Welcome to the American Journal of Sports Medicine's webinar presented in conjunction with the Pediatric Research and Sport Medicine Society. Thank you for joining us. Here are the learning objectives and the disclosures for our faculty and organizers. At the conclusion of today's program, we ask that you complete a brief evaluation to collect CME for this activity. Details will be given at the end of the program and in an email to attendees. At this time, I would like to introduce our moderator, Dr. Ryoichiro Akagi. Dr. Akagi is a director of the Knee Surgery and Sports Medicine Center, Oyomino Central Hospital, Chiba, Japan. He is also a member of the AJSM editorial board and will be moderating our webinar. And with that, I'll turn the program over to Dr. Akagi. Okay. Thank you, Christine. Thank you, AJSM. And thank you, PRISM for sponsoring this webinar. Thank you to all for your interest in sparing your time to attend this webinar. I'm Ryoichiro Akagi from Chiba, Japan. I'm a knee surgeon and the director of the Knee Surgery and Sports Medicine Center at Oyomino Central Hospital. It is a great honor for me to moderate this webinar, and we are very excited to have this discussion today on OCD with the great experts. Okay. So, it's my pleasure to introduce our distinguished panel. Leading us off will be Dr. Justin Arner from University of Pittsburgh Medical Center. He is a team physician for the Pittsburgh Steelers and the United States Ski and Snowboard Team. He will explain the clinical presentations, epidemiology, and etiology of OCD, followed by Dr. Meninder Kocher, chief of the division of sports medicine at Boston Children's Hospital and professor of orthopedic surgery at Harvard Medical School. Dr. Kocher will talk about the radiographic feature and treatment indications of OCD in the knee joint. Third stop will be Dr. Theodore Ganley, the sports medicine director at the Children's Hospital for Philadelphia and the Bisigmano Family Endowed Professor of Orthopedic Surgery at the University of Pennsylvania. He will give his talk about the treatment of OCD, mainly focusing on drilling and fixation. Finally, we will have Dr. Marc Tompkins, associate professor in the Department of Orthopedic Surgery at the University of Minnesota and a faculty for the Orthopedic Sports Medicine Fellowship at TRIA Orthopedic Center. Thank you all for being here and participating in this webinar. We really look forward to hearing everyone's thoughts and we will have some time to discuss and answer any questions in the end. I will now turn it over to Dr. Arner for the first lecture. Please share your screen, Dr. Arner. You already did. Go ahead. Thank you, Dr. Akagi, for your kind introduction. Again, I'd like to echo the thanks to AOSSM and PRISM and Brett Owens and the rest of the staff here for putting this on and inviting me and including me in this distinguished panel. I know all you guys and ladies are here to hear really from the best. I'm excited to learn about it as well. We're going to talk more about the background, as Dr. Akagi mentioned. We did write a Yellow Journal article about this topic that I refer you to. Again, we have no final disclosures. OCD lesions, quite an interesting history. In 1887, first was diagnosed by Franz Koenig. He really had it right all the way back then before x-ray and all this imaging and technology we have now. Thought it was related to trauma, bone bruising leading to necrosis, and possibly spontaneous separation. He described it as a subchondral inflammatory process resulting in loose fragments of cartilage from the condyle. Here's some text from his original paper, which I'm not a German speaker, but pretty interesting. We mentioned pathology to subchondral bone. We know it can be acquired, idiopathic. It's potentially reversible, which we'll discuss, obviously, today. The instability of the bone cartilage fragment, obviously, is what we worry about. We're discussing knee here, but obviously, it happens in the ankle, the talus, we see it quite commonly, elbow, shoulder, and hip. Age really makes a big difference. Typically, ages 10 to 20, two categories which really predict prognosis and treatment options. Juvenile, when patients have open physes, and adult with closed physes. Bilateral is something we always need to look for and think about. It's been cited to be 15% to 40% in the literature. The prevalence in juvenile OCD lesions, 15 per 100,000, 12 to 16-year-olds are the most common age. It's really rare before younger than six years old. Six to 11, it's a little bit lower incidence, 6.8 per 100,000. As I mentioned, 12 to 16-year-old, it really increases, basically doubles 11.2 to 100,000. Females is a risk factor, two to four times the greater risk factor in the literature. Being an African-American and having obesity as an issue increases that risk. We believe sports participation is important for this and developing these. As female athletes are becoming more and more common, we're seeing it in more and more females as well. It's a really interesting study from Dr. Coker and Journal of Pediatric Orthopedics from 2018 that talks about the increased load on the posterior femur in baseball catchers and how that's associated with the high risk of juvenile OCD lesions. It really makes sense and it was a well-done study there I thought was interesting. A multicenter trial in 1999 was really a large number of patients looking at the location of these OCD lesions. As we know, the posterior lateral medial femoral condyle is most common, as you can see in this picture. 51% in that lateral aspect of the medial femoral condyle and 77% of the medial femoral condyle altogether. Less common in the patella and trochlea, but do occur and quite a bit less common in the tibia. As I mentioned, being a bilateral disease is something we need to keep in mind. We really don't know the etiology of this disease. The pathophysiology is not fully understood. Like most things, it's multifactorial. Traumatic is something that's been looked at most commonly. 