All right, I think we'll kind of start, I'll start talking and we'll get into the meat of things in a minute. Good morning. My name is Alex Galant from NYU. Welcome to ICL 308. And let's see, make sure this advances. You said click. So if you click in the black space, then use the arrows. And then use the arrows. There we go. Yeah, yeah, yeah. There we go. Okay. So first and foremost, I want to thank you all for being here, rising up nice and early, 7 a.m. on a Saturday morning. I don't know. We'll have to talk to the program directors to revamp that. But a special thanks to my co-speakers and participants in this event. Very honored to have Dr. Lee Pace from Texas, Jackie Brady from Oregon, and my colleague Kirk Campbell from NYU who'll be helping educate us on patellofemoral issues, which are near and dear to my heart. So let's start by discussing medial soft tissues and patellofemoral instability. This is really an essential part of any surgical treatment of patellofemoral instability. My disclosures are not relevant to this talk. I'm sure you all know the epidemiology of patellofemoral instability. It's not a very common condition, but it is a troublesome condition, especially for our teenagers with a very high rate of recurrence, and especially if a second dislocation occurs. We know that there's a number of anatomic factors and patient-specific factors, such as young age, hyperlaxity, but also anatomic factors like trochlea, dysplasia, maltracking, and patella alta that can all predispose. And when you have three or more of these risk factors, then the rate of recurrence is extremely high with non-surgical treatment, and we move into the world of surgery. So now when we're thinking about patellofemoral instability, what it really is, it's a dynamic imbalance. It's a disruption of some kind of status quo. And the key thing there is the loss of soft tissue restraint. Even if you have the anatomic predisposition, you can have that knee teetering on the edge of instability, but never become unstable. So that's the quintessential, the sine qua non lesion of patellofemoral instability is the disruption either by traumatic injury or attenuation of the medial patellofemoral complex. So what is this medial patellofemoral complex? There are static and dynamic components to it. Obviously, we should never forget about the dynamic contribution of the VMO, which can also be treated surgically, but really we're going to be focusing on the static component of this, and specifically the MPFL and MQTFL are considered the most significant. So Jack Farr and others have taught us that the MPFL, and I would change that to say MPFC, medial patellofemoral complex, the image to it is the common denominator in patellofemoral instability. And so its treatment should be a part of any surgical procedure for patellofemoral instability. So what can we do to address this? And we have many choices. The first choice, the most obvious one, is do we repair damaged tissue or do we reconstruct it? And we're going to answer that question. Second question is if we are going to reconstruct, if you're going to repair, you repair whatever is damaged. If you're going to reconstruct, what exactly are we reconstructing? Are we treating the MPFL, the MQTFL, some of the other less known ligaments that are part of this complex, or are we doing a hybrid of things? Then we have options in terms of choosing a graft, choosing the technique option, double or single limb, and various fixation options. And it just, you know, sometimes when you think about it, it kind of makes you cry a little bit, too many choices. But because you guys made it out there and because I like you, I'm going to make it easy for you. And you learn nothing else. This is going to be a slide. Just, you know, remember it and you're done. And that's kind of the summary of this talk. Repair versus reconstruct. This is a no-brainer. You're going to reconstruct pretty much all the time. And I would say there's maybe one caveat to this. In my career, I've only encountered this a few times. So I call this the unicorn case. This is a very rare case where you have an acute injury, usually some kind of traumatic sports injury with an avulsion, typically a bony avulsion, and the patient truly has no predisposing factors. I think in that situation, you could try a repair, but you really have to convince me, I have to convince myself that there's nothing else going on, otherwise I'm reconstructing. In terms of the MPFL, MQTFL, or hybrid, thus far, we have no evidence to support one over the other. It doesn't matter. If you want to throw in MPTL, some people have done that. It's probably not necessary for most cases. And you cannot do that in lieu of the MPFL or MQTFL. But you can certainly add it if you want to get creative. Allograft-to-autograph, doesn't matter. Surgical technique fixation method, doesn't matter. Thank you for your attention. No, just kidding. All right. Medial repair, right? So let's, we started off, I told you, we can just, you know, we can just reconstruct. This is a patient of mine who I repaired, and he did well for about a year or so, and then he had recurrent instability. I got excited. There's a little medial avulsion. So it'd be really great if we could just throw some suture anchors for avulsions, or maybe mid-substance imbrication. There's arthroscopic techniques described, which I've done, just slick. Again, you know, the triumph of technology over reason, in my opinion, because when we look at even some of the older data, when they compared redislocation rates and outcome scores with non-op treatment versus repair, these are prospective randomized trial, no difference, which means the repair does about as well as doing nothing at all, or just doing some therapy. So, sorry, but it doesn't work. When you compare repair to reconstruction, you see the tremendous difference in failure rates. You have very low failure rates with reconstruction, and we'll talk about why they fail at all, and very high rates with repair. This study recently published out of Mayo with their 12-year follow-up on some of their repairs versus reconstructions, three times higher rate for failure for repair, more re-operations, although the PROs in return to activities were similar. And this study out of my institution, Dr. Campbell was the lead author on, or the senior author on, you know, showed that this is a meta-analysis of randomized trials, 2.7 total recurrence with reconstruction, 28% with repair, and non-op, almost 50%. So there's your answer. So now, we're going to reconstruct, right? And whenever you reconstruct, you have to respect the principles of really any ligament reconstruction, not just MPFL or MPFC. Graft selection, where to insert, how to fix, how to tension, and then obviously addressing additional pathology. And I would argue that the graft selection and secure fixation, obviously you need to securely fix, but it's not as big of an issue for the MPFC. Anatomic insertion and graft tension very much is, and so we'll talk about that later in the talk. And addressing additional pathology, that's really what the rest of this ICL is about. So we know where the MPFL and MPFC is located, second layer of the knee. It is a thin, you know, less than half a millimeter ligament. It has this kind of fan shape with a broader insertion on the patella and the distal quad, and a femoral location that is oft talked about. It has about a kind of 15 millimeter footprint on the medial femoral condyle between the medial femoral epicondyle and the adductor tubercle and the gastroc tubercle. And its position has been debated, but it's roughly two millimeters anterior to the adductor tubercle and then variable proximal distal, but anywhere between four and 10 millimeters has been described. Radiographic landmarks have been identified. We commonly speak about it at Chottles Point. Again, it's debatable whether Chottles Point truly represents the anatomic insertion of the MPFL. There's probably some variability. It is very, very important to have perfect lateral x-rays like you see in that picture there to have that point correctly. In terms of its insertion on the lateral side of where the ligament inserts, i.e. on the patella and the quad, studies have been done showing that pretty much in all cases the medial patella femoral complex inserts on the proximal half to a third of the patella with some fanning out on the quad or a little distal. And some surgeons, specifically Dr. Fulkerson, have taken that a little further and said, well, that's maybe an additional ligament or maybe another ligament part of this complex and called this medial quad tendon femoral ligament or MQTFL. So when we look at this anatomic dissection from Jorge Challa's paper, you can see that the footprint on the femoral side is similar. The femoral footprint for MPFL and MQTFL, whereas the lateral attachment is about three centimeters of the distal quad. MQTFL is considered because it attaches more proximal, possibly more active in early flexion angles, and it's been hypothesized that maybe its reconstruction can help address the issue a little better in patients with patella alta, and I'll talk about that in a bit. This is a picture from the anatomic dissections of Miho Tanaka. And that point marked with a star right in the midpoint of the MPFC, sort of kind of between MPFL and MQTFL, some refer to it as Tanaka's point, is basically the midpoint of the forces acting from the MPFC on its quad tendon and patella attachment. Additional contributors include the medial patella tibial ligament, medial patella meniscal ligament. This is a nice dissection by Leprod and Lazarent and other authors there. You can see the insertions on the small tubercle on the tibia for the MPTL and right on the anterior horn of the medial meniscus for the MPML. And they originate from the inferior aspect of the medial patella. In terms of their biomechanical studies and the strength testing, they've definitely been shown to be a less significant contributor, weaker ligaments compared to even the tiny MPFL. And in terms of treating them isolated, as I mentioned, should not be done. This was a study by Gamal and colleagues that showed that if you do an isolated MPTL reconstruction, you're not going to restore the stability compared to MPFL or MQTFL. So if you want to add it, add it, but don't do it in isolation, obviously. In terms of where is our femoral attachment, this is very important for getting the isometry of the ligament, whether you do an MPFL or MQTFL. I like to think of that little kind of triangle between the adductor tubercle, medial epicondyle, and the gastrocnemius tubercle, and the MPFL origin lies slightly in from the base of that triangle, that upside down triangle. Here it is, the anatomic dissection, again, from another nice study. And what they've identified is that the medial epicondyle, if you use it as a landmark palpate, is a little bit variable because of its oblong shape. So the tubercles of the adductor and the gastroc are a little bit easier to palpate as almost like single points, and you can see where that lies. In terms of the biomechanical testing comparing the MPFL and MQTFL versus the hybrid, this is a recent study from HSS, and essentially it showed no difference comparing the three surgical reconstructions. And what was nice is that they showed that without over-constraint, all three techniques were able to restore to the native state, the kinematics, contact forces, and contact areas. This study lends credence to the point that I made earlier, saying it doesn't matter what you do, just do it right. This study, on the other hand, had slightly different results, 2023, published in Arthroscopy. What they showed that of the three reconstruction options, and again, the techniques, the way they do these biomechanical tests are a little different, but they showed that MQTFL alone was the most similar to the native state, which can be good and bad. So if you're not addressing additional pathology, which in my practice I always do if I have a significant malalignment or significant displasure or alter, I'm addressing that. So for me, that's why MQTFL as a disclosure is my choice, because I feel like without over-constraint, it can restore to a native state. But if you're not addressing it and you're fighting some additional forces, it may not be enough, because the forces