Welcome to the American Journal of Sports Medicine's live online learning course. Thank you for joining us. I'm Alexandra Campbell, AOSSM Education Coordinator, and I will be the operator for the webinar today. Before we get started, I would like to take a moment to acquaint you with a few features. There are options for how you can listen to this webinar. If you have any technical difficulties hearing the audio properly, please try clicking the phone call option and calling in for the audio or switching the speakers that are being utilized. At any time, you may adjust your audio using your computer volume settings. To send a question, click in the text box and type your question. When finished, click the send button. Questions you submit are seen by today's presenters and will be addressed throughout the presentation. So please send those questions as you watch rather than at the end. There is CME available for this online activity. Here are the disclosures. At the conclusion of today's program, we ask that you complete a brief evaluation by going to education.sportsmed.org and logging in. Please take a moment to complete this if you wish to collect CME for this activity. At this time, I would like to introduce our moderator. Dr. Christopher Jones is an Associate Professor of Orthopedic Surgery at the David Geffen School of Medicine at UCLA. He serves as the head team physician and the Director of Orthopedic Surgery for the Los Angeles Lakers and as a team physician for UCLA Athletics. He has published over 70 scientific articles within the field of sports medicine and has a specific interest in the management of cartilage injuries. Dr. Jones is a member of the AJSM Electronic Media Editorial Board and will be moderating our webinar. And with that, I'll turn the mic over. Thank you, Dr. Jones. All right. Thanks, Alex. First of all, I'd like to really thank you, Donna, everybody, all the staff at AJSM for helping us organize this. We realize how, you know, big of a task this is to make these things go off without a hitch. So thank you for that. I promise you tonight that if you're interested in cartilage surgery, you're certain to learn quite a bit. We have the who's who of cartilage surgeons with us tonight. So I'll just start off by introducing them. So first, we have Dr. Andreas Gamal. He's the senior author of the AJSM Journal article that we will be discussing this evening. Andreas is currently an associate attending orthopedic surgeon at the Hospital for Special Surgery. With over 100 published articles, Andreas is widely considered an expert in the field of cartilage surgery. Next, we have Dr. Aaron Kritsch from the Mayo Clinic, where he serves as professor of orthopedic surgery. Having already been awarded several notable accolades this early in his career, Aaron's certainly a rising star in the field of cartilage surgery, and many of his scientific contributions have already influenced the ways that we approach some of these patients. So I thank Aaron for joining us tonight. And last but not least, we have Dr. Riley Williams from the Hospital for Special Surgery. Riley is a professor of orthopedic surgery and serves as the medical director and head team physician for the Brooklyn Nets, the New York Red Bulls, and the Iona College Department of Athletics. He has a unique cartilage referral practice that's comprised of a lot of high-level athletes, and I'm certainly looking forward to hearing a lot about his thoughts as we talk about cartilage repair as they pertain to this challenging population. So thank you for joining us, guys. And without further ado, I'll turn over the floor to Andreas to discuss his paper. Thanks. Alex, can you give me control to present everything? And while you do that, thanks very much for logging on, everyone, and joining us for this cartilage hour. It says we're waiting to view your screen. Let me try one more time. Oh, God. So screen come over now. Yes, looking good. We're looking at your presentation of you I'm not sure if you can make a full screen but we can see the slide. And it's the wrong screen. But. Let me check one thing. All right, guys. Let's just start in this one. Sorry, two screens. Sometimes this is always a little bit of a pain. So we recently published something I want to give kudos to Gergo, who was my fellow at the Brigham. And we looked into the outcomes of osteochondral allograft transplantation, specifically related to storage time. So how long can we store an osteochondral allograft prior to implantation and still get good outcomes? And just one slide on the basic science to this. A lot of this is old. All in all, back in 2004, I'd looked at conocyte viability over time, and that's the graphic on the top right. I mean, the gist is storage with salineness is a bad thing, lactate is ringers, but 28 days, more than 2 3rds of the graft are essentially dead. If you use specific culture media, and that's what most companies use nowadays, you can get sustained viability up to a month. So 83% in 28 days. And that's where this one month rule really came from, that was still pretty much a tier two. And this was also confirmed by Dr. Williams, where he looked at conocyte density with storage time and essentially showed the same, less than 28 days, good at 28 days, he started to see a decline. The most recent study, which was a preclinical model in a dog, actually it comes from Mizzou with Cook, Jimmy Cook, who published this a couple years ago, and they looked at conocyte viability specifically and clinical outcomes in dogs, and found that if you have conocyte viability less than 70%, you pretty much are guaranteed a clinical failure. So that then was followed by three papers that looked at the clinical outcomes. So out of the same Mizzou group, Noel and Jimmy Stannard published in 2017, they looked at 75 patients with ultracoronaviral grafts, not quite two years, overall had a 71% success rate. And if they compared patients with grafts that were older than 28 days, those were more than two and a half times more likely to fail than fresher grafts. This is contrasted a little bit by what Buckbee had published in 2017 when they looked at an early release. So the old days, 20 years ago, they did fresh grafts. They didn't have the same FDA requirements that we have nowadays. So they could release it very early. And they matched against 75 grafts that were later, which were released 20 days after retrieval. And this is mainly because the FDA had mandated that we need to do a viral testing and bacterial testing, and that just takes a while before these grafts get released. They had a really long follow-up time of 12 years and had pretty much the same success at five years, so 85 versus 90%. And they didn't find any differences between the early versus late release. But if you look a little bit more closely at that study, it didn't really compare apples to apples. The early release, that was in lactated ringers. And as a bunch of studies, including the ones I had just mentioned on the previous slide, had shown the lactated ringers, chondrocyte die off much sooner. And they also had a different technique. They used mostly shell grafts in the early days rather than the plugs that we use nowadays. And shells transplant more bone, a little bit more prone to failure. So they compared something that's potentially good, meaning an early release, but stored in a bad solution, stored and then implanted in a technique with higher failure rate, with something that's potentially worse, meaning a later implantation date, but better culture medium and better techniques. That's probably why they didn't really show much difference in clinical success. And then Dr. Williams had published something just last year, specifically looking at patients who had cartilage delamination, which is one of the failure mechanisms of OCAs. And this was really a case control study looking at the delaminated versus patients