60% of OCD lesions are in athletes and that gives us another reason to think trauma is likely related here. There are biomechanical thought processes behind developing these as well as vascular and genetic, which we'll go over. As I mentioned, traumatic etiology is the most common examined etiology and cause of these in the literature. It's been discussed, whether it be a single trauma or repetitive microtrauma. Repetitive microtrauma seems to be a more likely cause in a typically susceptible individual. The classic discussion point is that repetitive impingement on the tibial spine with the medial femoral condyle with flexion and internal rotation, you can see a picture here showing a prominent spine there and you can kind of picture how that may irritate that subchondral bone. So it leads to injury of that subchondral bone due to the stress on the immature bone and the growing bone, and without healing of that trabecular bone, it can become unstable. By mechanical factors, as I mentioned, obesity, alignment, including increased tibial slope, retrovotum, flattening of the condyle, having a discoid meniscus likely from that same thought process of the tibial spine, having a hypermobile anterior horn of the meniscus, again, this mechanical, biomechanical type combined issue leading to just trauma to that subchondral bone over many, many repetitive types of events, having meniscectomy and then joint instability. Vascular factors, as I mentioned, were also looked into quite early. In 1953, it was first described. There's a nice article in the Journal of Trauma and Acute Care Surgery from 1966 by Campbell and Ronawat that was really a pretty great study looking at the histology of these OCD lesions. So they found a characteristic bone infarct in these folks with OCD lesions, and they concluded that necrosis was the primary event leading to the unstable fragment. In a study in the European Journal of Radiology in 2012, they examined arterial end branches in the subchondral bone and postulated that that maybe started this process along with the repetitive microtrauma that compromised the blood supply during that rapid growth. We think that the growing young individual with that susceptible bone really does play an important role. Genetic and biologic, family history has been linked. 14% of folks do have a family history of OCD lesions, higher incident in twins. There's been some research that the agracan gene may play a role. You can see a picture of that here. A ribbing theory, which is basically the secondary ossification center in the distal femur may develop into an OCD lesion after trauma has been discussed as well. And other endocrine abnormalities such as vitamin D deficiency, human growth hormone deficiency, and certainly we have a lot to learn about this genetic and biological aspect of this. The clinical presentation as we wrap up here is quite variable. With a stable lesion, it's really difficult to really pinpoint specific reproducible presentations and complaints patients have. But a lot of times patients will have vague knee pain after sports and sometimes they'll progress to effusions or intermittent antalgic gait. Those lesions are stable. If they become unstable, obviously that mechanical aspect of the disease is what we typically see with catching, locking, swelling, classic Wilson sign and tenderness over the medial femoral condyle inflection is something, as you see in this picture, that we typically look at, but really has low sensitivity internally rotating that tibia from 30 to 90 degrees to try to impinge that tibial spine on the medial femoral condyle, that lateral aspect of it. Something worthwhile doing, but certainly not always present. As I conclude here, it's a disease of the subchondral bone. There's really a spectrum of disease where you have no osteonecrosis to bone resorptions to collapse to then sequestration. The fibrovascular tissue forms between that bony interface and has difficulty healing whenever you get unstable fragments. As I mentioned, etiology is logically multifactorial. We're learning more about it. There's a highly repetitive biomechanical type injury to this and factors related to sports and repeat instability. I'd really like to thank the ROC group that is led by the folks here giving presentations after me, and really thank them for all they've taught us, and I'm looking forward to their presentations as well. Thank you very much. Great. Thank you, Dr. Arner, for the concise overview of epidemiology and etiology and clinical presentation. We will have the Q&A time after everyone's talk, so let's now move on to Dr. Kocher for the next lecture. Dr. Kocher can you please share your screen? Thank you, Dr. Akagi. Can you see my screen? Yes, we do. Okay. Wonderful. Well, I want to thank you, Brett Owens, AOSSM, AJSM, and PRISM for putting on this webinar on OCD of the knee. I think it's a really fascinating condition with a long history and a lot going on in terms of current treatment and assessment. I'm going to talk really about assessment and treatment indications for OCD of the knee. Let's see. Okay. I have no conflicts of interest in this talk. I would disclose that I'm on the OJSM editorial board. I am involved in PRISM and founding of PRISM in Pozna and currently on the board of AAOS. AAOS is actually very interesting because we had this CPG for the diagnosis and treatment of OCD. This was published in 2010. This was actually a super frustrating experience. We had a clinical practice guideline group that reviewed all the level 3, 4, 5 literature on OCD of the knee. After a lot of work and a lot of money and a lot of time, we had a number of inconclusive conclusions about OCD of the knee. The only conclusions we could make were based on consensus, not on data. We really realized that we needed better data for OCD of the knee. That started the ROCK study group. This was founded in 2008 by Dr. Ganley, Walsh, Shea, and myself. We've grown into 23 centers with a registry and prospective data to try to better understand OCD of the knee. I think this is a great website, kneeocd.org. This is the ROCK OCD website. I'd encourage everyone to go there and take a look at it. There's some interesting information on the provider side. It's a good source of some information and tip sheets for patients as well. This can be a frustrating condition for patients, so this may be a resource for you. I do think it's a super interesting time to look at OCD, because there's a long history of OCD and a lot has changed. On the left is a picture of the treatment of OCD. This was actually at Boston Children's Hospital by Dr. Green. This is a bypass brace to unload this left knee, and he would put children in this brace for about two years or so. That'd be kind of hard to do now. When we imaged OCD, a lot was by bone scan and surgery was all open, largely removal of the OCD fragment. Where are we now? We're seeing OCD more frequently in younger patients. It was predominantly males, now more females as well. We have better ways of imaging with MRI. We've got open treatment with chondral resurfacing and arthroscopic treatment, and a lot more interest in biologics. I think this is a good time to be talking about OCD. However, we've got so much information about OCD, I think it actually becomes a little bit confusing now. This unstable lesion of the knee, do we treat this non-surgically? Obviously not. You've got an arthroscopic image. Fixation, drilling, do we bone graft? What about stem cells? Would we treat this with an OATS or an Allograft or Macy? I think we have a lot more options than we did before, and that actually may make it more confusing. In ROCK, we defined OCD in 2013 as a focal idiopathic alteration of subconval bone with risk for instability, disruption of the cartilage that may result in premature osteoarthritis. We just heard from Justin about the etiology of OCD, and we think this is really repetitive trauma, microfracture in an area that has a poor blood supply. I think this