Good evening. On behalf of the AOFAS, I want to welcome you to tonight's program, Foot and Ankle Injuries in the Athlete, an update from the expert panel. It will be moderated by Dr. John Kennedy. Joining him tonight is Dr. James Calder, Dr. Gino Kirchhoffs, and Dr. Ariana Gennacos. You can find their full biographies and disclosures in the program document posted in the chat box and also in the on-demand education center in this course listing. The 2023 webinars are provided free to AOFAS members and orthopedic residents and fellows with funding from the Orthopedic Foot and Ankle Foundation, supported in part by grants from Arthrex and Stryker. Just a few quick housekeeping items before we kick off tonight's presentations. For technical difficulties, try closing your browser and logging back in the same way you did the first time. Recorded physician attendees may earn one hour of AMA PRA Category 1 CME credit by completing an evaluation and CME claim form at the end of the webinar. You can find the link to the claim in the CME chat tab, and we will follow up with an email at the conclusion of this broadcast. We are recording this webinar, and it will be available tomorrow in our on-demand education center content library. We encourage you to ask questions during the presentations. To do so, click the Q&A tab on your navigation bar. If we can't get to your question tonight during the live broadcast, the faculty will reach out to you following the broadcast to respond. At this point, I'll turn the program over to Dr. Kennedy to begin. Welcome, everybody. We have a great lineup this evening. It is 9 o'clock here in Eastern Time in New York, and I know it's about 2 o'clock in the morning in London and about 3 o'clock in the morning in Amsterdam. So we have recorded talks from both Professor Calder and Professor Kerkhoff. But tonight is very, very exciting. We have Dr. Giannakos, who's our first nano fellow here at NYU, and last but not least, myself, and we'll be talking about specific topics in terms of foot and ankle injuries in the athlete. So I'll pass you over to Dr. Giannakos, I think she's going to give you a little intro on who's here, and then we'll start off with Dr. Calder's pre-recorded talk on navicular practice. Hi, my name is James Calder. I'm an orthopaedic surgeon at the Fortis Clinic in London. And I also work as a professor in the Department of Bioengineering at Imperial College in London. So the topic we're going to cover today is navicular stress fractures. And really looking at some of the newer ways we should be treating these, perhaps, as well as the original descriptions of open reduction and internal fixation or percutaneous fixation. My conflicts of interest are on the WAOS website, and certainly there are no conflicts with regards to this presentation. So we know that navicular stress fractures are difficult in the athletes. They represent a third of all the foot and ankle stress fractures we see. And the problem with diagnosis leads to a late diagnosis with a somewhat insidious onset of pain, making it quite difficult to ascertain exactly what's going on with the player. And the management has been well documented for many years now, and consists of non-operative management initially for the vast majority of these. And certainly if we go back to TORC's papers back in 1982, look at non-operative management for the non-displaced and incomplete fractures. So these are the unicortical fractures. You may consider non-operative treatment for the complete fractures when there's no sclerosis, but certainly in the athletes, we'd be moving more towards operative intervention in that scenario. So if we look at the results of non-operative management, well, various people talk about the results being promising as long as you can non-weight bear them. And certainly in TORC's classification back in, or TORC's paper back in 1982, he reported a 100% union, but 78% were unable to return to sport if they used a walking cast. So I think that really pushed out the boundary saying actually if we're going to treat them non-operatively, they should be in a non-weight bearing mode for certainly for about three weeks, six weeks. Kahn then went on and looked at 86 fractures and had an 86% return to sport, but it was a long time. It's about five, nearly six months if they are non-weight bearing for six weeks and then gradually building up. And then the meta-analysis, once again by TORC's group in 2010, gave strong support for the initially conservative management for these fractures. So what do I do and what is, I follow the, that has been described by others before me, and if I treat them non-operatively, I'll give them a non-weight bearing boot. I prefer not to have a cast, but that means you can get some mobilization through the ankle, but they remain non-weight bearing for six weeks. I think it's also important to check vitamin D because we know that a lot of our athletes are relatively deficient, so they may have a within normal range, but realistically having a vitamin D level of say 56 probably isn't correct for an elite athlete and they're probably looking to more towards 100, 120. I'll also give them a bone stimulator. There are various out there on the markets, whether it's Exogen or whether it's one by DJO, but I give them a bone stimulator. We don't know whether that works. There isn't a lot of clinical evidence for it and there's scientific assumptions going on there, but certainly I'll give it to them for certainly the elite athletes. And then during the six to eight weeks, they sort of gradually increase weight bearing as long as they're pain-free and also clinically they're non-tender. And then building up to 12 weeks, they may start weight bearing in a hard sole shoe and increasing activities as long as they're pain-free. If you've got access to an Ulta-G or an anti-gravity treadmill or a Hydro Works running underwater treadmill, then this is going to be helpful in gradually increasing the weight bearing status through there. And then at 12 weeks, we'll get a CT scan to confirm that there has actually been no propagation of the fracture. And then at that point, we may expect them to start resuming sports. It can sometimes be a little longer than 12 weeks by the time they actually get back into competition. But from about 12 weeks onwards, I'd say that that's when they can start resuming in more heavy load impact activities. My management for when it comes to operative treatment, let's really relies upon those that are complete fractures. So they're bicortical. They are fractures that are displaced or those that have failed non-operative management in the athletic population. So maybe during the 6 to 12 week stage, as you increase the activities, if they start getting pain again, that's the time when I tend to break away from the non-operative management in the elite athletes and move towards fixation. The operative intervention may be open reduction internal fixation, but by and large, percutaneous screw fixation has been shown to be adequate for the majority. And certainly, if it's a complete but undisplaced fracture, then that would be perfectly appropriate. There's very little evidence to suggest that bone graft is required, but I do use bone graft if I'm performing an open reduction internal fixation. So in the displaced fractures in the elite athletes, I will tend to open that fracture site up, debride, certainly if it's sclerotic, then I will perform an open reduction rather than a percutaneous fixation. And in that situation, I would then use bone graft. I also use bone marasperate from the Iliac crest concentrate. Once again, there's no evidence for that at all, but it's one of those perhaps percentage gains I put in there. And it certainly seems to make some scientific, there's some scientific basis for it, but it's unproven clinically. So the percutaneous technique I would use for those patients with a unicortical fracture that's failed to conservative management for the completely undisplaced, complete fracture with bicortical, that is once again, that's not got sclerotic margins. But if they've got sclerotic margins, then at that point, we want to consider open reduction with bone grafting and perhaps BMAC. So here we've got a 22-year-old footballer. This one failed non-operative management with pain after eight weeks of non-weight bearing. So in that situation, it's a professional soccer player, footballer as we call them in the UK. And in that situation, it would seem perfectly appropriate to consider a percutaneous screw fixation. Now, in this situation, perhaps I would perform screws going from medial to lateral and lateral to medial rather than two screws going across from the medial side, sorry, from the lateral side. But the purpose of this one is that generally speaking, just over the sort of lateral to lateral third to medial two thirds. And so I was worried about getting the cross screws, the cross threads actually across the fracture side. And this was a CT scan on the right hand side at 12 weeks confirming union of that fracture. This is a 19-year-old rugby player, professional rugby player. He'd had no pre-existing symptoms of pain and then suddenly got a catastrophic midfoot pain and limped off the pitch. And you can see the fractures on the x-ray and it's confirmed on the CT scan. If you want to get a 3D reconstruction, you can do on that. I don't find it