Welcome to the 8th webinar in the AOFAS 2020 Classic Webinar Series, TALIS Osteochondral Lesion Treatment. This webinar will be moderated by Dr. Eric Giza. Joining Dr. Giza is Dr. Dominic S. Carrera, Dr. Christopher D. Kruin, and Dr. Michalis V. Hogan. You can find their full biographies and disclosures in the program handouts, available for download by clicking on the handouts tab on the right side of your screen. The 2020 webinars are provided free to AOFAS members and orthopedic residents fellows, with funding from the Orthopedic Foot and Ankle Foundation, supported by grants from the following companies, Major Grants, Arthrex, Inc., Additional Funding, Wright Medical Group, and Envy. I'd like to run through a few housekeeping items before we kick off the presentation. Please make sure your speakers are turned on and that the volume is turned up. For technical assistance, you can reference the help tab at any time. If you have technical difficulties, your best bet is to close all your browsers and log back in the same way you did the first time. If you experience any buffering issues, please refresh your browser. Registered physician attendees may earn one hours of AMA PRA Category 1 CME credit by completing an evaluation in CME claim form at the end of the webinar. Links for claiming CME are provided in the handouts tab, and you will also be reminded at the end of the program. This webinar is being recorded and will be available in approximately one week on the Physician Resource Center at www.aofas.org. You are encouraged to ask questions during the presentations. To send your question to the faculty, click on the question mark icon on the bottom right of your navigation column. I'll now turn the program over to Dr. Eric Giesa to begin the program. Thanks, everybody. Sorry, I was just getting my presentation ready to go. I want to thank everybody for tuning in tonight, thank the AOFAS for putting this together, and also my fellow panelists. Hopefully, we all can update ourselves, learn a little bit, and go ahead and be able to answer some questions for you at the end. As we all know, talus osteochondral defects and injuries are often very difficult. It's funny, with the fellowship starting next couple weeks, I always think to myself, oh, this is the greatest thing. The fellow comes in, they're like, oh, we got an OCD case, that's going to be awesome. I'm like, yeah, they're not so awesome when you start treating them and following them for the long term. When patients do well, it's fantastic, but when they don't or they fail, they're often difficult to treat. Approaching it from an algorithm basis is a good way to go. These are my disclosures. Good reading, where pretty much the entire references for all this is in Volume 39, Issue 1, Supplement of 2018, and there's been a more recent supplement too. It's the consensus meeting of the talus osteochondral defect with treatment from around the world. This is good reading for the recommendations from the thought leaders and experts in the field. The talus osteochondral defect is something that is an ongoing clinical challenge. For many years, it was just thinking, oh, we'll just microfracture this and then it'll make new cartilage, but we really have to treat the bone underneath. The ones that fail are the ones that have persistent edema. When you look at the anatomy itself of the talus, there's three to six times body weight across the talus. There's no tendons that attach to it. There's multiple ligamentous attachments, and 60% of the talus is covered by articular cartilage. The mean thickness of this cartilage is a lot thinner, as you can see, than the femur or the patella. What that means is it has different properties. It also has a very tenuous blood supply, and the nutrition for the cartilage itself is diffusion through the joint. Because the blood supply for the talus itself isn't that great, once damaged, the cartilage heals with fibrocartilage. As we know, highland cartilage has a limited capacity for intrinsic repair. Because the chondrocytes are in their matrix, they are often unable to migrate to the site of injury for repair, and surgical intervention is often required. If you look and think of the pathology of this, of course, it occurs from ankle sprains, subchondral fractures. You have two main types where you have the cartilage and bone involved, and then the less common ones where, and maybe more acutely, where you go in and you see the cartilage is delaminated from the bone, and the subchondral bone is intact underneath. Obviously, microtrauma with chronic instability, acute ankle sprains, ankle fractures, a more recent study showed about 33% of ankle fractures have an associated talus osteochondral defect, and then there's some association with vitamin D deficiency for some of those that are more chronic or maybe the bone is just not healing itself. Certainly, we don't have time to get into it tonight in terms of ankle instability reconstruction, but if you have a patient like you see in this video here with gross instability and an osteochondral defect, you have to address that instability or a varus or valgus hindfoot at the same time. We have to think of this as an osteochondral lesion of bone marrow. For the last two decades, we were focused on cartilage, cartilage, cartilage, and once there was stable cartilage repair construct, the thought was the bone can then just remodel. I think in the next 10 years, we're going to find that perhaps we need to address both the bone marrow lesion underneath as well as the cartilage. If you look at the pathology, the micropathology of this, you have your injury, your inciting event, and then the bone healing response occurs because you're not getting a cartilage healing response as vigorously. Then the healing response fails after time, and then what you get is fibrosis, neovascularization instead of new bone formation. This then goes down the pathway that Nick Van Dyke described of almost like a pressure gradient which leads the fluid in the ankle, the synovial fluid, to then create subchondral edema and cyst formation. Then that's what leads to the pain, the bone marrow lesion, if you will. The subchondral bone itself supports the articular cartilage and absorbs most of the joint reaction force, but it dissipates the stress in an even fashion. It responds via Wolf's Law. If you have an injury to that, you're going to get edge loading, and you don't get the normal biologic process to promote healing. If you look at