concept of the secondary physis is very interesting, and so there may be an injury to the secondary physis. This is not the physis between the metaphysis and the epiphysis, but the physis that goes around the epiphysis, and injury to that secondary physis may be etiologically related to the development of OCD. So I'm going to talk really about assessment and treatment options. As we heard, the history can be quite vague, so it can be pain, stiffness. There's usually not a single traumatic event. Ask questions about overuse, mechanical symptoms. The symptoms will really depend on the stage of the OCD, so a stable lesion may be very vague. An unstable lesion may be more mechanical. On physical exam, they may walk with an external rotation gait or have pain with internal rotation. The so-called Wilson sign, this is probably because the most common location of OCD is the lateral aspect of the medial femoral condyle. So with internal rotation, that can impinge on the tibial spine and cause pain. The most common locations of OCD in the knee are the medial femoral condyle in about 64% of cases, the lateral femoral condyle in about a third of the cases, and then less frequently patella femoral in other locations. On x-ray, don't forget the notch x-ray. That's a key point. So the knee series in children and adolescents should really be four views, AP lateral, patella femoral, but include a notch view. And that's shown here on the left. So you can see the AP x-ray, you don't see a lot. But then on the notch view, which is an AP inflection, you'll see the OCD lesion. And that's because most OCD lesions are more posterior. So you will see them inflection and maybe not see them in extension. So that's a pearl is to get the notch view. OCD has been classified on x-ray based on its location. The most common location is shown here, a 2C. So that's the lateral aspect of the medial femoral condyle and more posterior. OCD has been classified based on x-ray. This is the Burnt and Hardy classification, but this is really not used very frequently anymore. I would say, don't forget to assess alignment. I think in cartilage surgery and cartilage resurfacing, getting hip to ankle x-rays and looking at alignment is very, very important. And I think that's the case in OCD as well. We may see medial femoral condyle OCD lesions that are in varus alignment and lateral femoral condyle lesions that are in valgus alignment. And that may give us a real opportunity for guided growth. So we can improve their alignment with a small plate and two screws compared to doing the big osteotomy of the distal femur or the proximal tibia. This is just an illustrative case. So a 13 year old with left knee pain, soccer player, they actually had Panner's disease of the elbow five years earlier. We don't really know of an association specifically with Panner's and OCD, but it's an interesting combination. These are the x-rays. And again, you can see it much better in the notch view. So an OCD lesion of the medial femoral condyle, fairly large and slightly posterior on the femur, open growth plates, MRI shows clear demarcation of a large OCD lesion, but it does not look to be unstable. These are the sagittal MRIs showing a large lesion with a slight cyst there anteriorly. This is the hip to ankle x-ray, and you can see the mechanical accesses in the very medial aspect of the medial compartment. So in this patient with open growth plates, I think guided growth is a great addition to treatment. We get a hand x-ray in this 13 year old, six month patient who shows plenty of growth remaining. So these are the arthroscopic pictures showing some furrowing, but the cartilage is intact. We treated this lesion with a bioabsorbable TAC and transarticular drilling as shown here. We went on to do guided growth in both knees because both knees were embarrassed. These are x-rays showing healing of the OCD lesion. You can see here on the notch view, our drilling, and you can see the lines of bone formation from the drilling. And then at one year post-surgically, you can see correction of the mechanical access, and because growth was remaining, we took out the A-plate. So again, don't forget about alignment. Old imaging included bone scan, and this actually was well studied and was shown to be prognostic of healing, but I bet you can't find the nuclear medicine department in your hospital anymore. I don't know where they all went. Cahill and Berg. Cahill, who was a professor in Peoria, Illinois and did a lot of work on OCD and actually was one of the founding members of AOSSM and the president of AOSSM was very interested in OCD and bone scan. This is the Cahill staging system. Again, we don't use this very often. You know, why don't we use it? Because we have MRI. I think MRI gives us a lot more information. And for me is sort of essential in every patient I see. We can get information about the articular surface, stability of the lesion and it's prognostic of healing. It's very sensitive and specific for OCD. This is the most commonly used classification by Fritz Hefti from Basel where stage one is a change in signal, but it's not marginated. Stage two is marginated, but not dissected through the cartilage. Stage three is dissected through the cartilage. Stage four is dissected and in situ and stage five is a loose body. We've looked at this classification. It's had really pretty poor inter and intra observer reliability. We modified a classification based on MRI where grade one is cartilage intact without a breach. Grade two is cartilage is breached, but this lesion is stable. And stage three is unstable, meaning there's true fluid between the lesion and the base. The lesion's hinged with partial displacement or it's fully displaced. This showed much better reliability and it was really related to treatment. So stage one lesions will be treated non-surgically. Stage two, typically with arthroscopic drilling, a small surgery and stage three lesions need a bigger surgery fixation, plus minus bone grafting or cartilage resurfacing. So again, MRI gives us much more information. This is a AP x-ray coronal MRI. This is a stage two lesion, lateral knee x-ray, sagittal MRI. You can see the fissuring in the cartilage, a lot of edema, stage three lesion. Other things we are interested in on MRI are the contour of the lesion. Is it normal? Is it concave? Is it convex? The interface between the cartilage and the bone lesion is there increased signal or focal increased signal? How about the signal between the OCD bone and the underlying bone? Is that irregular? Is it linear? And then the bone fragment itself, how big is the bone fragment? Is it comminuted? What are the characteristics of the bone? How much marrow edema is there? Is there edema around the OCD lesion? Is it in the whole condyle and findings of instability? So I think these are things that we're looking at on MRI to see if they're predictive of successful treatment with non-surgical treatment or with surgical treatment. We have an arthroscopic classification