particularly helpful, but there is obviously a dorsal fragment there and this has been hanging around for a while. So it's been a stress fracture evolving over a period of time. So in that situation, I performed screw fixation and I was pretty pleased with the pictures at 12 weeks. I performed a medial to lateral and a lateral to medial screw fixation and got good compression at the fracture site. I did an open incision there with bone grafting and felt pretty happy about it at the 12 weeks. Then at 16 weeks post-op, he'd started his rehab and he suddenly got pain again. And the CT scan at 16 weeks confirmed that in fact, there'd been a re-fracture and the thing had fallen apart. So what do we do then? Well, in this situation, I took the, perhaps the AO approach and used more metalwork. And in this one, I put, augmented it with a dorsal plate, with once again, with bone grafting and I was lucky. The player got back playing professional rugby at the elite level and the fracture healed up and he has done well. But it does beg the question as to whether that's the right thing to do, because that's not the case with all those, all the patients when I put a plate and screw fixation over the top. Because when we take it back to basic principles, I'm probably just stripping the blood supply or the remaining blood supply away from the fracture site. And since we know from the anatomical studies, the blood supply comes in from the periphery of the navicular, then we're probably, I'm probably doing the wrong thing by lifting all that periosteal layer up, debriding that, and then putting a plate on top of it, further compromising the blood supply. So in those cases that we looked at, where they'd actually gone onto a non-union and a recurrent non-union, having had a plate fixation, we decided to look at something, a different way of doing it. And if we look back to, this is a paper from Pitt Fishman back in 2012 with Jim Nunley's group. And they described eight patients with a vascularized pedicle graft from the lateral tarsal artery, either from the cuboid, the intermediate, or the lateral cuneiform. They also used it for tail and navicular joint fusion in patients with avascular necrosis. And six out of eight patients in this series healed, and they had a relatively long follow-up period. So I think this is worth exploring more, because that probably does suggest this is the, this is the correct way forwards for those difficult cases when you get a non-union. So once again, this is a 23-year-old professional footballer who had had a navicular screw fixation under my care, had healed, he'd got back playing, and then suddenly he had an explosion of his navicular following screw fixation nine months beforehand. And this is not a pretty sight. It was a, once again, he's a soccer, apologies American colleagues, but he's a soccer player, but he's an expensive soccer player. And I wasn't too proud of what had happened here. So in this situation, I took a different approach. And this is the approach I take nowadays, saying that we got an ultrasound identification of the medial lateral artery. And you can do this interoperatively just prior to the, just prior to making any incision and identify these arteries, which are pretty easy to pick up on the, on the ultrasound and mark them, can mark them out for surgical exploration. The first approach is to take the incision down onto the fracture site, identifying the neurovascular bundle, along with the deep peroneal nerve, identify the fracture site, and I removed the previous screws and debrided and packed the fracture site with iliac crest bone graft plugs, which were taken using a bone harvester and packed the fracture site accordingly. Then you can see here, there is the neurovascular structures go down there, and you can see there's also one of the arteries, arterial branches coming across. And in this case, this was coming across down to the cuboid and make a tunnel underneath there, following the arterial branch down onto the cuboid. And then placing a guide wires in the cuboid under image intensified control, and then taking an osteotome to lift a vascularized osteoperiosteal flap. Once you've got that up, you can then swing this round back underneath the tunnel you've made previously, into the dorsal wound on the midfoot. And then that then just lays into the groove where there's the previous fracture site. Now, I don't use loops at all. I get seasick from using loops. I think Jim Nunley, he was a hand surgeon in his previous life, and I think he does use loops. But I've done these without loops myself, and I've also performed them with a plastic surgeon in the past who has used loops. But it's a relatively straightforward thing to do, to either bring up the dorsal, either the medial or lateral tarsal artery branch. And then lay it down into the fracture site, and then suturing it in place, and it provides a blood supply to the healing fracture. I do replace two screws back in there again to hold the fracture site and support it. But otherwise, I'm not stripping. I'm trying to avoid any stripping of the periosteum away from the dorsal aspect of the navicular. So, I spoke to Jim about this some time ago, when I first thought about doing it, having read his paper, and he was very helpful and sent me the original diagrams. And by the time we got up to looking at a few of these vascular flaps, I said to him a couple of years ago, well, actually, you know, you haven't written up your series recently. So, last year, Jim and his team did publish this very good paper in Foot & Ankle International, where they looked at 43 navicular fractures and looked at what is the appropriate algorithm we should be taking. So, 15 of them were acute, and they went on to have open reduction in internal fixation, and they had an 80% union rate. There were 12 fractures that had actually had chronic changes with sclerosis as well, and that had arthritis and bone graft, and they went on to 75% union. But those 16 patients who'd had failed surgery with a very chronic looking and sclerotic fracture site, they went on and performed a vascularized graft, and they ended up with 100% union rate for these ones. And I can say independently, and I haven't published my results yet, I can say independently, I would agree with this in that I think it does provide very good symptomatic improvement, but also a very high union rate. And so far, so good, I've been lucky, all these difficult navicular fractures where they've had a nonunion or very sclerotic edges or re-fractures, they've also gone on to unite. So, the concluding, the conclusion from Jim Nunley's group was that vascularized bone grafting certainly appeared to be beneficial for those more difficult cases. And I would concur with this. I think it is the, probably this is the correct algorithmic approach to take for these difficult fractures in elite athletes. So, my conclusion to this talk today is that evidence would suggest that initial non-operative management is wise. But if you're going to perform non-operative management, they should be told that they should remain non-weight bearing in the boot for six to eight weeks. The evidence would suggest that if you weight bear them early, they're less likely to have a good outcome and they're less likely to heal and they are more likely to have symptoms once again when you reintroduce sporting activities. I think one needs to consider surgery if the fracture is displaced, sclerotic, or those elite athletes. I prefer percutaneous screw fixation for those fractures that are undisplaced. There's certainly those unicortical fractures that then have a recurrence of their pain having gone through a period of non-operative management and the pain returns. I perform open reduction with internal fixation and bone grafting if it's a chronic fracture or if the fracture is displaced. And I still use a screw fixation for that. And I prefer Iliac crest bone graft using some corers. And finally, I think vascularized bone pedicle grafts are useful and they have a very good success rate for those difficult cases where there may be gross sclerosis right the way down into the fracture site or if there's any evidence of avascular necrosis or those that have failed surgical management with screw fixation. And those are the difficult ones. And I have no hesitation in advocating vascularized bone pedicle graft. And they tend to get back. I'm happy that they heal up on the 12-week scan on the CT scan so far. I've got a series now of eight patients that have done this and they have been able to get back to professional sport. Thank you very much indeed. That was an absolute masterclass by Dr. James Calder. And those of you who don't know, James is a professor at the Imperial College. He's one of the founding members of Fortius Clinic and a great colleague and friend, as is Professor Gino Kirchhoff, our next speaker. Gino is a professor at AMC in Amsterdam. He looks after professional athletes from the Olympics, from the premiership, and from soccer clubs all over Europe and indeed over the world. And tonight he's going to talk to us about acute syndesmotic injuries in the athlete. Any moment now he's going to do that again. Gino is coming to us from from Amsterdam so he has pre recorded this. So hopefully, Alina is sorry I was having a little bit of computer problems but I think we're good now. That's great. Thanks so much. So