this very basic little graph, if you have bone rigidity, you have the inciting event at this point in time, and it tries to remodel. After time goes by, the remodeling kind of gives up, and it ends up creating this bone marrow lesion because you have inferior quality repair tissue. The osteoclastic remodeling and removal of damaged bones occurs, but you get mineralization in some spots and not in others, and it leads to this bone fatigue. Here's kind of a video that shows you a bit about the inferior bone quality. We've all been there and seen this. When you go to curette this bone, you notice that it's almost like chalk, and it's really filled with neovascularization and other factors. You can see that it's just not very quality. You can't leave that such as it is. When you look at these bone marrow lesions, again, you find this bone fibrosis and decreased mineralization. The other thing that we've started to focus on in the last decade was, what is the bone marrow lesion cause of pain? This study, of course, this was a knee study, but the ones with more bone marrow edema are the ones in the knee, in particular, for mild to moderate arthritis, were the ones that had increased odds of reported pain. I think we have to look at that as part of our treatment algorithm for the future. When it comes to workup of these, the X-ray imaging, you always get an X-ray, but you don't always see it. MRI, as we know, is very useful. It helps in your preoperative planning, determine the stability of the lesion. Certainly, when I go to the OR, before I go, I always like to get a CT scan, because sometimes the edema can be misleading, and the actual cystic change can be larger or smaller than you see. A nice study that was out a couple of years ago, for those of you who have SPECT-CT and 3D-CT, certainly that's an option to use as well. We won't go into the specifics, but there have been a couple of grading systems to help you with your management. We'll get into the algorithm, and then I'll turn it over to my colleagues for the way they approach different size lesions. We have to look at acute or chronic, where is it, what's the size, is there bone edema and depth, did they have a prior surgery, and then what's the coverage insurance issues, what's the cost, and international considerations from country to country of what you can use, allografts, autografts, come into your thinking. Your options are stimulation, like microfracture and retrograde drilling, your replace or repair with transplants and different cartilage grafts, or regenerate, where you're utilizing the patient's own chondrocytes that are being grown out in a lab, and then you're re-implanting. There are a lot of options still available, and we get into these debates at some of the academic meetings, and what you find is that so far, our outcomes, regardless of whether it's grafts, whether it's bone marrow stimulation, they're all hovering in that 80 to 90% region, so we know we haven't found the perfect answer for each one, and maybe what we're trying to figure out is that, or understanding now, is that size matters, and hopefully we can all agree on that, so many years ago, when I was training at Mass General, Tom Minus, who kind of pioneered the whole knee cartilage concept, he sort of said there's edge loading in a two by two centimeter lesion in the knee is what led to increased pain, and there's been some good studies now from HSS, as well as one study from Choi, is that this seems to be the number, and microfracture doesn't work as well when you have a lesion that's greater than 129 to 150 millimeters squared, so in that, and the reality is that's where most of these lesions fall, and so we're going to talk about the different areas, and we can think about it as this size-based algorithm, small, medium, and large. I'm just going to do a quick whirlwind around the world, because it does differ by country and experience, and there's been great papers reported from all. In Japan, they certainly used AutoGraft, and have talked about fixing unstable lesions with a little AutoGraft cortical spike. In Korea, there's been some good work about using adipose tissue to help import outcomes, adipose MSCs. Turkey, obviously, as we know, the early studies really pioneered the mosaicplasty, and then for revision situations with large cystic lesions, our colleagues in the Netherlands have reported the metal implant. There's going to be some other ones we'll talk about tonight. The juvenile allograft has been reported upon, and there's actually a study in this month's FAI regarding that. They're good outcomes, but there's a possibility that cost is an issue, and then in Australia, US, and Europe, a thing called MACI is available, and MACI itself is an AutoGraft cartilage, so you actually harvest the cells, grow the cells out, and then re-implant them as a second operation. There's been some good studies showing that it works well. However, it's off-label in the United States now. It's on-label for me, but the cost is significant, somewhere in the range of $40,000 if our American insurance doesn't cover it. So, are we confused yet? I am sometimes, considering to know what to do, so let's see if our panel can drop some knowledge, for those of you who are Hamilton fans, and then Dr. Carrera is going to start us off with microfracture, talking about sort of maybe some of the smaller lesions. We'll move into medium-sized lesions with Dr. Pruin, and then Dr. Hogan is going to tackle the tough ones, which are the structural allograft and AutoGraft, and then if we have some time, we'll get some case discussions and questions from the audience. I'll turn it over to Dr. Carrera. Thanks, everybody. All right. Thanks very much. Thanks for this opportunity to present before you. I'm going to focus on microfracture, as Eric has mentioned. I trained with Dr. Steadman, who originated this technique, and one of the things that I learned from him that I think is important is that microfracture of the ankle can be very tedious and time-consuming, and doing a good job, particularly in the tighter ankles, can be quite a challenge. In some cases, it can be a five-minute, easy technique, and at other times, it can be much more complicated than that. Here are my disclosures, none of which are relevant. As a background, the term osteochondral defect, or OCD, I will use in reference to all of these other terms that have also been used to describe osteochondral fractures or lesions of the talus. In terms of non-surgical