Just to try to provide a brief overview of summarizing a lot of things you've actually already heard, my disclosures are in the syllabus. So the first thing is these are very common. If you look across professional and even Division I sports, we know that the incidence in all comers in the 20 to 24-year-old age range is probably similar to what we see in recreational individuals at the ages of 40 to 45. So we know it's very common. We also know that the MRI often doesn't correlate with what we see at the time of arthroscopy. This is an interesting point because many of these athletes, when they come in, they often know they have chondral disease or osteochondral disease, and there's not a lot of evidence that shows that participation in sports will show that this will make them progress. So the threat of progression doesn't necessarily match with decision-making when it comes to treatment. So I often say that decision-making is not linear, and given the lack of correlation between the clinical symptoms, the articular cardinal status, and our lack of knowledge about natural history, most of us are in the business of treating individuals for the here and now. So this is one condition, especially when we're dealing with high-level individuals, and this doesn't necessarily have to be professional athletes, where skillful neglect may be acceptable. These patients often will have oscillating symptoms, and it depends on where we catch them in their cycle. So watching them is an option when they can achieve appropriate play and performance. So athletes, and this isn't always a professional athlete, it could be just individuals who desire to achieve high levels of activity, we have to separate concern from disability. We know that in some instances, their inability to perform makes them unemployable, they may not be able to get a scholarship. Treatment shows it may actually affect their asset values, so we're very careful about discussing the potential to burn bridges. We are pretty good at improving ADLs, but it's a little bit less predictable when it comes to return to sport. Our desire is to match the solution to the desired outcome and the available timeline. We may choose solutions that are temporizing given the athlete's timeline. And one thing that we are often asked is how do we actually predict the likelihood of success and how sustainable our results will be? I would just say anecdotally, when we can get a year, a full season, oftentimes that's pretty predictive in the near term that you can get a couple of more, okay? So immediate past performance for upwards of a season is actually helpful to know when you're gauging the relative risk if you're in a position to take one of these individuals, whether you're counseling or advising a school or other team or environment. So who gets what? Non-operative treatment is often appropriate for the acute onset of symptoms where performance is maintained, or maybe the performance is compromised and that's acceptable if they're actually playing for something, for example, a new contract or a scholarship. Operative treatment is more likely indicated when a performance is impaired, when they fail non-operative treatment, and maybe they're early in a long money situation. In other words, they have a contract ahead of them where they can afford the time required to actually get better. I think we're becoming much more thoughtful now on how we apply, for example, non-surgical treatment. We're starting to differentiate, say, the wet knee from the dry knee and to delineate who might be responsive, for example, like the one on the left, to orthobiologics, where on the right may be responsive to load changes, where they have pain mostly with load but don't have that achy, wet, synovitic knee. Chronology matters. Our older patients who come in who may have had the same looking diseases, our young patients often say, well, I don't understand. Why aren't you offering me cartilage repair or cartilage replacement? Because I think chronology really does matter. And I think the reason is that our older patients behave more like arthritic patients. I see them as being often less responsive to the same treatments that we can offer for the same level of disease in our younger patients. In the end, I think a lot of this relates to load, and that translates directly into the bone. And you've heard a lot about this, but in my opinion, I think while this entire session is dedicated to cartilage, the bone really matters most, and we'll finish up with that at the end of this discussion. So this is where we are today. These are the frequencies with which, they're pretty updated, with which these individual procedures are performed in the United States. And the algorithm is profoundly complicated, and certainly not the subject of this conversation, but I'll just say that we've become very attuned to how we match demand level, defect size, defect location, and comorbidities such as malalignment and meniscal and ligament status. Much like we've evolved in our thinking, for example, for rotator cuff repair, we've sort of thrown out sometimes primary repair, debridement, and so forth. Patients can do very well in that setting. Similarly, in the knee, debridement and chondroplasty can do very well. We first learned about this when we looked at our patients who were undergoing biopsy for future ACI, when about 40% of them never went on to reimplantation because they did well with their debridement. Similarly, we've learned that vertical walls can actually shield the normal cartilage in the periphery, and that defect can become less relevant despite not treating the defect itself. So, just a very simple example, patella defect with mechanical symptoms, and basically we'll perform a debridement. You can see flaps there. This individual is desirously getting back very quickly, has a relatively short timeline. Less concern about restoration, although it might stimulate the surface a bit with a curette, but we've treated this patient out of the gates just with a debridement, and maybe we'll add some type of orthobiology at the end of the case for inflammation and so forth. Neurostimulation as you move down the lineage has been well studied, and I think it still has a limited role for some defects, but it's interesting. When you look to the literature, the results are actually pretty promising across the highest level athletes. So, if you can get a good result in this population, we can often get a good result in our more typical patient who just desires to be active. We have recently shown that when you compare an awl to a drill, we actually do better in terms of revision rates when a drill is used, and I think that has a lot to do with the fracture response that's incurred when we use a microfracture awl. So some defects are tough to treat with other technologies, so we talk about size, but what about defect configuration? This is a very long, narrow defect. He has activated effusions. He has no real debridement potential to do well, so I thought this was a good one for micro-drilling, and we already heard from one of our speakers from Japan that adding a little bone marrow aspirator concentration may augment the results to this procedure. We can improve marrow stimulation with a variety of augmentation options, such as the orthobiology that you see here, scaffold augmentation, and then there's cell-based augmentation where you can actually use minced autologous cartilage or even allogeneic minced or surface treatments. This is a relatively new technique that I think has great promise