of OCD. This was from the Rock Study Group and a lot of credit to our colleague and friend Lucas Murnahan, who unfortunately passed away. But in the arthroscopic classification, this is very descriptive, which is a very consistent way to describe things from a heuristic point of view. But we've got cue ball lesions. We've got lesions, those look normal. We have lesions that have a shadow when you turn the light down, a wrinkle in the rug, but it's not unstable. We have locked door lesions where there's a fissure in the lesion, but when you probe it, it's not unstable. Trapped door lesions, when you probe it, it opens like a trapped door lesion and craters where there's a loose body. So Dr. Ganley and Dr. Tompkins are gonna talk about treatment. You know, this is our treatment algorithm. I won't go deeply into it other than we really try with most lesions to fix them and get their own bone and cartilage to heal. Now, when we can't do that, we have various options for chondral resurfacing. I think we use a lot of osteochondral allografts now because these lesions are quite big usually and need bone and cartilage. I think prevention actually is super interesting in these cases. We talk a lot about ACL injury prevention. What about OCD prevention? This is Wayne McElwraith, who's a good friend, who's the Jimmy Andrews of the horse racing world. He's a surgeon, a veterinary surgeon of horses at Colorado State University. And we're good colleagues and have talked a lot about OCD. And interestingly, OCD has been really decreased in racehorses and quarter horses because they look at the amount of activity, they warm up the horses, they look at nutrition, they get plenty of rest and sleep, things to reduce their stress. As soon as they have MRI findings, they get stem cell injections. And so, you know, actually maybe we should be treating our kids a little bit more like racehorses and quarter horses to try to decrease this sort of increasing incidence of OCD of the knee. This is a family picture of our two horses. And thank you very much for your attention and thanks for the organizers. Thank you, Dr. Kocher, for the fantastic overview of diagnosis and MRI classification. Okay, I think we should switch gears a little bit and get more information on the treatment. So let's turn it over to Dr. Ganley. Dr. Ganley, please share your screen. Excellent. Okay, I'd like to thank Dr. Akagi, Brett Owens, AOSSM and PRISM and our wonderful AOSSM staff. Look forward to discussing surgical treatment. I have no disclosures related to this talk. I was recently more prominently involved in our ROC group as has been in the past. And our goal's objectives will be to address OCD lesion drilling and fixation. And then Mark will address higher level lesions. We'll start with a case, 15-year-old catcher. Had a collision, medial right-sided knee pain and swelling, tenderness, otherwise stable and unremarkable knee, but presented with these images. And what we just say that these OCD lesions that present can be diversity in race, sex, age, activity. And again, it was mentioned that it's 60% sports and there can be a variety of different sports. And it's not just knee, but elbow and ankle, as you're well aware. When we talk about surgical treatment, I believe it's important setting expectations. I discuss with families that OCD is non-viable or dead bone. And as our ROC group has noted it, and or it's cartilage precursors. And our goal is to make that non-viable or dead bone, we can say become living bone and cartilage. And your ask when you speak to the patient is for us to bring, they're asking us to bring the dead back to life, literally. So I sometimes describe that as CPR on the bone. And so who are we discussing when we talk about drilling and potentially fixation of intact lesions or hinge lesions? So we'll start with those intact lesions that are persistent symptomatic juvenile lesions that have failed conservative measures and predicted FISO closure within six to 12 months. Our goal is enhancement of local blood supply in that scenario. And what are these non-operative scenarios? So articular surface intact and not marginated, non-operative treatment. There's a variety of different treatment measures. Again, our clinical practice guidelines that there's not a wrong answer if you treat it with activity restriction or bracing or casting. But if you go through these cycles, typically three month intervals, it's re-evaluated. And if it's not healed after one or two cycles, then typically that inter-articular drilling, retro or trans-articular drilling is offered. An excellent study, lead author, Ben Haworth, and you see that the list of authors, they are trans versus retroarticular, a prospective randomized controlled trial. That was, again, a multi-center study group. And that was published in AJSM this past year, 2023. And the end result of that is that both techniques demonstrated consistent interval healing, high rates of clinical improvement, return to sports, and excellent patient reported outcomes at six, 12, and 24 months with low revision rates of surgery. So both were considered safe and effective techniques for the surgical management of stable OCD. As a matter of fact, also, Dr. Ochi from Japan described excellent results in a retrospective study with intercondylar notch drilling as well, a small series, but the philosophy is bringing blood supply to that region. That's where that classic lateral aspect needle from a condyle location, which is typically on the order of 70% of lesions that are seen in the knee. What about trans-articular drilling? So it has demonstrated in that series, a little bit shorter tourniquet time, fluoroscopy time, bony healing was a little earlier, greater at the early intervals, but the same at 24 months. And again, return to sports slightly early. But again, both techniques were safe and effective, trans and retroarticular. But the transarticular, what do I do? I tend to create standard portals, but a smaller inframedal infralateral portal to get a little more perpendicular to that lesion. What are we seeing in those cases? As Min described earlier, this will be the cue ball or the shadow cases seen arthroscopically. They'll be immobile. Again, I will actually use a cord needle biopsy to serve as a drill guide. It helps prevent that fat pad from getting wrapped up and it keeps that K-wire perpendicular. And again, this is an example of that serving as a guide, keeping that drilling perpendicular so you can get these perfect circles as shown. I tend to use a 0.45 millimeter K-wires when it's transarticular drilling. A video showing fat droplets on the right, showing that you've reached appropriate depth. And again, when you flex and extend, you'd like to see those perfect circles on all areas that are those softened areas of the OCD lesion. When do you add resolvable tacks or darts? It is if the lesion is blottable. So you get these slightly blottable lesions. There's many different manufacturers. This is just one example