We're going to move on to treating OLTs with the SCOPE. We have a great lineup for you. First, we're going to introduce Eric Ferkel, who's a good friend of mine from Southern California Orthopedic Institute, and he's going to talk about bone marrow stimulation technique. Good morning, everybody. That was a phenomenal talk, Dr. Van Dyke. Thank you very much for all the insight that he provided. I want to also thank everybody for being here. Here's my disclosures. We thank Dr. Hogan, Dr. Kennedy, Dr. Hunt, Humbert, Gus DiGiovanni, and all my mentors and colleagues over the years. So, my talk today is going to be about microfracture, bone marrow stimulation, and the talus for treatment of osteochondral lesions. We look back at the history of microfracture, it begins with Dr. Steadman from Colorado in the 1980s, where he was beginning with the ice pick idea, and initially described this technique in 1992, published at a seven-year follow-up in the knee, 80% success rate. If you look at the idea of articular cartilage regeneration by stem cells, typically begins with cartilage formation at the edge of the cartilage, and if you look at how microfracture works, typically with fibrocartilage beginning with inferior stiffness, however, inferior resilience in weak and wear properties. However, there's improved function in patients over time, and a second look in 36% of patients at three and a half years in one study showed incomplete healing. Let's look at the etiology of a condal defect, typically due to trauma in 93% to 98% of patients on lateral talar dome lesions, and on medial talar dome lesions, 61% to 71%. If you look at the natural history at a two-year follow-up, 89% of these traumatic lesions were found. If you look at the treatment options for osteochondral lesions in the talus in 2022, obviously non-operative management is one of the options. The talk today that I'm giving is on microfracture, but there's multiple options, as Dr. Van Dyke just showed. Osteochondral grafts, MACI-particulated cartilage, even resurfacing implants, and if you look at the Venn diagram of treatment options for osteochondral talar defects, for one centimeter squared or less, you have multiple options, including microfracture, and then one to 2.5 centimeters squared microfracture, as well as one of the options. The factors influencing my choices on OLT surgical procedures are the size of the lesions, acute versus chronic, the location of the lesion, either shoulder or the containment, as well as the cystic status, as well. We look at the strategies on how we approach thinking about cartilage restoration, either as reparative or replacement, and in this case, we're going to discuss reparative options today. In the traditional elements for cartilage regeneration, you need the kind of holy trinity. You need the growth factors, the scaffold, and the stem cells, and we're going to begin talking about how you can help to bring all those elements to the area of healing. Looking at Dr. Van Dyke's study, that was one of the landmark studies with Dr. Van Bergen in 2013. It showed excellent return to sport, return to work, and 66% progression, limited or no progression to OA in his patients. So Laura Ramponi in 2016 further expanded kind of the size idea, where we can say the marrow simulation is the best, and in her study published in AJSM, she showed that 107.4mm squared or less really was the best size for marrow simulation, and 80% of the papers showed level three or level four evidence on that. So this gives us different technique options for how you can do microfracture. There's awls, which go back to the Dr. Steadman era. There's newer options, such as the nanofracture with either a smart shot, which is proprietary, or nanofracture technique, and then there's mechanical power tools, and then you can use a K-wire as well. My preference is to use a 0.035 smooth trocar tip K-wire, and the idea is to achieve vascular access into an avascular region. In the traditional microfracture, you have the cartilage trimming to the edges, have perpendicular edges to allow healing from the edges. And then the traditional angled awl is roughly perpendicular to the bone, you mallet it in, usually about two to four millimeters in depth, and the idea of the awl is it actually widens a little bit, which in my mind actually can contribute to further problems, which we'll show in a moment here. Another question is how deep is too deep, or is there deep enough? So traditionally, the awls went about three or four millimeters deep. Some studies suggest you need to go six millimeters deep. I think we're still looking at the data, but the consensus would show probably less than five millimeters of depth is the way to go for the talus. So for microfracture with a 0.035 smooth K-wire, I typically do it one to two millimeters apart, about five to six millimeters in depth. You can go a little deeper if you need to, if there's a cystic element to it. I don't use threaded K-wires, and you want to have the water on constantly to maintain the prevent heat buildup. The idea is you want to have smaller, deeper holes. And then if you're harder to reach zones, you can do trans-taylor drilling or trans-malleolar drilling. So there's a lot of different devices you can use in your arthroscopy sets to help achieve that. Another thing to think about is the idea of the surface diameter and how the compaction happens with your K-wire. So typically, in an awl, you're seeing here you have a border with a high regularity. With a nanofracture or a smaller technique, you have low regularity and a high regularity with the K-wire. When we look at the microfracture of the awl, the problem is that you're having limited trabecular channels, and you're having a more compressed bone deposit. When you look at a K-wire, you're actually seeing well-defined channel walls outlined by those fine osseous deposits. The problem is the trabecular channel access was limited, so you're not getting those marrow elements coming in to help bring healing. And then newer techniques using smaller devices, either with nanofracture device or a SureShot, you have less irregularity and more open trabecular channels, allowing for those marrow elements to seep in. So the idea with the SmartShot is you have less bone compaction, bone resorption, and better bone remodeling. And that's shown that you have improved bone healing at four months in this histology study on the bottom. So let's look at some of the studies of OCDs and microfractures. Dr. Van Bergen showed in his study that I mentioned, you have only about a third increase in OA, one grade, 74% good, excellent results. In another study in arthroscopy in 2008, showed lesions less than 1.5 millimeters had no failures. When augmenting with platelet-rich plasma, there was improved outcomes here in this study in KSSTA with better AOFAS scores, FAM, and VAS scores. Again showing PRP or hyaluronic acid as an adjunct to help improve