override the normal ligament. So the MPFL and hybrid are definitely stronger, at least according to this study, but may over-constrain a little bit. In terms of clinical, again, study published recently in Journal of Istiklal out of our institution, looking retrospective study, showed no difference in just about anything. Complication rates, return to the OR, et cetera, re-dislocation. This study just published out of, I'm not sure which country, but it was from Asia, I believe. No difference in PROs, patients achieving MCID, return to sports, very low recurrence in both cases. Here was a comparison between MPFL and the hybrid MPFL-MQTFL. They thought that maybe adding, doing the hybrid for patella alter cases would add some benefit, but it did not. So so far, that's more of a hypothetical situation. Now how do we reconstruct the MQTFL? I would say that this probably the technique used by most is the technique that Dr. Fulkerson described, basically passing the graft using a single limb going under the VMO to Tanaka's point and then looping it around the half to medial third of the quad. That's the technique that I use, and you'll see it in one of the videos in the case presentations that we're going to do. MPFL reconstructions, tons of techniques, kind of like, I don't know, like I guess the UCL, they've described a bunch of techniques. There's docking, there's buttons, there's screws, there's two tunnels in the patella, there's everything. And really, there's no difference, it doesn't matter. Whatever works for you, whatever you know how to do, do that. So it doesn't matter what kind of graft you use, allograft or autograft, they're all stronger than the native ligament. So I prefer to go allograft because why would I take something from the patient? But if the patient has a preference not to use, you know, dead person's tissue, you can harvest their gracilis, that's enough. Cortical button is strongest to failure, screws the stiffest, doesn't matter. Two limbs, one limb, doesn't matter. What does matter? What matters is graft position. If you get the position wrong, you're not going to have a good result, particularly placing the graft proximal and making it short as well as too tight. So the study from 06 showed, and studies since then have showed similar, that if you have an anatomic reconstruction, you have kinematics and forces similar to native state. But if you make it short and malpositioned, you may as much as double the compressive forces on the medial patella, and as we can all understand, that will lead to arthritis. So if in doubt, you go a little distal, a little posterior, that's been shown to be better, but it's not ideal to go too distal because that can make it loose. In terms of graft tension, that matters a lot too. So two newtons is what's been shown in studies to restore stability, normal translation without increasing contact pressures. If you go five times that or 20 times that, then obviously you're going to have issues and increased tilt, increased abnormal tracking. So but how do you know clinically or how to set graft tension? So the tricks that I would recommend is one, you can try to reference the contralateral side if it's normal. It oftentimes is not. So how else, what is normal, really? Normal has been shown to be one to one and a half quadrants of translation as the patella is just engaging in the groove. So you can do that. That's about 30% or so, 25% to 30% of translation. And I also like to look at it arthroscopically. This is a patient I recently did combined surgery on. So the first, the top picture is the patella translating before, before I did the reconstruction and the bottom picture is after. And same for the, you can see the patella sitting on the lateral wall and then in the groove afterwards. So I have my camera usually in the lateral gutter looking up and I placed the knee at about 20, 30 degrees and then set my tension that way. The additional thing that matters is the flexion angle, speaking of where to position the knee. We know that native NPFL is not isometric. It does have some isometry in early flexion up to 60 degrees and then becomes more lax. This is highly dependent on where you place your femoral insertion. And in terms of where to position the knee, there's a number of studies have basically shown that you don't necessarily want to be in full extension, but you certainly don't want to be in excessive flexion either. So to summarize that, I like to secure the graft in early flexion at around 30 degrees or so in patients with Ulta. Not Ulta, 20 may be sufficient, but in patients with Ulta, you probably don't engage until later on. So definitely don't want to do it in deep flexion, but full extension you can, before you engage in the groove or if there's dysplasia and you're not sitting adequately in the groove, then you may lateralize the patella as you're setting your tension. So go into a little bit of flexion. So to kind of summarize, medial patella femoral complex reconstruction is a very powerful, very important procedure for managing instability. But we can get into some complications. So fracture is one. How do we avoid that? Well, maybe avoid the tunnels. You can do the either MQTFL in isolation, or you can use an anchor, or you can even suture it to a strong periosteum, especially in children. Stiffness and over-constraint leading to arthritis. You want to avoid your proximal and anterior attachment with the high and tight and setting too much tension on the graft and obviously get your therapy started right. You don't need to lock these patients up for the MPFL alone. And then recurrence, we don't want to go low and loose. And the key thing there is, in my opinion, is to address additional factors that contribute dysplasia, maltracking, ALTA, et cetera. So this was a little algorithm that I keep in my head that was published in 2016. I've sort of adjusted it a little bit in my head, and I'll show you how I adjusted it later in the cases. But as you can see, MPFL or MPFC reconstruction is in every one of those boxes, and adding procedures then depends on additional pathology. So I thank you for your time, and our next speaker is going to be Dr. Jackie Brady talking about TTO. Okay. Okay. Thanks so much for getting up early this morning, you guys. Feel free to ask questions along the way too, and we'll get into some discussion on some cases. That was a great intro and a great starting point. I think most of us who treat patellar instability default to soft tissue reconstruction as our starting point, right? And I think there's abundant evidence out there that that works for most people alone. And so I am tasked with when do you add TTO? And I think there are still a lot of question marks around this, and I'll try to give you my interpretation of the current data and some idea of where we're going with some of the multicenter data that we're accumulating. But there are hints in the literature. Let me see if I can advance the slide. This was a study in 2021, prospective cohort of MPFL reconstructions alone, only a 5% rate of failure. The same is true of a study that I did with some of my fellowship folks at HSS, about a 5% rate of failure, so pretty low. But in their univariate analysis, patella alta and a preop positive J sign bore out as predictive of failure. Our group was not quite as clear. The numbers were pretty similar, but we weren't able to draw that out quite as much in univariate analysis. And I'll hint at that a little bit. Ours were more people who had a combination of factors. But pay attention to this preop positive J sign. We'll talk about that a lot. I think a lot of us hone in on that, especially if it's a significant J sign, as a sign that something needs to be realigned. Coronal malalignment did not come up. So the TTTG and the PTLTR in that study didn't come up. But in this one in 2018, if you compare MPFL-TTO versus MPFL, if you look at the combo group, they seem to do better if they had higher TTTGs. And so I think I could throw TTTG under the bus as well as anybody, because it's just a flawed measurement. I think the bottom line is this is a three-dimensional problem, right? And we're using these two-dimensional measurements to try to define this three-dimensional problem. But it's a hint. And so I think using this in your toolbox and sort of accumulating information on who this patient is is important. So TTTG is shown there on the left. You get that on cross-sectional imaging. You can do CT. You can do MRI. There's some studies on the differences between the two. And I think that's because what matters functionally is the patellar tendon insertion. And if you scrutinize your MRI, you'll see that that's a little lateral compared to the peak of the bony tubercle. Functionally, though, I think that's what matters to me. That's what matters to the patient. That's what's functionally affecting them. And then the PTLTR is the newer kid on the block that's shown on the right there. That's the vector that Dave Dedek loves to talk about. The patellar tendon, is it draping over the lateral trochlea? And is it sort of showing you that you need to line up this putt if you're a golfer? So let's talk sagittal plane then. Patella alta, most of us will measure it with a caton de champ. Again, a little frustrating with the measurements because the modified insole cell body keeps being the one that bears out as significant. But you can't tell what you did with that one because if you measure the tubercle and then you move the tubercle around, it's going to stay the same. And so most of us will use caton de champ as our measurement. We start to call it alta at 1.2. I think most of us wouldn't intervene until it's pretty well higher than that. But if you take patella alta, then you combine that with a short trochlea. So here's a dramatic case of trochlear dysplasia. And you can see that arrow showing you where the groove ends or starts depending on where you're looking from. So that kind of creates a pseudo excessive alta. And then if you add to that knee hyperextension, then you've got a really long arc of motion that your MPFL or MQTFL or sort of soft tissue reconstruction is going to need to stand up against before the patella is contained within the bony walls of whatever groove it has, right? So let's talk about J-sign. What's this thing that's not muted? Hang on one second. There we go. Just kidding. Oh, dear. There we go. The J-sign has been classified in a couple different ways. The number of quadrants. Some people have sort of a good, bad, and ugly kind of classification. It's been called into question because the inter-rater and intra-rater reliability has been poor. But again, I think this is a three-dimensional problem. And I think we can prove that to you. And we're using, like, video to get people to try to identify a J-sign. And video is a two-dimensional media. So you have to be careful about sort of throwing it completely under the bus. I think most of us know that something's going on if we see a J-sign, especially if it's a significant one. The Chinese have really done some great work on the J-sign, and especially the so-called grade three or the super ugly J-sign. And they found that femoral anteversion is a predictor of J-sign. External tibial torsion. So like axial plane, right? We're not always measuring that in our patients. Patella alta. And then there was a study in OJSM that said that it's closely associated with patella alta and trochlear dysplasia. So multifactorial. The Chinese, the same author Zhao in 2020, showed that J-sign is an independent predictor of MPFL failure. And then the grade three J-sign correlates with a lower Kujala score, more MPFL graft laxity if you're measuring laxity. Inferior clinical outcomes. I think a lot of us are very interested in redefining failure. Because if you just go with recurrent instability, you're going to get that 5%. And that doesn't really tell us what we need to know. And then J-sign and BMI correlate with disease-specific quality of life as of the 2022 study in KSSTA. So J-sign has a lot to do with outcomes, right? And we want to resolve that when we can if it's a significant one. There was a study that was pretty small. It was only 31 cases of a J-sign with patella alta. And 97% of them were resolved with a distalizing TTO. So you can see the TTO sort of comes into play when you start to think about malalignment. Rotational