of the placement of one of those devices. And again, they're resolvable. When do you add bone graft? If lesions have closed feces, marginated cyst, ovoid bodies, or that blottable types, then that combination of factors makes me lean toward adding bone graft to these cases. Can you add bone graft in a variety of different measures? You can add it in a retroarticular manner or in a transarticular manner. Here's an example of taking a 15-gauge core needle biopsy from the proximal tibia on the right, and then transferring that to that 0.62-millimeter, to a 6-2 K-wire drilling site. And I will show the size on the far left of the 6-2 K-wire and the 15-gauge trocar biopsy on the left. So that actually can be placed. This is an example on the left of a placement of that outside of the skin, and this is an example of that trocar placement. So it's a small amount of bone, but it can be placed into a slightly larger 6-2 drilling site instead of the 4-5 drilling site. So one example of just adding bone to something that we all agree would benefit from new bone, either by drilling and stimulating a bone to reach that location or simply adding bone. You can also add that in a retroarticular drilling, and you can add bone graft there as well. But retroarticular, the technique of drilling of intact lesions without adding bone is shown here. And again, this is gonna be on our hot, 60% of patients are athletes or high-impact activity-level patients. Here's an example of the monitor shown on the left, the CRM above the knee, and a drill guide shown on the below right. Again, this is a flag-shaped drill guide, which is quite popular for this technique. And again, if you look on the right, you'd like to reach just below that articular surface to stimulate that healing process. On the sagittal, and also you can see the AP coronal view here as well. And again, so you can see the drill guide on the left and that being placed. There's a variety of ways that you can obtain a bone graft. On the left is a curette, on the center is one of many commonly commercially available guides, and that can be placed, again, retroarticular edition of bone graft, or in this case, it's a hinged lesion, and that bone graft is added arthroscopically. But moving on to this location, harvesting from the proximal medial tibia, you can also take that from the iliac crest. But again, with a slightly larger drilling, that bone graft can be added in a retroarticular manner. Moving on then to unstable lesions, trapdoor lesions. So as Min had described earlier, and these are unstable lesions that can be made congruent and can be placed in an arthroscopic video shown on the right of that trapdoor lesion. And this is fragment detachment is the operative indication. And in this case, this lesion was curetted arthroscopically. You can see that after the fibrous tissue was removed, there's some bleeding bone, a small amount of drilling was done, but if that bone is completely sclerotic, I think that's the indication to open that. And Mark had wanted to talk a little bit philosophy about the more severe, basically sclerotic lesion. So he'll discuss a little more of that open technique. And this is arthroscopy, the principles are the same. Make sure there's appropriate viable bleeding underneath. And if that's not, then you curetted it out and add bone graft. This is an addition of, you can see compression screws. If you add these arthroscopically, I think it's helpful to have screw capture systems that make sure they maintain your screw and you can secure that arthroscopically. And I like these, some of these devices will have depths where you can see that you like to recess that two to three millimeters. This is a video showing a screw that is contained and captured when placed in a video on the right. And again, putting that a few millimeters beneath the articular surface. I like three millimeters below. And this is the screws in place. And then at the time of removal, you can see the images there. Again, you like to stay perpendicular with removal of these. Again, for trapdoor lesions with sclerotic bone, like open treatment and Mark will touch base on that. If it's an, this is an example of an unstable trapdoor and getting that fibrous tissues from underneath of the progeny fragment and getting it from the parent area below and make sure that there's viable bleeding bone on both sides. If you do have a locked door, it's just slightly mobile. There's a number of different treatment methods for that. If there's a break in the cartilage, a Osteocondyl autograft has been described. And the philosophy there is it creates a vascular access channel, it creates a biologic bridge of cartilage and bone. And that's again for fixation of these trapdoor lesions. Again, if there's a trace subchondral bone, flathead screws, if there's sufficient subchondral bone, then these are variable pitch screws can be helpful. Another method, if there's trace subchondral bone, instead of like a potted plant, it's like a manhole cover and there's just a small amount of bone on the base have described this suture bridge fixation for those. And again, just a simple example, this is done arthroscopically, but it can be done open if these lesions are not easily addressed based on their angle and position. And this is just an example of that open. And you can see there's a variety of different sutures and a variety of different anchors that are commercially available. And so we've addressed the shadow and the cue ball and the locked and trapped door and Mark will be addressing the crater lesions as found. And just like Min stated, I'd like to highlight that we like to address the principles of alignment and make sure we're addressing nutrition for these patients of ligaments and menisci and all other structures. Curls and pitfalls, we like to do the last procedure first. Do not perform procedure with low success rates because they're less invasive and avoid building a house on a bad foundation. Fixing OCD, you want to treat the progeny and parent interface like a non-union and remove that fibrous tissue. Like to thank my colleagues who I've consulted with regarding this topic over many years, including this large group. And thank you for your time and happy to answer any questions. Thank you, Dr. Ganley. Thank you for showing us so many great techniques and cases. Okay, let's move on to our final speaker, Dr. Tompkins, who will give us some more information on treatment and failed fixation cases. Dr. Tompkins, please go ahead. All right, thank you very much, Ryoichiro. I'm grateful to be part of this esteemed panel. I'm not sure how I managed to be on here, but I'm grateful to you and Brett, as well as the AJSM, AOSSM and PRISM staff for all the work that went into this in the background. So we've heard three great presentations. I'm hoping that this will kind of build on those presentations. My task is to talk to you about failed fixation cases or for salvage, as Ted noted. That includes the arthroscopic classification of