without delamination. And really didn't find any differences in storage time. I will let Dr. Williams talk more to that because he knows the study better than anyone. I would just say overall they had fairly long storage times. So 30 versus 31 days. And the time to failure was sometimes up to 12 years. But I'll let him speak more to that. So what did we do? We took 111 of my OCA patients and they were all single surgeons, same providers. So JRF Ortho provided these grafts with a minimum of two years followup. And we did an ROC analysis and based on that, then divided patients into an early and a late group. The early one being nine to 24 days and the late group 25 to 27. And this was pretty much 50-50 because we divided based on the median survival. And then did Kaplan-Meier survival analysis and a regression analysis to look at what, if anything, had an influence. So the five-year graft survival was really based on pre-implantation storage time. So early implanters had a 93% five-year survival in this Kaplan-Meier curve. While if they were implanted just a few days later, 25 to 27 days, the survival went down to 70%. And they were non-implanted later than 27 days because at least with this provider, 28 days is the max. And if you look at the regression analysis, so age didn't really have much of an influence with a hazard ratio of essentially one. Same defect size, no real interesting differences. But the storage, if you went to the late group, that increased the risk of failure by over three times. So what I've taken from that and hopefully what you will take home is you shouldn't accept any grafts that are older than 28 days. The upper limit really varies by company. There are some companies that go up to six weeks. So you can still tell these companies that you wouldn't accept any grafts that are older than 28 days. And even if you stay below the 28 days, really try and get them implanted as soon as you can. I know logistically that can be a challenge trying to coordinate between your time, patient's time, and hospital availability. There's a lot of research going on in this area, both to hopefully with the FDA change the donor and tissue testing so that we can release them earlier. Right now, as I had mentioned, you can't release them earlier than 14 days. Meaning you can't ship them until day 14. And then some groups are looking at better storage solutions so that you can hopefully extend the storage time with maintained conocyte viability past these 28 days. So with that, I'm done. And I'll turn back to Peter. I hope you were able to see this. And let's open this up for a discussion. Thanks, Andreas. I think you did a really nice job of summarizing a lot of the basic science data. I think this is a really interesting paper. It confirms what we already knew from the basic science data, but gives us some clinical data now to really sort of hang our hat on and say that we need to be implanting these grafts sooner rather than later. I wonder if based on your clinical data, which is pretty compelling, 70% versus 93%, it's a big difference. Should we now maybe slide the scale back a couple of days and now change the standard from 28 days to 25 days? It's a pretty big difference. Yeah, and the one thing is, I'm always a little bit reluctant to make changes based on one study. I believe the data, I think we were honest and included everything, but confirmatory studies are always a good thing. So if we can, Erin, you, I think, look at your own data, publish that. And I think if it pans out that this is true, then I would for sure say we should try and tip the scales a little bit. But Riley had looked at his data and there wasn't really much difference. So like everything else, let's wait, get this confirmed. But really, I think in general, it's better. Your study is a better study, much more comprehensive and germane to the question. My study was just an observation of specific phenomena of condor delamination, not disintegration or clinical failure. So it's really not, your study answers the question. I mean, anecdotally, I don't really accept graphs that are beyond 23 days, just because a quick look at the registry. And again, I did an interview today for the SMI just to kind of talk about the registry. So kudos to everybody involved here because you're enrolled already. It's the only way you can answer these questions, right? To be able to prospectively collect and look at questions, right? And this is like a really big question. This topic has been lorded over by industry as you guys all know, since the beginning. Cryolife said back in 1998 that you could put in graphs up to 38 days, I believe, and then they sequentially sort of bring it back down. And my question was always, what are the biomechanical properties and viability of what we're putting into people? Because ultimately as the captain of the ship, we're responsible. And it's one of the few types of implants that we really had no control over. So love the study. I think it continues to give us the mantle back in terms of determining what industry standards should be. And the reality is that two and a half week, two week QA model, the institutional programs at Toronto and San Diego, they never did that. They re-implanted and went in 48 hours based on a simple test that they did in the hospital. So there's probably a lot of discussion that needs to be had about where we are regulatory-wise with this particular approach. Thank you. Andreas, can I ask a follow-up? So you presented the 30% failure in the older graph group. You defined failure as graph failure, revision, or conversion to arthroplasty. But I didn't really see in the paper kind of the breakdown of that. How many of these were true graph failures, first of all? And then second, can you conjecture about that failure mechanism? I mean, were you seeing cartilage delamination in the older graphs? Were you seeing, you know, were creeping substitutions stopped and now you're getting some of the bone fragmentation? Or what did you exactly see there in terms of method of failure? So the vast majority ended up with revision biologics. So I think there were maybe two or three arthroplasties in there. When the, luckily you can revise a failed allograft within allograft, doesn't guarantee success, but at least there's a chance. And most of these are young patients. So I usually tell patients if this fails, the next step is not an arthroplasty. The failure mechanism is pretty similar to what Riley had seen in his study. So the majority is stopping of creeping substitutions. So essentially you end up with a pretty shallow, almost like an OCD lesion where it fails, not just through cartilage, but sort of through the subclonal plate. And sometimes they look pretty innocent first when you look at them arthroscopically, but as soon as you touch them, you see that the whole surface is really unstable and loose. But it is striking that there is some bone on that cartilage, you know, where it fails. So they're not true delaminations. So do you think that it's the poor cartilage that's importing or imparting higher stresses to the subchondral bone? Or do you think that we should be looking at the bone phase of these grafts as well in terms of aging and how it affects the, you know, kind of the cellular biology? Yeah, that's the part I don't think anyone really has answered yet, but it's a great question because we always talk about chondrocyte viability. And if it were just the chondrocytes and just the cartilage, you would expect to look in there. And it's almost like a failed Macy where you're looking at the subclonal plate and there's just no cartilage on top of the cartilage, just really didn't necessarily delaminate, but breaks down and becomes this loose fibrous tissue. And that's certainly a part of the failure mechanism. But I almost see more, I think, failures that also affect the bone and not just the cartilage itself. So one