we will put on a Gino's recording on cynicism moderate injuries. Thank you. Hello dear colleagues from the United States of America. This is Gino Kerkhoffs from Amsterdam, the Netherlands, Medical Centers. Thank you very much for this kind invitation to be part of your webinar. My disclosures, I work as a consultant of Artrax. This is a view of one of our buildings, Amsterdam, UMC, the Netherlands. So let's start talking about acute syndesmotic injuries. Acute syndesmotic injuries mostly occur in high energy sports. It's seldom as a result of an inversion sprain, but in a high energy inversion sprain, also collateral damage to the syndesmotic ligaments can occur. However, what we see more often is an axial loading and external rotation of the foot, with a foot flat on the ground. Considering that with only the forefoot on the ground, you could, with the same injury mechanism, have damage to your ACL. So in close up, if we look at this picture, you see what happens with this flat on the ground. There's an axial force and an axial rotation. So this is a typical mechanism, and patients as well as managers and team doctors will recognize it's not like a inversion injury, but it's a typical different injury mechanism that should make you aware of possible damage to the syndesmotic ligament. If we look at the anatomy, we see the anterior inferior tibial fibular ligament. We see the interosseous membrane going all up in the space between the tibia and the fibula. And what we can also see is the great amount of vessels going all the way down from the interosseous membrane to the anterior inferior tibial fibular ligament. And you see that the vessels going over the ATFL anterior tibial fibular ligament are going in different directions. So what brings us that good knowledge of anatomy on the anterior interosseous and posterior side of the syndesmotic ligaments. Makes it, if we have a look after an injury mechanism in our outpatient clinic, and we see the patient, that at first we see that there's a different pattern of the hematoma if we have a syndesmotic injury. A hematoma will follow anatomic pathways and you see some collateral damage to the deltoid and there's some pain as well on the medial side. And you also see hematoma discoloration there and going all the way up to the interosseous membrane. Then we have our positive squeeze test with a pain at the anterior inferior tibial fibular ligament and a little bit higher up at the interosseous membrane and not on the spot where you press with your fingers. Important detail. Then recognizable pain on palpation of the anterior inferior tibial fibular ligament and just a little bit higher up at the interosseous membrane. As in the syndesmotic joint. Then we have the fibular translation test as well as the cotton test or exorotation test. Then there's the ring tape test. So it's a circular tape one and a half centimeters above the joint line. Patient is asked to stand on the foot with slight exorotation for weight bearing with and without the tape. An immediate downscale of the pain experience gives you some information on the stability of the syndesmosis with and without the tape. And for me, it's an interesting test because if the tape doesn't do anything and there's clearly syndesmotic injury, then it's so unstable that you will have to do an operation. So an interesting subjective test on my behalf. Then if we look at the literature, what is the exact diagnostic value of acute clinical evaluation? We looked at that together with our colleagues in Qatar. And we looked at six syndesmotic tests, the recognizable pain and palpation, the squeeze test, dorsiflexion external rotation test, weight bearing and non-weight bearing, and fibular translation test as well as the cotton test. Thank our PhD student and now resident Thomas Baltus for his great work here. And he came up with a very helpful conclusion that the most discriminatory findings for syndesmotic acute syndesmotic injury is overall clinical suspicion based on the trauma mechanism as well as the appearance of all the clinical tests in your heads. Then a slight video to illustrate this. I'll play it twice. This is a game against Gibraltar in a workout for the European Championships one and a half, two years ago. I'll play it once more. It's about our Dutch player with the number 17. Here it happens. Then you see him going to his knee. I saw him at outpatient clinic. Sorry about that. First question, hey doc, can I play further? That's on pitch. Answer is no. Hey doc, yours in two months, two days later in the outpatient clinic. So, okay, how do we cover this? First we have to know, okay, what's the injury mechanism we saw? The axial compression load and an axial rotation of the foot. He pointed to his ankle joint over the syndesmosis. So, acute syndesmotic ligamentous injury. Stable or unstable. So, external rotation test, squeeze test, tenderness, cotton, ring test, lateral instability. So, everything positive, anterior talofibular ligament, lateral ligament complex, fully stable, not painful. All the other tests, positive. So, what else did we do? Weight-bearing x-rays, lower leg x-ray, ankle joint x-rays, through the good work of Noortje Hagemeij, also a PhD student and now a resident with our friends from Boston. She looked at normal variations in the syndesmotic volume using ultrasound, as well as the work from Thomas Baltus over in Qatar. We have an opinion of, can we rule out the syndesmotic injury with an ultrasound? Well, answer is this. If we look at a complete tear of the anterior talofibular ligament only, then we have a 100% sensitivity and specificity using ultrasound. So, yes, static ultrasound has indeed a good value in the initial evaluation of this ligament itself. So, what about MRI? Show the limited inter-rater and intra-rater reliability of acute ligamentous ankle injuries looked upon on 3D MRI. Let me explain a little further. You see the posterior syndesmotic ligament pointed out with green arrows. Then interosseous membrane with orange arrows and the anterior side with red arrows. So, this is what we looked at in this study. And what we found was for inter-rater reliability, digitized for complete discontinuity and was almost perfect for the anterior inferior tibiofibular ligament and moderate or even a non-existent for interosseous and posterior side. And same goes for the inter-rater reliability. Okay, so MRI useful if you say it's a complete or a tear or not of the anterior inferior tibiofibular ligament, even on 3D MRI. So, main question indeed still is, stable or unstable? So, the work we did again with Noortje Hagemeijer, friends from Boston showed a complete range of normal and abnormal of the syndesmotic measurement using weight-bearing CT, giving a lot of information also to set the diagnosis syndesmotic instability, the work that we also did with our great friends, Chris DG and others from Boston. So, main findings there helped us a lot in this case because we still had to distinguish stable or unstable and we had to prove it to a lot of people surrounding this player. Stable would have meant ring tape, boot or something else. And obviously the rise, the awareness, the first range of motion should be full, the flexion extends the strength of the back, then the proper set of imbalance, normal walking pattern, all the cheek, all the way to the return to the pitch at performance level in eight weeks. Interesting if it would have been stable, we judged, okay, instable would mean fixation. This is how the nanoscope looked like, instable on cotton test or X-ray rotation in dorsal flexion. You see the fibula moving out the picture. And this is what we did, placed a tightrope, looked on the cartilage, did some small dissection impingement of the anterior inferior tibiofibular ligaments, fibers that were impingement and not growing back. And this is the arthroscopic view with a needle arthroscope post fixation doing the same test. So what's the potential option if the nanoscopic view would have not shown a stable syndesmotic joint? Then you could place a second tightrope in a 30 degrees different position. You could also fall back to the old technique, the plantar standard reconstruction of the AITFL, or you could place an internal brace, the AITFL. I would say in European football, I prefer a slight instability over an overtightness of the syndesmotic joint, because of the flexibility that the players need for all the foot position and passes. Then important, we said already, is the needle arthroscopic check after the first treatment of the instability to check if it's really stable enough. Now come to needle arthroscope, come also to John Kennedy, my great friend from NYU, did a lot of work together on the safety and efficacy and then further in-office treatment with nanoscopes. So needle arthroscopy, I think a very safe tool for us also to treat the acute syndesmotic ligament injuries because what does the ankle joint inspection show us? Cartilage damage on the telodome. So we did a needle arthroscopy together with a tightrope fixation and professional athletes with acute syndesmotic injury. 