Chapters Transcript Is this the NEW Gold Standard Course: NYU Langone Orthopedics Webinar: Innovative Techniques in the Treatment of Ankle Arthritis So, without further ado, uh, we'll start on the current evolving strategies increase in treating cartilage defects of the talus. And this is in part about arthritis but also in part about Taylor uh trauma in the form of chondral defects and ostochondral defects. Right, so this is um our disclosures, arthrax and into bones are coned and this is the introduction uh concentrated bone marrow aspirate PRP HA scaffolds, and so forth. And for whatever reason, um, this is skipping ahead. So, nonetheless, osteochondral lesions of the talus, um, are more common than we thought. The ankle is the most commonly injured joint in the body. There's 27,000 ankle sprains per day in the United States, and all these up to 50% may result in cartilage injury. And unlike The uh ankle, or rather unlike the hip and the knee, there are no metallicoproteinases in the ankle to create idiopathic arthritis. So the vast majority of arthritic change within the ankle is from trauma or post-traumatic osteoarthritis. Now, this is Larry Bonasser's work from Cornell who we do a lot of collaborative work with, and this shows that the first 500 nanometers of all cartilage, whether it be from an elephant or from a mouse, is roughly the same in terms of its sheer dissipation, sheer energy force dissipation. So 90% of sheer forces are dissipated in that very, very thin layer. And when Henry Mankin says we're all gods, we all walk on water, uh, what he was alluding to is that there is a, there's a lubricine or a boundary lubrication on the surface of this. So if you damage this. Then the underlying cartilage surfaces are at higher risk of uh further damage and degeneration. And this is Etai Cohen, who works with Larry and some work we did looking at the injurious impact of an ankle sprain on cartilage, and looking at confocal microscopy here, this was a bovine etched cartilage, and you can see that what we're doing here is we're injuring cartilage in the same way that the talus would impact the tibia. Or vice versa, and within an hour, you can see that these cells um here are dead, and, and what we know about cartridge cells is um once they're damaged, they never regenerate in the same way. And this study here again from Fourtier's group looking at multiphoton microscopy. When we superimpose this on Anderson's um By modal distribution of regeneration and repair in cartilage, you can see that there's an initial phase of um cell death, and then that's followed roughly 2 weeks later, um by a catabolic rather an anabolic stage. But if you look at the multiphotonn microscopy, you can see that rather than these nice lacuar shaped chondrocytes. Most of the cells are being replaced um by proteo proteolycans or fibrous tissue, so it is not normal. And consequently, when you have large lesions, um, we are Then obligated to try to do something surgically about this because it simply won't repair on its own. So we look at reparative strategies, replacement strategies, and biological adjuncts. And I think now all of us agree that biological adjuncts are here to stay, um, and so that's what I will be talking about largely uh this evening. Biological adjuncts we're going to talk about are like that uh concentrate bone marrow aspirrate and uh and the rest as this slide has automatically moved on. Um, I will read out the laundry list, we'll get to it. Um, but nonetheless, this is what we're gonna talk concentrate bone marrow aspirate. These are the traditional elements, you remember, um, from medical school, you need growth factors, scaffolds in the stem cells in this Venn diagram where they will meet in the middle is the perfect milieu. Um, we're also gonna be talking a little bit about the These um names that we've borrowed a little bit from bone regeneration, and we're going to talk about chondroconductive, choroinductive, and chondroprotective. Chondro conductive is providing a scaffold for the ingrowth of cartilage. Chondroinductive are substances that initiate chondrogenesis in stem cells. And counterprotective will slow slow the degradation of the native articular cartilage, and each one of these topics that we'll talk about, uh, will be ascribed one or more of these characteristics. Now, the late great Arnie Kaplan has taught us all that the role of the stem cell was originally that if you have a multipotent, or pluripotent stem cell, and you put that into a particular biological environment, it will run down that path of differentiation, and it will create that. So we take a stem cell from bone marrow, we put it onto skin and it should reduce skin cells and so forth. And we realize now that there was And naive look at this, it was certainly the start of um cellular biology and regenerative therapies and MSK, but it, it is no long, it is certainly not the the end of it, and I think now we realize that there is a lot of trophic effects or downstream effects of stem cells. This again is uh Fortier's work on the secretome theory, and we will hear a lot about secrettomes and exosomes um in uh the coming, uh, in the future, um, in terms of how it affects our patients. Um, this is really what we're talking about. The secrettome, when you uh when you inject a stem cell into a particular environment, The macrophage or the um M0 cell will engulf that. Um and so if we were to radio label stem cells and inject them into a body or into a joint and look for them 24 hours later, the vast majority of these cells are gone. And where do they go? Well, this is what happens to them. They become engulfed by these microphages or monocytes, and then they become activated monocytes, whether they're M1 or M2. M1 are largely um pro-inflammatory. They're not good, so we want a good balance between M1 and M2. We want a greater number of M2 macrophages, and some of the stem cells that we use, particularly adipocytes, are M2 preferential, so they will create more um CD markers for chondrogenesis. They will have more anti-inflammatory uh role than the M1 macrophage. So this is what we call the secrettome. When you have a secretome or an activated macrophage and a small vesicle pinches off from that and goes into the extracellular matrix, that then can stimulate local stem cells to push down a path of differentiation. And they're the exosomes. They're things that industry is looking at very carefully to prevent arthritic change or address early arthritis, particularly in the ankle. Um, so that's going to be an area of interest and we should keep an eye out for it. And like anything in industry, we have to, um, We have to be somewhat weary. Right now in the MSK space, there's about 17 companies advertising that they have purely um chondrogenic exosomes. When you do a deep dive into these, there's just one company that truly has this, so be careful what's written on the package may not be, may not reflect what's truly um. Inside This was nicely um created by James Butler, our current fellow, um, and this again shows that when we inject conservative bone marrow aspirate, which has about 1% to 2% of stem cells, and it's taken up by the type A cells in the synovium, and it can produce either an M1 or an M2. CVMA pushes most of these cells on the M2 lineage, and so you can see that it produces the CD or chondrogenic um markers. It also has a very powerful anti-inflammatory, and many, many of these growth factors which responsible um for temporal sequence of cartilage regeneration and repair. But interestingly, the trophic effect on this is these M2 macrophages stimulate synoviocytes to produce hyaluronin and lubricin, which are chondroprotective. And also, if we extended this out a little bit, it'll also show that it turns off or it blocks IL1 and NKF cells which are uh pro pro-inflammatory cells. So it is a chondroprotective, um, it is chondrogenic in small amounts, and it is um. And it is an anti-inflammatory. So what's in a conservative bone marrow as, why do we use it in those patients who have uh early stage arthritic change or in chondral injuries? Well, it is um PRP on steroids, really, because it has stem cells, unlike PRP, it has a great greater concentration of this substance called IL1RA which is a very, very potent anti-inflammatory. It's like your own. Um, steroid in of itself, it's a very powerful anti-inflammatory and of course it has this multitude of growth factors of which responsible for regeneration and repair. So preferentially, if we could, we would, we would do CBMA in the office. It's difficult to do that, so that's why we use PRP which does not have the same quantity of stem cells nor uh IL1RA. We typically take it in the operating room from the Uliac