last question, guys, before we move on, you know, this paper is great for giving us some more insight into the effects of graft storage time. I'm just curious, you know, when we get a graft match, you know, we all receive the email from the tissue bank company. It has the patient demographics, it has, you know, the age of the patient, the gender, it has, you know, some graft characteristics, bruising, superficial fissuring, you know, all these things. For those people who don't do a lot of these, what graft-related factors, you know, on that email that these people get do you guys look at and consider important? I mean, usually, I match by size. I think most of us do that. Number two is compartment-specific. Riley had done great studies looking at the use of contralateral, and I think that's perfectly fine. That's pretty much it. It would be great if we could match, gender probably plays less of a role than things like blood type or tissue typing, but, you know, supply is already difficult enough, and I always tell our fellows that if you go into practice and you tell them, it has to be exactly this size, down to the millimeter, and this age, and you can wait, I mean, years. So, in a certain way, it's beggars can't be choosers. I hope that as graft supply becomes better and we know more what's important and what's not important, we can make the matching of the survival better, but that's what's really attracted me to osteocondylografts is because most of these things, us as clinicians have a chance of sort of solving. We can stick our heads together and look at what works for us, what doesn't work for us. Should we use bone marrow augmentation or not? Do we drill it? Do we pulse lavage or not? Like, these are clinical problems, and we can make changes and see what happens. You know, the tissue engineering implants, many of the tissue engineering implants, it's not something that we as clinicians can solve, that somebody in a basic science lab has to come up with some growth factor to make those tissue implants better. But OCA, that's sort of the end-user, that's us, has a little bit more of a say. Great. All right, well, let's move on. Aaron's gonna give us a talk about his philosophy of cartilage repair in 2020. Thanks. Okay, hopefully you can see me okay. My philosophy, of course, is to get it right the first time. That's my approach to cartilage. My disclosures. So I think it's important to have a standard approach for every cartilage patient, obviously a thorough history and physical, but imaging is really the main tool in our toolbox. And what am I looking for? I'm trying to decide, is this a focal or diffuse process? Why did this lesion occur, if we can answer that? And then some lesion factors for surgical planning. So when we look at focal or diffuse, it comes down to which knees are good candidates for cartilage restoration. And I live in Minnesota. I tell patients about the pothole test, and if you have one pothole on the road and the rest of the road is fine, that's a good candidate for cartilage. If you have more potholes than road, unfortunately, that's diffuse arthritis, and really, at any age, that might not be a good candidate. Take this patient, a 44-year-old, relatively youthful and healthy, with some early joint space narrowing, some varice mal alignment. When you look at that MRI, when you look at those arthroscopy pictures, that's diffuse cartilage change. To me, that's not a cartilage candidate, necessarily, and in this patient, we treat with an offloading osteotomy with a good result. When we look at different cartilage options, no matter what we're gonna use, no matter what tool we like to use, we need to understand what the background factors are, and we need to correct those background factors. We looked at cases that were sent in to us that failed cartilage repair over a six-year period of time and we found the most common reason for failure of the primary cartilage procedure was either unrecognized or untreated mal alignment. So, clearly, these are important issues that we must recognize. And then, what about lesion factors? Well, certainly, size matters in terms of what lesion we're gonna treat with what modality. I like to look at the axial MRIs. If you go very distal, you can often get the surface of the femoral condyle. Here, you see a long linear lesion, so this is one of the unusual rare cases where we can perform an autograft transfer with a couple of plugs, but it's important to know your size and geometry of the lesion. Then, I try to decide, is this chondral or is this an osteochondral lesion? Here's a trochlear lesion in a 36-year-old that's actually an OCD and has bone involvement, so my preference here would be to treat the bone loss with a bone and cartilage graft like in Andreas's paper with an osteochondral allograft. If we look at a companion case, this is a delaminating trochlear lesion, more a surface lesion. Subchondral bone looks really good, so I'm gonna treat this with a cell-based option here as an old ACI case. Acute versus chronic, I think, tells us a lot about prognosis. Take this apical patellar lesion. You can draw very well-demarcated borders. This is clearly an acute lesion. In contrast, here, you can see a lesion that presents with acute symptoms but is quite chronic based on the imaging. You can see the subchondral sclerosis, the irregular cartilage borders, the bone edema. This patient's not gonna have the same outcome as that previous patient. Then we have to ask, how does our patient compare to the literature? Is it that ideal indication on the left or is it a multifocal indication such as on the right? When you look at Dr. Williams' paper, the phase II neocard study, that study was designed with simple lesions only, smaller lesions. So that's probably gonna have a different outcome than if you're looking at more complex lesions with early arthritis in the knee. And then patient factors. I think BMI, we're seeing more and more issues with, unfortunately, in our practice. I think Brian Cole said it really well, where joint biologic preservation really starts in the kitchen for a lot of our patients. So sometimes just taking the extra time and teaching them about BMI and how it affects knee loads, et cetera, can be successful. I think we have to take the patient as a whole. If you're getting into your clinical room and the patient's family members are handing you sheets like this, maybe that's not the best patient for cartilage restoration, even though their imaging would suggest that they are. And then finally, we kind of drill down why these clinical results are variable. Certainly, Andreas' paper highlights some of the biologics part of it. But really, we're really operating on different knees sometimes. Take the knee on the left versus the knee on the right. These are very different environments. One's a good indication, one's more of a salvage. And then the concept of joint homeostasis, we're just starting to scratch the surface on. Sometimes we see knees on the left with this diffuse synovitis, maybe not the best environment for cartilage, compared to the knee on the right, which is very bland and just has that solitary lesion. And then finally, we need to manage our patient expectations. So we really want improvement of pain and function in our patients, but also durable long-term outcomes. Our patients sometimes expect to be pain-free. I think we have to really counsel them, let them know that they're gonna have improvement with pain during activities of daily living. If you look at Dan Saris and the Summit Group, I think this is one of the best papers in terms of midterm five-year follow-up of Macy versus microfracture. And if you really drill down and look, so this is their Kuh subscale pain, substantial improvement from baseline, an average score of 82. We ask ourselves as a clinician, what does a score of 82 mean or what does that look like? So this is a