healing. This is a prospective randomized control trial. And FAI showed at 15 months, better AOFAS scores in the PRP group versus HA or saline. Again, a more recent study, again, showing this is retrospective by Dr. Choi using this scoring system that there was minimal failures at second look and improved FAS and AOFAS scores. So augmentation has been shown, I think, to help improve your outcomes with bone marrow simulation. You can use concentrated PRP from the bone marrow aspirate. You can use PRP from the blood. And the idea here that was shown by Dr. Fortier in her landmark study that you have improved histology with the microfracture and the concentrated PRP group in the staining study that she showed in her JBGIS paper here. The idea is that you're creating this crimson duvet leading to improved fiber cartilage formation with the microfracture by augmenting it with the platelet-rich plasma and I'll typically activate it with calcium chloride and thrombin to help let it stay in the injury site after I've evacuated all the fluid. In this consensus statement by the ICCRA group in Pittsburgh in 2018, it concluded essentially what we just talked about here, that you should have less than approximately 100 millimeters squared for the bone marrow simulation, less than about 5 millimeters in depth, and you should use concomitant techniques if you're treating with greater lesions. Let's talk about weight-bearing as Dr. Van Dyck just showed in his previous study. Excellent outcomes with early weight-bearing and treatment of OLTs. For me, I typically will keep them non-weight-bearing for the first couple of weeks, begin active range of motion weight-bearing around two weeks, and then progressively out of the boot by about four to five, six weeks post-op. Just to switch topics real briefly here, talking about osteochondral lesions of the tibial plafond, microfracture is also an excellent option here in treatment of these injuries. Typically, for my patients with an OLT of the tibial plafond, debridement, microfracture with augmentation, but there are other options as well. Here's a quick case to discuss, and I respectfully would argue that you should consider arthroscopy with ankle fractures, and this is the reason why, because it's an opportunity here to perhaps treat an acute osteochondral lesion of the tibial plafond in this patient who had a bimalleolar ankle fracture. This is another patient here who had an OLT treated non-operatively for nine months, and after a conservative measure had failed, I treated it with a retrograde trans-tibial drilling here with bone marrow aspiration, and then returned to play at about six months. She was doing excellent, and I want you to call her a scholarship here. So just to review the literature in OLTs of the tibial plafond after arthroscopic microfracture, again, excellent study. This was done in 2019, showed that there are satisfactory outcomes here with improvement of activity and function, and then a second study also showed similar results in this 31 patients here. I think overall, if we're looking at bone marrow stimulation, it's an excellent way to treat your patients for specific kind of lesions. We still need to do further studies here, especially with augmentation, head-to-head comparisons of microfracture with augmentation need to be considered further, as well as concomitant studies of kissing lesions, as well, I think would be helpful to further improve our literature database. But I think consider bone marrow stimulation as an option for treating your patients for both OLT and tibial plafond lesions. Thank you very much. Dr. Ferkel, and it's my great pleasure to introduce a very good friend and colleague and long-time member of ICCRA, Dr. Eric Giese. And Eric is going to talk to you today about the defect that needs collagen, when and why I use allograft. And I think what we'll do, for the sake of conciseness, we'll ask questions from the audience at the very end of everybody's presentation. So, you know, the interesting thing about talus OCDs is when you look at all this literature And we're all talking about different techniques and things that you use and there's Macy and there's AC And there's all these things It's kind of like bunions, right? There's 85 90% good, but there's about a hundred different ways of doing it and I think over the years that's been kind of the You know sort of the the Don Quixote kind of thing where you're chasing What is gonna be the best technique and I've certainly done that myself and when it comes to talus OCDs I remember when I was a fellow I was like, oh man, this is great We got a talus OCD case and then you have your successes But then you have those patients who come back eight years later after their microfracture and you're like, oh man, it's back So so they are difficult to treat. I think so Okay So I want to thank doctors Hogan and hunt and all my AFS colleagues and all my colleagues from around the world We have I think we have a great community here. These are my disclosures So this is an osteochondral lesion of bone and as dr. Van Dyke showed that you know for years and years We always just thought cartilage cartilage cartilage But we have to we're really repairing the cartilage or doing something the cartilage so we can get the bone to heal And when you think about the way that this bone slowly remodels It's when the injury occurs and then there's some time period where you get, you know Abnormal cellular recruitment and they're replaced by inferior elements So the OCD algorithm for me is not just hey, I always do microfracture. Hey, I always do this It's it's you know, especially a subspecialist. We get to these folks come in here. Is it acute or chronic? Where is it? How big is it? Of course we can agree on that but it Usually by the time they get to us, they've had one or two prior surgeries So they've already had that microfracture and then you have to address. Geez. What about what about coverage and cost? Okay, so not every pick, you know I I mean raise your hand if Blue Cross said it was okay to use bio cartilage or micronized cartilage But you know, it's denied by Blue Shield or you know, it's it's kind of this random Thing that we have to take into account. I want to thank Dr. Ferkel senior for turning me on to this kind of Venn diagram idea But most of the ones that we're treating that we're talking about fit into this medium size. So we always get an x-ray It's not always that helpful. I find MRI Very helpful. Usually the patients will come with an MRI but but I would make the argument that you should also have a CT scan before you go to surgery so that you can really plan out how you want to address it and Certainly some good studies out of Europe have shown that that 3d CT Also can be very helpful. So size matters and I think that's already been mentioned. So I'll kind of go through Skip through that and and and Eric just gave a great talk on microfracture. I want to thank Jeremy