crest. You can take it from multiple sites. The UA crest has been shown to be one of the highest concentration um of stem cells from there. Everything we talk about tonight is going to be based on basic science and clinical evidence. So nothing we talk about will be experimental, or most of the things we talk about will not, will be um already plenty of clinical and basic science evidence. This was a nice equine model, um. That was published about 14 or 15 years ago to show that the CBMA on T2 mapping and on um microscopy showed that there was better quality and quantity of cartilage in those treated by bone marrow stimulation with CBMA in an equine model and then saw um showed the same thing, um, roughly around the same time in a goat model. So we can see there's good basic science evidence for the quality and quantity of cartilage regeneration. In our own study with Charlie Hannan, who was our fellow me many years ago, um, Hannan has shown that there is, um, when we look at this and Um, bone marrow stimulation with CVMA versus bone marrow stimulation alone. The clinical evidence is that they're roughly equivalent to 24 months, and you'd expect that, but the T2 mapping again, which is a qualitative analysis of this shows there's better quality um chondrogenesis in this area. So it is both producing small amounts of cartilage and protecting the remaining cartilage, um, which is a, a useful thing, um, in terms of protecting this against. Uh degenerative changes. Um, also, corroborating our own evidence, Saul and Kim in level 1 and level 2 evidence showed that when this was compared with HA and small Taylor dome injuries, and that it was, um, better than the equivalent, it was actually uh superior to these. If I could ask whoever is running the slides, um, not to do this, because this is advancing on its own and uh it would be helpful if if I could do it on my own. So when we look at this, um, in AOT or in when we use oats graphs, um, this was Chris Moroski, another one of our fellows who's now down in Duke, and we can see that it is, it improves the integration um of the of the host graft interface when we use CBMA by contrast, when we do not use this. And one of the problems with AOT is the prevalence of cyst formation. Um, you can see again a nice study here by one of our former fellows, shows that when we use um concentrated bone marrow aspirate, um, with oats grafts that it reduces, um, the cyst cystic rate by about 30%, which is useful. These cysts are typically not um clinically relevant but radiologically. Um, not necessarily concerning, but, um, oftentimes alarming to patients if they see cysts. Um, and when we use concentrate bone marrow aspirate, it speeds up, um, this. A creeping substitution that occurs between the hose graft interface so very, very useful there. And this I think is a good sign. This was presented at the recent AOFAS um by our current um fellows, uh, Sebastian, and what he has shown is that when you look at consulated bone marrow asberg with AOT, you get a 94% survival of mean follow up of 10 years. Um, that's, that's pretty good for joint sparing, um. Joint sparing surgery. So large chondral or osteochondral defects treated with grafts and with CBMA, the likelihood of survival is uh is fairly high. So we talk on uh PRP plate-rich plasma, which we take from peripheral blood, which we take in on the bedside manner here in the office. As we've alluded to, there are certainly up to 1500 and probably far greater growth factors involved in this. It is going back to our early slides as both chondroinductive and chondroprotective, um, and consequently chondrogenic. So it has all of these things, but it is no scaffold in it, so we often mix it with a scaffold in an operating room. Um, again, these are the uh unique proteins that are in there, and we won't go into the buffy code and buffy layer in great detail. And again, for some reason these slides are automatically advancing, which is, uh, gonna be difficult for our audience to, um, to get any meaningful information and that keeps going. Um, this is, um, a nice studies done by Neil Smyth, both a fellow of Dr. Schoon's and mine, and, um, then another study that we did with Brian Co's group in Rush to show that um PRP is both an anti-inflammatory, chondrogenic, counterprotective, and chemoattractive, and 85% of our patients are slightly over that. And then we looked at that again 6 years later, and we showed again the vast majority of these are anti-inflammatory, chondroprotective, and chondrogenic. So in patients who, who have a chondral injury, it is very useful um to administer something that's going to be anti-inflammatory and reduce the catabolic load on that joint, ultimately to protect. Um, the arthritic change or arthritic milio. And again, I would ask those who are running this slide show not to advance unless I ask to feed. Um. So if you look at PRP, um, in general orthopedic population, you can see that it is over the years, it is increasing by an order of magnitude in terms of its usage and predominantly in sports pathology and knee and shoulder, I think in foot and ankle, we have been leaders in this field, um, and I think now the vast majority of of us. Excuse me, um, are using this as an augment to our surgeries or as a preventative measure, uh, for those patients who have early degenerative changes. Again, this is an anti-inflammatory effect of PRP as I alluded to earlier, it decreases IL-1, which is the potent anti potent inflammatory mediator and TNF alpha. Um, produces hyaluronin and by the synoviocytes and therefore it is a very potent anti-inflammatory and tubologic agent. Excuse me. Um, this is, we alluded to this earlier that it is chemo attracted, so when we have these microfluidic devices. You put PRP on one side of the gated chamber, and you put PDGF on the other side, and stem cells in the middle, you can see once these gated chambers are open, that the stem cells are rush preferentially to the PRP. So again, showing that when we, even though PRP doesn't have stem cells, when we put into an area, it will attract those stem cells to there. Of course chondrocytes are very, very rare, um, so we're not suggesting that it creates a massive onrush of uh charging um chondrocytes within a joint, but it certainly will help in protecting. This was a nice study again done one of our previous fellows, uh, Yasui and and John Dankert from uh NYU. We looked at whether multiple injections were beneficial or a single uh injection in a rabid model, um, and we found that um a single injection was every bit as good as serial injections and there was a log dose response curve. Um, as you increase the number of injections, you actually ended up with a negative feedback loop. So for all those doctors out there who's suggesting their patients should have several injections of PRP, um, at this time there's no evidence that that is better than a single um injection. Again, um, constructing an evidence-based chain here, we're looking at Maidan and Gunny, both of which have level 2 evidence to show that PRP in a microfracture of bone marrow stimulation, um, was, um, better than the bone marrow stimulation alone or better than HA. So again, building up a body of evidence to suggest that PRP is useful, um, but at the time of surgery. And, and again, this was from the Turkish group again corroborating that evidence um in a level one trial, um, which I think is the best available evidence to show that PRP is useful to prevent cartilage degradation and in chondrogenic uh proliferation in small defects, these defects in the Turkish group were less than 8 millimeters. In our own group again, Neil Smyth once again showed that when we looked at a rapid model with AOT that PRP was very was beneficial at the hostcraft uh interface integration. So again, building up a body of evidence. And when we look at this, um, when we look at PRP overall, however, um there are problems with it because if we have any drug needs to be standardized both in constituents and in dosage. Um, by contrast, when we look at PRP, as we alluded to earlier, there's over 1500 growth factors alone, so it's difficult um to standardize that. Other influences are exercise, non-steroidal, uh, BMI, smoking, um, nutrition, and so forth. So everybody has a slightly different PRP and it's varied in terms of the time of day that it's taken and exercise and diet and so forth. So there has been a, a push to try and standardize this as much as we can in terms of Um, looking at the um protocols and, and um determining what in fact we are injecting before we can come up with definitive evidence. That's probably not possible because the FDA simply won't allow us um take out one of 1500 growth factors to determine what