a crater, but I'm gonna kind of expand on that. So you saw my disclosures at the beginning, but I don't have any disclosures relevant to this presentation. Here's what I wanna talk about. We'll start with a little bit of a case. I wanna just go over the rock definition of OCD again, talk about histology, and then we'll get into treatment options and I'll finish with the same case. So there's an 18-year-old male who pain began one year prior when he jumped into a shallow lake. So he had kind of an impact injury. And after that time, he started describing loose body symptoms. I think this history is pretty important and I'll come back to why. So on exam, as has been nicely highlighted by Justin and Min, the patient had sort of the stereotypical exam, which was tenderness right over that area. I always tell people training with me that if they don't have tenderness over that area, you do have to be a little bit leery, especially if they have tenderness elsewhere, because sometimes OCD is an incidental finding. Actually, not uncommonly, it's an incidental finding. So just quick MRI here. So these are obviously the T1s. You can see on the coronal. So you can see the lesion. There's probably a little bit of bone. Then if we look at it on T2 star bone windows, where we get CT-like imaging, we can see even a little bit more. We can see that there is some bone there, but you can see by all definitions, all the things that Dr. Coker went through, that's not a very healthy lesion. And so in many cases, that's a lesion that would get removed. The fragment would get removed and treated like a failed fixation or something that needs salvage. So while it's not a failed fixation in this case, I'm using this case as an example. So I just want to remind everybody what the ROC definition for OCD is. I want to highlight that in the last few years, we've added the part that I underlined, which is and or its precursor for subchondral bones. So again, both Justin and Min nicely highlighted kind of what we're thinking or historically what we've been thinking. I think we've been very fortunate here at the University of Minnesota with a multidisciplinary team to have some better understanding through pediatric cadaveric tissue and high-level MRI imaging to understand that this has a lot to do with what Min was, at least in, maybe not all, but we think most cases, what Min was describing as the epiphyseal growth plate. So it's right under the articular cartilage. And what happens, just to bring this up, I know it's already kind of been discussed, but I want to highlight this. So what we've seen in pediatric cadaveric tissue is that you get damage to this epiphyseal growth plate, and then the cartilage, you get necrotic cartilage, and that then does not become bone like it's supposed to from the growth plate. And so if that gets big enough, it actually can get into the bone, as you can see here in a manifesto lesion. And then if that's big enough, then you get to an area where the bone can start to become unstable and you'll have a fragment of OCD, articular cartilage, and possibly some bone superficial to that that can become unstable and start to become symptomatic. So here's a case of a 16-year-old that I took care of that had previously had fixation, really well done surgery with bioabsorbable screws. Unfortunately, it did not heal. And we ended up having to remove the fragment that you see on the left there. And then you can see the adjoining histology. We sent it to the lab to be evaluated. And what you see in the bottom left of that histology picture is this area of necrotic tissue. Really what it is, it's sort of the cartilage on logger that never actually became bone. And that's because the cartilage in the epiphyseal growth plate was injured. And again, if that becomes sizable enough, then the overlying bone and cartilage can become unstable and symptomatic OCD. I'm going to skip for the sake of time so we can get to some questions. So what happens though, when you get this crater, when you get a lesion that you think is unstable or excuse me, unsalvageable, or just you have no fragment, what are our options? So I think in the US, at least at this point in time, there are many different cartilage options as you probably all are well aware. But the three main that have the most study relative to OCD are OAT, osteochondroallograft and cartilage regeneration. I'll talk about each one of those briefly and specifically cartilage regeneration with Macy. So I treat these patients a little bit more conservatively than other like drilling or non-op patients. So it's a period of about eight weeks of protected or non-weight bearing, but it does depend on the graft choice. So if it's an OAT or an OCA, the weight bearing can be earlier. I sometimes employ an unloader brace and then we allow gradual low impact activities by three months and a gradual return to all activity by between three and six months, depending upon how they're doing both from a healing standpoint and from a mechanical and neuromuscular standpoint. So with OAT, I think everybody on the call likely knows what this is, but obviously we're harvesting from a minimal weight bearing surface and then implanting into the OCD. The problem with this is this is limitations of donor availability. Usually the OCD lesions are just too big unless you're going to do a significant mosaicplasty, which obviously has some downsides. So typically these are going to be smaller size lesions. So for the bigger lesions, which most OCD lesions reach this threshold, we're thinking about osteochondral allografts if we want a bone and cartilage structure. Obviously with osteochondral allografts, you have to think about disease transmission and cell viability. These are handled very carefully and well to maintain cell viability and the studies suggest that the cells do remain viable for a pretty significant amount of time. But that is some of the downside. I think you all know how the treatment goes, but you drill the defect. I'm going to highlight with the case here in a little bit, but the key thing is you have to, when you're putting in the OAT or the OCA, you have to get all of the crummy tissue out. So that cartilage on logger, and if the lesion has been there long enough, you have significant sclerotic bone. And so as Ted was alluding to, you need to be able to get all of that out. So you have healthy cancellous bone to heal into the OCA. It's a little bit different thought process than just a chondral lesion for OCA because normally we're trying to keep as little amount of allograft bone as possible, but in some cases you have to have a little bit of a deeper OCA for OCD lesions. So the most ideal patients here are the ones that with larger defects, sometimes uncontained lesions as well. And then finally, MACE. So the MACE, just like in, as I was describing with the osteochondral grafts, you have to prepare the lesion by removing all fibrous tissue and sclerotic bone, and then you can get cancellous autograft from nearby. Could