treatment options, generally, progressive mobilizations have been the key in terms of treatment with low success rates, generally with conservative treatment, in the range of 25% to 45% has been published. The one group of patients that I think should be looked at more carefully in terms of treating more aggressively, non-operatively, are those with acute non-displaced lesions. These, I think, should be treated with six weeks of mobilization. The report by Steele showed about a 50% success rate in these patients. Microfracture historically was used as the first line of surgical treatment following the failure of non-operative measures. The success was strongly and inversely correlated with the lesion size, and that's proven to be true over the years. The study that I think really has pushed me to do microfracture, especially early in my experience, was this study of 105 OCDs, and there were essentially no treatment failures with a small lesion of a diameter less than 15 millimeters, and with a single failure with a lesion greater than 15 millimeters. Whether the microfracture is a true gold standard, I think that's really been called into question, including for lesions smaller than this, and we'll talk about that a little bit more. In terms of indications, as I mentioned, non-operative treatment failure for three to six months, both tibial and tibial OCDs can be treated both of traumatic and atraumatic origin. The depth of the lesion generally should be less than five millimeters, and that was also based on the AOFAS consensus statement, and as mentioned already, lesions of less than 1.5 centimeters squared. Contraindications, depth of greater than five millimeters, any generalized degenerative findings such as with arthritis, patients unwilling to undergo non-weight-bearing rehab protocols, and any lesions that don't meet these criteria, really, there are many other options, as we are discussing tonight, that should be considered too. So the role of microfracture. Back in 2016, there's a statement that there appears to be consensus on the indication of arthroscopic treatment for those that are smaller lesions, and I would say that, particularly in athletes now, I don't think that's a consensus. I think there's been a trend away from microfracture that's followed the experience in the knee, particularly in professionals, and also based on the consensus statement that was published in the AOFAS. In talking about the physiology of microfracture, just getting into a little more detail, it involves punching holes, tiny holes, into and through the subchondral bone. This introduces bone marrow access to the chondral lesion, which leads to a repairative clot. This reparative clot is multipotent marrow-derived cells that heal and adhere to the surrounding area, including anchoring to the intact surrounding cartilage. The type of cartilage that is created is primarily type 1 cartilage and not the type of cartilage that we're born with, which is hyaline type 2. In terms of the technique, establishing good shoulders to the lesion is important. The standard arthroscopic approach is used. Loose body removal, debridement of any soft tissue or loose cartilage, and that can be done with shavers, burrs, curettes, both ring and cupped. Important is this removal of the calcified cartilage layer, perforation of the subchondral bone, the picker awl, and various angles can be used. I would encourage you to use ankle-specific awls because of the challenges of the access, particularly into the deeper recesses of the joint, and there are ankle-specific microfracture systems that help with this. Also, verifying that marrow-derived elements have eluded from the site is important. These are some additional pictures. A here shows removing that unstable cartilage, B showing shoulders to the lesion, following removal of calcified cartilage, C is penetrating into the subchondral bone. Most of the awls will have a color-coded section that gives you an idea of how deep to penetrate with it. And lastly, you can turn off the pump just momentarily to see if these bone marrow elements actually exude from the microfracture. In terms of looking at outcomes, a few different studies have been reported. Two-year outcomes, this particular paper had 95% good to excellent outcomes in 2005. The study that I previously quoted for small lesions, a meta-analysis of seven qualifying studies included 299 ankles in 295 patients. Good to excellent results were in 80% of patients. I generally tell patients that most of these osteochondral techniques have about an 85% success rate, although there's different indications for the different types, and I think microfracture falls into that as well. Here's a study reporting outcomes from 399 patients for tailored dome lesions at different locations, and what they showed was that the shoulder-type lesions had substantially worse clinical outcomes than those that had more contained lesions. They also reported that age did not affect clinical outcomes, although microfracture, particularly in the knee in several studies, has shown to have inferior outcomes in patients over 50. Finally, there's a second look arthroscopy study with MRI that showed that there was comparable tissue quality only in 64% of cases. 36% of these cases observed inferior tissue quality, though these patients were also shown to have functional improvements with the procedure. Thanks very much for your time. Okay. All right. Well, my name is Chris Krulin. I am sitting in the office next to Eric Giza over here in sunny California. Hope you guys are all doing well. I'm going to talk about augmentation of microfracture, more looking at what kind of scaffolding techniques you might be able to use, and look at some of the literature out there as well. There we go. All right. So, as we've already discussed a few times, there are multiple surgical options. From debridement to marrow stimulating, we have cell-based therapies. We also have different types of oats. But I'm going to be talking more about the different types of scaffolds that you can use. So, the overall goal of any augmentation or scaffolding used in an osteochondral defect is, one, to improve on the microfracture treatment, two, to encourage the integration of the cartilage, and also encourage the cell inoculation and migration, and then to do it with minimal risk, and then also to try to be cost effective. So, first one I'll quickly talk about is micronized cartilage matrix. And the principles behind this is