10 European elite athletes. And so obviously all athletes have had an initial 3-Tesla MRI. And we asked for a diagnosis, asking for a syndesmotic ligament injury and other ligamentous injuries. Didn't specifically ask for an opinion on concomitant cartilage damage, obviously. There's always a wide view on the ankle joint when this is evaluated, but initial percentage was 13% on concomitant cartilage damage on the initial MRI. What did we find in our literature study together with Chris DG and John Kennedy and others? We found 21% of patients with isolated syndesmotic injury cartilage damage. And so what did we find with our nanoscopic evaluation of the cartilage damage in the ankle joint? Up to 90% partial surface or full surface cartilage. So nine out of 10 patients showed cartilage damage using our needle arthroscopy. So important to know, has obvious prognostic value for patient rehabilitation, physical trainer, small pains, and maybe even a period of weight bearing just after the operation. So needle arthroscopy professional athletes with syndesmotic injury after tightrope fixation showed a return to sports for 10 weeks with a range of five to 12, and return to performance defined as the level that would have been expected of these players without having had the injury in their own sports ranges from eight to 24 weeks. So quote from the Dutch national players at the bottom side, two months after ankle operation, I was with the team playing for the Europeans. That item here says everything. So another few quotes here, look at the dates. So within eight weeks, return to full performance. So your take to work messages are acute syndesmotic injury, you're close to very good diagnosis if you go for your overall clinical awareness, be aware of all the six or seven or eight good clinical tests are out there, know the injury pattern, and then you'll be making wise decisions. So important, obviously, stable versus instable. Stable means conservative treatment, instable means fixation using whatever device you need, and a needle arthroscopy to check the quality of the fixation as well as the cartilage damage, the concomitant cartilage damage, be aware of that. So I wish you a great webinar. Sorry that I'm not live. I hope to see you all soon, maybe in Las Vegas for the AOS or at the AFS. Thank you very much, everybody. Happy to be welcomed in Amsterdam city. Ciao. Well, another great masterclass there from another dear colleague and friend, Gino Kirchhoff. And our next speaker is Dr. Ariana Giannakos. Ariana is our first nano fellow here at NYU. We've been doing nanoscope or in-office needle arthroscopy now for the last three to four years. It's been really popularized and pushed forward both in Amsterdam and in London and here, and indeed in MGH. And Ariana has had the opportunity to travel all around the world to visit these great surgeons. And she will then start her practice in Yale in the next month or two. And so without further ado, I'll pass this over now to Dr. Giannakos who will talk about Iona arthroscopy and the athlete. Thank you to the AOFAS for hosting this webinar and for having me here to speak today. Today, we'll be talking about the utilization of the nanoscope and foot and ankle surgery, particularly when managing the athletic population. These are my disclosures. I'll be presenting on the use of needle scope, particularly in the office setting and discussing some examples of how we've been using this technology in certain athletic injuries. The nanoscope is comprised of a handpiece with programmable buttons for image and video capture. It utilizes a chip and tip technology. The evolving nano needle is pictured to the right of the screen, which is becoming more popular, particularly in the office setting. We typically use a 4.0 millimeter arthroscope with a 5.9 millimeter inflow outflow sheet. The nanoscope camera consists of a 1.9 millimeter diameter with a 2.2 millimeter inflow outflow sheet. Therefore, the size of the camera is significantly smaller. The needle scope attaches to a portable monitor, which makes set up a lot more efficient both in the OR and in the office setting. This is a photo of a basic nanoscope handpiece kit, which is comprised of the handpiece itself, obturators, both sharp and blunt, which are in a disposable kit. The cost for each is about $500, but the new ones that are being developed are going to be reusable up to three to four times initially. In addition, we have variety of peel packs that include graspers and biters and whatever you may need. For over 20 years, we have still been utilizing arthroscopy for various foot and ankle conditions. We have evolved though from using a 4.2 millimeter scope with either an epidural or general anesthetic in the OR to now using a 1.9 millimeter scope with local anesthesia in the office. So ultimately we're doing similar operations with smaller instrumentation in the office setting. The ability to utilize these smaller instruments during arthroscopy allows us to expand indications for diagnostic and follow-up arthroscopy. This ultimately can shift some procedures from the operating room to a procedure room that is in the office. The nanoscope can be used in various joints, including the ankle, knee, shoulder, hand, wrist, elbow, and so on. By utilizing instrumentation that is significantly smaller in size and diameter and also consists of less instrumentation and equipment, this type of technology has the potential to make ankle and tendon scopes less invasive and more accessible. Previous studies have demonstrated iatrogenic articular chondral injuries during ankle arthroscopy when utilizing the 4.0 millimeter scope. Vega in 2014 reported an overall injury rate of 31%. And we know that cartilage doesn't heal or survive injury. 24% of these were superficial lesions and 6.7% of these were severe lesions. You can see in the depiction on the left the size of the scope within the ankle joint, even when patients are under distraction. And even with the 2.7 millimeter scope, there can still be iatrogenic injury due to the scope rigidity. The nanoscope is 1.9 millimeters and is a semi-rigid piece. So how do we go from the office to the OR? So obviously the surgeon has to adopt different steps, you know, going from diagnostic OR asleep, therapeutic OR asleep, diagnostic procedure room awake, and therapeutic awake. And patient-specific anesthesia progression goes from general anesthesia to spinal anesthesia to sedation and then awake under local. Dr. Kennedy created this setup depicted in the photos here at NYU. There is an OR monitor, underneath is the fluid which can flow through a pump, usually about 45 millimeters of mercury. Everything is done under a sterile field and it's exactly the same as you would have it in a normal OR. The procedure itself is very similar to your standard ankle arthroscopy procedure. In the office though, we utilize 1% lidocaine and 0.25% marcaine around standard arthroscopic portal sites and then directly into the joint. The same portals are just like you would use in a normal OR setting. So if you're doing an anterior ankle scope, you'd use your anterolateral and anteromedial portals, just like you would in the normal OR. Listed here are some of the various foot and ankle procedures that Dr. Kennedy has been training me to perform using needle technology. So how can needle arthroscopy be used in the management of athletic injuries? I wanted to include this case. This is a case that I actually did with Dr. or Professor Calder in London just this past December. So it's a 26-year-old male professional footballer who presented after sustaining an inversion injury during one of his games. He came in with lateral ankle pain and instability. His MRI showed lateral ligament disruption as well as cartilage injury to the anterior tibial anterior plafond. The plan was to do a lat leg repair along with the scope to assess the joint. We were in the normal OR at this point and we initially started with the standard scope. Unfortunately, we were unable to find the loose body that was from the tibial plafond. Being the nano fellow and having the nano needle with us, we ended up opening up the kit and we use the small needle scope to get to the back of the joint where the loose body actually ended up. So at this point, we were able to obtain the loose body, clear out the joint with no issues. Now, Professor Calder has been using this in his athletic population, especially when he's doing a diagnostic scope or if he needs to get to the posterior aspect of the joint. So what are some common ankle injuries that athletes sustain that we can use this in, particularly in the office setting? So anterior ankle impingement, it's common in athletes who sustain repetitive dorsiflexion movements. Impingement can either be bony or soft tissue and can be either anterolateral or anteromedial depending on the injury. Athletes who fail conservative measures typically benefit from arthroscopic intervention involving debridement of the areas of impingement. So this is a case. It's a 26-year-old male who presents to the office with five months exacerbation of right ankle pain. The patient had a previously failed debridement and microfracture at an outside facility that was done in 2020. The patient underwent an OATS procedure here at NYU in 2021 and did well, but unfortunately developed scar tissue. These are MRIs demonstrating his OATS graft, which is a 10-millimeter graft. Utilizing the nanoscope, we were able to identify complete integration of the autograft, but an abundant amount of scar tissue that was causing him ankle impingement symptoms. So this is in the office and this is performing an anterior ankle