be distal femur, could be proximal tibia, or your choice, but then you fill that with, to a level of the adjacent bone. By the way, thank you to Ted for letting me use this. I will admit that I utilize this very infrequently for OCD because I think that there are other options, particularly OCA is the main thing. So these are images from Ted. You can, in order to help facilitate fixation with the matrix, you can put anchors and then seal the bone at the edges in order to avoid any bleeding, getting into the cartilage cells, and then you place the matrix and secure with both suture and fiber and glue if necessary. So similar ideal patients. This has already been mentioned by I think everybody, but don't forget about alignment and it's important to remember that alignment can be managed in multiple different ways. So what happened in the case that I presented before? So in contrast to all the stuff I just highlighted, this patient underwent curatage, proximal tibial cancellous bone grafting, and then open induction internal fixation with headless screws. So here's what I wanted to highlight when I was saying before about cleaning out this stuff. So this is an 18 year old, if it's been there long enough, and most of the time we think that this is something where this is developing probably before the age of 10, but presenting later on. And that probably matches with some of the epidemiology that Justin was highlighting. The problem again, though, is you get this area deep to the lesion where you have fibrous tissue and deep to that you have sclerotic bone. And you got to get that out is the, I think the take home message that I would like to pass along. If you do, and then if you fill that with good, healthy graft that can help bridge the gap as well as keep your fragment congruent with the surrounding cartilage. We've been following our patients, unfortunately not yet published, but we're working on gathering the data. So far, a very high healing rate. So you can see at the bottom there, the fixation of the fragment that effectively was a loose fragment. Here's an intra photo. Here's what it looks like at three months. I think it's important to note that this will heal, but it can take some time. It can be adequately healed by three to four months. But if you have the opportunity to scan it again, it's even more healing takes place over time. So you can see how that's nicely integrated at a year and a half. I think again, another take home message I want to pass along. This is a study that we published a few years ago, noting that the cartilage on the OCD fragments is most of the time, maybe if not all of the time, normal. Again, we think the problem is probably subchondral, whether it's bone or whether it's the epiphyse growth cartilage. Again, it's probably a combination of those things, starting with the epiphyseal growth cartilage in most patients. But the articular cartilage is normal and there's nothing better than we have than putting our own articular cartilage back in. And so I'm really aggressive with trying to salvage fragments that have been floating around in the knee for a while, because even in those cases, most of the time the cartilage is healthy. The tissue behind the cartilage is not so healthy. So you got to really clear that out. I employ a number of things, including kind of drilling all of that to allow for bone in growth channels. But the vast majority of the time it can heal. And so I think to the degree that you can, try to save the fragments. And it's not so much failed fixation, it's failed biology. So we need to make sure that we are thinking about biology and then also the stability of the fragment until it heals. And then once it heals, should be good to go. Thank you very much. Thank you, Dr. Tompkins, for the wonderful talk, again, with very impressive cases. And that was very informative. Okay, I thank the panelists for their wonderful presentations. And I do know that we're pretty much running out of time, but I've been told that we're allowed to run over a bit more than an hour. So I'd like to take a couple of time to answer the questions and discuss a little bit more. So to start the Q&A session, I just want to give a quick case presentation. Christine, can you share my slide? All right, just a quick case presentation to stimulate the discussion. Okay, so this 13-year-old boy came to me for the right knee pain lasting for like three months. Something wrong went on. So can you go back to the first slide? Oh, okay. So he had been playing basketball for three years, but he didn't have any event of trauma as far as he could remember. And he felt pain on running and squatting, and he had a fusion but had no catching or corrective pain with motion. We performed MRI and CT as well and found an osteochondral defect in the lateral facet of femoral trachea. And first, I thought I don't see any free body originating from this defect. Can you move on to the next slide? But by further investigation on the one before, yes, that's it. There was a suspected free body just behind the tibia. In the hiatus, which was actually arthroscopically confirmed and retrieved. And so the next slide. Since there was a thin layer of subchondral bone attached to the free body, we performed an open reduction and fixation for this free body using bioabsorbable pins. And the postoperative course was uneventful until one year after the surgery, and he was able to return to basketball. Actually, I'm starting jogging by like three months after the surgery. But after one year and two months, he had recurrent pain and swelling, and he returned to my office. So I sent him for an MRI again and confirmed the chondral defect at the fixed OCD site. And so for this case, at this point, he's 14 years old. His face is not still closed. And I would ask the panelists, what will be your next treatment option? Any thoughts? I think, Dr. Akagi, these lesions, you know, patellofemoral lesions in jumpers or in children are not uncommon. And so this is because jumping has a high patellofemoral force. Many of these lateral trochlear lesions are very shallow. So they're mostly cartilage and not a lot of bone. And I think that's what you saw in this piece. I agree strongly that you need to fix the lesion, even if it looks like it's only cartilage. It often has some, you know, subchondral bone or a zone of provisional calcification or something on it. And there have been a number of papers showing that, you know, gross chondral-only lesions can actually heal in children because they often have some calcified cartilage layer. You know, I think now you're dealing with, you've already fixed this, and now you have a chondral defect in the lateral formal condyle. So I think you have to do some sort of cartilage resurfacing procedure. You know, that could be MACI, that could be allograft, that could be, you know, a particulated cartilage. I think you also have to think about the patellofemoral alignment because this kneecap is a little bit tilted and maybe