that it's an allograft cartilage extracellular matrix. So, it's decellularized, then dehydrated, and then micronized. It's a scaffold for cell attachment. It's relatively cheap and it's easy to use arthroscopically. You don't have to cut anything. You can just kind of squirt it into the area after microfracture. Typically, people are mixing it with PRP or bone marrow concentrate. And the idea, like I said, is you're trying to improve the cartilage regrowth or the tissue quality within, after a microfracture. Some people also like to refer to it as microfracture plus. So, when it came out, there was some supporting data looking at animals showing that there was, filled with this micronized cartilage particulate being in place. And when they did histology, they saw that new cartilage cells were present, and there was some relatively normal proteoglycan appearance. Our lab was able to look at the use of the mesenchymal stem cells mixed with this cartilage matrix. And when, after only three weeks in a chondrogenic media, you were able to see that there was cartilage matrix, which was dyed blue in this picture. There were live cells around the cartilage matrix. And so, this kind of proof of concept showed that there was some differentiation of cells around the cartilage matrix, and that it could potentially lead to an improvement of the fill of the defect after a microfracture. So, you know, micro cartilage matrix can be used as a scaffold to help grow cartilage. There's been one article a couple of years ago that looked at 30 patients with OCDs less than 1.5 centimeters. They had a mean follow-up of 20 months. And there we go. And then what it showed was that their pain scores went down and their functional scores went up. So, that's a good sign. And a recent abstract that was at the AOFAS in 2019 from HSS looked at 197 patients with one-year follow-up. And there were three groups. One group had microfracture with micronized cartilage matrix and bone marrow concentrate. One had just bone marrow concentrate, and one had microfracture alone. Then they used MRI to evaluate these patients. And overall, there was not a significant difference in MoCART scores. The cartilage matrix ones were a little higher, but not significantly higher. But what they did notice, which I thought was quite interesting, was that the revision rate was much lower with the cartilage matrix compared to the other two. And overall, they saw that the outcome scores were the highest with the cartilage matrix and the bone marrow concentrate. And they felt that it improved the radiographic and functional outcomes of patients, and it had relatively low risk. And therefore, they thought it was a good idea to use it with microfracture. So again, with the technique, so always, we all know that we recommend a preoperative MRI to help plan and identify the lesion and help understand how deep it is. It helps you show the need for bone graft if needed. And then also recommend the CT. Standard setup, I typically have the leg externally rotated off the side of the bed with a leg holder. I use a non-invasive distractor to help distract the ankle once I'm doing the microfracture and cartilage work. I like to use a 2.7 millimeter scope. Some people still like a four, but I find it's just easier to move around the small joint with the 2.7. I have a 1.9 available for tighter joints. And then I've also started to really use the 70 degree lens and find it much easier since so many of the OCDs are on the shoulder. I found 70 to just be a lot easier and I don't have to fight as much to get a good view. So if you haven't tried that, I recommend it. It takes a little while to get used to, but you'll find it to be much nicer. So then you can curate the lesion back to a stable border. You microfracture, then turn off the inflow and you dry out the joint. If you need to extend the portal, you can do that or you can, and you can also apply a little more traction at this point. I like to use these sponges to dry out the joint. Sometimes the sponges even can hook up to suction and that really helps it out as well. Then here's the cartilage matrix being mixed with the PRP and then it gets applied. And here it is getting applied. And sometimes you have a paddle, sometimes you don't. But once you feel the lesion, you can then pat it down with a freer elevator. I recommend not having it be as high as the surrounding native cartilage being a little bit lower one. You're going to get a little hypertrophy of the tissue in the fill of the defect, but also it helps you hold in the fiber and sealant that you're going to place afterwards, which you can see right here in this video, placing it over the lesion. So after a while of using micro cartilage matrix, we had also had some acute ones where we would cut up the cartilage and place it back in and not use anything else. And so we got to thinking, well, what if we took that damaged cartilage? We know from a previous study that we did with our mentor in Australia, Martin Sullivan, that the damaged cartilage that is taken for Macy, because they were doing a lot of them in Australia, was very viable and the cells all lived. So if we cut that up and put that back in, maybe we could create an even better construct. Jeanine also showed this in 2005. So we started to work on a technique called, which we now call AutoCart. We used to call Pacey or Particulated Autologous Chondrocyte Implantation. But you take the chondrocytes from the OCD, that the damaged cartilage is viable. You use a matrix to provide a scaffold and then you combine these two and you created a nice, relatively inexpensive, single stage matrix augmentation of your defect. And here's a picture of what it can look like. So here's the old method. We'd send the resident or the fellow onto the back table, use this little cutting board from an eye tray. And they would do that while you did the rest of the work in the ankle. But recently we've been able to use this cartilage collection device where you can resect all the cartilage here using the shaver. And this device hooks up to the back of the shaver and catches all of the cartilage fragmentation. And it basically creates this nice kind of articulated matter that's much smaller than we could do with a knife and forceps on the back table. So then you can take that and mix those two together. And here it is getting injected into place. And then you can pat it down with a freer. And you can see you can get a very good feel of the defect. There's actual