patient who had a score of 82, that's how they would fill out the form. So they still might have weekly pain in their knee. They might have some mild pain with activities of daily living, but overall substantial improvement. So I think we have to really do the work upfront in terms of counseling them that we can improve their pain, but probably not a pain-free knee. So in conclusion, I think it's important to develop a standard approach for every patient. I think x-rays can really help us determine focal versus diffuse lesions, as well as background factors. Really, I think we owe it to ourselves to study our MRIs carefully. We need to optimize patient factors and then manage our patient expectations. Thank you. Thanks, Aaron. I think that was a great, pretty comprehensive cartilage talk in six minutes. So thank you for that. I noticed you were really concentrating on getting it right the first time using MRI, x-ray imaging, obviously your physical examination and advanced imaging MRI. I'm just, I'd like to get a sense from the panel here, cause I know what I do. How many of you guys are still doing diagnostic arthroscopies for some of these patients before you make a decision as to what type of cartilage repair procedure, if any, you're gonna do? And if so, in what case do you do it? I'll start with you, Aaron. So I think over time, less and less, I think MRIs have been very good. I think you really need to owe it to yourself to study that MRI. Previous studies have shown maybe there isn't a great correlation of MRI versus findings at the time of arthroscopy, but I think we're relatively good at predicting. So I think few surprises. Cases where I'll still use diagnostic arthroscopy are if they've had a previous failed cartilage procedure, and there's some question about the integrity on the MRI. If there's some question about meniscus status in terms of amount of meniscus, I don't want to necessarily go into a situation where I would need a meniscus transplant, for example, and I don't have it. So sometimes the complex multiple revision cases that can be beneficial, but as routine, I don't typically use it. Riley, I think I know what you do. What's your take on it? I came up, I'm a little older than everybody here, and one of the metrics that I fought against early was this idea of these diagnostic arthroscopies being done routinely. It was really at the nascency of ACI, so this sort of gave surgeons an excuse just to go looking around. MRIs were of questionable quality around the country, so it was definitely in play. So my bias was to do less. I had the benefit of Hollis Potter, who had a big interest in that, and it really helped from the diagnostic side, and as our registry and many others have demonstrated, a duration of symptoms, which arthroscopy can obviously help to delay and extend the amount of time, as well as just the intervention itself. Those are all negative predictors for clinical success moving forward with these procedures. So I will do it in cases where I think, obviously, I think a MACE is appropriate. You kind of have to just to verify the lesion and to verify the suitability of that patient for that procedure. Just as an aside, and I was talking about it a little bit during my talk, I think 10 years ago, I was all allografts all the time, and I think in 2020, I'm like, hmm, they're good, they're not perfect, and when you're successful with something, you see more of it, and I'm just thinking a lot more critically about a 22-year-old with an articular cartilage problem versus a 42-year-old. They're different, different set of decision-making, I think all of us would agree, and in those patients, maybe I would be a little bit more careful and perhaps use a diagnostic just to confirm what I'm thinking. I think like Erin and Riley both have said, if it's a straightforward case, let's say it's someone who has an OCD lesion and have a good MRI scan, I think a diagnostic scope doesn't really add too much, but the two instances where I think it's helpful is a meniscus, because a meniscus transplant is good, but it's not perfect, so if you have some meniscus remnant that is not perfect but might be good, then the question is should we spin our wheels to a meniscus transplant if what we do mechanically may be not better than what they already have, and for that, I think that's really hard to get from an MRI scan. You want to go in there and prod that a little bit, especially lateral meniscus right at the pulvoteus hiatus. It's hard to see sometimes, and then someone who had a prior ligament, so sometimes if you have a once, twice failed ACL with cartilage, just having the chance to do an EUA really adds, I think, helps me with my decision process. Last follow-up question, Erin. I noticed, so in Andreas' study, if you look at the data, it was almost about 10% of his patients were treated for bipolar cartilage lesions, and 16% were treated with multifocal grafts for multiple lesions. We all love that cartilage patient who comes in through the door young, healthy, great alignment, solid, contained lesion. What is your take on the treatment of young patients with what we would obviously say if we see these lesions as more advanced degenerative disease? How do you approach that patient? What's your take? Yeah, so, I mean, you have to make a decision there. Is it worth doing or not? And I think you have to compare it to other treatment options available. So for the older patient, maybe it doesn't make as much sense to push it, but that younger patient you're talking about that's getting into trouble with bipolar disease like after they lose their lateral meniscus or something, those are very difficult. Typically, the ones I worry about are especially ones that are in multiple compartments. That being said, if you have a single lesion in each compartment, I think you can still get a good outcome. But those patients you spend a lot of time counseling that we're just trying to buy them a little bit of time and symptom relief. The bipolar cases, I mean, clearly a salvage situation where you just don't have other good treatment options. So for example, like some early patellofemoral arthritis in a very young patient, for example, you might consider that. But I think those circumstances are few and far between. I think those are cases you have to think and discuss with that patient multiple times before making a decision. Yeah, I think you hit the nail on the head towards the end of your talk where you said it's all about managing expectations, right? Riley, what are your thoughts on those types of patients? I think you can be aggressive at treating them with OC grafts and Macy because that's really where we are right now in terms of the literature which supports that. I'm just much more circumspect at this point. I'm much more about why. Why does this 22-year-old have a trochlear lesion, a medial femoral condyle lesion, and start to lose their lateral compartment? Some of that is joint homeostasis which I'll chat about a little bit. And some of it is maybe a genetic predisposition. A lot of it's gonna be alignment. That's why it's good to have Andreas around and Scott Rohde around because we hammer each other about principles, right? It gets drilled into your brain. I can see you guys when those patients come into my office even 22 years in. So you just need to have an understanding of what you're treating. Why did this happen? And how am I gonna make sure it doesn't happen again? And that just means being honest about osteotomy, being honest about the likelihood that they're gonna need some metal bridging procedure at a premature age. It doesn't mean don't treat them. It really annoys me when these guys just send people away. They don't refer them and tell them, well, you're 32, you're gonna need a knee replacement. Come back when you're 50. That's ridiculous, right? That's where we come in. And so that's where we try to come in