for for this slide You know just kind of looking at this argument back and forth. Should you should you not I would I would Can make the argument that if somebody comes in and they have a failed microfracture and they have this persistent edema You know, it's less optimal to do a repeat thing and that's it's hard to sell to a patient, right? Like Einstein said help. Well, you've already micro fractured. I'm gonna do it again and hope for something different. So These cell-based regeneration things. I've you know been in various studies over the years Trying to prove which one's good which one isn't is, you know, and we want to help our patients But they are expensive and some of them require two surgeries. So scaffolds do work There's been a couple of studies showing that so the concept is what are we going to do here in 2022? What's the most cost-effective and arthroscopic approach? So what I've settled on to my partner Chris crew and have settled on to is using a micronized cartilage scaffold but adding autograph to it, so This stuff actually came out of a tumor surgeon at Miami And it is a commercial product. I have no financial interest in it but it does it's this dehydrated micronized cartilage that can be used as a scaffold and it's only $750 but Chris Krulin and I really wanted to prove that you know, because everybody said oh it's acting as a scaffold It's acting as a as an attachment site. So we published this study where we created a little mini joint and We found that it does actually act as a scaffold for for for neo chondrocytes So the short-term outcomes from that Have been shown also in a follow-up study 31 patients You know showing improved promise scores and then this one with larger study From HSS showing short-term outcomes in a large number of patients So I think there's a reasonable argument to use it because it's pretty cost-efficient and you're really just Augmenting what is your bone marrow stimulation technique addition of bone graft? There the concessions statement was that if it's four to five millers deep consider I use calcaneus autograft Just to put in before you add whatever you're going to use on top So for me the future for medium-sized lesions is using the patient's own cartilage and adding it with a micronized cartilage scaffold And you're able to take the cartilage from the patient because if especially if it's a primary lesion Why I just feel like why would I just throw out that that cartilage cap? So I set it up. I usually do use distraction when I'm doing cartilage procedures There's some commercial products out there that have like basically a little stiv so you harvest it it chops them up They did some studies to kind of show that it does not Is that video gonna play there there goes? It chops up the cartilage and it only had you know, obviously some of the chondrocytes are gonna die We know where they where they were cut But at the same time it's about a nine eighty five to ninety percent viability of the cartilage cells And so you have yourself some nice graph there and it only only cost you the cost of a shaver Um, so then you cure at or do your micro fracture or whatever you decide turn off your inflow and Then here's here's how it's kind of mixed up and you mix it with BMAC PRP. Whatever your choice is And then dry up, you know, obviously you need to dry the lesion And then apply the graph to fill the defect and here's what it looks like going in Pretty easy to do And you only need two portals. I find rarely Do I need a posterior posterior lateral posterior medial portal and smooth it out with an elevator? And then apply some fiber and glue wait a few minutes and then check your range of motion So that's what it looks like after you're all finished So Auto cartilage or whatever you want to call it. It's less than $2,000 American and all done in one step So the future I think may this may be one of the techniques. Obviously, we need to have studies There's been some some, you know level four evidence here. We described the technique in 2018 Here's a case example, this was a 26 year old male. He's a professional volleyball player He had an ankle sprain and they finally got an x-ray because he was you know Didn't didn't rehab and you can see that he has that lift lesion the lateral intracondylar fracture of the talus and so that that fragment was completely flipped around 180 degrees and It was too small to fix. So do I want to walk away and leave a professional volleyball player with basically a 20 by 15 size lesion So what we did was we chopped up that cartilage mixed it with the micronized cartilage scaffold Added a patient's own PRP and then put that back in there There's a fiber and glue going over top So rehab protocol I am now Start starting to weight bear a little bit earlier. I'm starting at four weeks, but it sounds like there's a good I'm now convinced that we always like to learn at our at our symposia. So I guess I'm gonna start at two weeks This was before he could I also did a arthroscopic lateral ligament on him The the team wanted a follow-up MRI before they'd let him back to play So there's kind of need to have a follow-up MRI at five months, but he was back doing his thing. So in summary Scaffolding does enhance your micro fracture in my opinion single a it's a single stage autographed added which is low cost and low risk and Again want to thank everybody for their attention All right, so next up we're going to see Dr. Collins going to come up and talk about when to use an osteotomy. Just a brief announcement prior to the next speaker. We are definitely aware of the construction and the some of the banging that everyone's hearing and so we're working on that and thank you for your feedback on it. We're aware of it and the society's working on it. Thank you. Hi, Nick Cullen. Nice to meet you. I've come over from the UK and I'm going to be talking about osteochondral lesions, know when to hold them and know when to perform an osteotomy. So disclosures, this is the Royal National Orthopaedic Hospital from where I work and this is a picture that was taken a hundred years ago aerially and this is a picture of it today so not much change but we love working there and if anybody's over in sunny London then please feel free to drop in and see us. So let's talk about the osteochondral lesions and considerations for surgery. As we've talked already that the indications for surgery are patients with persistently symptomatic lesions who failed non-operative management and it presents a significant impact on their quality of life. So we've got a couple of pictures here of examples of a couple of patients we treat who are playing really good high-quality sport who have osteochondral lesions. They're managing very well with these osteochondral lesions being monitored on a regular basis and these have little impact on their quality of life and they're able to perform to a good level. So these aren't the patients that we're looking