cartilage cells in there and then mixed with a matrix to try to help encourage some migration. Add some sealant and then here it looks quite well. And the patient at one year had this MRI. I recently just saw this gentleman and he was doing quite well and back to running on a daily basis. So here's another case example, a 29-year-old student who was a PhD student. She was bouldering and fell and presented with this MRI. To understand what that line was in the subchondral bone, I also got a CT and it didn't necessarily correlate as well to the MRI as I was hoping. But I knew that she was going to need to go to the operating room. So upon evaluating this lesion, it was found to be unstable. You can see if I push on it right there, boom, it pops up. There are different kinds of techniques to treating this based on its location and the instability. It felt surrounding area that there was still some loose bone underneath that needed to be addressed. So the lesion was then or that loose flap of cartilage was then removed. And in this case, we had to bring it to the back table and cut it up. That ended up being the lesion. There was a lot of fibrous bone underneath this. I think that flap of bone was and cartilage was acting like a one-way valve. So then in this case, we injected some of the micro or the particulated cartilage, added a little. In this case, we mixed them together in the patient and sit on the back table. And then that's what it looked like in the end. And then added some sealant to cover it. Typical rehab protocol for these is probably fairly similar to a lot of us. Non-weight-bearing for 10 to 14 days in a splint. And then around that time, put them in a CAM boot, start physical therapy and range of motion. I start progressive weight-bearing at 25 to 50% at four weeks, depending on the location of the lesion. And then I want them out of the boot at about eight to 10 weeks. And then I don't let them run until about four to six months. Here was that patient at 11 months post-op. So still had a little bit of a defect in the bone, but we typically can see that in a lot of these. But she had no pain and had returned to activity without restriction. I think that increased signal seen there on the T2 images just represents some ongoing remodeling of the area. So there's been some literature on this autocar technique in FAS. Dr. Sullivan was able to do that on a acute lesion in a rugby player and had him back at playing at 23 weeks, which was pretty good. So some other scaffolds that are out there that aren't really used in the U.S. as much in the ankle as they are in Europe and other locations. So I'll go back. The top one is your HIAF it's called, which is a heliuronic acid matrix that basically creates a heliuronic rich bath of fluid and material within the Taylor defect. And people can impregnate that with cells as well. And the one below, which is used with a lot with Macy, this is the cartilage or the collagen one, three, type one and type three matrix. This is used for Macy in the knee and in the, you can use it in the ankle, but it's also got some other uses where people just use the actual matrix and don't have it impregnated with cells. So we'll review that. So one term that's commonly used in the literature is this amic or autologous matrix induced chondrogenesis. And basically you're performing a micro fracture and then placing a piece of that collagen one, three membrane over and then sealing it in the place. There's been some literature from the Italians on this technique. It's gone to an arthroscopic technique and a two-year follow-up. All the patients were improving on their outcomes. And then also you can see there was an improvement in the findings seen on CT and MRI. In Germany, Martinus Richter has had a couple of papers regarding what he calls his mast technique. And this is basically taking micro fracture with bone marrow concentrate from the iliac crest and then adding the collagen one, three matrix. And this is a continuation of his two-year follow-up study. And he had a hundred of 124 patients follow up in five years. So pretty good. And the average lesion was 1.7. If you've ever seen him talk about it, he can do quite a large lesion on this. As you can see, the range went up to six centimeters. And preoperatively you see their VAS scores and they improved. And he has a pretty good discussion in this five-year paper talking about the role of MRI and how to take good MRI images. But what he also noted was that if you looked at MRI from two years to five years, you continue to see improvement in these patients. So it looks like there's probable remodeling that continues for a lot longer than we probably follow these patients. There's another similar to the mast technique called the BMDCT or bone marrow derived cell transplantation. Again, it's bone marrows, but this one, you're in one of the articles, they use multiple different types of matrices, but primarily heliuronic acid or the high up graft. And what this article looked at athletes, so 140 athletes, and again, their outcome scores improved. And by 48 months, 72% of them had returned to pre-injury level. One interesting finding they had was that patients that required removal of spurs or had noted fissuring within the cartilage around the lesion representing arthritis did not return to sport as easily as patients who had no arthritis or no bone spurs. So in summary, I think it's clear that scapulting does enhance microfracture and you can do it in a single stage, which I think everything's going to move towards single stage just because of cost and simplicity compared to a two-stage procedure. The goal is to make sure it's low cost, low risk. And the three most common are this micronized cartilage matrix, the heliuronic acid one, and then also the collagen 1,3 membrane. And then while I was preparing for this talk, Dr. D'Ambrosio and Ussuelli in Italy quoted, this is from one of their discussions talking about, it's important to find scaffolds that are able to promote regeneration of the subchondral bone as well, because in the end, that's the fundamental piece that is needed to create a coating that is more similar to hyaline cartilage. Because I think we are doing a pretty good job of trying to address the cartilage and getting these hyaline-like fills, but we still have a lot of problems with the subchondral bone. And I think that's what we really need to talk about. And so that kind of leads into what Dr. Hogan will talk about with plugs that