and be honest brokers of information based on the literature. And it's very pleasing to sit here with these guys because in year 2000, we really didn't have any literature. It was like freewheeling and people kind of doing what they felt. And it was largely a cult of personality driving clinical decision-making because famous people were doing things and now we have better information on which to treat it. So I think it's our responsibilities as subspecialty carless surgeons to take on these cases, but to do so, just being honest and creating level set expectation the right way about what's likely gonna happen. These are like diabetic patients to the endocrinologist. You never really get rid of them. You just have to have in mind another bullet in your gun for the next time they come back. Yeah, well, I think that's a perfect segue to your talk. So we'll get into cartilage repair in the high-demand athlete. Should we even be doing it? I don't know if that's the title of my talk. All right, great. So I've given this talk in a number of different ways. Dr. Jones, I think we just lost Dr. Williams. He might be trying to get back on right now. Okay. While we're waiting for him to come back on, just to follow up that last comment, I think we sometimes, success I think is a different measure for those younger patients with salvage issues as well. So someone, if you're able to do a cartilage procedure at the age of 30, if you buy them eight years until that cartilage repair fails, that's considered a failure in the literature, but I think a success depending on the discussion you have with that patient up front. All right, looks like we have Riley back. All right. So I'll turn off my camera here. Great. Does that look clean to you guys? Great. Looks great. Okay, awesome. So if you guys indulge me here a little bit, I've been giving this talk for about 10 years now in some shape or form. So I'll just show a quick case, which I think kind of illustrates where I am right now. So this is a elite level division one basketball player who presented to me after landing awkwardly after a layup, had pain and swelling. And as you can see here, developed this shear lesion in the lateral compartment. It was a little bit of meniscal pathology. This athlete had some aspirations for play beyond college and wished to continue. This was an in-season injury. And so basically I was trying to be as minimally invasive and manipulative as possible. So I did a simple little procedure, did a very light cleanup of the meniscus and dripped some bone marrow aspirate concentrate in at the lesion site and did a postoperative PRP three times starting at week four. So week four, six, and eight. And told Tim to plan on coming back to me for an autograft procedure at some point later. And lo and behold, two years postoperative, you can see this near complete lesion fill, relative lack of edema on the fat suppressant views if I had those to show you. And basically the take home message here is the more experience, the less I feel I know. So what are the challenges in general for trying to return the cartilage injured patient back to sport? Well, first is obviously is the return of functional tissue, the restoration of functional anatomic cartilage or cartilage reparate at the lesion site. We know that it's near impossible to create new cartilage because of the lack of articular cartilage support. The conditions that support the development of articular cartilage do not exist ex-utero as much of the vascularity that supplies the articular cartilage layer in the womb disappears soon after birth. There are no validated treatment algorithms, although we're better. And there's really no evidence that we can create functional articular cartilage at all. The second and probably the most challenging is the restoration of joint hemostasis. We don't say it, but articular cartilage injury is really a massive change to the catabolic and it creates a catabolic environment in the knee. It's a massive change. It creates an imbalance where a breakdown exceeds synthesis. And as a result, there is the creation of a synovitic response commensurate with really what this is, which is an early arthritic response. And so that effusive has pro-inflammatory manias and the persistence of said manias can be harmful to articular cartilage and is, especially upon the reimplementation of load to that joint. And then finally, the restoration of fitness and that's aerobic fitness, strength fitness, the return of proprioception and the sense of the joint and its position in space and mental factors, depression, fatigue, loss of confidence, these things, there's a big psychological component to this that the longer you have symptoms, it may be more difficult for you to overcome. So an extended duration of symptoms and long post-surgical recovery is some of the things I think about when I'm talking about returning these affected athletes to play. So in 2020, what am I thinking? I'm gonna go through this very quickly. I'm thinking non-operatively, I really like the biologics. I like visco-supplementation and platelet-rich plasma. Hyaluronic acid has many positive anabolic components and property that make it an attractive option. And it's been shown in a number of studies and spent analysis that it has some effectiveness with intra-articular therapy, especially when you're trying to, for example, get a cartilage injured patient through the season. So in those cases, I would strongly recommend a consideration of that. Platelet-rich plasma, bone marrow, aspirate, concentrate, and adipose-based stromal grafts are things that are in my armamentarium. Platelet-rich plasma probably has the most support. We know that it increases GAG, type II collagen, and decreases cartilage degeneration, induces chondrogenesis from poor potential stem cells. There's a lot to like about platelet-rich plasma for which leukocyte-poor preparations are typically the best. And we are getting increasing numbers of studies that support that. Bone marrow, aspirate, concentrate is something that people are using. I use it on occasion, mainly as an adjunct to bone incorporation for osteochondral allografts. But bone marrow, aspirate, concentrate also contains these progenitor cells, which can be helpful in helping to, again, modulate that joint homeostasis that I mentioned earlier. I use it in lesion debridement surgery as an adjunct to micronized cartilage repair or biocartilage in osteochondral allografts. And for the subchondroplasty or calcium phosphate injection, which I'm now starting to use a little bit for treatment of some persistent bone bruises in this patient population. But there's really very little data at all for the use of BMAC as a go-alone in the joint. Adipose tissue contains high concentrations of pericytes, much more than you would find in bone marrow aspirate. And as such, these anabolic cells can be helpful in modulating the negative inflammatory response that we see in some of these cartilage-injured patients. We know that these adipose-based cells can help increase functional scores when used in the treatment of osteoarthritis patients. We can see in some studies an increase in cartilage volume. And as an aside, it's helpful in the treatment of epicondylitis and helps with decreasing retear rates following rotator cuff repair. So here again, an anabolic-type cell that you can use as an adjunct. So as we slide into the palliative option, again, that first case was a palliative option, but I added biologics to it. And in terms of maybe sliding the expectation from an in-season short-term management study, maybe with increasing observation longitudinally over time, an option that we could use to help decrease the likelihood that we have to use these bigger reconstructive procedures in some of these athletes. Dennis Crawford out in Oregon basically demonstrated that the palliative option is pretty good. He had a very