malalignment is elusive. I think here in the States, we're trying to, like when you're doing these studies, do you get everybody to take some sort of rotational measurement? The bedside rotational measurements of the sort of estimated femoral anteversion, those are fraught with reliability issues, as are all physical exam findings. And then are you going to CT young people across the board? If you get an MRI, are they going to move in between the hip and the knee cuts? So it gets tricky to measure it. But we know in some literature that the patella femoral contact forces start to go up at as little as 20 degrees of anteversion. And I think a lot of people would consider that sort of high normal. I feel nobody on this panel will probably derotate a 20 degree anteverted femur. And so is TTO a middle ground there? If you think about this three-dimensionally, can you bring the train back to the track, so to speak? And I think that's where we're sort of outside the evidence we do not know. But this is absolutely how I think about my patients. I think about them in all planes. I think about their entire anatomy. Their ligament is laxity. What do we do with that? It all gets very confusing. But if I've got enough sort of hints that something's malaligned and there's a J sign and I can't convince myself to do anything more extreme, I think a TTO is a nice starting point to realign someone. And as we know, these factors don't exist in isolation. This is a couple of biomechanical studies that showed that the MPFL isometry of your reconstructed ligament can be disrupted by ALTA, high TTTG. And if you have both of those things, it's worse. It sort of passes the common sense test. These are sort of synergistic. This is that prospective MPFL study out of HSS that I was talking about. Again, 5% recurrence. But if you have a post-op J sign that you didn't fix, worse PROs. And so we're trying to understand failure a little bit better. Are these the patients that won't get back to the activity they want to do? Are these the patients that still have some apprehension, don't trust their knee? And oh, by the way, post-op apprehension plus hyperextension, lower rate of return to sport. So you get hints that maybe soft tissue reconstruction isn't enough if you're really trying to get them back to trusting their knee. So this is the Jupiter study that I mentioned. I think the jury is still very much out. We have like 2,000 patients and counting, but we're very limited by the radiology part because these poor radiologists are having to review all the images. And so we hope to have some powerful information comparing the groups. I gave a presentation yesterday on return to sport. And the return to sport after MPFL and TTO was a little lower, but I feel like that calls into question like, well, who are we doing that on? It was not a directed study at that point. You just sort of did what you would do anyway. And so are we treating more malaligned people? Maybe they're at higher risk for not returning, or is it a factor of like it's harder to recover from a TTO? We don't know. So I think in all, I think we have a pretty good case for TTO for malalignment. In the coronal plane, however you're going to define that, if you just look at that patellar tendon drape, I think that's a good starting point. Look at that PTLTR. If you like TTTG, I think there's a little evidence for it. We sure wish there were more because it's an easy measurement to get, but it's two-dimensional. And then rotational plane, maybe if it's not enough rotation to do something about it from a derotating the femur standpoint. And then the J sign, pay attention to the J sign, especially if it's anything more than just a glide. And I think the practical advice that I would give right now with the data that we have, which is sort of woefully inadequate, is if you're worried about the vulnerability of your MPFL graph, so like the hyperextensile knee with the dysplastic trochlea with maybe a hint of patella alta, but not enough to do something about. Or if you're asking your MPFL to pull the patella back into the groove, you got to consider realignment. And usually for me, the starting point is TTO, unless I'm going to think about doing something more drastic. And in general, in high-level athletes, we trust their build, we trust their mechanics, we trust their soft tissues, bottom line. And so less is more. So you'll see us stretching it a little bit more and doing soft tissue reconstruction alone in a high-level athlete, as opposed to like a person with collagen that we don't trust. Like an Ehlers-Danlos patient would be my classic example. I feel like all of those patients live in Portland, Oregon. And then I'm going for bony realignment. I'm looking for excuses to move those bones around because I don't trust those soft tissues at all. And I think if you see asymmetry, it's worth looking at that. If they have asymmetric symptoms and asymmetric anatomy, it might be worth making that more symmetrical and unload the chondral lesions. And we'll get to that in the next talk. So speaking of which, TTO for overload, I think is a concept that's been proven for a long time. This was Fulkerson's group in 1997, showing that the antramedializing tibial tubercle osteotomy unloads distally and unloads laterally in a very powerful way. Corey Edgar had a cadaver study that really called into question distalization in the setting of overloading the patellofemoral joint and showed it in a cadaveric model, that you're going to increase the contact forces in early flexion if you distalize that tubercle. But that was in a cadaveric model. I think the problem with all of our biomechanical studies in patellofemoral is like, they're not dysplastic. They don't have all to, I mean, heck, they all have Baja because they're not connected proximally if you're not careful about it. And so translating that to a clinical population, I think is inappropriate. And actually, in patella alta, if you look at this x-ray, that patella is edge loading distally. And so if you distalize, you might have a shot at more uniformly distributing those contact forces and not overloading it and helping with the overload problem. So I think I learned in early practice not to be afraid of distalization in the setting of that very typical chondral lesion that people have from instability. So lots of smaller studies for overload, positive outcomes, reasonably safe. There are complications of TTO that you really want to take into account and not sort of be flipping about. But I think it's a reasonably safe procedure if you need to realign someone. But there's no RCTs. And I think the Jupyter data will help. But again, it's not a randomized controlled trial. I think the prospective studies that are looking for failure of MPFL give good hints. And then you have to take that and sort of study that group and figure out what failure is and how do we get the risk factors there. But don't be afraid to add it. It's a powerful procedure. Thanks so much for your time. All right. Well, thanks for coming, everybody. I want to thank Alex for putting this together. And I also want to say that I like the way these talks are set up because I think we're at an interesting time at treating patellar instability in this country. And I think that I want to present this as a sort of a point counterpoint because I obviously have a very different take on my algorithm, which I think more closely aligns with a lot of European thought on this. So let's dive in here. So when I think of patellar instability, I like to look at it as a symptom of a problem. Similar to how a cough is a symptom of an upper respiratory viral infection, an unstable patella is the result of some underlying anatomic risk factor. It is the end result of something else. It's a manifestation of some pathology. And so these have, I think, very aptly been coined anatomic risk factors, ARFs. And so what are these ARFs? Trochlear dysplasia, which is going to be the focus of this talk. But we have patella alta, which is due to an abnormally long patellar tendon, as well as some short trochleas on rare occasions. We have the axial malalignment, the thermal antiversion, and the external tibial torsion. Again, it has been discussed. We also have genuvalgum as a known but rare risk factor for patellar instability. What about the lateral tibial tubercle? I'm going to pause it to you guys now based on recent literature that there is little to no difference in the position of the tibial tubercle on the proximal tibia in patients with or without patellar instability. And I do think that TTO should be viewed as a compensatory procedure. It does have roles. I do think the notion of offloading, like offloading a chondral defect, I think that is correct. I don't think it has a routine role in treating instability because the lateral tibial tubercle, in my estimation, is not a problem. And here are some of the studies to show it. I've been the first author on a couple of these. But here are some other studies out of Japan and China, which all have come to similar conclusions that the lateral tibial tubercle might not be a real pathology. So I have a whole talk to give on that. But obviously, for the interest of time, I can't go further into that. But when it comes to trochlear dysplasia, it is almost hand-in-hand with patellar instability, given the frequency that it is present in this patient population. And this was first shown in the mid-'90s. This was Henri Dijor, Dave Dijor's father, who was the lead author on this study. And he showed, comparing a control group to a patient with recurrent instability, that on X-ray, roughly 90%, maybe 95%, had at least one sign of trochlear dysplasia present on a lateral radiograph versus only 6% of a control population. So it was everywhere in this surgical population. And its association with recurrent instability has been shown time and time again to be very strong. These are all studies between 2010 and 2020, all different types. So they looked at different factors and different ways of looking at things and different odds ratios and this and that, whatever. But dysplasia was either the only risk factor noted, or it was the strongest risk factor noted for recurrent patellar instability. Furthermore, what is the association with trochlear dysplasia and cartilage injury in the patellofemoral joint? So these are a few studies here showing that the natural history of trochlear dysplasia is early cartilage damage in the patellofemoral joint with progressive radiographic and symptomatic arthritis. And the Mayo Clinic also showed this in this study here, looking at a 25-year follow-up after a first-time patellar dislocation, showing that fully half of those people had radiographic and symptomatic arthritis on X-ray. Because they have that Humboldt County or whatever it is where Mayo is, they just have this database. It's amazing. And it's also a condition of younger people. Most people were under 25 years of age when they first popped out. But they looked at the risk factors for arthritis. It was osteochondral injury, recurrent instability, and trochlear dysplasia. We know that trochlear dysplasia is associated strongly with not only osteochondral injury, but recurrent patellar instability. So the natural history of this, for at least a majority of people, is early arthritis. And here's some clinical examples. This is an 11-year-old female. So this is a fifth grader with high-grade trochlear dysplasia. This is what her patella looked like. Here's a 16-year-old female with the more rare trochlear lesion. Most of these lesions start on the patella. The trochlea is less commonly affected early. Here's a 13-year-old male who had failed a few prior just soft tissue procedures. Here's a 14-year-old female who had failed an isolated either MPFL re-feeing or MPFL reconstruction. So you can see these are none of these people are even seniors in high school. And they have severe chondral injury present in the setting of trochlear dysplasia. So when we talk about operative intervention, I do agree that I think the soft tissue reconstruction has a role in everybody. But I think we have to understand why we do it when we do it. But the next thing that typically comes in line is the tubercle osteotomy. And then we have disease-specific or anatomic-specific treatments after that, which I agree with. I do all that