already have bone in them. Great. Thanks, Chris. I'm loading up here as we move here. So, you know, inherently what we're talking about. There we go. So, great tee up for this and as we really talk about the problem of the subcontra bone, which is one obviously we've been talking about for some time now and that we continuously are trying to meet this challenge. No disclosures with this. And so, a little bit on the background. I mean, we recognize that we have improvement FAO, FAO scores with osteochondral autographs in some cases. And so, being able to optimize this is what we're speaking toward. This ties directly into, again, one of the position statements that came from our consensus meeting here in Pittsburgh, and from our international college group that all the faculty here are part of. And just really how do we continue to drive this from the bodies of work that are being done to really look at how we can do this better and continue to improve. But what's special about the ankle is the differences, the pathology that we've discussed, the architecture, also the access to get to the ankle to address these problems, complex problems, and also the natural history of disease. But also the thickness of the cartilage, and this speaks to, you know, that variability of the knee versus the ankle that we all recognize as foot and ankle surgeons and adds that layer of complexity. But it also brings into play more readily the subchondral bone and how important it is for recovery here. The concerns that we have with marrow stimulation long-term, some have been mentioned already, of fiber cartilage is biomechanically inferior to type II hyaline cartilage. I believe all of us are likely advising our patients, I can help you and make it better. Hopefully, I can make you, but I won't make you great, and I won't be able to provide you with what you were born with. And this progressively degenerates over time in response to mechanical loading of the joint. When we look at microfracture as well, that number of the 150 millimeters has fluctuated. It's likely gone a little lower between 100 and 150, but again, as these lesions increase in size and also as we can recognize more subchondral bone involvement through our preoperative assessment and evaluation with MRI, with the edema patterns that Dr. Giese spoke to, but also with the CT scan, it gives us more information. When we talk about osteochondral autografts, it involves transplantation of one or more tubular units of cartilage harvested from the ipsilateral knee in the majority of cases. I had a patient the other day, which has been interesting. She had a complex PCL injury on that knee, and the parents asked me to use the other knee, and I said, so I'm going to give you, now you may have two bad knees for the sake of making your ankle better, but it's a complex discussion. And mosaicplasty is one form that was mentioned in some cases just by Chris, highly cystic lesions or secondarily after they failed index procedures. But I believe, as has been alluded to here, more and more we're considering, should we be thinking about a primary OATS procedure and some of these lesions that we know the subchondral bone is involved, and we're hoping that it will help us heal these lesions, but not necessarily sure. And when we look at this, the inherent advantage here is to include replacing the defect with viable hyaline cartilage and also with an adequate bone plug with a subchondral bone construct. The potential issues that exist, need for graft harvest and donor site morbidity, differences in the surface curvature between the graft and the host tissues, particularly when you have to take from the knee to place in the ankle, poor potential for spontaneous healing at the cartilage interface of the graft, and a lot of our work in biological adjuncts are really looking to address and optimize that. And also the possible need for an osteotomy, as Dr. Krulin mentioned, I think as our techniques and surgical techniques continue to be enhanced, even using different arthroscopy, different angles, I anticipate that over time, our ability to minimize the need for an osteotomy will continue to be the case, though it is a technique that we all should know and understand and the implications of that. The biomechanics of osteochondral grafting, with the autologous grafts, you do get partial restoration of contact mechanics. This study was done in 10 fresh frozen cadavers with a degree freedom robot and showed that. And when we really look at this, you have to place the graft in a congruent position, as congruent as possible. And as we look further, studies have shown medial and lateral grafts across a variety of graft heights, peak pressure with one millimeter proud graft. And you get 675% more pressure with a lateral that's proud one millimeter and 255% for a medial and 56% versus 23% respectfully for countersunk. And so you want to err on the side of countersunk as opposed to proud. And, you know, for, I remember when I was a resident, you know, this is over a decade ago, and individuals would say, well, leave a little proud so that when someone weight bears, it'll actually sink to the appropriate level. I've erred away from that based on this study and others. You really want to have this at the surface or just a little countersunk if you can't get it perfect. A good medium to long-term outcomes of the systematic review, Bazagary and his group show clinical success of 87% with donor site morbidity of 12%. Another study by Hagedy and his group, a thousand bazaplasties, 98 of which were in the talus, 90% good to excellent results based on the handover scoring system, 3% donor site morbidity in the knee. And the study by Murawski and Kennedy and his group, good results with 72 patients at 28 months and also less than 5% donor site morbidity at the knee. And again, I think this has improved as our techniques with knee harvest have improved and respecting the soft tissues of the knee when you harvest the graft. And when we look at this study, looking at oats in an athletic population, 38 amateur and professional athletes, a greater than 150 millimeter lesions, follow up of 45 months. This is by James Calder and his group, and 87% return to their previous level of play. A very impressive, strong correlation between their MoCART scores and ability to return to sport. Two patients had donor site knee pain and three had plugs and both had three plugs harvested. So there potentially is a small correlation with the number