low re-operation rate, around 15% at a 31-month follow-up. So definitely one that you can use as an option moving forward. Marrow stimulation is largely for historical context. I put it in here because there's still a number of surgeons who are doing this procedure. The problem with microfractures, many of you have heard me say over time, the longer you observe it, the worse it looks. And it pretty much loses all head-to-head performances against other repair methods. The true return to play a number based on our perspective that is 22%. And as such, I don't recommend it. Whole tissue transfer is really where I'm thinking most of my focus is right now. I've really turned back to the use of osteochondral autographs. I do a procedure now where I'm using 10-millimeter pre-cut allografts to backfill donor grafts from the femoral notch to treat bigger lesions, and perhaps sometimes using biocollage or other types of adjuncts to extend my indications. Because as I look at my population of osteochondral allografts about which I've published a lot, I'm just finding that at a midterm follow-up, despite the early follow-up that typically reigns in from two to five years in my hands, you just start to see an increasing number of these clinical failures that Dr. Gamal was talking about earlier. So it's really had me stepping back a little bit and sort of thinking, hmm, maybe I should be trying to do autographs like you see here on the screen as much as possible. And that's really where my head has been over the past five years. So there's really good support for both autographs and allografts. The expected range of return to support with the allografts ranges anywhere from 75 to 80%, which is pretty good. It's just that, again, as I get older and I see some of these patients down the line getting a decade out, there's just a lot of subclinical failures where they do activity modification and change their sort of activity based on deteriorating functions. So you can use the biologics that I talked about. I'm very enamored with them because I think the homeostatic environment of the joint is really where the problem is right now. And I'm trying my best using some of the tools that we have to modulate that a little bit better. So to finish up, I'm just gonna hop up with a couple of meta-analysis that sort of discuss these things in terms of what the best options are. And a couple of studies that looked at this. So in the first one, which Dr. Critchlow was lead author here, this is kind of enough to include me, looked at over 2,500 patients. It looked at three, excuse me, four specific types of approaches. Osteochrono-autograft, osteochrono-allograft, ACI, the classic, and microfraction, basically showed that osteochrono-allograft, OCA, and ACI were over 80% of the time very effective at under a year at returning patients back to sports in some fashion. That doesn't quantify the performance, it just quantifies the patient's self-describability to participate in their desired sport. With microfractures, as is typical, coming in a poor fourth place. Another meta-analysis done with slightly fewer patients, but again, over 20 studies looking at the same metric, pretty similar results in this meta-analysis, osteochrono-autograft, 89%, OCA, 88, ACI, 84, and microfracture, 75, with decreasing effectiveness and functionality in the microfracture group subsequently. So, pursuant to what you've heard here today, I would encourage you to try to understand your leads and etiology so that you don't repeat the sins of the past. Doing cartilage repair surgery should be about what you can do. Some of these procedures are technically demanding, and as much as you can, the labs offered by the Academy, AOSSM and Anna are very helpful in getting your hands dirty and getting comfortable, not only with the repair, but some of the requisite osteotomies that inevitably will be associated with some of the procedures that you do. And again, I can't stress this enough, you need to think about joint homeostasis. You cannot return an athlete to play at high loads with a swollen knee. It is full of bad actors, which are ultimately gonna lead to a generalized joint deterioration from which the patient may never recover. So you have to have a dry knee at the end. Set physical and psychological expectations from the outset, and then again, just always be mindful of maybe using biologic adjuncts proactively before the patient runs into trouble. And thanks for your time, and I'll stop there. Great talk, thank you, Riley. We actually have had some questions pop up from the audience, so I'll start with this one. Do you treat cartilage lesions in the femoral-tibial joint differently than the patella-femoral joint, given the fact that they have different mechanical environments? And if so, how do you treat cartilage lesions in the femoral-tibial joint? Given the fact that they have different mechanical environments. Why don't we start with you, Riley, your approach to condylar defects versus more patella-femoral joint. What's your take on that? I'll try to be as straightforward as I can. I know both of my colleagues will have some thoughts. You gotta think about what cartilage lesions are. They're either a result of an OCD, which is congenital from some sort of instability, such as patellar instability or from overload, right? So there's usually some mechanical actor at play. So it's the same whether you're in the tibial-femoral joint or in the patella-femoral joint. Unstable patellas need to be stabilized. If there's a cartilage lesion, you fix it. People talk about the geometry of the trochlea. I don't really have an issue with the geometry of the trochlea, quite frankly. I can pretty much do anything anywhere. You saw a stealer's choice, that's just me. But you have to just think about like, all right, how did this happen? And how are we gonna keep it from happening? Because the cartilage is just a secondary effect of the problem, right? So I mean, I went through that in the late 90s, just sort of filling holes, and that ultimately ends in sorrow and pain. So you just have to be proactive about kind of understanding how we got here so that we can get out of here, and then you sort of fix the cartilage around it. So I don't have any dogmatic approach about a specific approach in a specific geographic location. What I will say, again, I said it earlier, and I'd love to hear what Aaron and Andreas think. I wanna use autograft tissue. That's where I am. I wanna use it, I wanna extend it because your cells, the patient's cells, I think in terms of durability are gonna give them the best shot at hopefully not needing you in the future. Andreas, what do you think? It's funny to hear you because what Bugbee, who's a friend of ours, has said that we sort of start life as carpenters where we just see a mechanical problem and then you fix the mechanical problem, and he feels that he's become a little bit more of a gardener, meaning more of the biologics that joint homeostasis that Riley had referred to. And it's true. Initially, you just see a whole bunch of things and it's true. Initially, you just see a hole and you wanna fill it, and then at some point, you realize there's a whole lot more going on than that. But I agree, I'm not, well, in the past, I would have said ACI or MACI more for the patella-femoral joint, while osteocolon autografts, in my practice, certainly more for the femoral colonnales. And part of that was based on, it's just technically a little bit more challenging in the patella-femoral joint. But as Riley has said, once you've done a few, that doesn't really hold you back. The one thing I would say, allografts in the patella, that's still something where I think twice, just there's not much bone. If you put a big plug or especially a shell on a patella, if that fails, it becomes a little bit more of a challenge. Having said that, I do do OCAs in patellas as well, but maybe