impingement debridement. We used ablation actually due to how thick the scar was. Once again, you can use smaller shavers as well, but you can use ablation and the patients surprisingly tolerate this pain free. This was a study recently published by Colasanti and Kennedy at NYU, which demonstrated improved pain promise scores and a 96% return to previous sporting activities following in-office arthroscopy treatment for anterior ankle impingement. Mean return to play was approximately 3.9 weeks, but what's important to note in this is that 94% of the patients expressed that they were willing to undergo the same procedure again. In addition, the patient had a better understanding of pathology and therefore they were able to understand the rehab protocol better. They felt more involved in decisions and with their treatment. To the right is a video of Dr. Kennedy performing anterior ankle impingement debridement in his office. Another common injury is posterior ankle impingement. This is typically affecting athletes engaging in repetitive plantar flexion. Once again, impingement can either be bony or soft tissue in nature and posterior ankle arthroscopy is often indicated as a definitive treatment. This is a 12 year old male who presented with a three month history of right posterior ankle pain. X-rays demonstrate an osteogona. After injection, the patient did not have any alleviated symptoms. The plan was then to perform an in-office posterior ankle scope for osteogonam resection and FHL tenosynovectomy. This is a video of thus debriding the os before removing and to the right is a video demonstrating an FHL tenosynovectomy. All within the office, all under local. This is a 17 year old male tennis player who presented with posterior ankle impingement due to a CETA process that was also causing FHL stenosis and tenosynovitis. After physical therapy as well as shockwave therapy, the patient unfortunately continued to have residual symptoms. The plan was to undergo FHL debridement and removal of the STETA process. He was able to return to playing tennis within a week. And this is reflective of a lot of the good outcomes that we are going to be publishing in posterior scopes. Once again, recently the NYU team published outcomes following in-office intervention for posterior ankle impingement and demonstrated improved clinical and functional outcomes and a 100% return to sport in the 10 patients that they looked up at four weeks. Lastly, Iona can be used as both a diagnostic and therapeutic intervention, particularly in peroneal tendon pathology. Peroneal tendoscopy is often indicated for peroneal stenosis, tenosynovitis, luxation, either intrasheath or luxation for a lax SPR, or small tears that require debridement. Obviously, if the patient has a larger tear, that would be indicated for an open procedure in the LR. Our group's prelim data evaluated 15 patients. 12 patients underwent successful debridement and groove deepening with significant improvements in FAOS scores and mean return to sports at three weeks. Of note, three patients had much larger tears that was unfortunately not picked up on MRI, and those three patients were then indicated for an open repair in the LR. This last case is a 59-year-old male runner who had a chronic history of snapping and swelling with pain over the peroneal tendons. He had a past surgical history of ATFL reconstruction and CFL reconstruction, as well as a syndesmotic tightrope. His MRI demonstrated interstitial tearing of the brevis and tenosynovitis. He had felt that there was squeaking of the tendon, and therefore, our working diagnosis at the time was possible peroneal tendon stenosis. He underwent an in-office tendoscopy that demonstrated a very tight stenotic tendon sheath. Therefore, in addition to debridement, a groove deepening was performed, and the patient did well postoperatively. And once again, the patient tolerated the groove deepening, which is the bony procedure, all under local. So in summary, nanoneedle technology can facilitate the diagnosis of intraarticular pathology and a simple bedside procedure under a local anesthetic. The simplicity of the procedure allows for patients to observe their own condition, and therefore, better understand treatment and rehabilitation protocols. This is important, particularly in the athletic population. Patients can buy in and therefore become part of the team and understand how to get back to play quicker and more efficiently and safer. This type of technology can become the future of arthroscopic intervention. Thank you. Thank you, Arianna. That was a very educational talk. And I think for us that are in this space of looking at in-office nanoarthroscopy, it becomes de rigueur. It's what we do every day. And of course, we have to understand that most people looking at this haven't had the opportunity to use it yet. But I think over time, that will change because patients will demand it, insurance companies will demand it. And there's so much that we can do in an office that we don't need to bring to an operating room. There'll always be a need for an operating room. But I think a lot of these cases that we do now with big ORs and a big staff and a big cost can all be done very simply. And the great thing is that the outcomes are even better. And patients do want to know what's going on. And I think, as you quite rightly said, when they know what's going on, they do pretty well. So without further ado, I'm going to talk much about nano as well. But I will also talk about osteochondral lesions in general. And so we'll have James, our fellow here, is going to... We can work in nano, but I just can't work a computer. So here we go. So this is Innovations in Treatment of OCLs. These are my disclosures. Arthrex is the company that actually makes the nano equipment. I was looking at Iona way before Arthrex were. There was other companies doing this, but I decided that I would go with Arthrex simply because they were the best at that time and currently still are. I don't get any royalties from that at all, but it is important to put that out there. Interbones, RegenerMed, and Isto have nothing to do with this at all. This is what we're going to talk about. And we'll spin through these fairly quickly. We may not have time to get to ankle instability. I know we're coming up to 10 o'clock Eastern time here, and we'll try and get through as much as we can. So ankle OCLs are much more common than we thought. In the United States alone, there's 27,000 ankle sprains, and up to 50% of these may end up with some form of carpet injury. And we've even heard from Dr. Kirchhoff's talk today that 90% of syndesmotic injuries will end up with some form of carpet injury. Now this was something that we, this was a study we performed with Larry Benassar's group up in Cornell. We tried to see what would happen, bovine cartilage, if we used an impactor that had the same force as a normal ankle sprain. And you can see this is bovine cartilage here, and 60 minutes later, you can see where that impactor has occurred. These cells are dead, and these cells will simply not regenerate to normal cells. And again, this was a nice work done by Kira Novikovsky. And you can see this is using multi-photon microscopy. You can see this curve here shows that you get initial cell necrosis. These are chondrocytes up on those top photomicrographs. And then you'll see the lacunae, they're dead cells. And instead of the regeneration and repair that you would ordinarily think, it actually is mostly proteoglycan synthesis that you get, or matrix synthesis. So, the normal chondrocyte, of course, never has a capacity to repair. Now, this work was all done, or a large majority of it, was done by Paul Glimcher and Frederic Shapiro, who were my bosses many, many moons ago in Boston. And really, it was what they showed was, when we have these cartilaginous injuries, they initially fill in, if they do go down to the tide mark, they will fill in with type 2 cartilage. But ultimately, that de-differentiates into type 1 cartilage after about a year. And that is important when we talk about bone marrow stimulation, and why ultimately that will fail. So, the knowledge that osteo… and the cartilage never really has the capacity to repair or regenerate, we now need to look at seeing how surgically we can intervene. And there's two broad categories in how we do that. Using bone marrow stimulation, ACI, MACI, and AMACR, outside the bailiwick of what I'm going to be talking about today, but I will talk about bone marrow stimulation. And then we'll talk about replacement strategies using either an osteochondral autograft or an allograft, and extracellular matrix scaffolds. The proprietary one here we'll be talking about is biocartilage. And then we'll talk about biological adjuncts to this also in terms of PRP, concentrated bone marrow, and so forth. So, reparative strategies go way back to the 1980s. Stedman and Inee was using these large balls or picks and creating this… these passages into the subchondral bone to allow stem cells to migrate and ultimately proliferate in this area. And when you look at this, it seems like a very interesting and useful procedure. And nowadays, we've moved away a little bit from microfracture. In fact, we've moved away a lot from the actual term microfracture. But… and we ask why do people do it? Well, the reason it's done is because it's simple, and because