effect it has. But ultimately we do need to standardize this more and um a large a group from the Members of the biologic Society, um, looked at this and published um uh from Owen Hurley's group, again, one of our previous fellows. Um, and what they only achieved 62% consensus on this, um. I'm not sure what time, OK, and uh. And you can see the ideal dose of PRP is undetermined, and the minimum volume required is unclear and may depend on pathology. So really what we're, we have achieved the consensus of we really don't know very much about this other than there's good basic science and now an amassing body of clinical evidence to show that PRP when used in a certain range and when when strictly um adhered to, is beneficial, both in chondrogenesis and small defects and chondro protection. By having trophic downstream effects within the joint that will prevent arthritic change uh downstream. So we move on then to HA which is less contentious, this is a carbo protein or uh polysaccharide native in synovial fluid. It's um it stimulates chondrocytes. It does actually reduce pain by blocking substance speed um and it does have an anti-inflammatory role, and there's some very nice and elegant. Um, basic science evidence on this to show that it will inhibit uh metal metallic proteinase 13. That's one of the metallic proteinases involved in arthritic change which we have in the, uh, in the knee, and it is, um, it will reduce pain, provide a viscoelastic supplement supplementation. And how it's uh biological effects were reducing inflammation and promoting chondrogenesis. So a little bit more powerful, we used to just say it was the WD-40 um of the joint. I think we now realize that HA is a lot more to offer. This was a nice study done by Eric Strauss and his group here at NYU to show in a rabid model, um, when they had full thickness cartilage defects, and they were treated with um HA after BMS. There was greater infill and those treated with um the HA than those not. And uh his conclusion was it is counterprotective and anti-inflammatory. Clinical evidence for bone marrow stimulation again shows, and in this nice study there were better AFAS scores and decreasing VAS scores um in the, in the group with HA by comparison to those who were not treated with HA in terms of um tissue remodeling. So it has a triviological effect which we all knew of. It has it reduces pain and I do think that it has a um An effect on chondrogenic, um. Proliferation in small areas. Now we go on to scaffolds, um, we'll talk about ECMA and BJCA which is a buy cartridge and Daovo, which is their trade names. Um, So the composition of ECMA or bio cartilage, um, it's a dehydrated all allograft, it's extracellular, so there should be no MHC mismatch, and we use that as a scaffold. So this is um chondro conductive, and we then we use this for either PRP or CBMA or now with fat cells, um. And it lad is a biological info, um. In this area, so think of it as a physiological route. Again, the equine studies on this show that there is both a qualitative and quantitative improvement when bioc cartridge is used as a scaffold in those patients or in those um horses treated with uh 4 osteochondral defects. And the clinical evidence of this, again, Ahmed and our own study here, uh, which are both level 3 and level 4 studies, so that when we use bi cartilage versus just CBMA alone. And by a cartilage with better infill, as you'd expect on Mokarts scoring and T2 mapping, um, is ultimately better in this group. And again, I think that's probably a harbinger for poorer outcomes in those patients who are not treated with this, with just bone marrow stimulation alone. And you can see the difficulty with this is it has to be put in in a dry scope and then carefully molded into the shape and probably counter sunk so that when the patient moves fairly early, even though it's a congruent joint, that it doesn't uh shoot out. Uh, this is a nice study by Nate Mercer again, one of our residents here showing that uh when we used, um, CBMA with bio cartilage in larger lesions, um, that it was a better outcome again from providing better infill that uh chondral interface. Uh, by contrast, this is a cellular graft, um, this is a an offering by Zimmer, um, where they use 1 millimeter cubes, and the idea of this is that it would, um, provide a cellular milieu for early integration and better quality integration than an acellular graft in larger lesions. In a recent study by James Butler looking at a systematic review of this. Um, it shows that there are certain centers and certain surgeons, um, who are very proficient at using this, um, but it's that old thing that Graham Mapleley used to say that an average orthopedic surgeon is an average orthopedic surgeon, and by and large, the outcomes of this, uh, were not as good as was initially indicated. So, um, this probably should be indicated only for surgeons who are getting, um, who know how to use this in terms of Making sure that it's not being used to fill in bony voids or bony defects, that is used in combination um with bone grafting and then careful um application of this. When it is done so, it gets an equivalence to bio cartilage, and when it is not adhered to those strict principles, it does not. So there's a great wave of enthusiasm. I recently was at um AFAS and then the um offset. Conferences um where there is a a large amount of interest now in uh FA grafts or MAT. Um, a large number are, are a large part of this work was done by, um, Farsidla many years ago and Duke, and where he looked at The multipotent. Stem cell um colonies that are formed by fat, by contrast to bone marrow or other areas, and, um, so they exhibit this multi-differentiated phenotype, so this truly is a multipotent cell, and there is a predilection for these um cells to to go down the um chondrogenic path pathway by comparison to osteogenic or neurogenesis. Um, so it is very, very important for um for any sort of cartilage. Defect, um, and particularly I think in, in the area of non-surgical applications for arthritic change in the ankle. The big problem is in the nomenclature and what is available in this country by FDA regulations. So ADSCs are cells where we um harvest the cells and we grow them, and they are not available um for uh clinical use in this country. SVF is a required centrifu centrifugation, and more importantly, um, colagenase, which digests the matrix around them to release the um. The the stromal fraction. Um, that is what a large number of papers that you read, particularly from Kim and Korea are using HaSVF. Um, we are not yet allowed to do that in the United States, we use MAT or micronized adipose tissue. This is the microdermal uh structure with MAT. Um, and so that's when you're reading papers just to to know what you're reading about, uh, it's useful to look at this. And again, one of our previous fellows looked at this in terms of the limited evidence because the evidence was all over the place, and this was in conjunction with our friends from Amsterdam. You would think that um the results from Korea are so good that perhaps we're we're missing out on that, but I think that when you look at the advantage of MAT or other harvesting methods methods, there are many other things other than parasites, um, and so we have this extracellular matrix, which is, which contains a multitude of growth factors, not just stem cells or parasites. So I think we get this biological milieu that is probably even better um than the SVF alone. So I pose some some. Based therapies, these parasites are adherent, they're almost like pre-stem cells, adherent to the adventitia of um of blood vessels. And they're an order of magnitude greater, um, an order of magnitude greater than um stem cells found in bone marrow alone. Um, what we have found is that these parasites have preferentially are engulfed by the M0 M0 uh macrophage to produce an M2 secrettome. So again, going back to those early slides, when these cells are engulfed by the host macrophageal monocyte, they tend to produce this M2 secrettome by comparison to M1, which is pro-inflammatory. So these are very powerfully anti-inflammatory. Recent work work again done by Larry Banasser showing the tribological properties of MAT and to show that they do act um to reduce friction within the joint. So all of this is very useful, particularly in early um arthritic change. This is what it looks like when we started off using this, and I think it's fair to say we're probably the first, um, in terms of NYU in our, in our group, we're the first to use MAT in the ankle in this country. Um, oftentimes we get a yield like this, which is 30 ccs of of fat or MAT, and then we thought, you know, 1 teaspoon of sugar is good in your