stuff. But I think that with this algorithm, that we are treating the symptoms. We're not treating the problem. So this is what my sort of ladder of treatments looks like. I do agree everyone gets an MPFL reconstruction. But if the most common anatomic risk factor in patellar instability is trochlear dysplasia, then trochlearplasty is going to be my most common procedure to treat that problem, whatever that problem may be. And then I will treat ALTA. I will treat valgus, rotational abnormalities, et cetera. And so I have TTO at the bottom of the list. So overall, what is my surgical treatment algorithm? So first, I try to make this as simple as possible. Identify the problem. Determine the severity, which that is the absolute controversy gray area where our research should be focused. You can compensate for mild pathoanatomy. So I do plenty of isolated MPFL reconstructions. And I also do lateral lengthenings with that. For mild disease, whatever that disease, whatever that risk factor may be, most of the time it's going to be for dysplasia. If that anatomy is more severe, then I'm going to fix that direct problem, directly fix that problem. And then I will still rebalance those soft tissues because those soft tissues have been made abnormal secondary to that underlying anatomic problem. So they do not reset themselves. So you do have to address them. And that's why you still add it on. Okay. So before we get into trochlearplasty, let's talk about compensatory management. So there is a role, as I've said, in doing MPFL reconstruction in patients with trochlear dysplasia. This was a study by Bob Taiji, 34 patients, about five years follow-up, a hundred percent follow-up and no repeat dislocations. They had good improvements in tegner, kujala, lysome. The issue with this study is that they used a very early form of the du jour classification. So you really couldn't specify how bad the dysplasia was. It was very, very qualitative. It was almost binary. They had it or didn't have it. So you couldn't say this, they had severe dysplasia, mild dysplasia, whatever. But it does, I do think it does show that there is a very good role for compensatory management in patients with trochlear dysplasia. Okay. This study by Laurie Heimstra, and if you guys are interested in instability, I highly recommend reading Laurie's work. She's a very good researcher. She showed that she was able to quantify dysplasia a little bit better, mainly by measuring the height of the supratrochlear spur on the lateral x-ray. And she found that spur height greater than five millimeters was associated with lower, what are called BPI or Banff-Patellar instability instrument scores. And the Banff score is a disease specific patient reported outcome that she validated. So she found that these BPI scores were lower in these higher grades of dysplasia. And this is a Japanese study that showed similar findings. They did du jour A, B, C, D. Again, I don't love, I think it's a very elegant way to qualify dysplasia, but I don't think it's a great way to indicate and stratify how you treat somebody. Nevertheless, this was a study that showed that with increasing degrees of trochlear dysplasia, that was associated the most with recurrent patellar instability with an odds ratio of three. So not insignificant that at some point your compensatory tools stop working so you've got to do something else. Now let's look at this. So there's been a couple systematic reviews. This is a systematic review only looking at what role or what benefit did a TTO add to patients with instability. And they specifically focused on patients with elevated TTTGs above 20. And what was interesting, probably the biggest interesting finding for me was that there was only nine studies found in the literature on this. Less than 200, less than 300 people elevated TTTGs between 16 and 20 actually. And they found that there was really no difference in outcomes and they didn't even have enough numbers to perform a meta-analysis on it. Min Kokerv then published this. He was able to drum up a few more studies I think that you could call into question maybe some of the studies that were put into that. But he got enough to do a meta-analysis, quote unquote. Same thing, 400 knees, TTTGs above 20, NPFL alone versus NPFL with TTO. And basically no difference in relocations and sort of spotty PROs reported, but really no consistent significant benefit from adding a TTO to these patients with instability. And one last thing is I do think that the TTTG has been shown. A high TTTG is highly correlated with trochlear dysplasia. So the higher the TTTG, look at the trochlea. Okay. So this, I will not get into techniques today because I want to focus on the literature. If you guys want to see my technique, I'll be presenting as well as Jack will be presenting her technique for TTO. This afternoon I'll actually do a pure technique on my thin flat trochleoplasty. But my indications for it are this, simply put a flat or convex trochlea. Convex I think is easier for people to stomach. The flat ones I think is definitely an area of controversy. But that's what I do. And that's fairly common in Europe. And what that translates to in numeric ways, what's called the lateral trochlear inclination angle, which is a numeric way to quantify trochlear dysplasia. So a normal LTI is between 18 and 20 degrees. A flat trochlea is zero. A convex trochlea has a negative number associated with it. So zero to five, roughly flat is when I'll pull the trigger on a trochleaplasty or at least have a discussion with the family about it. And then when you examine them, if they have patellar apprehension in higher degrees of knee flexion, that is also, that supports my indication. There are two, I would say these are the two most common types of trochleaplasties performed nowadays. They are both what are called groove deepening trochleaplasties. On the left is the thick flap technique that Dave DuJour and Dave Dedeck do. On the right is the thin flap technique that I do. These are both technique articles available in arthroscopy techniques. The thin flap technique was designed by a guy named Hans Bereider in Switzerland. So I am merely mimicking what I've learned from these people. So one of the big questions about trochleaplasty is you're going to kill the cartilage, right? You have to kill the cartilage by doing this procedure. So Philip Schottel, who is the person that I directly learned from on how to do trochleaplasty, did a study showing when he did these post-op biopsies of trochleaplasty patients, they got stiff. So he needed to take them in for a license of adhesions. And he took these little osteochondral cylinders and showed that the cartilage viability was normal or nearly normal in all of the specimens. So osteo, in the osteochondral junction, excuse me, was normal and nearly normal in all specimens. So this was several months out. So the cartilage lives quite nicely. And then this will be proven out in some of these clinical outcome studies. So this is hot off the press. This is Dave DuJour's average 15-year follow-ups. This is long-term data, minimum 10 up to 20-year outcomes of his thick flap technique. Forty-four patients all had an NPFL reconstruction. He does a lot of TTOs as well. I don't do any TTOs. He had only mostly primary procedures. You can see only five had prior surgery. They had one recurrent dislocation that was managed non-operatively. But the big takeaway here is that 38% had no osteoarthritis at this follow-up. And then the rest of them had low grade, grade one to two. So no high-grade arthritic knees at average 15 years. And he made the comment that they were not able to correlate the radiographs to preexisting cartilage damage at the time of surgery, which is the key point. They don't know if this was due to the preexisting cartilage damage or the trochleoplasty that caused this. And that, to me, is the big one right there. So this is my personal favorite study. This is by Hans Bereiter as a senior author. This is also a short-to-long-term follow-up of patients with a trochleoplasty. These people had combined surgeries. They had NPFL reconstructions as well as trochleoplasties. Higher numbers of revisions, 15, a third of them had prior surgeries. They had no repeat dislocations. They had about 30% of more high-grade cartilage lesions at final follow-up. But if you look at this, overall satisfaction was 100%. Everyone said they'd do it again. Level of activity went up in all but one patient after the procedure. And they made the comment that we didn't understand the significance of the preexisting cartilage damage. So we were unable to correlate that with the radiographic findings. But almost everyone had at least some degree of cartilage damage on the patella present. And then we have Dave Dedick's study here that he published a couple of years ago. He had about a similar number of knees. This is more short-term follow-up. You can see he had, this was a lot of revisions. 45 had failed prior procedures and were revised to with a trochleoplasty. But you can still see, even despite in the revision setting, good improvements in IKDC, good improvements in Kujala. 80% had at least rated their satisfaction at 9 out of 10. 2 had persistent J signs. This is another study. To me, this highlights the importance of making sure that you address the soft tissues. A fairly large study of trochleoplasty done in isolation without soft tissue retention done at the time of the initial procedure. There was a 14% reoperation with 8% redislocations. They had to do something to stabilize them. But the other takeaway is the durability of the PROs. He had very, very good PRO follow-up on this. And with the patients that were followed up longer than 8 years, the PROs were durable with significant improvements. It was the WOMAT and the Kujala and the IKDC. All stayed durably improved into the long term. This is one looking at return to sports. And most patellar instability patients are not athletes. A lot of people cannot be athletes because of their trochlear dysplasia. But just when we look at this, this showed that in low activity patients, they were able to be more active after a trochleoplasty. The higher activity patients, because there are some that are athletes that deal with it. There was no change in that, but they were, they did not typically lower their activity level after a trochleoplasty. Over two thirds returned to a previous activity level or higher. So you can get people back to sports. I mean, I've got multiple college athletes playing sports after a trochleoplasty. In fact, it was a trochleoplasty that I will humbly suggest. I can't prove it, but that allowed them to do it. So, and then there are other, these are other studies. So there is a body of literature. There is a body of peer reviewed evidence out there in support of trochleoplasty showing it has favorable outcomes and has a very clear role in treating patellar instability and a central role when trochlear dysplasia is present. Now the last bit here is trochleoplasty with cartilage. So there are no published articles on combined procedures. So this is purely my experience. Okay. So this is all anecdotal. Um, the most common thing that I do is treating a patellar chondral defect at the same time as a trochleoplasty. So that's been a patellar osteochondral allograft in most cases. And I've done at least 25 to 30 of those. Um, there's no change in the rehab with this. Um, this is, um, I think I've done six to eight of these this year. Um, uh, and it's, um, we've had no, uh, no failures, no increased complications, no increased risk of stiffness, anything like that. Um, uh, trochleoplasty with patellar Macy, I've done two, I think I'm going to start doing more of these, um, especially for the younger patients. Um, and you can see, this is actually the, this was a rare case of Macy hypertrophy. Um, uh, but this, uh, but this worked out very well. And I think that this is going to be for cartilage only lesions in a younger patient. I think I'm going to probably lean more towards the Macy, uh, just because I can, when it fails, I can revise that to an osteochondral graft. And when you put an osteochondral graft in a patella, the only revision is a bigger graft and you run out of real estate really quick. So, um, now on the other side of things, um, chondral defects on the trochlea more rare. Um, I have done now two fresh OCA's in combination with the trochleoplasty. So I do the trochleoplasty first. Um, and then this is the same patient, uh, both knees where he had a large, uh, unstable irreparable OCD lesion, osteochondritis dissecans. So we were able to put a fresh plug in there. Uh, and, and he's been very, very happy. Again, this is very anecdotal. This is just, you know, one patient. I have done three patients with the, with that flexible, um, osteochondral graft that that's cryopreserved, um, that, that has worked out well, but I don't think you get the same type of highland cartilage out of that. Um, so I don't, I think that that might be better for a smaller trochlear defect. Um, it's easy cause you can just mold it to fit in, cut it and mold it to fit. Um, but I think that's going to play a lesser role for me in treating these cartilage defects on the trochlea going forward. Um, uh, but the patients that I had had done well. Um, so in conclusion, trochleaplasty, it's reliable, has high satisfaction and I, and I treat it as a primary procedure. Um, I do consider it a joint preserving procedure. Um, at least if we indirectly look at the, at the literature on this. Um, I think anecdotally it can be performed at the same time as cartilage resurfacing. Thank you. All right. So, uh, I'm going to be, uh, finishing up, uh, and then we'll get into our cases. We're gonna talk about cartilage restoration options, uh, for the patellofemoral, uh, joint. I have no relevant, uh, disclosures. There we go. No relevant, uh, disclosures. So here's a brief, uh, overview. We'll start with a clinical case, uh, talk about some background, uh, review the different cartilage restoration, uh, options, uh, that we, uh, have and then talk about clinical, uh, outcomes. Here's a typical case that comes to your office. 