at doing surgery for. When we look at osteochondral lesions there's a huge amount of procedures that we can consider. So some of these are arthroscopic and there's a whole multitude of open procedures that we can consider. So from my point of view I try and divide these into a small and a medium and a large osteochondral lesion. I think the central bit here, I'm afraid the images have been overlapped, looking at this as a volume is quite helpful. So the small lesions are those that are less than a hundred and twenty-five millimetres cubed. The medium ones are 125 to 1,500 and the large much much bigger. And it's these large volume and medium volume lesions that are where we're controversial. So the question we ask ourselves is size everything? Well just the size we need to take into account other things. If we've got a loose body, an unstable lesion that's causing mechanical symptoms we may prefer arthroscopic treatment. In those patients that we see polypathology with impingement lesions, instability we've talked about, it may vary our treatment. The kissing lesions, we all have patients who've had failed surgeries for osteochondral lesions and even in those lesions that we feel they may respond well to arthroscopic surgery. You can't keep banging your head on a wall repeating arthroscopies. So those patients with one, two, three failed arthroscopic treatments provide a treatment conundrum. So the management of smaller lesions less than a hundred and twenty-five millimetres squared or cubed, I think these tend to respond very well to arthroscopic treatment and there's very little controversy with this. Those small number of patients who might have an intact cartilage cap we could consider subchondral drilling, although in my practice that's something that we see relatively rarely. So where the controversy starts is for those medium lesions moving on to the big lesions and we know that these have poorer results with arthroscopy and the bigger the lesions are the poorer the results. What are the issues? We've got to address not only the articular surface but with a lot of these a big bony defect as well. So in the ideal world we're looking at a large to medium osteochondral lesion we need a reproducible procedure that produces some kind of high-quality cartilage lining that can be used across whether it's a shoulder lesion, a cystic lesion, very deep lesion and ideally not involving adjacent joints of damage to these. So we've traditionally had the ACs and MACs as a more complex procedure but this is a two-stage procedure which makes it difficult. We'll come on to the matrix-induced chondrogenesis. The oats has been a successful way of treating the osteochondral lesions but those of you who do this procedure, sometimes it's quite difficult to get a decent match of the cartilage to the surrounding cartilage to get a nice smooth surface and with the shoulder lesions it can be quite challenging because we really find it difficult to harvest an oats where there is a shoulder lesion. The allografts, if you can get these in the very big lesions, can be helpful in the UK. We struggle a little bit. We've just heard about the particulated juvenile cartilage as a reasonable option. And then we've got various resurfacing techniques. I put a star for arthrodesis. So once we get into these bigger lesions we're talking about joint salvage surgery and I tend to talk to my patients that if a joint salvage surgery fails we may need to think about something definitive such as an arthrodesis or a replacement. I think it's helpful to have these conversations early on in the management. So what problems do these advanced techniques, whichever one we choose, pose for us? Well in summary it's really access to the lesion and its visualisation. When we look at the bigger osteochondral lesions then most of these, four out of five of these, are going to be in the medial or post-remedial aspect of the talar dome which makes access particularly difficult. They're challenging lesions for arthroscopic management and trying to get in to access these to confirm that you've debrided the deep cystic lesion and then to be able to confirm that you've impacted your bone graft and you've got a nice smooth lining of what you're laying on top is really difficult. One of the silent things that is very difficult to quantify is once we're trying to get bigger lesions in and debride these deeper in the joints what kind of collateral damage are we incurring from getting the cartilage in and providing a good cover here. So the alternatives, well a step medial cut malleolar osteotomy provides excellent access and there's a pretty low morbidity from this. So you can see on the blue line here, this is the pattern of where we get the osteotomy and we can fold down that medial malleolus. Do we need a medial malleolar osteotomy? Well there are a few studies that show with the more anteriorly based, so those one-fifth of lesions that aren't post-remedial, you can get a pretty good access with a wire distractor and you can open the joint with an arthrotomy. You can see here this is the Polish group who've had some success with these at the anterior aspects of the joint. Once you do a medial malleolar osteotomy in a fold down then sometimes the access appears a little bit limited. You have a sweaty period where you can't quite see you have a good access to the joint and I've found this wire distractor is really helpful. You can get it right down deep at the insertion of the deltoid ligament so you're not in the non-articular area and you're just into the plafond. When you jack out that wire distractor you can really see the medial 50% of the joint and get an excellent access. The first thing to do is debriding this osteochondral lesion which you can do with curets and a small osteotome and scalpel, a periosteal elevator and we tend to try and puncture down into the subchondral plate. We tend to do that with a wire. You've often got to go a bit deeper than you expect. You feel a little give as you get into the subchondral plate so you get down to those nice mesenstymal stem cells. Managing the lesions, well traditionally we've used oats. More recently we've tend to move on to the matrix induced chondrogenesis in our unit and this shows that various reports of pretty good results from the AMIX and the HAMIX. Again with size these can be used across the board with the smaller and the larger lesions and the results seem to be maintained whether in a smaller or larger lesion and they can be used in the cystic and the shoulder lesions as well. So it comes as a small pad here. You can see this is being laid over the osteochondral lesion itself and then it's carefully cut back until you get it to be exactly the right size. Once you've got it to the right size we tend to soak these in bone marrow aspirate that we've aspirated from the ipsilateral pelvis and then it's glued on with this some T-seal glue which we glue in place and you can really