cup of tea, then 10 should be better, and we injected this into the ankle. And of course, um, it caused capsular distension and pain. So now for the ankle, we've come up with Adons. That usually about 5 cc's is more than enough within an angle. Um, this is what it is. Uh, while I was doing my residency, I enjoyed my, uh, plastic surgery rotation. So here I am back doing, um, liposuction. We typically take it from the abdomen, you can take it from the buttock or thigh as well, um, and Then we, this is the mechanically agitated, so this um releases a lot of the um adherent parasites. And then we um we sent or we, we don't centrifuges, we simply get it from mechanical agitation and then you can see our yield here. So for any one person we get either 10 to 30 ccs of of fat and then inject it in. Most of this work, original work was done in uh the Rizzoli in Italy, and you can see their patients here have done very well. Um, they get improvements up to 2 to 3 years, which you may not think is a lot of time, but if that's you or that's your patient, that is a significant amount of time, so they don't need to have surgery and they can get things lined up for surgery. We're not in any way saying that MAT um is going to take the place of surgery, typically doesn't. What it does, it prolongs. Uh, the interval between the patient coming to your office and requiring surgery so that they can get everything uh squared away and they can maximize or prehab and throughout that time. So this is chondroprotective, it's anti-inflammatory, and it's chondrogenic in small areas of cartilage defects, um, but in large cartilage defects, obviously it is not gonna restore the joint. Um, this was a, a case in point. Um, this is when John Danker looked at our, our studies here. We had, uh, 19 patients, uh, with high grade, or many of them had a high grade arthritic change within the ankle. Excuse me, and you can see that. Their AOAS or FAOS scores improved, um, really not that much, um, only up to about 61%. So if you think about this, you think, well this really didn't work, but if you're in that group and around 60% of patients do well from this, and then that's a win. And it's certainly um better than multiple steroid injections and better than PRP in these patients. So, um, but where it works far better than the higher grades is in the lesser grades. So if you were the KL2 for instance, uh what we found is that now that this is where this is optimized, so we will protect the cartilage to allow greater than 2 years. Uh, from this. So MAT in the knee, again, it's the same thing. You can see a large part, a large number of um works using MAT came from the Rizzoli initially, and they had a 100% stress. Um, and our own study was um. less uh encouraging, and when we use MAT in the knee again with high grade arthritic change, most patients did well up till about 2 years and then it started to drop off. But 2 years pain for return to to function um is pretty good for these patients. So innovative biologics will go through this very quickly. This is lubricin, um, let's say or lubricin memetic, it's an endogenous cartilage surface, uh, proto glycan 4, it's decreased in arthritic change. Um, Scott Rodeo did some nice work on a RAT ACL model on this to show the better RC scores. Here at NYU we're doing some nice work within the, uh, rabbit model, and we will be presenting this and publishing this shortly to show with it on. Um, friction testing, histology, and I I she scores all patients, all animals treated with this and did far better. So again, a good, um. Something good for early arthritic change. Polyacrylamide hydrogels are being used in Europe. They're not FDA approved. They're all label in the United States. We've been using them now in ankles. And um so this binds to the synovium and produces a tribological effect as well as in reducing the pro-inflammatory markers. It stays there for up to one full year. The original work was done on an equine model showing that uh. Again, over 80% of these did well. This is the original um study, which is just published again show improvement in WOMA scores in 4 months and maintained. When we look at the um histology of this, these cells are maintained within synovium for up to 1 full year. Very quickly, CardiMax is a viable cartilage fiber, uh, with, with cells. Um, we're beginning to use this limited evidence, this is the mechanical evidence showing that it stays in a defect when put in there, and this is the original carttridge allograft in a goat model again showing. Good H&E scores, suffering those scores, and this is a study we're undergoing right now, again, looking at the biomechanical and cellular response, um, show, showing that there is a mitochondrial um connection to this so down regulating kibolic uh proteins. So without further ado, I think that's enough, uh we can leave cases for the end. So I think there's an exciting um A future or a cartilage, people will say, are we ever going to be able to protect cartilage from um from degeneration? I think the answer to that is probably yes at some point now the answer to that is no, but we can prolong the life of the joint. Remembering that post-traumatic osteoarthritis is the single biggest cause of arthritic change in the ankle. And I think for those patients who have repetitive ankle sprains or ankle trauma from uh fractures, we need to follow these up carefully before they become significantly arthritic, um, so that we can use this array of um biological adjuncts um at our disposal. So thank you very much. I think questions will be sent to um Doctor Walls, and without further ado, Uh, I do, uh, we'll, we'll move on now to ankle fusion from one end to the next. This will be, um, the eminent Steven chestier, um, traditional standard for end-stage arthritic change, ankle fusion. Can you hear me? Hello, yes, carry on student to say hi. This is um This is just a breakaway from uh Doctor Kennedy's talk, had a lot of research, a lot of numbers and Personal research, etc. But um, as the oldest member of the foot and ankle staff, I, I was uh assigned talking about one of the oldest procedures in orthopedic surgery, which is uh fusions. So, uh, ankle fusions were first described in the German literature back in 1879 by Albert. Uh, I couldn't find the article or pictures from it, but that's what the literature says. But the, the person really uh brought forward a fusions and a lot of the principles that, um, that would seem simple what he did. If you look at any technique of fusion or ankle fusions, if you don't follow a lot of the standards, uh, or the principles that Charley uh showed, it will potentially lead to increased numbers of uh non-units. So the basic principles of diffusion and healthy casts his bone to cancel his bone. If you can get that, that's usually the best. Uh, Charley said it did it under compression, and that's what the Charley clamp was. It literally clamped uh the joint down and opposing two cancer the surfaces the bone, um, doesn't know the difference between healing. To itself or healing to another surface, and so that's uh at least the basic principle behind it. Of course there are rankle and there's a lot of other bone morphogenic proteins and stimulators, etc. We're not gonna go into that. Yeah, there has to be fixation that's stable enough and strong enough to hold the bows in opposition sufficiently long enough to obtain union. Uh, the fusion rates of all of the Uh, techniques that I'll briefly go over in uh the name of time um ranges from 83 to 99. It has a lot also to do with biological factors, uh, that most of us are. Have at least a glimmer of knowledge of this. Time in ankle fusions usually is about 4 or 12 weeks plus reminder 4 weeks. However, it's a general principle, uh, in patients with neuropathy, particularly diabetics, since they don't have the Because they have neuropathy, they can't tell if there's pain or motion at a fusion site. So the, the rule of thumb is just to double the time to fusion, mobilize them longer in the name of uh in the name that they can tell you that things are going wrong or slow. Obviously, the most important thing, since there's so many techniques of uh ankle fusion is to have something to do with the position. You can get the bones to heal, but if they healed the wrong position. You can cause multiple other problems. So, in general, uh, ankle fusion. Is uh 90 degrees to the table shaft, and I'm talking about, you took a, a block of wood or something that is available during the surgery. I usually put it under the foot there. Uh, this also stabilizes uh the midfoot joints, which also can lead you to think that you have a fusion in the correct position, but there's actually up to 10 to 15 degrees of motion