of plugs necessary in the amount of residual donor site morbidity or pain that may occur. Single and double plugs, 14 patients at five year follow up mass controls, equivalent results, both clinically and radiographically with a single versus a double plug, particularly when you take the crescent type technique that's listed here versus two large plugs and shaving back. And when we look at, obviously the discussion always is, are you robbing Peter to pay Paul? I am from the camp, and I think many with the literature would agree at this point that autograft transplants do function better than allografts, particularly in the talus. But 26 patients with 26 studies with 915 ankles were included and 6.7% assuming that patients were lost to follow up and 10.8% that were. And we looked at this estimated 2.8 to 5% of donor site morbidity. So is the osteotomy a concern? I believe with the right techniques, the concern can be minimized and mitigated. It does add to the recovery and it does add another variable that you have to monitor during the postoperative recovery period. And so you just need to face that. And it does add a component for the patients. But it's very important, if you feel you need an osteotomy, to truly give them the best shot at the title and a positive outcome. You need to be comfortable moving forward with doing that. So 62 patients underwent a Chevron osteotomy. The median amount, 34 and a half month follow up, 32 MRIs, 94% of the patients were asymptomatic at the osteotomy site. And also T2 mapping revealed restoration and relaxation times in the tissues at that level. Are cysts a concern? Again, a lot of the work around OATs coming from a group in New York, 37 patients, MRIs in mean 15 months. About 65% had some evidence of a cyst. There's variability with symptomology with this. Increasing with age showed an increase in cyst formation. Again, speaking to that subchondral bone deficiency. So clinical impact was not found to be significant in this case. So what do we know? There are some concerns with OATs. They do well in larger lesions. It may be a great option that you want to consider, even in a primary setting. That's how I approach patients in a unique fashion. Can we improve the outcomes? We're doing a number of these things that Dr. Krulin and everyone here has spoken about. Trying to enhance the biology of bone marrow aspirate cells, bone marrow aspirate concentrate. Some are still adding PRP. I usually use bone marrow aspirate in isolation with this. Autograph and allograft solutions as well as growth factors. My usual cocktail is a combination of bone marrow aspirate concentrate. And occasionally I will add some minced cartilage, juvenile cartilage or minced cartilage to that bowel cartilage. And so, as you say, what else are kids good for? The cells, the umbilical cord, blood studies are really expanding more in Europe than here. We'll have to see how that expands going forward. So keep your biological adjuncts and adjuvants in mind. I add these in all the cases of OATs. I'm really trying to optimize that interface healing in the scenario where I have a OATs procedure where there is a significant cyst. I will also bone graft from the calcaneus to fill that bone void up to the subchondral plate until I have my plug to make up the difference based on the depth. So so it may be due to the shortcomings inherently of our ability to move with it. So remember what matters. Thanks and great group. Looking forward to the discussion. There we go. Yeah, the mute button was sticking. So, I'm just going to show, we have a couple of cases. There were some questions in there from good ones from folks. Somebody asked what is the sealant? And that at this point in time is fiber and glue. Tisial is the commercial name. And the other one was about the harvester that Dr. Kroon had presented on. And its name is the GrafNet. And that commercially, this isn't a commercial promotion of them, but that's made by a company called Arthrex, specifically for that purpose. And so, I have a few, we don't have that many questions and we've got a few minutes. So, I was just going to stump the panel for the next couple of minutes. And then we can answer more questions. Here's a case. This is a 17-year-old girl. And hopefully our panelists are off mute here. She had pain after a ballet performance. She fell and she had this. And her MRI showed this here. So, I'll start off with Dr. Hogan. What would you do in this situation? So, thanks. So, I would obviously want to assess and examine for concomitant pathology, instability, impact of the perineals. But looking at this image, in my mind, it's an unstable lesion. It's a lateral lesion, likely did occur from this acute event, significant inflammation and acetylbitis in the anterior aspect of the joint, as well as posteriorly. So, in my mind, that's unstable. I would want to move forward. The edema pattern, again, as you mentioned, sometimes it overreads, but in the acute setting, you should expect an edema pattern of this size. In some cases, I may get a CT scan based on the amount of time from the time they presented to me from injury. But otherwise, I would just move forward with this, in my mind, with arthroscopy, debridement, with the initial plan of microfracture, with bone marasper, concentrate augmentation. But to have everything else ready in the event, it's more than meets the eye. Okay. So, definitely take to the OR. And so, this is what it looked like. It actually was one of those that had bone and cartilage. It was a big enough flap and it was still, about half of it was still attached. So, in this case, I'll switch over quickly to Dr. Krulin. If it's not detached and there's no plastic deformation, what's your choice here? Would you take it out and do the auto cart, Chris? Yeah. So, I haven't had good success with trying to push them back in. If it will fit in place easily and I'm not fighting it, I might try to debride a little bit of fibrous tissue underneath it and then try to secure it in place. If it still is kind of attached but I can't get it in the place and it doesn't look that symmetrical, I then just remove it and cut it up and glue it back into place. Which is what Dr. Hogan mentioned. This was one of those rare ones where I was able to push it back into place. And there, I had put one dart there and then I was putting a second one in. And she did really well. You're not going to see that very frequently, but just keep it in mind. As Dr. Hogan mentioned, kind of