have an excellent access from the osteotomy and see that you've got that well aligned and well seated down and flush with the articular surface. The osteotomy is closed and fixed with a couple of screws. So the larger lesions we tend to have a bigger cystic component and the bone defect is the problem here. So people have tried trephines, oats procedures we've talked, tricortical blocks from the pelvis. If you can get fresh allograft that can be helpful as well. These are the kind of lesions we're talking about. From our modified technique with the medial malleolus osteotomy we've usually got a really good supply of corticocancellous bone from the metathesis. So we tend to use the trephine 10mm that we use from an oats and we can use a 10mm drill hole right into the middle of that osteochondral lesion. We overtake some of that bone from the metathesis so we can leave it a little bit proud. Then you can trim that down so it's absolutely flush with the articular surface as you've impacted it and then lay your haemic on top. So these are the types of arthrograms that we look at. They're big deep cystic lesions and after a haemic with bone graft we can see that the articular surface is reasonably well restored. And finally in the future we've been looking at using some of these 3D mapped replacements such as this which is an EpiSeal where you can have these 3D devised and patient specific instrumentation with a surface that really moulds perfectly to each individual's articular surface. Perhaps this could be the way forward. In summary, symptomatic osteochondral lesions are amenable to surgical treatment. Small lesions, there's little debate, probably respond best to arthroscopic debridement and bone marrow stimulation. Medium lesions and revision lesions will need some regenerative or replacement technique. The higher lesions require bone graft and the vast majority of these are there over the posterior medial talus. These are difficult to visualise, difficult to access so I would suggest that you consider an osteotomy which has a lay morbidity. Thanks very much. Very well done. We all know those are challenging cases. So next up we have Mark Dracos from HSS and I think as you can see there's a big interest that some kind of biology is going to be what the key is for the future for treating these lesions. Hello. Thank you for the intro and the intro music. So I appreciate the opportunity to speak today. Thanks for organising this and the invitation from Dr. Hunt and Dr. Hogan. So today I'm going to talk a little bit about biologics. You're going to see a lot of repeating themes here but it makes me actually feel a little bit encouraged that I'm not on an island. These are my disclosures. So the focus of this talk is basically going to be on how can we improve outcomes and I'm going to focus specifically on BMAC and PRP and ultimately what some future directions are going to be. So not to rehash this but the current status of cartilage repair due to the avascular and acellular nature, this complicates its natural capacity for regeneration upon damage. As we've heard about multiple times when trying to categorise these, this is really a mixed bag. So if you look at the picture on the top left, this is really what I would call an osteochondral lesion that involves both the cartilage on the bone. The picture on the top right is more an osteochondral fracture which could potentially heal by fixing it. The one on the bottom left is really a delamination where the subchondral plate is intact and the one on the bottom right is really like an osteochondritis desiccans which I think of more as a nonunion. So the point is besides size this really can be a mixed bag in terms of what you get. And as we've heard about there are a number of current surgical options which include reparative and regenerative and replacement strategies. Now the biggest challenge I think for me and for us is that there's such a big divide between doing something arthroscopically and a big open approach. If you can do it through a minimally invasive approach and get a similar result that would obviously be ideal. So we talked about microfracture. The biggest issue is that it heals with fibrocartilage. So if you do these second look MRIs you'll see the picture on the top right. So essentially it has a different texture. Multiple studies have shown 60 to 80 percent having cracks and fissures. Long term results are mixed and larger and shoulder lesions do poor. And I really appreciate Dr. Van Dyck's talk. Ultimately though if it feels good that's great but I would hope that it both looks good and feels good. And for the people that are you know ardent microfracture protagonists I would argue get post up MRIs and maybe you don't feel so good about it anymore. Now long term that may or may not make a difference in terms of arthritis but ultimately if we're trying to correct the pathology we'd like it to be as normal to a normal anatomy as possible. So let's see. So how can we improve outcomes? So I believe the focus has shifted from procedures to biological interventions. And there's a whole host of biologics that we can discuss. And again I'm specifically going to discuss BMAC and PRP today. So this is a really important slide. So what I would argue is that there's a healing triad for these lesions. So and that involves three major things. So stem cells or progenitor cells growth factors and a scaffold. And in any bioengineered environment these three components I believe are optimal to necessitate cell regeneration and renewal. So what's BMAC? BMAC has emerged as an important regenerative tool containing mesentimal stem cells and growth factors for cartilage repair. So there are cellular contents including these mesentimal or progenitor cells that can be obtained from bone marrow. But with the current technology we can only get a small concentration. So this is what I usually do. We usually get about 60 cc, spin it down to about 3 and then mix it with something. And you're only getting 0.01 to 0.1% of the cells that in theory have the potential to become the tissue that you're looking to regenerate. However there are also growth hormones and cytokines including PDGF, TGF-beta and some other things that may be useful for healing as well. So one of the other things that's difficult when dealing with specifically BMAC and PRP is that the BMAC itself is a mixed bag. So there are cellular contents as well as the growth factors. But very few of the studies that I'm going to discuss right now actually look at what they're injecting into people. So they inject it and see how they do. But not many of these studies actually take what they inject and put it in flow cytometry and do an analysis of what they're actually getting. And when you get kind of nitty gritty into the weeds on this stuff there's a very specific set of criteria for what qualifies as a mesentimal stem cell. It involves some specific markers and a lot of what we