in Europe where they have less access to allografts and offers a very economically responsible option here in the United States as well, and it basically involves obtaining normal articular cartilage, minced cartilage in the adult. It's been shown to be biologically active. There's apoptosis at the edge of the minced cartilage, and it's basically combined with bone marrow aspirate and maybe a scaffold, such as allogeneic anhydrous collagen, and it's placed arthroscopically, and we place fiber and glue over the top of it. So this is a relatively new technique that's, I think, cost-effective. It doesn't require a lot of planning if we're in a situation where we want to do primary off-the-shelf treatment. OxyContin autograft is a dominant treatment strategy for a single defect in a high-level individual where the defect size is around 10 or 11. So I think the literature is very supportive of this being an excellent technique. So case in point, this is a WNBA player with a focal defect that already was debrided, has a little bit of tibial wear, but has that focal defect, and it was very simple and straightforward to treat with a single plug. So I think the literature does support this as an excellent option in this situation. You've heard a bit about MACI. It can be performed arthroscopically now. There's excellent return-to-sport data. In the highest-level athletes, I would say personally, I've had less experience, but it can be done. One of the issues is, I think, the time to feel better can be a little bit longer than some of the other techniques we use. But I think there are clinical situations where it may be optimal to use MACI, such as bipolar defects or multifocal defects in very young patients with intact subchondral bone as primary treatment. So it does have a role. OxyContin autografts in the isolated situation in a high-level individual has had return-to-sport rates, as you see here. So I know we're talking about an autograft failure, but I would tell you that this is a very durable, sustainable operation. It's supported by our experience. It's supported by the literature from multiple centers. So especially with an isolated defect that is symptomatic, this is an excellent treatment with an intact graft that can get an individual back predictably between six and eight months. This is just an example of a hockey player who has a very large trochlear lesion. This was the only defect there that failed the treatment, and you can easily size match topography. You can match it with an osteochondral graft, as you see here. Another example of a patella defect in an individual who's towards the end of his career could not play patella grafts, as you saw Tom DiBernardino did a great job explaining how we can do an excellent treatment for these defects, especially when the subchondral bone is involved. I'll just finish up with the importance of comorbidities. We've talked a lot about how we treat the cartilage, but when it comes to load and correcting comorbidities, especially malalignment, that's the lowest hanging fruit we have. In addition, doing these procedures in meniscal deficient patients often presents a challenging treatment situation. Meniscus allograft transplantation, much like osteochondral allograft, has excellent reports in the literature of survivorship. Our initial concerns with meniscus allografts were, look, if we let these individuals go back to high-level sports, certainly the first thing that's going to happen is they're going to destroy their meniscus. It's interesting that that has not been our experience, so it can be done in high-level individuals who do cutting and pivoting sports with good results. Similarly, osteotomy, as I indicated, this is the lowest hanging fruit we have. If you can reduce load, that's sometimes maybe all you need to do in these individuals, and the return to sport rate and return to work rate with osteotomy is actually very high, and it mirrors cartilage repair in the same population. Another example, and it's been said, well, look, you can't do an osteotomy on a professional football player. It just won't work. I would argue if you don't do it in certain instances, they will never get back to play. So I don't think there's anything inherent in osteotomy that prevents an individual, especially in a professional football situation, from getting back. You might argue that the biomechanics in the soccer player or other might change, but if you're not going to get them better with a graft alone, you have to consider unloading procedure. A similar example, valgus disease, lanofilm condo, simple to correct and can improve your likelihood of getting an individual back. This is probably the most important slide in this issue of managing expectations. We've learned a lot about non-operative treatment, and as I've told you, because we are not honed in on the natural history of these issues, I've told you that sports participation doesn't necessarily make it worse. There is absolutely a role for non-surgical treatment for this patient group. We have to get a handle on our successful outcomes, but I think it's become even more interesting to figure out why we're failing. So we focus much more on our failures than our successes to figure out how can we do better. You heard a great talk on gender matching for osteochondrographs. Maybe that's the key to improving our outcomes in that setting. So something we have to really pay attention to do better than this 75% overall. And then I'll just leave you with this final concept. We're spending a lot of time talking about cartilage, but what about the bone? Why do these patients present with load-related pain? It probably has little to do with the cartilage itself, but the fact that the cartilage has failed and load is being transmitted to the bone itself. So lots of novel techniques out that only address the bone and do nothing to the cartilage. This is a situation where putting a bioabsorbable pin that turns in the bone in the subcondal region where you have isolated edema with relatively healthy cartilage, active implants and others which are trying to get through the FDA process, really purport to unload the joint and do nothing for the cartilage. And their clinical data, phase three data, randomized studies have shown that they get excellent results even when ignoring the cartilage itself. So it's food for thought. And my final comment is this. We have to be very cautious when we're using the literature that's in the public domain in interpreting return to sport. There are a number of factors that have nothing to do with the condition we're treating. And when we borrow from the literature and say, look, look what happened here, what's public in the public domain for players getting back to sport after Tommy John or after analog after other, there are so many other variables at play that make it very difficult for us to determine the success rate and the timeline that they get back to sport. So I think we have to be a bit careful when we're making these judgment calls in terms of the percentages of those who get back. Thank you very much. So in conclusion, large instance of cartilage abnormalities. The plan must meet the athlete's expectations. I do believe skillful neglect is an option in this population. And my general philosophy is we do the least amount necessary to achieve a successful outcome and narrow the risk profile. Thank you very much.

cartilage and osteochondral disease

MRI and arthroscopy correlation

treatment decision-making process

treatment options

load and comorbidity correction