not quite as easily as in a femoral colonnale. How about Aaron? Yeah, I think you both said it very well. I think we used to be maybe a little bit more dogmatic about it, but now I think it's just, it goes back to what are the lesion factors, what are the lesion characteristics, what are the background factors? So I don't think there's a one-size-fits-all approach. I mean, sometimes a two-stage approach with a patella-femoral disorder for MACI is fine. Sometimes you wanna do it in one stage with whole tissue or whole tissue transfer. I think as a cartilage surgeon, you have to know and understand the nuances of every tool in the toolbox. And for certain patients and for certain lesions, one's gonna work better than another in your hand, so. Another question that came in, guys. I'll direct this one first to Riley, because I know you actually have a paper on this. Are any of the panelists using juvenile cartilage grafts? So I think they're probably referring to DeNovo. You still using that at all? Yeah, I mean, there's a fair amount of good evidence that DeNovo, in terms of fill, is very good. Pursuant to what Andrea said, I got really cavalier with these grafts, and listen, I haven't had a whole lot of failures per se, but if you fail a patellar osteochondral allograft after having drilled a lot of bone out, it doesn't leave you a whole lot of obstacle out of autograft, grafting your defect, so. Particularly juvenile, particularly cartilage in the patella is a winner over and over again. If you have a well-shouldered lesion, and that's really kind of the differentiator, you cannot use it if you don't have a well-shouldered lesion, don't even try. It would just wipe away. But if you've got a nice bowl or host site that you can clean, create nice sharp edges, it seems to work very well. We've shown that over and over again. I think we're near about a seven to nine-year follow-up for me on these that we can sort of talk about, but I know as part of my routine for clinical follow-up, I do MRIs. I do MRIs on everybody, so all the time. On a DeNovo, I would do one at three years, and I do one at two years. So we've got pretty good longitudinal data on those. I can endorse it unequivocally for that location. Not had the same success in other geographic areas. Okay, so for the patella, you'd like it in the patella femorals, right? Okay. How well? Got it. Aaron, are you using DeNovo at all? I have a hard time getting it reimbursed in my area. That being said, I agree with what Riley said. I mean, the evidence has been accumulating over the past 10 years. I used it in the beginning when I could have it reimbursed. I thought it performed very well, especially in a patella for a contained lesion. I see no issues with it. It's one of those things where we don't quite know the biologic value of what we're putting in. Is there some variability in the samples that you get? I don't know, but overall, it looks like the clinical results are very reasonable. Andreas, anything different? No, same. It's just most insurance companies don't pay for it. So if you get your hospital to eat the costs, then I think it's a good single-stage option. Okay. Hey, guys, while we're talking about this, and I'm just sort of thinking about this, I will say anecdotally that the use of the DeNovo does seem to calm the knee down. Not a lot of post-operative effusions with DeNovo. Has that been your observation? It's certainly kind of been for me. I wonder if there's something about the biology of those cells or something that they're kicking out that has sort of some anti-inflammatory properties in it or paracrine effect, just locally in the knee. Thoughts, observations? I mean, that would be a really interesting research question to look at. I have to look back at the ones I've done. I have to say the majority of DeNovo's for me probably were more as an adjunct, where let's say I did a medial femoral condyle, something, let's say a failed microfracture with an OCA, and then they also had a trochlear or a patella, for which I didn't want to use an OCA. So that makes that a little bit more hard to distinguish. But yeah, could be. Jessica. Along the lines of getting insurance companies and reimbursed for things, one question is how is the panel handling the cost of biologics used in conjunction with cartilage surgery? Private pay. So I guess what they're getting to there is are you having the patient pay for it beforehand? Are you having insurance somehow reimburse it or other routes? What are you guys doing over there at the Mayo Clinic, Aaron? Yeah, I mean, I've definitely had some denials of intraoperative biologics. I found that if I bury them deep within the body of the operative note, that sometimes those will get approved. So it's a discussion with the patient that they could get denied on the back end. So if they're concerned about it, I don't know if there's enough data that I can say it's necessary or will have a definable benefit for that patient. So it's case by case for me. Private practice setting, you guys over at HSS doing anything different? And Robbie, why don't you go ahead? Do you use that a lot? I don't have a simple answer. It's, I essentially charge patients the cost of the kit for PRP, a semi PRP in doses of three. It has not been a big issue intraoperatively for us at HSS to do PRP. I'm not sure if they get paid for it or not. I'm not charging for it in the OR. BMAC does not get reimbursed or Bulmar Aspirin does not get reimbursed. Listen, it definitely has some value. It's just hard to universally apply it in some standardized fashion because of the spurious nature by which it's covered. That's just the bare facts. I have a hard time in the era of COVID now too when I see people, I'm just sort of doing it for them. At a post, all right, whatever. I'll get paid $80 to do a lipogen, but I don't care. I mean, if I think they need it and it's something that I think will work for them, I do it. Because my hospital's supportive and I understand that's not the case everywhere. It really bums me out to hear that de novo is still getting denied. It's summarily ridiculous. You know, we can publish 10 papers on how it works, but yet they can publish one paper about how doing a knee scope and a 50-year-old may be funny and they don't wanna pay for it. So, I mean, it's just this spike that we're in right now with regards to coverage. So that's just, but listen, again, you've heard it. You're gonna play in this space. This is what it is. So I don't cry over spilled milk. You just take care of the patients and keep rolling. Yeah. One question from another person here is dealing with the patellofemoral joint lab, patellofemoral joint questions. Are you guys treating patellofemoral lesions at the time of an NPFL reconstruction when present, even when the patient's symptoms are primarily instability, not necessarily pain? I mean, I think, you know, we, I can speak for myself. I see a lot of cartilage lesions in people with patellofemoral instability because they tend to come to me after they've had 10 dislocations and the joint is not looking so great. I think the ultimate question there is, you know, pain, instability, or both. That's kind of how I approach it. And then in those three questions, those three buckets, and depending upon what the answer is, is kind of drives my decision-making process there. What's your take on that, Andreas? Yeah, no, I just laughed because this is, we can fill a two-hour panel with that question alone. I think overall, I've become a little bit less aggressive with cartilage lesions from dislocations, at least the ones that are just inframedial patellofacet and don't really affect the median ridge. Those areas tend not to really develop into much. So those, I wouldn't. I mean, if it's a fixable defect in terms of repairing something, I would always try that. But if it's a small piece that's not repairable and it's just inframedial, I