may be injecting does not even qualify for that. So this is the study that we did where basically we looked at comparing the functional outcomes of Taylor osteochondral lesions repaired with micronized allogeneic cartilage extracellular matrix and bone marrow aspirate concentrate and we compared it out with a microfracture and the reason that we started doing this is I had kind of been taught like many to know that microfracture was appropriate and you know again there's nothing like follow up to ruin surgery and some of the patients weren't doing so well and some of those patients I made worse and you know I didn't feel great about starting off with a hole and sometimes making a bigger hole so the question to ask was what could we fill this with something that would actually improve the outcomes so what we did is we compared both patient reported and MRI outcomes for OLTs similar size groups similar ages tried to make it as close as possible and versus microfracture and what we basically found is then we when we looked at the post-op MRIs the MoCART scores for the group that we included the BMAC plus the extracellular matrix did better from a radiographic standpoint and also had a lower revision rate so we lowered the revision rate by about 15% and I think it was because we had better fill so we our conclusion was that the use of this adjunct therapy and the treatment of OLTs improved the repair of tissue when compared to microfracture alone and there are other studies in different areas which also corroborate this was a study by Gobi looking at the knee where they also involved you know a scaffold plus BMA and had better results specifically at the quality of the tissue repair now this was a really nice review by Dr. Kennedy and his group and leave it to him to rain on my parade if you just look at the title limited evidence of adjuvant biologics with bone marrow stimulation for the treatment of OLTs I'm just kidding I know he's a big biologics guy too but basically the important part of this study which is very very valid and very very astute is that there's not a lot of evidence to support this right now there are only two studies which looked at bone marrow aspirate plus a bone marrow stimulation procedure versus bone marrow stimulation alone and both of those studies ultimately showed no difference in overall complication rates this was similarly a corroborated by a study that had a little bit larger inclusion criteria by Dr. Clanton and his group which also suggested that you know the evidence at this point doesn't support just the addition of bone marrow aspirate you know in fairness in our study what we did when we had our microfracture group what we did is we split it into two arms so one arm was just microfracture alone and the second arm was microfracture plus an injection of bone marrow aspirate and when we did that if you look at the slide on the bottom left the MoCART scores were no different between the microfracture alone and the bone marrow aspirate group it was really the scaffold that improved at least what it looked like on MRIs and by the way when we did the scaffold it still wasn't normal hyaline cartilage and you know one of the challenges is if you look at like the picture at the top the MRI again a lot of these lesions of cartilage and bone and even if you bone graft it it's really hard to reconstruct that subchondral plate predictably and have it look normal on MRI but this is what it looked like from a clinical perspective so when you do this type of procedure you usually get good fill so I would argue and then when we looked at our outcomes of microfracture versus the microfracture BMAC there was no difference as well so I would argue our study kind of supported that the scaffold was really a critical component to all of this as well so moving on to PRP so what's PRP it has a high number of platelets and it has a high number of biologically active factors including growth factors cytokines lysosomes and adhesion proteins and the way it basically works is it involves the action of these growth factors which are released released from alpha granules of activated platelets these components are believed to be responsible for initiating the hemostatic cascade the synthesis of new connective tissue and revascularization and there's over a thousand growth factors and these are just some of them you know listed on the top right but again we get into when once we get into the weeds on this what is the optimal composition for PRP there's been a lot of focus on whether you use leukocyte rich or leukocyte poor with leukocyte poor PRP its clinical applications may be to reduce inflammation and this may be good for things like arthritis whereas the leukocyte rich PRP may be useful in things like tendinopathy where we want to increase inflammation so again not only just saying we're going to inject PRP in people but what type of PRP are we doing and what are the actual components of what we're injecting I think are really important there are studies that suggest that PRP strongly enhances the recruitment of stem cells so even though PRP itself may not have these mesenchymal stem cells or progenitor cells which can potentially aid in healing what they can do is if the cells are in the surrounding tissue it can attract those cells to the area that you want to have heal or regenerate and there's some data to actually support that so looking at the PRP clinical outcomes again there's not there's really a plasticity of evidence when it comes to this you know there's some data that suggests it's more effective than HA there are really two studies these middle two studies by Gunny and Gormelli looking at microfracture with PRP versus microfracture at alone where it suggested some improvement in clinical outcomes but again the the rigor which we studies were done wasn't great they're using AOFAS scores and also not a lot of radiographic or long-term follow-up so there's some suggestion it may help but again when you kind of hold it to the fire now how much is it really actually doing and I actually had trouble finding a lot of PRP studies with scaffolds with good results long-term as well so one of my issues with PRP and I kind of have a be fair I have limited experience is that the half-lives of these growth factors can be very very short some of the most important ones have half-lives that are in the order of minutes so you kind of wonder if after you inject it it's already been metabolized and this is where again I think a scaffold would be very important so it's something to consider so in conclusion I think we should all have a cautious optimism about biologics I think right now the hype exceeds the science but I do think ultimately we want it's both to look good and feel good and to get that we need this healing triad I think there is significant promise for the use of orthobiologics to augment soft tissue and bony procedures just because there's no evidence that yet