26-year-old female, uh, soccer player, uh, two months out from a right patellar dislocation, comes in complaint of pain, recurrent instability. Her exam, uh, positive, uh, patellar compression, uh, three plus, uh, quadrilateral translation, positive apprehension. She did not have a, uh, J sign. Here are her, uh, images. X-rays are, uh, nothing, uh, significant. Here's her MRI, uh, large medial, uh, patellar facet, uh, osteochondral, uh, defect is, uh, noted. So we'll come back to the case, uh, at the, uh, end. Let's first review, uh, some background. So patellofemoral joints, most, uh, complex, uh, joint, uh, in the, uh, in the, uh, patella cartilage, uh, fitness range anywhere from four to five, uh, millimeters. On arthroscopy, 34% of the chondral defects that are seen are usually patellofemoral, uh, compartment. The majority of these defects are usually incidental findings. However, a significant amount do become symptomatic, uh, over, uh, time. Common causes of these, uh, chondral, uh, injuries, patellar instability, uh, similar to the patient I just, uh, presented, uh, osteochondritis desiccans as well as degenerative, uh, changes. Uh, recent systematic review, uh, showed that after a first time patellar dislocation, 85%, uh, of patients had signs of patellar chondral, uh, damage that goes, uh, to show, uh, what Dr. Pace, uh, said in terms of, uh, not knowing, uh, if patients had preexistent, uh, damage in those, uh, trochleoplasty studies that he showed. 47%, uh, of them had, uh, trochlear, uh, chondral, uh, where it says very high incidence of, uh, chondral damage at a time of, uh, what first, uh, patellar dislocation. So the patellofemoral anatomy is quite complex, which means treating, uh, these, uh, injuries quite, uh, challenging through a variety of different factors, uh, that have to be, uh, addressed in order to have a successful, uh, surgical outcome. You have to address, uh, any kind of lateral tilt, uh, instability, maltracking, alta or, uh, baja, as well as, uh, underlying trochlear, uh, dysplasia. So a successful surgical approach, uh, you know, usually involves concomitant, uh, procedures in addition, uh, to your cartilage, uh, respiration. So different modalities, uh, marrow stimulation, uh, that's more of a historical, uh, relic, uh, osteochondral autograft, uh, you have, uh, MACE, uh, you have particularly juvenile cartilage allograft and fresh osteochondral allografts. We'll review, uh, those in a little bit more detail. And literature has shown that these techniques have resulted in lower rates of success when using patellofemoral compartment compared, uh, to, uh, the tibiofemoral, uh, compartment. Uh, more recently MACE and osteochondral allografts have become the two, uh, workhorse procedures for, uh, patellofemoral, uh, cartilage, uh, respiration. So in terms of indications, usually high grade, uh, lesions, uh, load-bearing, uh, surface, these patients typically have, uh, failed non-surgical management, uh, physical therapy, uh, oral anti-inflammatories, uh, you know, some have tried, uh, different injectable options such as HA or, uh, PRP and or, uh, bracing. Contraindications, advanced osteoarthritis, uh, low grade, uh, lesions, uh, infections or inflammatory, uh, disease. Uh, I alluded to, uh, the need for concomitant procedures. These typically include, uh, offloading to real tubercle, uh, osteotomy, uh, and addressing any, uh, patella instability that may, uh, exist. So, uh, chondroplasty, microfracture, again, older, low demand, uh, patients is just to, uh, eliminate any unstable, uh, you know, lesions, uh, remove any unstable, uh, flaps. Uh, Federico, uh, et al, uh, showed that, uh, these patients, uh, had decent, uh, results, uh, about, uh, 58%, uh, of traumatic, uh, uh, chondral, uh, damages had good to excellent, uh, reported results in the short term, uh, that went down to 41%, uh, when it's more of a traumatic. So with microfracture, uh, or our bone marrow, uh, stimulation, uh, the goal or the hope, uh, is that, uh, stem cells, blue point stem cells will migrate from subchondral bone, uh, into defect. However, this only forms fibrocartilage and after two years, uh, the results, uh, definitely, uh, get worse. And a couple of years ago, uh, Jack, uh, Bird, uh, pretty much put a nail in the coffin, uh, when he, uh, wrote a article about abandoning, uh, microfracture. So there have been, uh, historically, uh, decent results. Uh, Dr. Stedman looked at his 11-year, uh, outcome, showed improvements, uh, in patient reported outcomes, uh, scores, uh, systematic review by SMOP also showed, uh, some, uh, improvements, uh, when used in a patellofemoral, uh, compartment. Moving on, uh, to cell-based, uh, cartilage restoration. So autologous chondrocyte implantation initially described, uh, by Lars Peterson back in 1987, uh, first, uh, generation, uh, he sewed a periosteal patch, he injected cells, he sewed it back up, he added some fibrin glue, uh, they had, uh, fantastic outcomes, 19% satisfied, uh, and would undergo, uh, surgery again, uh, at, uh, 10 years into a long-term study, uh, all had significantly, uh, better, uh, outcome scores, uh, when compared to their, uh, pre-op, uh, scores. Uh, Ebert et al., uh, looked at, uh, Macy for the patellofemoral, uh, compartment versus, uh, femoral, uh, condyle, and in this, uh, short-term, uh, study, uh, they found that Macy in the patellofemoral, uh, joint with concurrent correction of any underlying patellofemoral, uh, abnormalities led to similar, uh, outcomes, uh, both clinically and radiographically, uh, as, uh, Macy, uh, done for the femoral condyle. So the important thing is here, uh, is that they addressed any underlying, uh, abnormalities, uh, concomitantly. So in terms of, uh, outcomes of Macy with and without a tibiotubal, uh, osteotomy, uh, this is a short-term, uh, study, looked at, uh, up to 24, uh, months, uh, out, uh, they found that, at, uh, 24 months, uh, you know, both procedures, uh, Macy with and without tibiotubal osteotomy, uh, led to improvements, uh, in, uh, patient reported outcomes. There are no significant differences, uh, between the two, uh, groups. Again, uh, to stress this is just in the short, uh, term, long-term studies have, uh, shown that TTO, uh, certainly, uh, adds, uh, you know, to the, uh, outcomes. So looking at the 10-year, uh, outcomes of prospective study, uh, and what they, uh, found, again, 90% were satisfied overall, 76%, uh, were able to return, uh, to sports and were satisfied with sports, uh, participation, only 11% had clinical, uh, failure. So at 10 years, they found good clinical scores, high levels of patient satisfaction, and acceptable graph, uh, survivorship. However, uh, they did note that, uh, the patellofemoral, uh, Macy, uh, patients were not as happy, uh, as, uh, those, uh, with, uh, the tibiofemoral. Another, uh, cell-based, uh, option is particularly juvenile allograft, uh, more commonly known as, uh, de novo, uh, and this is similar to Macy. It's a matrix-associated chondrocyte allograft, uh, taken from donors who are less than 13, uh, years, uh, old, uh, initially, uh, you know, developed in 2007. There've been, uh, series of, uh, small studies, uh, shown, uh, significant improvements in overall, uh, crew scores, but there've not been any large randomized, uh, studies, uh, supporting, uh, its, uh, use. Here's one of the largest, uh, studies where, uh, they, uh, found in 27 patients, uh, post-op MRI showed majority lesion fill, uh, in about, uh, 70% of their patients, uh, significant improvements in pain and, uh, function, uh, with its, uh, use. For smaller lesions, uh, that also have bony involvement, osteochondral autograft, uh, is an, uh, option. Uh, typical places that we would get these graphs, uh, we're all familiar, uh, medial lateral trochlear margins, posterior femoral condyle, uh, or inter, uh, condylar, uh, notch. So a lot of small, uh, series looking at, uh, these, uh, uh, outcomes, right? All reported improve, uh, patient outcomes. One study at 10, the other at seven, uh, this one had, uh, 14. The largest study, uh, is by Moses, uh, Coyne, uh, out of, uh, Brazil, and he looked at 33, uh, patients and all of these patients had relatively small, uh, defects. The important findings were, uh, all patients had improvements in their outcome scores. However, lesions less than two centimeters did significantly better than those greater than two centimeters. Patients who had a single plug, uh, you know, did significantly better than patients who had more than one, uh, plug. And all of their post-op MRIs, uh, demonstrated, uh, RCSI integration, uh, at one, uh, year. So it is a viable option for a small, uh, lesion, but you, uh, should keep in mind that you are essentially robbing Peter, uh, to pay, uh, Paul and donor site morbidity, uh, is something that is quite significant. So osteochondral, uh, allograft, several advantages, uh, over, uh, macing off the other cartilage restoration procedures that we perform. This is essentially the salvage for anything else that has failed. And it's now becoming more and more used as a primary procedure for telopharmal cartilage restoration, especially for larger lesions and those involving subchondral bone, osteochondritis, death scans, or post-traumatic defects. These grafts should be used within 28 days of being harvested. They do better when they are sized and location matched. So more and more studies are coming out showing that orthothopic grafts, i.e. a patella for a patella, trochlea for a trochlea, does significantly better than when a condyle is used as your telopharmal compartment. So advantages, it's a one-step procedure. You have fresh, viable living cartilage, excellent time-zero durability. It addresses any underlying bony pathology that may be present. You're able to match the condyle thickness, especially for the patella. Disadvantages, donor, unfortunately, is required. It's difficult to exactly match, especially your central patella defects, your central trochlea. These are extremely difficult to match. And it's challenging when you have uncontained defects. So outcome studies have been, fortunately, quite good. Isolate patella osteochondral allograft survivorship was found to be 78.1% at 10 years. However, it did decrease to about 56% at 15 years. 