wouldn't do anything. Defects that are a little bit bigger, crossing the median ridge in young patients, none of us want to treat asymptomatic patients. So it's a hard question that I can't really answer in a minute, but anything where I think this is substantial enough that I would worry about progression, I tend to treat at the same time. Yeah, I think you said something interesting and it goes back to what Riley was saying about de novo. Those lesions tend to be more on the inframedial facet of the patella. And what I've noticed when I have to go and treat them because their chronic lesions in patients definitively have pain, anterior knee pain along with instability, I feel like I treat that best with some sort of OA graft, whether that's an OATS or an osteochondral allograft because they're often uncontained. They're never contained on that inframedial facet. What's your take on that, Riley? Anything different? No, I think I agree with what's been said. I think there was a case in that presentation that I didn't show, it was a basketball player. He basically sheared off 75% of his particular surface. You have to treat that. I mean, these sort of small and uncontained reason, I mean, if that are clinically, once you put the patella back, they're not engaging anything. They're not going to hurt. It's probably fun to leave those. What we're talking around, which we never really got to is, just sort of dogmatically, what I would say is, again, if you're going to treat patella from McCarver's lesions, you should be facile to be able to have osteotomies. Just get your mind around it. You have to do them, right? Especially if you're talking about any kind of cell-based Macy type approach, which a lot of us are advocating in that part of the body. So that's the more important thing about whether or not to treat a small lesion with an MPFL. If you're doing MPFLs, you better know how to do TTOs. And if you're doing TTOs, you better know how to do cartilage to be comfortable with that. That's why I think de novo NT has a role. If they have a lesion that does go across the median ridge and it is contained, de novo is easy. You're not drilling bone. You clean it up. You throw a little of that stuff in there. It takes 15 minutes and you keep going. You know, I've had a lot of success with that. It doesn't take a lot of time. It's not particularly morbid. And you can do it all in one setting. And it takes the whole idea of do I or don't I? Is it symptomatic or not? Especially when you're dealing with a really traumatic injury first time and it allows you to cover all your bases. Last question to the panelists. We're sort of running over here. I think it gets to a little bit of what your talk was about, Riley. And I'm always sort of curious about this as I deal with these athletes who have these issues. What is your return to sport criteria for different cartilage repair procedures? OATS, OCA, MACI. Is there any role for cell-based procedures in these high-level athletes given the whole point is to get them back to the field as quickly as possible because that means dollars? There's a lot in that question. So I'll speak as plainly as I can. I'll speak as plainly as I can. The data presented says that all four of those work. Microfracture even works if you're looking, if you like numbers that range from 55% to 75%, technically it works. The MACI definitely works. It's just gonna take a year, maybe longer. Maybe longer. It's just the nature of the rehab. And so there's not a lot of interest in MACI from these dollar-making athletes, but for like a sophomore in high school, you need to calm down. It's gonna take a year and just do this MACI, right? That's where we are. So it's not your job to be a cheerleader and rah-rah them to a six-month return to sport, which we all know is a lie. So your job is to be the truth-sayer and do what you think the best thing to do. And I'm just gonna say it again. I've evolved from the Ossicano Allograft crew. Not that I still love them, they're great. But for a young patient, I see those increasingly. You need to take a hard look at autographs. It has a quick return to sport. And regardless of what approach you use, you have to use some verification of the physiology of what you're doing. If you did an autograph, you damn well better verify that those damn autographs are healed before you have them start running around. So that's when you pick it, you can do it. I typically do mine at three months, because typically when they're feeling good and they want to start to load a bit. And then I do another one at a year. And everyone's all about it. Because as we know, these recoveries are never linear. They're always meandering. So I love the autographs. Listen, you have an MRI, it's fine. Keep going, right? So and it gets them through the rough patches. So whether it be ACI, I'd say personally, I'll do MRIs at my Ossicano Allografts at six months as a precipice of clearance. On my Macy's at six months. On my PJAX at three months, just to make sure it has some fill. I do three months, not because I think it's all done. There are a few that don't work. And I want to know at three months if it didn't work. Because if it didn't work, I can tell the patients it didn't work. Do you want to keep rolling with it? Or do you want me to do something else? So it just gives them an opportunity to participate in their own care. So there's a long-winded way of saying, you have to use some verification objectively with imaging to help you make that decision, which I do for all my patients. Great. You don't sound excited. Well, I mean, listen, you do the same stuff. I mean, Andreas and I share patients. And I'm like, what do you think? I'm like, well, you can do it. I can do it. I mean, we both can do it. Like, it may not change how you do. No, I mean, Chris did it with poison, you know? So it's a great field. I mean, I'm just going to say something as the older guy. I have affiliations with everybody on this screen. And I think that's very telling. Like, it's a small group. These are hard cases. But we do such a better job now than we used to. Like, I really would be saying, like, wow, like, I'm out here in the wilderness. I'm drilling. Chris, you'd be in my hour. You'd be like, oh, man, we're drilling condos. It was a little crazy, right? Just kind of going for it. So, you know, it's great to have some camaraderie and hear people's experience with it. Because what are we? We're not chronic surgeons. We're early degenerative surgeons. That's what we are. We're trying to effect some change longitudinally, make patients feel better. But we're also trying to help their joints to survive, which is really the challenge. So my hope is the next time we talk, we have a little bit more color around the biologics involved and maybe getting those covered. I mean, this is just a tough environment to be practicing medicine. You know, the last cynical thing I'll say is, you know, it's very galling when you see the graft and the facility and the repair device, they're getting paid five times more than you get paid for this. But you're shouldering all the load of it. It's really, it doesn't make sense to labor a love and you do good work. But at some point, you know, we got to take this mantle back. Because we are kind of operating with one hand behind our back with these patients. Yeah. Well, thank you guys. I appreciate it. We ran a little bit over time. And we only lost a few people. So it speaks to, you know, what people value here and how well this went. So thank you. Good to see you guys. It was great. Thank you. Thanks so much. Thanks, Chris. Thanks so much. And thanks, Chris, for putting this on. Thank you. All right. Thanks, guys. Thank you.

cartilage repair

online learning

surgeons

patient expectations

evidence-based decision-making

joint homeostasis

biologics

autografts

allografts

patellofemoral joint

individualized treatment