doesn't mean it's not a good idea you know some of the other speakers talked about the cost related with these things you know I think some of the costs are reasonable and as long as we're studying it I think you know this is how we push the science forward so I routinely use them I would encourage everyone to do them and use a scaffold and publish your results to help us out thank you okay so to conclude this session we've got dr. Porter he's going to talk to you about all you need is bone arthroscopic autographed of Taylor osteochondral lesions thank you it's certainly a pleasure to be here and be able to distinguish symposium and so I've been challenged to talk about something a little simpler and we've heard a lot of sophisticated approaches to this I want to kind of talk a little bit about just bone grafting itself these are my disclosures so I should kind of relations of the Taylor's are common so we're all dealing with them a great deal about one second in the United States there's an ankle spring and lateral or at least some type of osteochondral lesions are common with ankle sprains so we see it a lot the question I think has been kind of brought up some we can talk more than the discussion is it a problem of the cartilage or is it a problem of the bone or is it the bone supporting the cartilage we know that with osteochondral lesions irregular surfaces create irritation and like a pothole in the road it becomes an irritant inside the ankle so it causes pain it can lead to loss of function and arthritis so the loose debris the irregular surface probably causes synovitis and irregularity causes problems with inside the ankle small osteochondral lesions do well we've heard that already micro fracture allows them remove some of the irritability remove the loose parts of the cartilage there's a low recurrence rate it brings in blood products but really all you're getting is scar we call it fibrocartilage but it's basically scar the larger ones we worry about so what do we want what is our goal what are everybody up here talking about we want a smooth durable chondral surface with firm subchondral support preferably bone and a stable ankle with the small shallow ones we know we do well with micro fracture they do well even long term as we've heard the larger ones that you've already been discussing are the challenging ones the ones that one and a half to two centimeters and greater than the ones that are deep if you take asphalt and put it in a really large pothole it fails over time because the lack of the support and softness micro fractures very similar in a large lesion where you have like a high high recurrence rate and there's just not enough support so what do we do with these medium and large size osteochondral lesions you've heard a lot of different options I've been charged with talking about micro fracture and autogenous bone graft alone a couple things just want to mention as many many studies dr. van Dyck mentioned several up here have been mentioned but a couple one this was a study that I think is very interesting because the cartilage is it was still viable lifted up the cartilage bone grafted with autogenous bone graft let the cartilage remain in the cartilage lived and became good and when they compared that with just removing the cartilage do a micro fracture the bone grafting of the underneath the cartilage was significantly better in all aspects the others just I think we if you think about oats and what is an O's for do we think about the cartilage and then and the auto autograph cartilage that you're bringing but it may be the bone that's most in support most important in an O's procedure you're re-establishing that good subchondral bone the bone quality looks better on on evaluation but the clinical outcomes are the same but there's decreased edema there's lower reoperation rate and so maybe what on an O's procedure and a lot of these procedures doing is bringing in new bone so what are we trying to do we're trying to fill up the hole with something that's sturdy that's that's durable and that is low friction so it acts like a cartilage and preferably is cartilage so the cartilage we think is injured because of poor bone foundation or subchondral bone so this is what we do we do this fully arthroscopic we we do a typical approach to the osteochondral lesion get it cleaned up do micro fracture and then kind of shuttle in the bone graft into the area of the defect we generally fill up the bone up to the level of the subchondral bone but not all the way up to the cartilage it's probably not a big deal if you do fill it up to the cartilage in our experience in my is my own personal experiences in Indianapolis we've done 234 osteochondral lesions of the talus over the last seven years that's a significant number 141 we did micro fracture alone 93 we did micro fracture plus autogenous bone graft we did broson reconstruction if the ankle was loose in order to give them a stabilized ankle and in the bone grafting group we had one that both medial and lateral three I'm sorry they're both medial and lateral osteochondral lesions which are particularly difficult lesions to treat so one of this is this is trying to articulate to you like which ones do we do bone graft from which do we not so the upper right hand panel you can see that's a fairly small lesion has been debrided just with dorsiflexion looks almost normal with plantar flexion you see it but it's shallow and it's relatively small but on the bottom lesion what you can see you see a very large lesion with a very large cavern and then we so in those lesions we do bone graft we bring in autogenous bone graft into the portal and then impact it with it with a freer elevator and I'll show you a video of that later just looking at our lesions and again we don't have all the statistics done I just didn't have time to get that done for this talk between the 93 micro fractures with bone graft and my micro fractures alone one of the things you have to remember is that with these large ones we bone graft they are large lesions they're all one and a half centimeters or larger they're deep they're probably four to five millimeters deeper greater and if you look at just their subjective outcome it's very similar between those small micro fracture only lesions that we all feel pretty good about when we walk out of the OR was also interesting to note that when we looked at doing a reconstruction versus ones that didn't require reconstruction doing a brostom brought them baked basically in the same type of results of ones that that weren't unstable to begin with this is just a couple slides to show you so here's a pre-op with a fairly large cystic lesion and this is surprising enough at about three and a half to four months post-op and again from a subchondra bone reconstitution I'm pretty pleased with how that looks this is one I just decide I'm not going to just cherry-pick and take just the very best one I said when's