patients do well initially, and then they start to drop off over time. But if you look at these two studies here in athletes, 96% return to sports at 15 weeks, and 26… in 26 athletes by this is Saxena on the East Coast. And then here again, in six soccer players, 94% resumed activity at pre-injury level. So, this is really compelling data. But if you look a little bit downstream from that two-year mark, particularly in competitive athletes, it starts to drop off. So, we started to look at that. In the old days, it used to be anything less than 15 millimeters, you would consider bone marrow stimulation. And then Laura Ramponi from Rizzoli came visit us in New York, and Laura then presented her data to this international society that we had at UPMC. This is ICCRA. And we had a consensus meeting, and the consensus meeting really decided amongst the world's leading experts that bone marrow stimulation should be performed only in lesions less than 10 millimeters, and anything greater than 10 millimeters, you must consider replacement therapy. And that's important. It's not just in terms of boards questions, but that's important because it's a paradigm that leads to greater success when you are considering bone marrow stimulation. So, here's the problem with bone marrow stimulation, that when we breach the subchondral plate, the whole idea, as I said, is to recruit these stem cells, and it forms a fibrin clot. Then you get this type 2 collagen. That's what you want. That's what we think is going to be there. And Laura Micheli has shown that that does happen initially. And as I said, Fred Shapiro shows that, however, because the subchondral plate is damaged, we get proteoglycan depletion chondrocytes out of that, and de-differentiation of type 1 collagen. And that doesn't have the same mechanical properties as type 2, and ultimately fails. And the proof is in the pudding. So, when we look at this, it's not only in terms of what we look at in terms of arthroscopy. This is Jin Wu Lee, the second look at arthroscopy. 30% of repair tissue, greater than 12 months post-op. That's not great. I mean, 70% has. Clio Thurman looked at this five years post-op in MRI. 100% had cracks and fissuring, and all by his group. Again, at eight years, almost 80% had signs of surface damage and incomplete integration. And Rick Ferkels' group then looked at this clinically, and 35% of these patients with bone marrow stimulation had deterioration in outcome scores at five years. So, both clinically at second look arthroscopy, an MRI, and patient-reported outcome scores, these start to fail any time after two years. So, for an athlete, that's not very exciting, or for anyone. But why do this? Why does this happen? Well, one of our previous fellows, Dexter Tsai, who's now in Singapore, Dexter looked at a systematic review of animal models to see what happens to subchondral plate. The subchondral plate is really like the scaffold. It's really almost like the rafters in a roof. And if you think of cartilage as the tiles, if you don't have rafters, whatever tile you put on there, it'll collapse. And so, Dexter wanted to look at this subchondral plate. It absorbs 30% mechanical load, and of course, cartilage will only absorb about 3% or 4%. So, you really need strong rafters in that joint. And he showed that 100% of the time, subchondral plate never restored to normal, 100% of the time. So, we looked at this, and we looked at C, but Gene Kirkhoff's group looked at it in CT scan and showed something the same in their group of patients. And we wanted to go a little bit further in terms of MRI. What can we find in this? Is it a predictor of outcome that subchondral bone fails, or if there's a large area that's missing? And we found that it was. It was also, when we looked at subchondral cysts, subchondral bone plate, qualitative quantitative analysis of bone marrow edema, we found that as you progress in these in terms of the size, quality, and quantity of these, so too is the likelihood of failure of bone marrow stimulation increased. And patients often ask, and indeed, radiologists often ask, well, how long is normal to have an increase in bone marrow edema after bone marrow stimulation? We found in two years, it was relatively normal to have a slight increase, and it should be getting better from the initial time of surgery. But in four years, if you have bone marrow edema, then the likelihood of failure is high. So, in summary, in terms of what's going on in the MRI here, we can see that if there's a, the subchondral plate is damaged, and if there's bone marrow edema, the likelihood of a good outcome, long-term clinical outcome is poor. So, we do bone marrow stimulation, and here you can see we still use an awl. We don't go down six millimeters. We do one or two small nano-awls. These are just one millimeter in diameter. We've seen from work by Jinakis and her group that when you do multiple small penetrations into the subchondral plate, you create sclerosis, you reduce neovascularization, and ultimately, the bone will die. So, we just do one or two in a small surface area, and then we use a burr to remove the calcific zone, like Takao and his group in Tokyo do, but we do all this in the office, and just like Dr. Jinakis said, these patients are awake. They have no general anesthesia. They have an intra-articular injection of lidocaine and marcaine, and we're able to perform this procedure. We're able to show them the lesion, and we're able to show them what we're doing for the lesion, and therefore, patients really understand what's going on and buy-in in terms of their rehab and their expectations and so forth. So, the reason why we feel that nano is very useful, and this is some nice work done in North Carolina by Ned Amendola's group, and it really shows that if you get patients up and moving quickly with an ankle bone marrow stimulation, the likelihood of success is just as high as if you have them non-weight-bearing for a period of time, and the reason we know this, and again, this is work done by Nick Van Dyke's group. The ankle, by comparison to the knee, is a very congruent joint, so if you have a contained lesion and you have bone marrow stimulation, plus or minus a scapula in the biologic, once you get it moving, whatever you put in there is going to stay in there because there's no way it's going to get shot out, unlike a CAM joint as in the knee, whereas in this joint, it's very contained, and that mechanical loading will help stimulate the bone to heal and stimulate cartilage to heal also. So, in terms of microfracture, then, the summary for this is bone marrow stimulation alters the microarchitecture of the subclonal bone plate, which will most likely degenerate over time, and this will ultimately affect clinical output. Therefore, the lesion size for bone marrow success may be closer to 10 millimeters rather than the original 15 millimeters that is popularized in much of the literature. We feel that athletes may benefit from two years after bone marrow stimulation, but I think to prolong that, we're looking at biological adjuncts, and I'll get onto that a little bit later in the talk, and that most of what we can do in terms of bone marrow stimulation can be done now with in-office needle arthroscopy under local anesthetic, without the need for a big operating room, with early return to function. So, we'll talk a little bit about orthobiologics. These are the traditional Venn diagrams that we've all been taught that you need growth factors, you need stem cells, you need a scapula to hold it all together, so it's inductive, conductive, and osteogenic or chondrogenic, and this is what we were all told years ago when we were in medical school that this is the traditional role of a stem cell. You put a stem cell or a multipotent or three-potent stem cell in a particular area, and it'll follow a path of differentiation, and it'll produce any of these phenotypes here. Well, that probably isn't what happens, and I think now most of us who are in this field are looking at really rethinking the MSC. The secretome theory is slightly different, and what that means is that the macrophages, when you put an MSC into a particular area, the macrophages engulf that MSC, and they then become activated macrophages, and they have a stimulatory effect, not just in terms of the path of differentiation, but immune modulation, recruitment of endogenous stem cells, angiogenesis, and other trophic effects, and I think this is really the key to how stem cells work because when you inject a stem cell and you radiolabel a stem cell into a joint and you come back the next day, less than 1% of them remain there, and the reason for that is because they've been activated by the macrophages into this secretome. So, there's various ways that we get stem cells. One of those ways is concentrated bone marrow aspirate, and Dr. Calder has alluded to that earlier on when he uses this when he's doing navicular stress fractures or navicular fractures. So, the contents of concentrated bone marrow aspirate are not just mesenchymal stem cells. It also has interleukin receptor antagonist protein, or IRAP. This is one of the most powerful homologous anti-inflammatories that we have. It reduces the concentration of IL-1RA. It also has these growth factors and stem cells, as he alluded to earlier on. We typically get this or harvest it from the iliac crest. We put it