through the midfoot, so this has to be in contact. When you're engaging whether it's at 90 degrees that you um Arranged the the flatness of the surface actually to go with the calcaus which then in part indicates where the tail is uh the the degree of external rotation, uh, well, this is just a basic. Principle if you Allow it to be in internally rotated. That is an absolute. Uh, negative and make it very difficult to walk. Uh, putting the foot straightforward is OK, uh, but it's been shown in the literature that anywhere from 5 to 15 degrees of external rotation gives you the best. Moving forward, uh, so you don't have to vault over things and it avoids the the um Intolling of the foot. Um, some people use that they put the external rotation equal to that of the opposite side, and that's one way to think of it, and at least the, the 2 ft look the same versus the patient complains that 1 ft is duck, they're walking like on a duck on one side, if it's too externally rotated. The other concept too is they need to bring the foot posteriorly. Uh, versus allowed to slide forward because there's less foot to vault over, and that's part of the thing too, because the patient has a a a stiff hind foot. And if you put it forward, then they have to somehow jump over the front of the foot. If you put it backwards, and the, I mean, if you put it backwards. 90%, they would be like a peg leg. And others, they don't have to jump over the front of the foot cause it it doesn't even turn it into a factor. And so, the other thing is that a little shortening is OK, because this helps the foot to swing through instead of, uh, and some patients, if the, if you've uh augmented a fusion uh and try to make up for Lengths, which I try not to completely um Um, OK Put into the factor, uh, I will. Let the leg be a little bit shorter, so the leg can swing through. And not hit the ground versus having to take your foot and swing swing the leg out. Uh, the, the hip out, and so, uh, they have a better functioning to walk with. The indications, uh, and each has its own specific indications and indicators, but the majority ankle fusion's done. In the United States and around the world post-traumatic, that's at least 75 to 80%, maybe 10% of the Fusions are primary from due to primary arthritis. Uh, the rest of the make up with the infectious, um. Arthritis, neuropathic, chart, which they're gonna talk a little bit later in the talks today, uh, uh, failed ankle replacement, yes, those happen and there's some congenital reasons where the person has a flail, uh, ankle, and it's easier than trying to put transfers of tens that don't exist, particularly as somebody uh as uh. A spina bifida. Now, there's a whole series of approaches to the ankle, and sometimes it has to do with the type of uh implant that you're putting on. It also has uh whether it's uh Interior, which is the most common, there's lateral approaches, posterior approach, which is not very often often used, and also you have to look at what the soft tissue envelope with the ankle is, and then you, a lot of times you have to Jury ring, which approach you're gonna use depending on if there's soft tissue loss or problems with skin, etc. Now the oldest uh fixation, as mentioned, at least we have in the literature that we use is the Charnley clamp. Another other types of fixated intermele rod, useful, particularly if you're doing a panel a TCC fusion. There's anterior plates which there's abundance of, uh, I just thought it. Since I'm old enough, and that's one of the reasons why they gave me this talk. There have been people, I myself have used if the soft tissue in the front was no good, and this before we, I was using screw fixation, is to go posteriorly and use a a pediatric uh hip blade plate. Uh, there's a various amounts of uh Screw configurations, and of course it's arthroscopic. These are all types, but they all use the same basic concepts that Charnley uh put forward to us, which are, there's a tension side. And a compression side. And so, if you look at uh when Charley talked about putting the clamp on, he made sure that The the one in the tibia didn't, it was sort of in the middle, but the, the pin that went through the tails actually had to be uh anterior to the center rotation, and this allowed this only works, of course, and people will have an a tension or an active uh Achilles tendon. And you can see, uh, or at least the people as you begin to do ankle fusions, uh, that are open and you're using screws, etc. If you do not put the screws in to this axis of rotation, you will absolutely get it anterior gapping in the front of the fusion. This was taught to us in 1951 by Charley, and you have to respect that in all the types of fixation you use that. Depend on compression. Why would anybody want a primary fusion? Well, you have to explain options to the patients. Uh, and the, the most important thing I say to older patients, at least, it's one and done. The uh longevity of an ankle fusion is that the failure rate in general is about 5% in the first year, and if you do a graph of 15 years, there's very few reasons that the ankle fusion will fail if it goes to union. Um, if a patient has a little motion, little motion to start, and almost none, then it's easy to convince them to do an ankle fusion because they already have accommodated their life, their lifestyle, their activities, their rock bottom shoes, etc. to accept. A fusion which what it does, it gets rid of the pain. And a lot of the initial studies for ankle replacement in general, you can promise the patient they'll have 5 to 10 degrees increased range of motion. But anything beyond that, you're You're not particularly uh if they get more motion than that, praise the Lord. It also has to do with the age, uh, younger people, we have a tendency that since the, if you look at the longevity even ankle, uh, replacement, you know, it trails off, uh, every year, and then their only ankle replacements only been around uh the the type that we have right now, as research up to Uh, 1520 years, which has about a 15% failure rate, meaning needing a revision. Or a fusion, but if you fuse it, it's unlikely to need to be refused unless it gets infected or there's some problem with the initial union. Uh, and, um, Many of the surgeries, particularly ankle replacements. contraindicated, a soft contraindication if there's neuro neuropathy, because they, once again, they don't have the protective function that uh a person has to protect whatever surgery is done on their ankle. Now, what is the effect of fuchsia? Well, there's less pain, you end up with a stable ankle. You can walk faster once it, it's healed, you have an increased stride, uh, and usually not noticeable if you walk in at normal speed. It becomes obvious when somebody walks quickly because they're, they've lost the uh The flexion portion of their ankle, which is always used, uh, like, particularly when if you run, but if you're walking faster race walk, it's still a difficulty, and a lot of these people, fusion will have problems on stairs, so they'll be going up and down one stair at a time. Obviously there are screw techniques. You look in you look in the literature, you will find 15 different ways. To screw across the ankle, but the concept still is the axis of rotation. If you put screws like you see in the the center picture top, like this, these screws are anterior at least. 2 out of 3 or entry of the the axis of rotation. And so, but what you have to do is you have to, no matter what screw technique is, the first screw has to be the one that is anterior to the axle rotation, cause you try to, if you don't get it clamped in the front, and no matter what you do with the other screws, other than putting bone graft in an area that should have been under compression. And uh opposing the cancerous bone, uh, you're gonna end into trouble. And one way to do that is show is using a uh posterior to anterior screw that always goes in front of the axis of rotation. Now, of course, uh as I said, I'm one of the older people in the In the the funaglo service here, and I presented back in 1992, 193 at Joint disease. It was not the lying bone, he didn't get a hold of my slide at the hospital joint disease. Uh, and what I did, they, we didn't have at that time we didn't have any fancy plates like we have now. There's a myriad of plates that are put in the front, but I would use. A 3 hole DCP play. And using this as a tension band, I'd make a little cut in the neck here, and I put two screws approximately and 1 screw. Uh, into the tailors, and that's all it took, if the, the articular services were, uh, prepared correctly. To hold it, and I had a 90 92% fusion rate using a three hole DCP plate. Now, obviously, uh, when