89% of patients were extremely satisfied, were extremely satisfied or just satisfied with their results of osteochondral allograft at long-term follow-up. This study by Brian Cole and Rush Group looked at about 50 patients comparing plug versus shell allografts. And what they found is that plug allografts had significantly better survivorship than the shell allografts with 100% at five years survivorship for the plug, 66% at about 10 years, while the shell only had 65% survivorship at five years. And that went down to 37% at 10 years. So the summary for this is that you should certainly consider more of a plug rather than shell. You'll get better outcomes. Systematic review looked at eight different studies on 29 patients. Similarly, excellent outcomes at both short and longer term, 80% at five years, 77% at 10 years and 15-year survivorship was found to be 56% in one study. With 52% re-operation rate. However, majority of those re-operations were for removal of heart rate and or stiffness. So some of the less common surgical options for cartilage repair, we're not going to spend a lot of time, but you have the single stage autologous cartilage repair. You know, that's becoming more and more common. We have the cartilage allograft options. There's cartomax, there's cartiform. There's also the agility, which is the coral. And, you know, this is used more for the femoral condyle and trochlea. It is not approved for use in the patella. On the horizon, Novacart, Neocart. So the world of cartilage restoration, especially for the patellofemoral compartment, lots of exciting stuff coming down the pipeline. Quickly review clinical outcomes. Most patellofemoral cartilage restoration procedures do result in clinical improvements and outcomes. This systematic review looked at over 1900 lesions involved in patellofemoral compartment and found most of these were cell-based just because of the overall topography. And they did find that patellofemoral cartilage restoration leads to improved clinical outcomes, low rates of both minor and major complication. They did note the osteochondral allograft had a higher failure rate than the cell-based, and it's unclear why it didn't really get into it in the study. Osteochondral allograft in Macy had similar outcomes. This is a study, you know, from our group at NYU, had similarly low arm return to support rate, about 54 percent. Patients had similar improvements in their PRO scores. However, we did find that patients had worse outcomes when they were older and for larger lesions. This study hot off the press, looking at de novo, and they found in this study that they had a 100 percent return to support rate in their patients who played sports. So 17 out of 17 patients they reported were able to return to sports. So that's certainly quite promising. So bipolar lesions are always extremely difficult to treat. And Mizarin et al., back in 2018, looked at 18 patients with bipolar patellofemoral lesions, and he found that these patients, you know, had significant improvements in their functional outcomes, relief of pain, activity, and also reduction in recurrent instability, and those that had concomitant patellar stabilization procedures. Our group looked at reasons why patients would not return to support. We found that a lot of them had cases of phobia, which is a fear of injury, and they also had increased pain catastrophizing behaviors, and this is the reason why our ACI patients did not return to support. A similar study looking at the osteochondral allograft and had a similar reason. Here's a study we presented, you know, still under review, looking at patellofemoral OCA with and without tibiotubal osteotomy. We found that they had a similar return to support rate. So a lot of people concerned about the tibiotubal osteotomy. It did not significantly change outcomes. And although we did not find any significant differences in failure, it was trending that way. The one patient who failed in tibiotubal osteotomy group, and there were five that failed in a group that did not have a concomitant tibiotubal osteotomy. So there may be something there. So again, wrapping it up. Debridement and microfracture no longer plays a significant role. A more historical relic. May see as excellent short and long-term results. Novo has been shown to have good short-term results, but large studies are needed. Osteochondral allograft is a rapidly growing area in cartilage restoration. Keys to success, careful patient selection, orthotopic grafts, and correcting any underlying abnormalities. A variety of emergent options for cartilage out repair. However, more studies are needed. So getting back to our case. She had a diagnostic arthroscopy, very large osteochondral defect medial patella facet. She had a osteochondral allograft and MPQ TFL. Was able to get back to soccer at around six to eight months out. Now doing well a couple of years out. Thank you. Yeah. So let's, if anyone has any pressing questions, let's, you can go ahead and ask them. Otherwise, uh, uh, we'll go right into, we'll go right into the cases. This is the fun part of this. So thank you for sticking around. This is this. Yes. Um, I will typically, that's a good question. There was a study published on that. It showed that patients had two years or less of growth remaining with a thin flap technique that there was no growth disturbances afterwards. Um, I currently, um, will say if they are, with growth remaining that I would do it. I do have a male, um, the youngest patient I've done it on is a nine-year-old female, but she was physiologically 11. She was already like puber, puber, right? So she was an odd one. I had a couple 10-year-old females, both premenopital, who wanted to take the risk of possible growth disturbance to get fixed, um, to get it fixed. Because I do have a lot of pre-pubertal patients that I temporize with an MPFL alone, and then have to revise them when they get a little bit older. Um, I do have one male, um, and this is, this is what's driven me, who's, I think, was 12 at the time I did it. He's got some rigor bottom. He has a growth disturbance from my trophic lymphocytes. He hyperextends more on that side. So, um, but pubertal, if they've got secondary sex characteristics, um, I have never had a growth disturbance from that. I've done, I mean, 70, 80, 90 older feises trophic lymphocytes, so. When you say you had to revise the people who had soft tissue later, was it because they became recurrently unstable, or because you were planning a second operation? They all, well, that was the discussion. And it's played out in almost every instance that they did become unstable again. I mean, when you've got someone that's that young, that's unstable, pre-pubescent, their dysplasia's massive. I mean, otherwise they wouldn't dislocate so early, right? So they just had these raging degrees of dysplasia. So, um, they just have always tended to pop out again. Yeah. All right. Speaking of raging degrees of dysplasia, let's jump into our first case. You're going to like this one. All right. So patient ND, patient of mine, 16-year-old female with a recurrent, not lately. No, the right side's my good side. So she has recurrent instability. She's 16, uh, five years since she was 11, since she was pre-pubescent. Dislocates three to four times a month, like full-on dislocation, failed bracing, PT. She has no real family history and she is essentially a mature, skeletally mature, first menstrual period at age 12. This is her exam. That's her unaffected side. This is her affected side. So I would argue that that's that classic jumping J sign. She has three quadrants plus of lateral translation with a lot of apprehension, no endpoint. And you can, this is what indicates to me that there is a big issue with the trochlea is, uh, she continues to be loose in terms of that translation in, uh, 60 degrees or even more flexion. So not in there. So there's no engagement essentially. She had a little bit of a lateral tilt that corrects, otherwise her stability is normal and her hip rotation is fine. So we're looking at these films, Jackie, what, what do you think? She's very dysplastic. It's not a perfect lateral. And I kind of wonder if this is one of those ones where the radiologist would really struggle to get a perfect lateral because it also looks like she's got some rotation. If you look at the AP and the tibial spines relative to the condyles. So this, this seems like multifactorial malalignment. Yeah. So I think that's a great point with Dr. Brady is pointing out is when you look at the AP films or the alignment films, you see how the femoral condyle overlaps the spines. And that's probably an indication of some femoral rotation. The question is, is that compensatory or does she have true and aversion, aversion issues? And based on my hip exam, this is a patient that I don't remember if I had aversion study, but there was no major concern for de-rotating, which I've gotten into over the years. But you're absolutely right about, about her dysplasia. You know, the way we look at it as the supratrochlear spur is pretty obvious. I think even if we had a perfect one, that would not disappear. And we had some advanced imaging to look at that. She has that double, you know, the crossing sign, right? Which indicates a trochlear, that floor that rises above the walls and the double contour sign, which I look at a little less, but could indicate the medial hyperplasia and the classic de jure classification that our lead doesn't love. So, but also the other thing on this lateral. Okay. Okay. Fair, fair. Next, next ICL will have him and you on the same panel. A debate, thin flap versus thick flap. But anyway, but I think everybody would agree that this patient has ALTA as well. It's pretty dramatic. I don't think you can prove it though without an x-ray. No. Disagree? Yes. I would make my text, repeat that. Okay. I would not, I don't use x-rays for, to indicate ALTA. It's always MRI plus clinical exam. Okay. Fair enough. No, I think, I think, I think those are all interesting points to, to, to argue. So, so Jackie, with a 1.5 measured on this one, how big of a difference do you think we'd get with a, with a perfect lateral? That's a really good question. I think. You think it dropped down to 1.2? I don't think we know. Okay. I think it depends on which way that, that varispalgus is swinging. But yeah, that's a high number that you're measuring there. And I sure would be suspicious. Sure. Look at the amount of overlap between the patella and the trope there. It's almost a hundred percent, right? That is not ALTA. That patella is, looks a little bit high because the patella is a little bit lateral. And Dan Green has the best photo ever of, it's like a clock face. When you look at the medial, as the patella translates medial to lateral, you know, it's got a fixed point from the patella tendon down to the tubercle. And under normal situations, the patella is located in the trochlea. The patella is slightly medial to the tubercle, right? So it's a little bit down this clock face. And as it goes lateral, you know, you've got this, you've got this quad pole that's going to keep the patella tendon under tension, right? So if you've got this fixed point on the tubercle and it translates lateral, it doesn't just go in a straight line. It actually kind of goes up a little bit. So the patella kind of moves like this medial to lateral, down medial, up lateral. And so when you've got these people that have a baseline translated lateral patella on a lateral x-ray, it looks a little bit higher. And that's why that study showed that after MPFL, the patella was more medial. It brought it down and effectively reduced or improved some of this mild ulta. Yeah, the picture's worth a thousand words because it's so hard to explain. But that's one of these x-rays. I do need to see that picture because that confused me more than Adam's mathematical presentation yesterday. But also, like, if you're taking an x-ray uphill, I don't think you can... No, I understand what you're saying. Yes, I am raising eyebrows at this. So I understand what you're saying. Yeah, and that's very poor overlap. Yeah. So what do you think about that? No, it's probably still... I mean, I use MRI, I use what's called the patellar trochlear index. Yeah, PTI. Yeah. She's probably... I bet her patellar tendon measures probably 60 millimeters or something like that. I don't think that... I would not still consider distalizing her until I had an exam and probably even an intraoperative exam. Okay, fair point. Quick word about patellar trochlear index. So that's a described measurement on MRI. Roli Biedert from Switzerland is brilliant. He knows as much about patellar height as