overloading that area. So those are some, just some of my thoughts. Okay. Any other thoughts? Yeah, I would add to what Min said. So going back to the first surgery, I may have missed whether you talked about graft, but I think I emphasized in my talk that grafting for something like this is super important. And the base of the lesion, getting all of that stuff out is really important and can make a big difference. The other thing I would add is that I have definitely favored metal implants over time. And partly because I think that especially if we're pretty aggressive with getting all of the tissues out and we put some cancellous graft in there, I used to think that we could use the headless compression screws and get compression. I'm not so sure about that now. I think of it more as anchors. And so I make the screws a little bit longer because I think they're really there just to hold it in place while biology runs its course. So that would be some thoughts I would say to throw out in terms of the management of that. Obviously, that does leave metal in there. So I usually take those out, which means a second surgery, not so ideal. But I think it's a much more stable construct than an absorbable construct when I'm thinking about it being an anchor as opposed to a compression. And then I totally agree with Min in terms of everything he said about management now. But I favor osteochondral allograft in these. Great, thanks. All right, so let's move on to the next slide. So in Japan, we don't have real access to allograft. So what I did was I did an autologous chondrocyte implantation here. I triaged all the remaining cartilage, and it was this big. So I implanted the cartilage tissue. And can you click on it? So what I see here, this is actually three years post-operative MRI. And he's now 18 years old, doing completely fine with a smooth surface and good integration of the surrounding normal cartilage. And he's playing basketball twice a week. So his revision surgery, I'd say, went pretty good. But I agree. Maybe for the first line surgery, I should have made more stable fixation with maybe metal graft and metal implants. And applied grafting was another option. OK, so having these kind of cases. Actually, this boy was 13 years old when he came to my office. But do you ever change the treatment strategy if the patient is skeletally immature or more mature? Do you still go for fixation for the skeletally mature patient if this boy was already 20 years old? Well, any thoughts for that? I would say the principles are the same. I think the dialogue that we have with patients tends to change about the potential for success or the potential for something to be fixable. I tend to say everything that's fixable gets fixed. Everything that's not fixable gets removed. Regarding the original lesion that you had when they're traced subchondral bone, I completely agree with everything that Mark and Min said. And that's been a case where for acute fractures, we used this basically suture bridge fixation. And Henry Ellis and Phil Wilson kind of adopted that and published for OCD lesions. And the principle there is that that creates a large footprint for fixation. And then there's a second surgery four, five, six months after where the sutures are removed that gives an opportunity to go back and potentially add more drilling or anything else. And if it's not fixable and if it didn't heal, it can be removed. So that's an incidence where suture bridge fixation can be used. There was a question to the group, when do you use Macy versus Allograft? And I would say if there's a need for an immediate fill, I had a special needs patient that had a meniscus was dropping into a defect. And so I used OsteochondroAllograft because I felt that immediate fill was in particular helpful for that patient. But Macy certainly has been used for amyocondylesions and telatricular lesions with success. And great, thank you. Justin, do you have anything else to add? No, I don't. I was just thinking that I do like the suture fixation like Ted was talking about. I don't know what your thoughts are. If everyone is removing those sutures, do you think that's necessary? I feel like I've heard people leaving them. With trochleoplasties, people leave some of these sutures. Do you think that's an issue with walking on this? Obviously, that's different than the trochlea and amyofemocondyle or something. Yeah, I don't think we have a definitive answer for that quite yet. I wouldn't necessarily fault people if they're not. And I wouldn't fault people for using. Some people have doubled up on micro sutures for OCD lesions and saying they're adding some integrity there, but they're not going back for second looks or removing them. I think it's not an answered question like that. Right, that's great. All right, so I've prepared a couple of more questions, but I think we do want to answer some from the audience. There's a question unanswered. Does anyone use hyperbaric chambers as adjuvant therapy? I don't have any experience myself, but any of you? Same for me, I have no experience with that. Not for pediatric patients. No, no experience. I think there's no real data to support that. I don't think it's going to be harmful. And I think that sort of adjuvant things that we can do is actually an interesting question. The patients often ask that. And instead of dismissing them all outright, I think we should be kind of thinking about these things because they're interesting. You know, calcium, vitamin D, I think we really should be supporting that in these patients. I think bone stimulators, maybe that has a role in OCD. We just don't have data one way or the other. Hyperbaric oxygen, PRP or stem cell injections. So I think those things are all out there and we need better data. I think it's a great area to honestly study. Great, totally agree. Okay, so with that, I think it's time we have to wrap it up. Again, I appreciate all the panelists for the fantastic talks and for answering all the questions and thank you all for participating. This webinar will be available for viewing afterwards, so please review it again if you have anything you want to check out. Christine, do you have any additional messages to wrap up? I do, thank you. Yes, I'd like to give a big thanks to our panelists and presenters for their works on tonight's webinar and thank you attendees for your participation. On behalf of AOSSM and PRISM, we hope you enjoyed this webinar. If you're interested in CME or would like to view the recording of this webinar, please go to education.sportsmed.org, log in, click my resources, and then click the course title. You can then complete the evaluation for CME or view the recording, which will be available by Friday. We thank you again for your participation and have a great rest of your night.

knee pain

osteochondral defect

surgery

bioabsorbable pins

chondral defect

revision surgery

autologous chondrocyte implantation

MRI integration of cartilage

treatment decisions

adjuvant therapies