you go up into the right hand corner, there's a myriad of anterior plates, and they have holes here and there and da da da. But still, when you put that on, you still have to get This situation where you put the most amount of tension on the Achilles tendon, when you put the first screw in that uh that is in right this position to hold. The tension ban here and uh finally Arthrex a couple years ago came out with this, was thousands of dollars. This is a 3 hole DCP plate. Now, um, there's arthroscopic techniques and many open, um, the arthroscopic technique, what you're doing is, these are for ankles that are not, do not have any major deformity. If you want to get a good union rate, you go in, um, you can put a distractor on it, you. Cut off the cartilage, uh, back to cancerous bone on both sides, and then you use the three screws usually that we showed here, uh, previously, uh, respecting which Where the center of rotation is and how you're gonna clamp it down. Another way to improve this is some people make bigger cuts here and uh put uh a sort of a mini open, and regardless, you're still clamping this together, and because you can't see everything there, you're usually ending up put it in some form of a Biologic and uh bone graft slurry. Now I am rods are, uh, have always been in vogue, particularly a lot of these people with ankle arthritis have a sub subtalar uh either arthritis or Uh angulation, and so there are IRM rods here, there's at least 3 or 4 companies that make IM rods, and the newest thing in IM rods to me is going back to. An ankle or a fusion site under compression. So there, I think DOJ or Arthrex have, uh, and you can see in this one here, have developed uh IM rods that are, they have a knital core on it that are tightened and will actually give up to 6 millimeters of compression after the original setting of the IM nail. Uh, but of course, Uh, since the rods are, that's Solid. You can get into a fracture. Occasionally. Uh, usually IM rods too, uh, when you have a big, uh, bone defect, that's not a case where you have Kansas bone to Kansas bone. Um, they're made, uh, there are a lot of companies like, um, Uh, 4 Web and Pargon 28 would make custom cages to go and make a hole for the rod to go up and through the other add-ons or corrective osteotomies and custom graph cages like this is an example of a Something referred to me where I had to remove actually the talus and a majority of the calcaneus. I offered the patient to shorten them about 4 centimeters versus doing a 3D reconstruction cage and that I'll put a rod up through, but since this infection here, there's always the possible these type of things will end up with amputation. So this is something I and this um and I'm telling Doctor Kennedy this, many, many, many years ago at a orthopedics foot and ankle Society in Ireland, and they were going over ankle fusion, etc. I said, so what if Uh, when you do the fusion, you have respect for the fact that you may want to change it at some point to an ankle replacement, and I got left out of the room. Well, to tell the truth now, people are taking ankle fusions and taking them down and putting ankle replacements in, particularly in patients that when they were in their twenties or something like that, they would say, well, you'll outlive your ankle replacement. And so on those patients, what I offer them is to fuse their ankle using an anterior approach. Uh, and I maintain the malleola and I maintain the ligaments, and I don't fuse them on the sides to the media malleus or the fibula, and at that point there, uh, if you take it you take it straight down, you could have a a computer generated total anchor replacement, uh, you know, versus people that are take. A lot of people still take off the fibula, and then they moalize that or is it in one of the earlier pictures showing that they use that instead of a metal plate laterally, etc. And so that's why I advise young patients to To fuse and potentially leave structures there for the next surgeon when they uh go to total ankle replacement. I just want to tell you one thing, to all the orthopedic doctors out of there, when you go and look online for techniques for ankle fusion. Within the first click, you'll be barraged with total ankle replacement, advertisements and studies, etc. And so, uh, it's like nobody does an ankle fusion, but as I mentioned previously, when it's a patient who is too young, Too sick Have other uh factors that uh like they don't have any motion to start with, and ankle fusion pri primarily is usually the best. And I just want to show you, Doctor Charley is a this is in the literature, a way to fuse the shoulder joint. Thank you. Steve, that was excellent. Thank you very much. Um, so in the interest of time, we're going to keep on moving and we'll do questions at the end. Uh, so the next up is, uh, Doctor Luun and We've had ankle ankle fusion, which was for a long time considered the gold standard, but ankle autoplasty really is accelerating and growing and in fact, many studies are showing that there's more ankle autoplasty now being performed than ankle fusion. So the question is, is this the new gold standard? So I'm gonna pass on to Doctor Shonan, take it away. Yes, um, I'm not operating, there we go. I'm trying to go back to the beginning. I'm in the middle of the talk. There you go. OK, thank you. Um, OK, so question is, is this the gold standard? Is this the new gold standard, the fusion was, but now maybe the arthroplasty is going to be. My disclosures is that I'm co-inventor of the Zimmer total ankle, which is the lateral ankle replacement. The disclosures are not particularly relevant. Um, for this talk. Here's my team at uh Langone Orthopedic Hospital, wonderful partners. I couldn't be more blessed. We just had an edition of Kevin Schafer, the, uh, young guy with the, uh, blue surgeon's hat there, and you'll see him in a bit. Uh, I just want to say that we appreciate foot and ankle, but we were not the first. Leonardo da Vinci said the human foot is a masterpiece of engineering and a work of. And we feel that this is definitely the case and all of us love the foot and ankle, um, maybe more than uh Da Vinci loved any of his other, uh, inventions. He loved the foot and ankle, so do we. So, um, this is the normal ankle, normal motion of the ankles dorsiflexion plantar flexion. These are the hind foot joints. So a lot of people don't realize that the hind foot joints go side to side. They do do some dorsi flexion plants. Reflection. These are different views of that height foot joint motion. But a lot of people, I get confused when you talk about ankle. Are you talking about this motion? The answer is no. We're talking about dorsiflexion, plantar flexion, but, but yes, when you affect one, you affect the other. That's important to know. So here's the normal ankle joint dorsiflexion plantar flexion, and this is a motion CAT scan that we uh did with some studies that I was doing with um. The uh cardiac CAT scanner, which does motion. Now this is the arthritic ankle, and you could see the osteophytes and narrow of the joint and the osteophytes are developing at the tailor navicular joint. So, in general, how do we choose when we have this sort of end-stage bone on bone between arthroplasty and fusion? Well, specific conditions, lifestyle of the patient, so it's a custom decision. The goals of the patient, again, very custom, and the surgeon's preference, of course, has a way with influencing the patient. Now, uh, the indications for the fusion, I'm gonna just highlight this because I think many of us would agree that the ankle arthritis with a neurologic deficit, and ankle arthritis with infection, arthritis with inadequate bone and a failed total arthroplasty, those are. Probably now the best indications for a fusion, and we still do ankle fusions, even though I have done over 700 ankle replacements. I still do some a uh fusions. They are durable, long lasting, eliminates pain by eliminating motion at the joint, suitable for some high demand uh activities, but not necessarily all. Disadvantages will lose the motion at the ankle joint. And many can lead to arthritis, or they may lead to arthritis in adjacent joints over time due to altered mechanics, and that's been shown with longer term studies that people will get arthritis. So, it improves ankle pain by eliminating motion. It does correct deformity, which is very nice, but you do get it at the price of the motion. And we'll stress the subtalar joint which then can lead to arthritis and this is my motion CAT scan showing. A patient that I've fused about 1215 years earlier, and now she has horrible end stage arthritis of the hind foot joint. So what are the indications for an