into one of a number of proprietary machines, which react with the centrifuge, and we take about four to six cc's from a 40 to 60 cc draw. Everything we do has to be based on basic science, and this was one of the first studies that came out looking at an equine model from the 48 group at Cornell, and it showed that there was good T2 stratification with MRI, and there was good histological integration, better than when CVMA was not used in a microfracture or bone marrow assimilation group. Saul showed the same thing in a GOAT model. He also showed it in arthroscopy in the talus, where he showed that when he compared microfracture with CBMA and HA versus HA alone, and MRI improves clinical scores in the stem cell group. Kim showed the same thing when he used microfracture alone versus microfracture and CBMA. So there's good evidence, both in the basic science and clinical science. And of course, we want to look at this ourselves. And so we looked at this, this is Charlie Hammond, one of our previous fellows who looked at this, and he looked at 22 patients with CBMA and bone marrow stimulation, and then with just BM and bone marrow stimulation alone. And while the clinical scores were roughly equivalent, what he noticed in this was that the T2 mapping, the qualitative analysis of T2 mapping showed that there was better cartilage stratification in those who had CBMA group, indicating that the lack of CBMA was a harbinger of a poor outcome downstream. So we've also used this in our AO2 groups, in AOT groups, rather, and where we're using OATS grafts. And this was, again, one of our previous fellows, Chris Morosky looked at this in 72 patients and showed that color stratification would be a really good integration in and around the OATS graft itself. One of the problems, of course, with using OATS is that oftentimes, and you'll get a report from the radiologist that there is subclonal cysts, and patients get very worried about it. We don't particularly get worried about it because we know these cysts are there for about 60 to 70% of the time, and they resolve over time, or many of them do. But it's still a little bit concerning why they're there. And of course, one of the concerns we have is this 20% cell death around the host graft interface, and we'd like to incorporate the cartilage and bone to the host as quickly as possible. So when we use a concentrated bone marrow aspirate, we can see that that bony and cartilage integration is far greater than when we don't use it at all. Of course, PRP is used in an in-office setting. PRP is taken from venous blood. There's no stem cells, and no stem cells we're talking about in PRP. So it has all the same growth factors, really, as concentrated bone marrow aspirate, and it's used to augment healing and increases chondrocyte synthesis, biopregnate as in the gene, and pro-glycan production, and so forth. So we use it a lot in the office. We use it in various things, in terms of both bone tendon and cartilage. One of the other things, of course, about PRP is it is a very potent anti-inflammatory. So again, when you inject PRP into a joint, it won't just go to that focal cartilage defect. It turns on the actual joint to become far more chondroprotective, and it reduces the normal inflammatory mediators of inflammatory milia, where there will be a chondral injury. So I think it has a chondroprotective role. And so therefore, it's very commonly used. This is a very nice microfluidics picture, which shows that when we use this membrane, and you put stem cells in the middle of this device, and you put PDGF, which is a very potent chemoattractant, in one cell, and you put PRP in the other cell, and you then open them with a charge, you can see that the MSCs, they preferentially rush towards the PRP, indicating, again, a chemoattractive effect. So we want to look at this. Oftentimes, when you have one teaspoon of sugar in your tea, it's good, and three or four teaspoons may not be as good. And the same thing, of course, is for PRP. And we looked at this in our lab and to see whether there was any difference between a single or serial platelet-rich injections with osteochondral lesions and the WASM. So we typically do one PRP injection, and then we will do another one within six months, but no sooner than. We also wanted to see whether it had any effect on the integration, just like CBMA did, in terms of the integration of the host-prompt interface with AOTs. And it did, it increased graft integration and histological scoring on those patients, on those rabbits, rather, that were treated with this. There's also very good clinical evidence of this, and this is both level one and level two clinical evidence to show that PRP is beneficial, and more beneficial, indeed, than no treatment alone or, indeed, HA. So therefore, PRP is something that we use at the time of surgery in the office because it's easier to get than CBMA. Problem, of course, is anytime you talk about PRP, it's not a standardized treatment. PRP taken from me today will be different than it is tomorrow and different than anyone else in the room. So one of the problems we have when we're trying to evaluate this in any sort of meaningful way is that there's no good evaluation of what we're injecting. So I think moving forward, we need to be very clear. There are now three or four different ways that we can categorize or rate the type of PRP that we're getting. I think we have to standardize that and when we're certainly talking about publishing the effects of this. So that's really sort of gone through the two biological elements, but to hold those together, we're just going to talk today about an extracellular matrix cartilage allograft, ECMA. It goes under the trade name of biocartilage. It's an arthritic product. Again, I do support Arthrex in large part because I believe a lot of the products they have worked very well. And for me, this works well and there's nothing else out there right now. And I know there will be, and we'll look at that when there is. But right now, when I use this scaffold and mix it with CBMA or PRP, I think we can really provide all the elements we need for chondro regeneration repair. It really provides this scaffold where we add our CBMA and MSCs. Again, everything we do has to be evidence-based. And when you look at this again, there's a good work at the Cornell Group to show in the patella femoral joint that when we use biocartilage or this extracellular matrix in combination with bone marrows concentrate, that it produces better quality and quantity cartilage. This has been supported not only in the knee, but also in the ankle. A nice study by Ahmed, she looked at 30 patients with biocartilage with 90% satisfied. And our own group showed it in a level three study. And again, our MOCART scores were better in that group and our teaching mapping was better. This is what it looks like. It looks like garlic powder. You mix it and you put it in under a dry scope into the joint, flatten it down and you secure it in place with fiber and glue. Dan Grandy has turned us onto this idea that fiber and glue, of course, pushes those cells, those MSCs down the path of producing fibrous tissue. So judicious use of fiber and glue is important here. This is when we looked at AOT with and without extracellular matrix cartilage for augmenting osteochondral lesions. And this was a nice study. We found in fact that if you have a good integration between the AOT group, the AOT and the host and graft, using biocartilage was actually of no great benefit. And once you were using concentrated bone marrow, you really didn't need the extracellular matrix in a well-fitted graft. But those grafts that have cartilage degeneration around them, then certainly that's a different story. But I think for a well-fitted oats graft, you don't need this. So that brings us to the role in the management of ankle OLTs with nanoscope. I think since the introduction of this, we've been able to look at a lot more secular carthroscopy in the office. We can see what's going on in terms of secularization of scarring at the front of the joint, which is not too uncommon in AOTs or indeed in any of these. And so here's a couple of interesting, this is an ionoclastic resuscitatory treatment of ankle OCLs in the office setting. This is one we just did the other day. This is actually a very laughable lesion. We wouldn't have been able to do this without traction and so forth. You can see the patient is looking at everything here themselves. Until we do 1,000 of these, we're going to treat it as if it's in the operating room in terms of sterility, but this is probably overboard. We probably don't need to do that. These are just small two millimeter incisions. We don't even use sutures. We just use steri-strips at the end and an ACE bandage. And they get off the table and they walk back to the room. And this was one of the things that we were always worried about when we get an MRI report back and how do we differentiate? If it's sort of an eight or nine millimeters, is that something that would work for, will that work for a reparative or do we need to go on and think about doing an OATs or an AOT on this? Well, one of the ways that we can see this in a way that's better than MRI, which I think overestimates these a lot, is we can just simply stick a needle in the office and we can see truly, and not just the size of the lesion, but also