having everything ready to go in these scenarios. Okay. So, this is the one that I think we all mentioned. In the interest of time, I'll just show you what we did. This is called a lift lesion that Dr. Ferkel had mentioned. And this one was flipped 180 degrees. And just like Dr. Krulin mentioned, this was one, when I went to flip it back around, it had undergone plastic deformation. And you can see here, it just, it didn't fit. It didn't fit back in where we wanted it to fit. So, we took this and we did the technique that Dr. Krulin described. Okay. We'll move to our last one real quick. A couple minutes. We have Dr. Carrera. I have this poor unfortunate soul who, a 40-year-old golf pro, had a microfracture. Didn't do well. The operating surgeon decided to do an allograft OATS. And you can see here, the OATS wasn't integrated. Probably wasn't deep enough of a drill. And he had pain for 14 months. So, this is what it looked like. Thoughts here, Dominic? Yeah. So, it clearly looks prominent. And so, it needs to be removed. There's a base to it also that's concerning with somewhat of a sclerotic base to it. So, I think in terms of options, I think the base of that bony lesion, I would want to prepare in terms of penetrating it and trying to create a better healing environment with an overlying micronized cartilage probably is an option. But I would personally go to a revision autograft in this case. Okay. Dr. Hogan, because you gave us such a nice presentation on OATS, would you go to... This was an autograft. Would you go up to the knee on this one and then get a plug? Redo? In the redo, I would go to the knee, you know, talk to them about it. I would go to the knee and redo. These sclerosis that I see there at the interface, right? Right at the interface of the normal talus seems pretty significant. And that's just concerning to me. I would lean toward a plug if the patients were open to it. Great. So, I get in there and actually the OATS plug, the top, the cartilage, just lifted off. So, it was unstable. But underneath, some of the bone had integrated. So, Dr. Kuhlman, what would you use in this situation? We don't have that autograft, autocartilage here. So, in just a 10-second thing, what would you use? I would try to do just a micro-anodized cartilage matrix with some microfracture and add a little PRP or bone marrow concentrate. I still see people do quite well with the, with that technique. I try to avoid doing the osteotomy if it's possible. And if they then don't do well with that, then I would look more to something that needed an osteotomy. Okay, good. And those are the options. This one, I actually used some bone graft. This was a mix of calcaneal bone graft mixed with some de-mineralized bone matrix. And I went ahead and did the juvenile allograft over top. And this was one that did well for that. So, I appreciate the panel's input on all this. I'll turn the screen back over to our colleagues at AOFAS. And then we got just a minute or two left. And we'll scroll through and look at some of the questions here. And let's see. We talked about alignment of rear foot for chronic osteochondral lesions. I don't know if the other panelists can see all this. Obviously, in the setting of malalignment, definitely you need to correct the malalignment if you're going to fix an osteochondral defect. And then we talked, somebody had a case about the lateral ligament stabilization. Certainly, we do that at the same time. There are lots of different techniques and commercial products available for the lateral ligament stabilization. So, that's dealer's choice. I often reach for a product called the internal brace, but that's my preference. I'm sure others have ways to fix it as well. Anything else? Anybody else want to answer? The juvenile cartilage, you do have to plan ahead. It takes a couple weeks to order. And you have to get insurance approval. Tom, there's one question in the last second about microfracture. Do you want to take that one? How deep do you go? What size microfracture all do you use? Yes. So, the depth of penetration has been studied at three to four millimeters generally. And in a one square centimeter area, the spacing between the points, the microfractures can be as close to two millimeters. So, they're actually, there's a lot of penetrations. I'll try and get even seven, eight, nine in that small of a space with care not to over penetrate as it widens the holes. And that's based on the basic science that was done in horses at the time that microfracture was developed in part. And then it was further studied in some comparative work where there was a difference in the number of holes that were made in the early clinical experience in the knee. Great. Thank you very much. And I think we're about ready to wrap up. Somebody did ask about cost and I had mentioned that in my slides in the beginning. And it's really going to vary by state. I wish I could tell you that I had a bat in a thousand for every single one I tried to get approved. And sometimes you're shape-shifting a little bit. The insurance company will approve one thing and not the other thing. So, I wish I had an easy answer for you, but you still at least have, you can rely back. The micronized cartilage that Dr. Pruan talked about is only about $750. So, the mix of that with PRP is probably the lowest cost. And of course, the autograft knee that Dr. Hogan mentioned is also cost-effective as is a micrograft. So, I think that we are out of time if I'm not mistaken. So, we welcome more questions. People can certainly email me directly. It's eGiza at UCDavis.edu. And I want to again thank our panelists. I want to thank Julie and everybody at the AOFAS. And we look forward to virtually seeing everybody at the AOFAS meeting this fall. Thank you, Dr. Giza. We have come to the end of tonight's webinar. I want to thank the faculty for their excellent presentations and discussions. To claim CME or CE credit, please click the link located in the chat box on the right side of your screen. To receive credit, you must complete the evaluation first, and then you may claim your credit. On behalf of AOFAS, thank you for spending time with us tonight. Please visit the AOFAS websites to learn more about other upcoming programs and activities. Have a good night. Thank you again. Thanks, everybody. Thank you.

webinar

Talis Osteochondral Lesion Treatment

osteochondral lesions

talus

microfracture

chondrogenesis

OATS

subchondral bone

case examples

healthcare professionals