arthroplasty? Well, there's been a lot of advances in arthroplasty over the last half century for sure, uh, over the last 50 years, a massive the last 25, and really the last 15, we've taken off on our designs and things are radically different. So, I do it for all indications, all arthritis, osteoarthritis, rheumatoid arthritis, post-traumatic arthritis, people with end-stage osteochondral defects that Kennedy couldn't fix and the joint went on to complete arthritis, ankle arthritis with subtalar arthritis because if you fuse that ankle with ankle. Arthritis and it has subtalar arthritis, then the subtalar joint goes bad, it hurts a lot. Ankle arthritis with deformity, great indication for the replacement ankle arthritis with minor neurologic deficit. If the foot is floppy, no, but if the foot is just weak, yes, it can be very good. Ankle arthritis with eliminated infection, not active infection, you can still do a replacement. Failed total ankle arthroplasty still can be fixed with another arthroplasty. Bilateral ankle arthritis is pretty bad. People get stiff, they have trouble getting up from a chair. So we want to do one side at least with the replacement so they could do. Flex to get out from the chair, ankle arthritis for patients who don't want to sacrifice motion is a good indication. The issues with the uh ankle replacements that preserves motion at the ankle, provides better functional outcomes for certain patients, especially those with bilateral ankle arthritis or subtalar arthritis. It reduces pain by maintaining motion at the joint. Higher risk complications such as implant loosening, infection, and the need for revision. Especially true with the older implants, the newer generation has better outcomes, which I'll discuss in a bit, and there's a need for maintenance, not a turbable as fusion, especially in younger patients who are more active. If people want to run and jump, no procedure is good, but if fusion won't break down, but the subtalar joint will break down. But if you Do it in a replacement, you will have increased poly wear and maybe bone metal delaminations and cysts. So an ankle fusion for infection, here's some examples of some of my ankle fusions, poor quality bone, a charco, which Kevin Schaffer is gonna talk about in a bit. Patients with a very bad obesity and deformity, you could see here is a patient with some obesity and severe deformity. You could see a lot of pain in this patient. The bone quality was actually pretty poor, and uh her deformity was really bad. So here's what she looked like. He was what the tilt was. This patient again, bad bone quality. I did a fusion, and uh that's what it looked like, and here she is doing much better, walking better, and she's low demand and actually very happy. Um, this is another case this patient had an ankle fracture fixed, failed, and went on to uh a revision, progressive deforming. Now it's draining, so here it is initially, they fixed it, it fell apart. They, uh, revised it, it fell apart. She came in right before she was going on a cruise and she said, could you help me out? I said, uh, you're infected and we have to do an emergency fusion because you're on the verge of sepsis. So he took her to the OR. I cleaned it up, took out the joint, put on a frame, squeezed it together, put her on IV antibiotics, and we got a successful fusion, and she's very happy. It's a limb salvage procedure. Another patient, severe ankle fracture, chemotherapy, not a great host, a lot of wound complications. Things fell apart, bad bone quality. Here's her deformity, bad varus. Here she is, really twisted. Very unstable, bad bone quality, not good biologic health, um, and she's really struggling with pain and deforming. You'll see, look at that, it's falling over the edge. Poor one. Anyway, so that's what we did. Uh, we took her to the OR and this was a bad case for replacement because of bone stock, and I cut the bone wedge like this and closed it. To, uh, get a realignment of the ankle, cleaned it up, uh, squeezed it together, and put in some screws to get a fusion. Here we are in the OR looking through and through, and we got some screws in it and got her realigned and there she is, uh, very happy and working, walking much better than she was before. So, and that's her uh long term. So I like fusions. I want to tell everybody gold standard is dependent on the condition. It's all custom. Let's not forget about fusion, but arthroplasty, I believe, will address these problems very well with the exception of the cases that I showed you, uh, and preserve motion and improve function for a longer period of time. So I'm gonna go through some of the uh problems with the fusion you can see here. This patient's moving, but not at the fusion, it's moving through the bad arthritic hind foot, and the foot could deform after the fusion. And people with fusions, they will have difficulty on even uh uneven surfaces, difficulty with stairs and aching with prolonged activity. So this is a study, uh, showing uh patients with 22 year follow-up, they had uh arthritis in the adjacent joints. Here's a host of studies and basically you see. Here, really good rate of healing, but not everybody has beyond a 90% happiness. So we have overall 75% to 90% happiness. But uh again, this also does deteriorate with time. And then we found with other studies more recently done in 2015, they looked at fusions uh over 11 years, uncomplicated case. They had a nice fusion rate, 91% fusion, but 9% non. Union and the risk for non-unions for people with subtalar fusions and people with bad Va. So it's not a perfect thing, and people can sometimes do sports, but usually their sports activities deteriorate. And as I mentioned, they will get uh uh alteration of stresses and their hind foot joint will go bad. And then if you need to fuse their hind foot, then they have trouble healing their hind foot. So these are my patients, 2012, you can see, I Had to add more screws and more screws, and more screws and more screws, and at some point, you get tired of putting screws in. So, uh, this especially true in a patient with bilateral fusions, they don't do well. They can have significant joint arthritis, and their function is very limited. So these devices came on the market progressively over the last, uh, say 30 years or so, and uh they are good, uh. These are the, the, the implant that changed things, uh, was the uh uh the implant that was by a company, Depew, and it was a semi-constrained implant approved by the FDA. But the problem with that implant is it wore out and by 8 to 10 years there were big cysts and the implant was loose, and the plastic was worn out, and it was a huge hole. So that was a big problem, and there were many other uh new designs that were launched as a result of those problems. One of them was this design, which uh is a very large stem device that takes away a lot of bone. That's one I'm not gonna mention company names. I'm being kind of uh neutral here, but these are a lot of these are the common designs, um, and uh the ankle replacement takes away bone, but you want to preserve as much bone as possible. All of them are anterior ankle designs. Some of them have a piece of plastic in the middle that allows some pivoting. Uh, but only one is lateral, uh, that is the one that I, uh, co-invented. So we'll talk about the other models. This is one of the models out there. It's a 33 piece replacement with a mobile bearing. It's been around for a long time, and uh the results are pretty good. It was a flat cut on the tibia and a curved cut, um, with a uh resection of a lot of bone on the talus that was kind of capped uh over the talus that you prepare. This captail was problematic because underneath it there was they were developing cysts and they had some problems with the plastic fracturing and uh there was uh edge wear on the plastic plastic wear out and there was some uh degeneration. Let's look at these are the anterior approach. Here's uh a model, and you can see it's a two fixed uh two piece fixed bearing. In other words, this one does not have that pivoting surface. It had a very large stem that you could jack up and put more and more stems up even high to mid tibia. It was a flat cut tibia. It took away a lot of bone, it replaced a lot of bone. You had a flat cut talus again, taking more bone, and uh it had a uh crossli poly, but not highly crossli polyethylene, and the plastic uh is potentially a problem. Um, this is another model of a popular model two piece fixed bearing. Um, and they have a 3 piece mobile bearing in Europe. They did a side by side comparison to see is that mobile bearing better or not, and actually the fixed bearing turned out to be better. You're still doing a flat cut on the