the quality of the cartridge that's there by probing it. And I think that's really, really important. And therefore the patient knows also, the patient sees what it's about rather than trying to explain an MRI to them. They truly see it themselves and understand. Of course, one of the things that we're always asked about is what's the cost of this? Well, if you look at the knee and the shoulder, we are working right now to see what the cost of it is in the ankle. The cost of an MRI is far greater than the cost of a nanoscope for these joints. And we will find that also for the ankle and joint. So it is cost-effective. I think it gives us greater imaging of the surface. Of course, it won't tell us what's going on underneath the cartridge, but by and large with CT and x-ray, it can do that. And again, this was a nice study that was done by Gino Kirchhoffs and his group in AMC. And it looked at, can you use this to direct, can you use a nanoscope to direct during cartilage injections? And they were able to do so without any difficulty. And again, without traction and just under local anesthesia. We're going to spin through this very quickly because we're running out of time. These are replacement strategies. This is AOT. This is typically on a medial side. You can see here, we have a two plug on the medial tailored dome and a medial tailored osteotomy. This is how we do it. We use a Chevron osteotomy. We take from the lateral femoral condyle and then we fix it in place, spending a long time to get the congruency just right. And then use a three-screw fixation technique for the back. The surgical outcomes of this are excellent. All of these are over 80%. Patients do well, not just in terms of the short-term, but long-term. And they also do well in terms of their MRI analysis. Again, T2 mapping for us right now is a possible standard to measure cartilage integration and longevity. Other surgical outcomes in athletes. Well, Paul has looked at this. And again, almost, well, he had 75% were satisfied. Hangudi, again, over 90%. In our own study, we looked at a group of Brazilian soccer players. And again, 90% of these were professional athletes and they returned to their normal sport. So again, even though we're taking from the knee and transplanting to the ankle, soccer players are expected to get back to their previous level of sport. Predictors of outcome of this, another nice study by Keir Ross here at NYU showed that BMI and previous microfracture. So it's not good enough to say, well, I'll try microfracture and if it doesn't work, then I can move on and do an OATS. Really, we shouldn't be doing that. If it's the right size and it looks right, then we should do the OATS for the next procedure. Chevron osteotomies, people that were complaining, well, maybe you're causing a pilon type fracture to the tibia. No, you're not. This is a nice study by Josh Lamb to show that really, again, there's really no harm done when you're coming out to the non-articulating portion of that tibial profound. The next areas of OATS always talk about Victor Valdivano's study where 50% of patients had knee pain in a study of 12 patients. Well, in a study of over a thousand patients, this was a nice study in core that our group published and this was not me, this was a whole group of us involved in this. And it showed that in fact, the overall donor site mobility was less than 5% and that dropped off over time. As patients move further away from their procedure, their donor site mobility reduced down to about 2%. So it's very, very low in those patients that know what they're actually doing. One of the other concerns, as we alluded to earlier on, was trying to get the articular congruency just right. If you're a millimeter beyond the normal congruency, you'll get up to 79% increase in contact pressure. This was a nice study done by Easley's group and Ash Franza, who again was one of our previous fellows using a robot here. You can see this pressure mapping. So we spent a long time getting it just right. And this is again, a couple of cases. This is a nanoscope looking at the second look at OATS. Here you can see that it's integrated nicely. We look around, we push down on that integration because that's really where the problem with OATS is. It's not the graft itself, it's the integration. This is an allograft. Several years ago, we started to move towards allograft as we did in the knee also. And we thought that we should have the same results. Al Rashidi had showed that 11% is failed and Achmed had showed that about 20% is failed in their group. And so we'd want to look at our group. And again, we found that roughly 20% of the allograft group failed, which was just an unacceptable number comparing to two or 3% in the autograft group. So we no longer use that as there's a high rate of failure in the allograft group. And we don't have time to go through ankle instability. So I'm going to spin through a couple of cases. This is a male triathlete who had a long, he was running seven marathons, seven days, seven continents. And so he came in with, he came in with ankle pain and a osteochondral lesion. This is what we did. We put a cartilage in there. And again, we thought that looked pretty good. He got back to running. And several months later, he started having pain again. And this just shows you, not everything works. So we looked at the wire cartilage here and it's failed. This is just simply fibrillated. And this is not sufficient to allow him to get back to running. But again, it just shows you with a nanoscope, you can get in there in the office and tell, sorry, we're going to have to do something more. And we went on actually to do an OATS. This is a soccer player. He had an OATS five years ago. He developed antramedial pindrin. We find that oftentimes so that they do develop antramedial pindrin. And then we were able to put a nanoscope in there and we were able to try that. There's the original OATS graft that looks pretty well incorporated. A little bit of fibrillation at the cartilage surface as well. We were able to get in and clean off all the scar tissue at the front of the joint. And he's back out doing all the things he wants to do now. I think Ariana went over this patient before and he had an OATS in 2021. He developed well, or he did well, but he developed a scar. And this just shows the first time. Again, you can see the complete integration of the autograft. But he had almost an arthrofibotic appearance to this. And because the shavers are very, very small, he could be in there for a year and a day. They're trying to take all this out with a 2.8 shaver. So we tried the ablator, a thermal ablator. And again, remember this patient was under local anesthetic. That's all it was. We were able to use a thermal ablator sporadically and removing the scar tissue and they did very well. Now this is again, is a patient who had a three month history of right ankle pain. She had a tailor dome OCL on the other side and the lateral tailor dome before. And now she's a new tailor dome lesion. So we decided we would do Iona or anal fistanoarthroscopy with higher cartilage implantation. And this was a couple of months ago. And you can see that we're just shaving away. And there again is that, as I said, it looks like garlic powder in a dry scope. A little bit difficult to get the suction in. We are developing a better suction tip to get a dry scope in the office with the type of suction that we have. We don't have a strong suction habit in operating, but we're able to get a dry scope. And again, we put it into that detail. So in summary, osteochondral lesions. The lesion size is a key factor in deciding management. As I've alluded to already, anything less than 10 millimeters should really be treated with bone marrow stimulation. And we believe with biological augmentation and the addition of a scaffold that may improve that local biology and output integration. Anything greater than that 10 millimeters are squared warrants replacement, including AOT with biological augmentation. And we found that Orograft is far superior to Allograft and we have abandoned the use of an AOT in Allograft. Scaffold-based therapies are not useful unless there's significant cartilage loss around your AOT. We've also found that I think the future of this, not in terms of diagnosis alone, but evaluating outcomes and ultimately treating these is Iona are in office now on osteo-bedside assessment and treatment of osteochondral lesions. So that concludes my talk. I think that we have run over time. We're getting signals from the powers that be that we will have to cut it off here. I know there are many, many questions. And what I would ask you to do is send us those questions and we'll ask what Professor Calder and Professor Kirchhoff and Dr. Giannakis and myself, and we'll answer those individually. I think that's probably the better way of doing this than now. So without further ado, I'd like to thank all those at AOPS who asked us to participate tonight. I think this, I've learned a lot. I hope you have too. This is always educational. And so many thanks and be careful out there. Thank you.

foot and ankle injuries

athletes

navicular stress fractures

non-operative management

surgical options

acute syndesmotic injuries

nanoscope

in-office arthroscopy

anterior ankle impingement

posterior ankle impingement

biologic adjuncts

osteochondral lesions