anybody. But the thing is, you need a central slice. And so the big downfall of making all your decisions based on MRI is that the lateralized patella won't give you the information you need about the interaction with the groove, if that makes sense. Right. And so I think if you're going to use radiographs or imaging to drive your decisions about ALTA, you've got to do both. Right. Because the MRI will tell you a lot about three dimensions, but the x-ray will tell you more about strict height. And you're right, it varies whether it's medial or lateral. But I think in this case, this is my favorite situation where there's a big bump, but there's ALTA, and I can jump the bump to get it back into whatever groove is there. Yeah. So we just finished our data collection on this, looking at height measurements, sagittal height measurements on MRI, one image versus two image, to capture that mid-portion of the trochlea, and taking the patella's medial or lateral. And it's always different. Yeah. It's almost always different. Like, if you do a two-image measurement, there's almost always less height, less ALTA. Right. With that. So we still have to write it up, but that's what we showed. All right. Well, in the interest of time, let's move on. We can debate. We've spent a lot of time on imaging. I'm going to call an audible here and just tell you it's ALTA. She has tilt of 22 degrees. She has a high TTTG, which I know Lee doesn't love, but it is high. Her cartilage is pretty normal. And obviously, I don't even look at the MPFL or MQTFL on the MRI, but let's assume it's stretched out. So here's that algorithm that I showed you before. And I think in the past, trochleoplasty considered salvage. My thinking is, you know, I put it in the same line with all these other procedures. I know Lee's a big trochleoplasty guy, not a TTO guy. Jackie maybe is a more TTO. Kirk, I think you're also in the TTO camp. And I will kind of do the a la carte approach depending on what I think is an issue. So that's how I approach this patient. So here's her arthroscopy. She has some cartilage wear on the medial facet, actually. I think her lateral facet's okay. You can see pretty severe dysplasia. And we did the case summary was that we did the TTO with anterior medialization. We also distalized her based on my calculations of the CDI. And I do it intrapartly. I get a perfect lateral. I make the rep basically measure my CDI. It's a lot of yelling going on at that point. And then we did a lateral retinacular lengthening and the MQTFL with a graft. And there's a quick, I made the video guide. He did this for me yesterday, which is amazing. He shortened our 10-minute video to one. So that was, first thing I do is I attach the graft to the femoral side. Then we cut our TTO, expose the joint. There's that cartilage wear. Maybe it's a little more. Here's a pretty severe trochlear dysplasia. Call that a convex. She has a super trochlear bump. Do a thin flap technique using the proprietary guide. I use a lot of osteotomes other than just the guide. The guide can slip. I think I have better control of the osteotomes. I create my groove based on the pre-op planning. That is a tamp wrapped in a moist lap sponge to help me reshape. And then using the anchors. And then we proceed to pull the graft up to the quad. Do the classic focusing technique. I amputate the distal tip to advance. She was only needed to be medialized a little bit. Combination of the trochlearplasty and TTO. You need to take that in consideration so you don't over medialize. And here we're closing up the MQTFL after we do the lateral lengthening closure. And then she had very nice tracking afterwards and nice stability. This is the protocol. The limited weight bearing is mainly guided by the TTO. Made a full weight bearing by six, a good range of motion. She was a little stiff in the beginning, but came around and this is her six months follow-up. She's now, I think about nine months and doing well. You can still see a little bit of a J sign, no longer a jumping J. Her, I would argue that her Ketone Deschamps has been improved. Her glide is normal, you know, we didn't over constrain her. Can you play that video again? Sure. I mean, it seems like it jumped proximal, you know that, okay. I don't think she jumps anymore. I think it's definitely different. Her quad is definitely at this point is under, with all these surgeries, it's a lot of surgeries, the quad restoration takes some time. And I think her VMO, which we don't really talk about as much as we should, is under re-upped. Up and down a little bit more, not so much off to the side. I think you're just being overly critical of my work. I think that's a pretty damn good result. Let's play that again. We might take a vote here. I feel there's some microaggression going on. I don't think that there's really much lateral translation of that. I just wanna know from the trochleoplasty expert, did I do a good job? Yeah. Thank you. So that's mission accomplished. And what do you think about the x-rays? The spur is gone. Spur is gone. Would you like to see the floor deeper? And again, these are not apples to apples. They're still not a perfect lateral, but I think it's a little bit better. Yeah, it's hard to say. Obviously, trochleoplasty is a part form because we don't have guides that just give you a specific groove depth or- That was the question I was gonna ask you. How deep do you make your groove? Your picture seemed to show almost a normal groove, and I make mine a little shallower. I started off, I think that that's something as you get into this that you're always gonna err on the side of being shallow early because it's just, the biggest challenge is getting comfortable getting the flap thin enough to mold it if you do a thin flap technique. And I think, I know I took a lot of high-grade dysplasia to low-grade dysplasia early on. And as time went on, I now just am more comfortable getting it thin. And now I pretty much almost always only accept a normal, it's about four to six millimeters. Okay, okay. Yeah, I was gonna call out the bump too. I think it's too early for press really, but the Jupiter studies, as we try to look at dysplasia, we're taking all the measurements, like the trochlear depth and the lateral inclination and the sulcus angle and all the things. And the thing that really seems to matter in our preliminary data is the size of the bump. And so I think if you're going to go for anything with a trochleoplasty, get the bump flattened. And then we get in the weeds on the art of, do you do a thick flap? Do you do a thin flap? And I hope what you're hearing here is that the goal is stability, right? If we can solve the stability problem, I think that's victory. And I think like your point about dysplasia and arthritis is taken, but I think the cartilage injury that you showed in your talk is from the instability, it's traumatic, right? Like if you solve the instability, you stabilize the joint, then we've won at least half the battle. And I think- Why are they unstable? Well, because of their anatomy. I'm gonna let you guys battle it out in the next one that you have. Let's show at least one more case. All right, Jackie, do you want to present it? Either way. I'll run through it. Can you talk from there? Yeah, so this- This is Dr. Brady's case. This is a case from my early practice when I was a fraidy cat about trochleoplasty. It is something I learned on a traveling fellowship and I had done it by this point, but I hadn't done it a lot. And I think it was still very much my dogma to avoid it if at all possible. I think like full disclosure, if I saw this case now, I might have a different discussion with the patient. So I think it's worthy of discussion from the standpoint that one of my partners says, if there's lots of ways to tackle a problem, either all of them work or none of them work. And I think there are lots of pathways to stability in patellofemoral. So this is a 13-year-old. She started subluxating at age eight. And so this point about like secondary dysplasia, worsening dysplasia, I think all of us would agree that the worst dysplasia we see is in people who dislocate when they're very skeletally immature. So she was good motion, terribly apprehensive, wouldn't let me complete a real translation exam, but had a dramatic J sign. I couldn't feel an end point, but she sure wouldn't let me test quadrants. And her internal rotation versus external rotation of her hips was off, right? This is the sort of like raise an eyebrow, wonder about rotational anatomy. And then you can see here, I couldn't get the text to get a lateral, like there were so many attempts at a lateral X-ray that we finally just gave up. You can see her profound dysplasia. You can see that there's a little asymmetry even on the AP. I didn't think she was terribly high on that measurement, but again, not a perfect lateral, so you can't really say. And here's her asymmetric trochlear dysplasia. Like you can really see the effect that early instability has on a knee versus the other knee started at age 13 with a subluxation. So I was getting imaging. Here's the problem with the like, the patellar trochlear index. Like you can't find that patella anywhere if you're looking for your central slice and your trochlea is just sitting in the gutter. But her TTG was high. Her bone age, thankfully, was 15. She was more than one year postmenarchal, so we could sort of put all options on the table. She's like a little bit valgus, but not enough that I was thinking about correcting that. But she did have a lot of femoral antiversion. And I think Bob Taiji is definitely the level five evidence source of this, but I don't think about correcting femoral antiversion until it's well above 30, because there's room for error in that technique, right? Like we're looking at pins and things, but she was pretty high. And so she has severe trochlear dysplasia. She has a high-ish TTTG. She's pretty normal, ALTA, thankfully. Very introverted, a little valgus, bone age is 15. What are we gonna do with it? I feel like would all of us on the panel now suggest trochleoplasty? I would do a trochleoplasty. I would, 32 antiversion, if I'm doing a trochleoplasty, I might not, I would think about it versus moving the tubercle, you know? I think higher, like a 40 antiversion, I would derotate plus trochleoplasty plus MQTFL. So you're not moving the tubercle here? With a TTTG19, if I'm also gonna lateralize her trochlear groove when I do my trochleoplasty, I don't think it would be needed. Really? And especially if I'm rotating, moving her trochlear center, I would not touch the groove. I'm shocked it's only 19. I know, right? That patella's in the gutter. I would expect that to be 25. It's probably higher than 19. Well, I think it's because she's tiny. This is the thing with TTTG. They don't adjust it for patient size. She was a tiny human. And so I think in a seven footer, that would be like a 30, you know? Exactly, plus it's on an MRI, so that 19 is, you know, 23. So let's see what Dr. Brady did. So I talked to her at length. We talked about trochleoplasty and I expressed my hesitation with it. And so I think I steered them away from it. I think, again, if I talk to her now, we might have a different conversation about that. I felt like she needed soft tissue lengthening or release laterally just to get the patella to sit back on the trochlea. We did an NPFL reconstruction and a tibial tubercle osteotomy. So you can see that empty groove, the patella's just sitting sort of over the ridge of the lateral trochlea there. So I did a mid femur derotational osteotomy. The problem there is it's hard to compress because osteotomies wanna go home, so it'll sort of find its way back home if you try to like backslap or anything with a nail. So we ended up dynamizing this later, but she did really well. She had this brief increase in thigh pain, interestingly, with dynamization, then healed really well. She was a patient who was miserably maligned at first. And when I saw her post-op and she was all healed, she was thinking about trying out for lacrosse. And I think if you go one more slide, there's like an axial, yeah. So you can see her patella's more centered there, still dysplastic, but no more apprehension, amazingly, and like, you know, a nice solid endpoint. So I think this is a good illustrative case for me in early practice that