tibia and you are still doing a cap talus, so you're secting a lot of. Bone on the talus, that's what this implant looks like. It also has a spine in it that helps hold the implant in place, but it's in the orientation of the range of motion of the joint, uh, and, and, and sometimes it prevents the implant from getting bony integration onto the tibia. This is another model, a different uh device uh developed. It was uh introduced as a mobile bearing with a little piece of plastic in the middle that switched around. It was not approved for use in the US with that, so they made one that was uh constrained, that was uh fit that that was fixed two piece design. It still is a flat cut and it also caps the tailless. Um, and this is another newer one. It is a fry cut on the tibia. It has pegs to fix into the tibia bone. This one is a more clever in that it curves around the surface of the tus following the natural talus anatomy, and is not removing more bone. So I think uh a kudos to them for designing one that is following the the surface of the bone versus cutting into it. Uh, this is uh the model. There's another model. It's very similar to one I just showed you. This company had instead of pegs that were going obliquely, hasn't coming out perpendicularly, um, they, it's, it's a two piece model. It also is a flatcutus, but as you can see, flat cut tibia, but you could see on the tailus that is more of a curve cut on the tailus. Um, this is another one very similar to the other ones. Um, it has again more of that curved surface of the talus, but a flat cut tibia. And it's used with patient specific implants. This is the only lateral replacement, again, this is the one I co-invented. So this one, you can use the old incisions that were used for trauma. 90% of my cases are old trauma. So if you've had a lateral incision, use the old incision. Uh, it uses different materials. All the other ones are made of titanium. This one has tantalum, and tantalum has better bony ingrowth. This is from a study in JB Jazz, and you could see the barn integration with the implant. Here you could see that closer view of the metal and barn interweaving and uh. That is a metal that attracts bone into it. We also used a highly crossing polyethylene, which was unique and that had 5 times better wear uh than the other polys, the conventional poly, when we did wear testing. So here's a patient with an ankle fracture, malunion, widensydysmosis. Tilted ankle, long fibula, uh, in uh my device, we put it in the frame, we jack it open, hold it all in proper alignment, and then we mill away the surfaces on the talus and on the tibia, and we put in the implant, and that straightens it up and puts the surfaces on the surface without gouging away more bone. We take away the least amount of bone than all the other replacements on the market. And that way we were able to correct the valgus, the sagy rotation, translation, syndesmosis, and gave her good range of motion. Here's my um minimum 5 years we've been presenting this, and it was recently accepted uh to JBJS 130 patients follow up, minimum 5.9 years, 5 to 10 year follow up. Uh, it was my patients uh uh from 2012 to 2018. We have full data on these patients. They most of them, as you see, where um. Uh, were post-traumatic arthritis. Uh, some of them had multiple prior surgeries. They were not the smallest patients. Uh, some of them were smokers, some of them are foreign smokers. We had, uh, diabetics, we had people with cancer, we had ASA one was 10, and ASA 268. So, uh, a very high number of patients at ASA 341. So these were not the healthiest patients. We got uh good scores on the patients. Physical function and uh and pain, drop down, disability, uh improved quite a bit. The patients uh had really good outcomes and improved range of motion. This is range of motion, as uh as we will, as you'll see published in the literature. Um, this is, uh, the dorsiflexion, plantar flexion that we see with the ankles is a patient with pre-op arthritis. You could see from 2013, I did the replacement and um, This is now 8 years later, um, about 2013, actually 10 years later, 11 years later, and then, um, here he is, still doing well, excellent function, excellent range of motion, no cyst, no lucency. I here's another patient with excellent range of motion, and these are better things than we've had with the older designs, better range of motion, and less wear. We looked at our implants very carefully because we wanted to see, is there any area on the side view where we could see that there is some lucency, and we did find some lucency, not cyst, not lysis, but a zone which didn't necessarily heal in. And so we have these 12 zones and in our patients, we had uh these were the the these zones were defined before. The literature and in our series, my series, we had 26 patients, 20% had a single zone, one out of the 12 with some lucency. 7 patients, or 5.4% had 6 to 7 zones. None had more than 7 zones. There were no cysts, there were no subsides, no septic or aseptic loosening, no fibular malunion. Uh, we did have 3 cysts. I will show you. Cysts. Here's the cyst. These were not structural cysts. They were progressing probably from the subtalar joint. This was a cyst along the screw. Again, not structural, and the patient uh did very well. And uh you could see here good range of motion and no problems. Um, and this one was a cyst that came off the subtalar joint. And, um, and this is the, this is my, one of my most active patients. Uh, and he is also about 11 years out, and he has some cysts, but no pain whatsoever. It is highly functional, and you could see this isn't beautiful, but his metal and bone bonding is actually quite good, um, and he's got really good function. We corrected a lot of deformity, here you can see some bad varus which we tilted out of varus and got them into neutral alignment. Here's a valgus, a tilt the other way than Veris, and we got uh basically everybody that was tilted became untilted and uh life was good. We also had people with sagittal plane deformities, and we got them corrected to a uh corrected sagittal position. Here's one patient, pre-op and you could see very weird mechanics, and here they are post-op with uh. More normalized mechanics than what they had before. Um, and so again, we had excellent retention, uh, retention of implants, metal components, plastic components, 100% retained. We had two cysts that we packed. We removed some fibular hardware, and some medial gutter debrismen. We had a section of 3.8 treated IND and metal component retention. These are the categories of the operation. Uh, which basically nothing to remove metal or plastic components, just to uh deal with some arthritis that developed around it, or, uh, to take out the plate. As I mentioned, most common was the medial gutter debris. Here's our Captain Meyers uh survival uh score uh graph, you can see it's flat line. So we are not seeing the deterioration that's been seen in the past. 90% satisfied with minor or no reservation, 8% satisfied with major reservations, like a pain or swelling or stiffness, but they're happy, 2% dissatisfied, and my results are not the only ones with this replacement that have shown this sort of results. They are uh in Italy, uh, where Federico as wellli looked at 89 patients all. Had excellent survival ship, uh, with, uh, very few complications. He had 2.3% in, uh, with some loosening, but basically, uh, had a, uh, 7, 97.7% implant survival ship and, uh, other studies done, uh, at special surgery where they had done this implant, uh, and they looked at it, they actually had really good sur. Rivalship of this implant in particular, um, although it was found to be challenging for them to do, and it took longer for them to do, so they generally don't do it at this point. Uh, the outcomes in Sweden and in Scandinavia also show very similar survivorship course, uh, uh, graphs, um, like mine, and, uh, so I'm very pleased about that. Of course, I'm biased. I know how to do it, but I could uh correct severe deformity. I could deal with complex cases, durability is excellent, technique is different. There is a learning curve, and I'm going to cut my talk uh shorter uh so that uh we could get onto the other talks, but I have more literature to support the fact that implants are here to stay, the survival ships are much better. We're taking much less bone. We're having lower rates of infection, lower complications. We're correcting the formities way better, and the fusions are being outperformed by the replacements. And I'll give it a pause there. Thank you very much. Published September 18, 2024 Created by Related Presenters Lew Schon, MD View full profile
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