but. And the problem here is, if you're looking into the small, medium-sized defects, that's a playing field for a lot of different technologies. The problem is, is a lot of these technologies do lack evidence. And that is okay if you're playing in that particular area, because to tell you the truth, a lot of these will do well. Because we are dealing with the unicorn defect here, these are small defects, pretty much anything in that environment will work. However, if you are working in a large defect, that's different. So what constitutes a large defect? There's three different concepts that I want to share with you. So first of all, anatomic location. Does this actually, or actually lesion size, does it actually matter? Well, the interesting thing is, is there's actually not as much clinical difference in terms of the symptomatology between large and small defects as you may think. And, you know, the Aransberg out of Norway showed that very nicely. But what is very impressive, if you look on the right side here, that cartilage lesions are very close in terms of their symptomatology to patients that are undergoing total knee replacements versus the other typical sports symptomatologies that we see with ACL injuries or MPFLs. They are functionally doing much better, even preoperatively. But cartilage lesions tend to not do that, and that is largely because they go along with a lot of swelling and pain and not so much instability portions. What about lesion size when you're looking at the larger literature? There is evidence that larger lesions have a significant harm effect, so to speak. However, the data is not clear, and it is still at this point assumed that larger lesions are the worst actors, but small lesions can be equally symptomatic. The relative size matters. The relative size matters as it shifts the contact point when you are creating even small lesions in the lateral condyle. It shifts your overall load point posteriorly and slightly laterally. That is actually exactly the area where you don't want increased loading in the lateral side, and the overall rim pressure increases significantly. Ko showed that very nicely. And this is that situation. We just saw some pictures of that. This is the end situation. You lost your meniscus. You have that lateral femoral condyle lesion that is developing there. Those are the lesions that are different animals because those are what we call high-traffic lesions. Now we are getting stuck here. There we go. The high-traffic areas are exactly those that are sitting mostly on the lateral edge there, as well as in the center of the medial femoral condyle. If you have typically additional injuries like ACL injuries or so, very often you have subtle anterior medial or posterior medial instabilities, for example. That increases the overall rotational forces on your repair. So the central medial femoral condyle is one of those areas where you have to probably need more structure than just biology when you repair. The edge of the lateral femoral condyle, which I just pointed out, is another one of those, particularly if you are adding meniscus transplants or something to that very high mechanical area. Then the lateral trochlea in patients who have lateralized patellae that also do need reconstruction or alignments, those are these three areas of high-traffic areas where structural support is as important as just the biological support for large lesions. So large defect reconstructions require data. If you look at that, there's really only two of the traditional. That's the OATs, the osteochondral allografts, and the MACI that really has data in those kind of defects. That is why in the algorithm you see basically those two showing up dark blue with appropriate data behind it. You need to manage your expectations in these patients. That's what I have learned. Tell them up front that there will be differences in the outcome when they come up with expectations that are out of the line. You also have to be more aggressive rather than not. If you see here the blue outline, that was a lesion that was previously treated. A year later, the second lesion here showed up. So that was probably a mistake on my part. I should have been more aggressive at that point and treat the actual defect larger. You have to also understand that this is not the time to be cute with incisions, exposure, or complexity. You have to really address what needs to be addressed. That can be a whole bunch of different things at the same time. Also, look at these patients yourself. These are examples of patients that have been sent to me after a previous scope saying, oh, all they need is a cartilage repair. One of them has a chondrocalcinosis, which is a complete contraindication, and the other one is basically significant OA. That is often something that is hard to assess just by an MRI or if somebody else failed to show you those lesions on the scope. The biology never stops to surprise me. If you look at lesions like this one here, this is somebody who had an overall 13 centimeter square size defect. This is actually one of my athletic trainers, and the other day we were at a game, and he starts doing this a year after the procedure. So I didn't think that was possible. The quad is key, and weight-bearing needs to be accelerated. There's some really good work by Rolf recently that showed that if you look at the rehab protocols, we have gotten more and more aggressive with equal outcomes, and I think this is a real key going forward. These long immobilization times are horrible for our patients. And then the other thing that I think is a game changer is looking at the musculature. Things like blood flow restriction really need to be looked at. So take home, treating cartilage defects requires planning, data, and technical skills. Know your limits and the limits of the procedure that you are working with. Understand the factors that are involved, alignment, defect location, biology, and the actual demand that you are preparing the patient for, and make sure to discuss outcomes and expectations. And then you'll find the right door for the exit for this patient and don't come back to the operating room every other year. Thank you. Thank you, Christian.

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