what's the last CT we've done an osteochondral lesion of the talus here's your pre-op imaging with MRI and the CT here's where we take the bone graft from the calcaneus and again this is not perfect but there and this tends to mature over time the bone does but it has a significant improvement and some reasonable bone in that subchondra bone to support the fibrocartilage on top this is the technique again the the area we go in the calcaneus about halfway between the tip of the fibula and the lateral calcaneus you can use a handheld seven millimeter trocar or you can use one of these motorized ones you'll get you can get up to probably two centimeters of bone graft is cancellous it's fairly morsel eyes you can see that's about little over one and one and a half centimeters of bone we didn't take the bone and we actually use the chromanizer cannula so it's already you've already used already paid for it and if you work really fast like this you can put it inside the cannula really quickly then you got it just in the end of the cannula like this go back do this go confirm that the rest of your your cartilage looks good go to the medial side is a medial side lesion here and you'll see a fairly cavernous about a 1.3 1.5 centimeter lesion that we again you want to get all the loose fragments out clean up the edges with the shaver and and then you'll see that we microfracture it after that so you've got some nice stable borders but that's a pretty deep lesion that's gonna be a lot of scar there if all you do is leave it just like that it will fill in with scar but is that really the best thing long-term so we've harvest our bone graft we shuttle our bone graft right down directly into the hole into the the pothole in the in the talus we do this still with the with the water on in this situation we do turn the water off and this is obviously an allograft video but in a true autograph we'll let the water off so it gets a lot of egress of blood up into the lesion which acts kind of like a fiber and clot for it we mash it down and really try to get it nice and smooth with a freer elevator so why why consider just an autogenous bone graft for osteochondrolysis cost-effective you're gonna scope the ankle anyway it's a $250 added charge in Indiana for Medicare reliable small puncture wounds your small bone graft harvest site other entities certainly are significantly higher cost one it's available you don't have to get a rep to come there you don't have to get special considerations we've never had a problem with insurance to date anyway you're doing the standard arthroscopy portals it's a low donor site morbidity uses seven millimeter trocar to harvest and you can choose your own site we think we can take a medium or or worrisome osteochondrolysis and basically convert it to a really small cartilage that do very very well with microfracture alone right so you've taken a bad lesion and made it a good lesion and it's low-cost and it's a very available so I use this now for all my initial treatment of osteochondrolysis they're greater than a centimeter deeper than three millimeters I use bowel cartilage only in some of the professional athletes and high-level athletes or one that there's no insurance issues I like it if there's containment but I've used them on shoulder lesions also I am a little more aggressive with weight bearing than what you heard on some of these other talks because I think the tibia acts as a kind of mold for the for the bone graft and the fibro cartilage so hope all your osteochondrolysis heal well thank you very much that's great so we've been told by the powers that be that we don't have an enormous amount of time for questions but but I think it is important because the panel has been discussing osteochondrolysis just to reemphasize that microfracture is part of bone marrow stimulation and I think our knee surgeon friends and those of us here who do a lot of this would agree that microfracture is probably not the right way to go in most of these it's easy patients do well for a few years and then they come back and so what I'd like to and I really like what dr. Porter was talking about in terms of putting in a bone graft in there because you really do need a structural scaffold in there and that's because the subchondral plate never restores after microfracture never it's very few absolutes in orthopedic surgery never restore so once you damage it it doesn't come back so if you don't have a subchondral plate whatever you put there ultimately will fail if the volume is large so for that reason I'd like to ask Eric how do you do your microfracture yeah and I agree 100% with what you said that microfracture is very for a very specific population of patients who have these small lesions like we talked about for me right now I'm using either a very small K wire or I'll use one of the devices that allow you to do a very small nano or the microfracture with a very small trocar tip it's really important like dr. Kennedy mentioned that you have to keep them spaced out and you maintain that subchondral plate is that really is about 30% of the compressive mechanical load in the ankle or in the talus is where the subchondral plate is so we want to maintain that prevent further collapse and the all's I think do create collapse and compression so really space them out keeping them very thin very small and having them go deep is important as well that's very well said so dr. Dracos you talked a little bit about BMAC I think it's important also BMAC really is a trade name it should be CBMA concentrated bone marrow aspirate how do you think CBMA works by comparison to PRP you talked about stem cells and do you think stem cells have a big role or you think IRAP has a role in I think it's probably more the growth factors as we said there's such a small concentration of it ideally we'd like to be able to manipulate those cells and expand them in culture unfortunately now it's still illegal to do that in this country because of limitations but I think that part of it is the growth factors in the cytokines and the chemotactic effect as potentially as well as an anti-inflammatory effect as well yeah I think that's important to know this there's a massive volume of IRAP interleukin receptor antagonist protein in concentrated bone marrow whereas by contrast in PRP there isn't so it has a trophic effect so I think it's an immune modulatory effect within the joint and chondro protective as well as chondro regenerative so I'll ask dr. Giza you have any questions we have looks like we're out of time so I do want to thank our panel all the speakers dr. Kennedy and of course dr. Hunt and dr. Hogan for having us all here and if the audience has any questions for any of us just come find us find me in the audience later happy to answer any questions

osteochondral lesions of the talus

OLTs

microfracture

bone marrow stimulation

autogenous bone grafting

biologics

BMAC

PRP

individualized approach