there are more than, there are more pathways than we think to stability. And if you're thoughtful about it, you can achieve it. I think here in the States, the leaning, generally speaking, is to try not to touch the trochlea, but I think we're increasingly following the trend of the Europeans and some of the Americans who are leading the charge that it's a safe thing to do, if done carefully. And so I think not an unreasonable plan for this one. Johnny, if she had a valgus in addition to the, which I do see a lot combination of valgus and rotation, would you go distal femur? Yes, and try to do both. I've had a case that, I'm not gonna get to it here, but with a, Biplanar. With a biplanar, and I think some of the new PSI from various companies can really help with the plan and execution of that, because that's a complex procedure. Over a nail is a relatively easy, I wouldn't say easy, but it's a relatively safe procedure. I had another case also with delayed healing like that, that I dynamized and did great. But you can also kick them into valgus with those, especially if you don't get your starting point right. So you have to maybe get your trauma partner in, whoever is- I grabbed my pain's partner, yeah. I was still doing level one trauma at that point. Let's do one more. That's a very interesting case. I think there's a lot to discuss there. So she's doing well, which is great to hear. How long of a data do you have on her? Probably about five years now. We'll be curious to see what her cartilage looks like. That's true, maybe I should bring her back. Because I think that kind of displays you, even though they're stable. I always wonder what displays you, what effect lead to your point as long-term. Yeah. And again, these are all signs that you can use compensatory management to do it. I just have, my philosophy is fix the problem. What's the problem, right? And so I don't disagree with the outcomes. I don't think that that's a fake outcome, right? I just obviously would handle it differently. Any questions from the audience? All right, let's just do one more quick case. We have a couple of minutes left. We're happy to stay a little later. I'm happy to stay a little later, but just wanted to show you, kind of getting a little bit crazy here. This is a patient that I had when I was in my practice in Queens, where I was for 13 years with New York Presbyterian. And definitely a different patient population than you get at NYU in Manhattan or Brooklyn Heights, which is like where Matt Damon lives and stuff. So let's paint some happy little trees here. This is a healthy male non-smoker. Not your typical patella patient. He just, it's a worker's comp injury. He twisted his knee in IHOP cooking, fell first time. He says it's the first time this happened, but he's had this cracking and discomfort in the knees his whole life. He's from Ecuador and he's very, very limited right now. He's, like I said, unremarkable. Not your typical patella femoral patient. BMI 30, not loose at all. He comes in ontalgic. He's got a little gene of valgum, no recurvatum, normal hip rotation. His knee is very painful, tender laterally. He's got some crepitus. He's got a J sign and two quadrants of a lateral translation and pain with patella grine. His quads are weak right now from an acute injury. So you look at this, he's 21. I'm not gonna ask you guys. I think we can agree that he's got some pre-arthritic or arthritic changes in his knees. He's some loose fragments and such. He has dysplasia. I think that's a pretty good lateral. He does have a crossover sign and something happening in the supratrochial area. He just has this weird look to his knees. So then we do this MRI and you get a little nauseous when you're looking at this MRI because the kid's 21 and you see that. You see it on the lateral side. And I think to Lee's point, this is, in my opinion, this is an effect of dysplasia from a young age that's been completely ignored that is having him track laterally. So whether it's the instability or instability plus a very abnormal shape to his patellofemoral articulation, I don't have an answer, but it's certainly a combination of the two. You see people with dysplasia that don't have instability that have cartilage damage. And I think the guys, if they've got more dynamic control with their stronger quads, keep their knees in a little bit better than the girls do, but sometimes they pay the price for it like this. Yeah, well, so as I started out my talk, it's a dynamic imbalance and there's a combination. His knee was obviously teetering and deteriorating for years. So this is a view from the superior lateral portal, which I like to do both for educational purposes. And then you can also do this and you can actually watch him track. And no, I'm not pushing it with my hand. This is how he tracks. And you can see why he has that severe cartilage damage, both on the trochlea and on the patella. This is his natural tracking. We're just moving his knee flexion extension. And I was going to fix that, which is why I'm doing it over and over again. I'm not sadistic or anything like that. But you can see how he probably had the hypoplastic medial trochlea that he formed, that spur. So 21-year-old kid. So we just went in for a loose body removal. And, you know, Kirk, you gonna harvest some cartilage from Macy for him? What do you think? I think he's- I know you're not supposed to use- Yeah, so- Are you gonna use autogenous cartilage implantation? No. So I kind of wanted to. I kind of wanted to. You know, if you went back to his MRI, he has cyst- So I harvested, right? You know, so he has cyst formation, you know, on his MRI. So he has both a bone and cartilage problem, you know, in my hands that requires a bone and cartilage solution. Could you do Macy? Yes, more data's coming out. So let's ask for who would just go non-op and just tell this kid, there's nothing I can do for you. PRP, maybe pay out of pocket with your IHOP money. AJ, right? So he wants something done. This is his films. By the way, that's a nice picture of a difference between a Merchant and a Lauren View, and a Lauren View, which is less flexion. He's sitting very out. So who would do a cell-based repair? Something on the surface. Nobody. Who would do an osteochondral-based repair? The attraction of cell-based is it's not shouldered, right? Is that fair to say that, like, if you don't have a shoulder, it's kind of, like, cell-based, I don't feel like needs a shoulder in the same way. So I don't think it's unreasonable to talk about. Who would do an osteotomy for him? You guys aren't doing anything for this kid. Lee, trochleoplasty. Trochleoplasty on this guy. Unloaded? Why would I unload with a trochleoplasty? Anybody would just tell him patellofemoral arthroplasty and forget about it. I think that's a little too young at 21. I do arthroplasty all the way to total knee, but I think for this kid. So what I decided to do is, and I'll be honest with you, like Jackie admitted that she wasn't really doing trochleoplasty early on. I wasn't really doing osteochondral at that point for patella in my career. So I was a little hesitant and I decided I'm not gonna burn any bridges by doing a cell-based. It might not work, but I was going to do an osteotomy. So these are his lesions before I started preparing them and then after preparing them, measuring pretty large. And so what we did, we did a tibial tubercle osteotomy with a 45-degree cut and a lot of translation, 12 millimeters medial and anterior, no distalizing obviously here, soft tissue stabilization for instability. And I used the particulated juvenile cartilage implant, which Dr. Campbell mentioned in this talk. So that's DeNovo. And he had a 20 by 20 lesion on the patella, 20 by 12. And we did a lateral lengthening. And these are his pictures. Sorry, was there a picture of the, yeah, that's a picture of the DeNovo in the lesions. And you know- And you don't move him, right? You hold him still? What was your immediate post-op rehab? Like extension? So in terms of motion, just a couple of days of no motion, and then just- Really? Just like I treat the, you know, Macy and others, same thing, I let him move. I agree, it doesn't feel as good the way it sits in the lesion compared to Macy, compared to something that is on a patch because you're just fiber gluing over this minced cartilage. So not my favorite thing, but I think this kid, there was no way we're going to get Macy approved. So this is what I chose to do. You could probably finagle it. What's that? The Macy. Get it approved in Queens? I think so. Come over and help me get it done. I can't get it in my head. It's very helpful how you describe the chondral defects because they will, I mean, I have resurfaced patellar and trochlear defects, right? Yeah. You know, bipolar, but I just described them in a way that doesn't sound very bipolar. That's not the problem with this kid. This kid's insurance sucks. It's not going to cover it. Oh, yeah, it's about insurance. I'm not talking about the bipolar, yeah. Oh, no, I've got the proof of that. His reference to Queens is that it's shit insurance. Yeah, but no, he won't, if it's government insurance, you're not going to get it. Yeah, correct. You can't do, yeah, in my hands, I would have done bipolar osteochondrographic. And I think now I probably would have done the same. This is like a full disclosure. I just wasn't as comfortable with patella. And I still think that to Kirk's point, the patella osteochondrolographs are a tough case, especially when they get close to your border. You have no border. Now you start playing around with putting screws in. It's tough to fix them with screws. And, you know, the key is, well, obviously it depends on where it is, but like restore the median ridge. Yeah. And if your borders aren't perfect, rats, I think that's the trade off. So again, to Jackie's point, that there's many ways to arrive at stability and good function as this guy, this is four and a half months. And I, you know, I asked him, show me what you can do. I thought he was just going to like stand on one leg and do a mini squat. And he went all the way down. You can see he's still offloading a little bit to his normal side, but he did remarkably well. And I'm curious to see what his arthritis is going to be like in the fall. There's no doubt in my mind he will have arthritis, but I think we bought him, you know, a decade or more at least before we need to do anything else. And because we didn't burn any bridges with a subconval bone, I could do an OCA in the future. So I think that was a win. I don't think I would do a trochleoplasty on this. I think I would do this today. I think you can absolutely unload that and centralize that patella and get your tracking better and let your cartilage restoration heal in. I think if he had less arthritis. Right, the arthritis I think is the- No changes on the trochlea. I know you're pretty ahead of us in terms of the indications for trochleoplasty, but I think if he had no, if he had a normal trochlea and a bad patella, then I would, you know, what you showed earlier, patella cartilage repair and the trochleoplasty, I would definitely consider that. I just think improving the congruency between the patella and trochlea is the, and I agree that there's no question that the TTO is based on what you did. That is the essential offloading portion of what you did, right? Yeah. And the data, I agree with the data that the TTO offloads the cartilage surfaces. I don't disagree with that. In that region, lateral. Yeah. Especially here. Yeah. Great. But I'm going to pause it to you that probably improving the congruency between the patella and the trochlea is going to offload that even better. I don't think, I think there's a whole subset of people that say that you mess up the congruency if you change the shape of a trochlea that- I think they're full of it. Yeah. This is where the debate is. We can sit here for hours. I love it. Well, thank you all for coming. Does anybody have questions? I mean, we're out of time, but we're happy to take on a few questions. All right. Thanks everybody. Appreciate your time. And thank you to my speakers.

patellofemoral instability

Alex Galant

NYU

Dr. Lee Pace

Jackie Brady

Kirk Campbell

medial soft tissue

reconstruction

MPFL

tibial tubercle osteotomy

trochleoplasty

cartilage restoration

clinical cases