Thanks panel, appreciate it. We're gonna invite up our next moderators with is Dr. Cassandra Lee and Clayton Newell to give us our meniscus session. Alrighty, good morning and welcome to our session on meniscus and cartilage. First up, we're gonna go a little bit out of order. So we're gonna start with Rachel Frank talking about cartilage algorithms. Thank you very much. I'd like to thank the program chairs for having me and our moderators for moderating this session. We're starting with cartilage because it doesn't matter if the meniscus is working if there is no cartilage. So it's clearly king or queen, however you wanna call it. I do have some disclosures, none of which are directly relevant to the content of this discussion. So we know cartilage pathology is common in the knee joint. In fact, when you scope the knee, two thirds of patients that you scope for any reason whatsoever will have a cartilage defect. The big question we have to ask ourselves is do all cartilage defects need treatment? And when we think about that, we have to think about what do our patients really wanna know? And what they wanna know are these four things. If I have surgery, how long does it last? If I have surgery, can I get back to doing what I love? If I do nothing, is that okay? Can I live with my cartilage lesion or my meniscus tear? And can I simply live with my current symptoms? And can you promise me, doctor, that nothing will get worse if I go ski this weekend? That's what they wanna know. And the key is to manage their expectations because even though we have a lot of tools in our cartilage toolbox, not all of them can get the patients back to what they want to do. When we think about cartilage restoration, we have to consider these critical things for joint preservation as a whole. We have to think about the patient's alignment, their ligament status, and we just had a great session on ligament status, the cartilage, of course, and the underlying subchondral bone, as well as the meniscus status. And we're gonna hear a bunch of great talks on meniscus and meniscus repair techniques coming up. And the last thing we have to think about is biology because with all of this, we can fix all of the mechanical problems, but we need a safe and sound biologic environment for any of these individual procedures to succeed. When we think about our cartilage restoration algorithm, there's a lot of tools in our toolbox. We range from simple cleanup scopes all the way to reconstructive scopes, reconstructive procedures. What are the important factors and how do you decide? Well, these are the things I think about when I think about what to do with my patients with a cartilage defect. I think about the defect size, location, and containment, the depth and involvement of the underlying subchondral bone, their alignment, meniscus status, and stability, as we just mentioned in the previous slide. Have they had prior treatment and has that prior treatment made any future treatment possible or impossible? What are their goals and expectations? Are they in season, out of season? Are they in a contract year for my professional athletes? And then what about the cost, the safety, and the availability of the implants and grafts? And in 2022, this is incredibly important. I can only do certain cartilage procedures in certain facilities in my practice where I can do other cartilage procedures in other facilities simply due to cost. And so that's a major consideration and will only continue to be a bigger consideration. Don't forget about the staging scope. If you see a juicy cartilage lesion on MRI, it does not mean you can order a cartilage graft and just take them for surgery. You've got to consider the staging scope. I've actually started to do this more frequently now in the office, and you can see here in one of the patients that I've done this on with needle-based arthroscopy systems. And you can do this very easily under local. This now, at the beginning, took a while, but now it takes about five to 10 minutes after a good setup with a team that knows what they're doing. And here on the screen in just a second, you're going to see a picture of a picture. So you're watching a video now of my video, and I would argue that this is a pretty good, high-definition view of that cartilage lesion. In this case, I was able to scope the whole knee, confirm the tibial cartilage status and meniscus were intact and say, okay, I'm going to take this patient for a fresh osteochondral allograft. I ordered it that day, and we were in the OR in three weeks. And so you can do this in the office setting with the right procedure. You can also do this in the operating room if the patient is not necessarily a good candidate for an in-office-based arthroscopy procedure. And so here, a similar patient, similar defect, but she just did not want to do this. She did not want to be aware of what was going on. So a little max sedation, no general, and local. And again, as long as you numb up the capsule, you can actually probe everything you want to in the joint and even do a complete synovectomy completely under local, as long as you have enough local and the patient is cooperative and understands what's happening. So don't forget about the staging scope. When we get into the actual treatment for the cartilage, I'm going to run through all of the different options in the next two minutes. So we have palliative options where that's our simple scope. This is my workhorse for in-season athletes, particularly those with mechanical symptoms or loose bodies. This also allows me to stage the lesion for future cartilage restoration. There's a lot of data around, not much of which is published. We're working on a current paper right now. Approximately 40% of patients who undergo this so-called cleanup scope do not require a second cartilage procedure. So just because we can, doesn't mean we should. And sometimes simple is enough. When simple is not enough, we can think about more reparative procedures, such as marrow stimulation or microfracture, and certainly augmented microfracture with biologics. The challenge with microfracture is it's not very durable. Yeah, it's safe, it's easy, it's cheap, it's single stage, but durability is of a concern. And so adding a biologic may be the solution to help improve the durability of microfracture. We think about restorative options, including MACI, or formerly known as ACI. And this has advantages and disadvantages, but namely it's a two-stage operation. But most cartilage procedures, at least in my practice, are a two-stage operation because I'm very frequently doing a staging scope. MACI's great for those irregularly shaped, full-thickness cartilage defects, big cartilage defects, and occasionally bipolar cartilage defects. Other restorative options include minced cartilage products that come off the shelf. These are challenging due to cost and minimal outcomes, but the outcomes that are there are pretty favorable. So it's another tool in our toolbox. Finally, two reconstructive options, including OATs, or autograft osteoarticular transfer. And this is where we take a piece of bone and cartilage from an area of the knee that we don't need it and we place it into the area of the knee that we do need it. This is limited by defect size, so certainly you can only take so much before you cause donor site morbidity, but does have the best outcomes with respect to return to play in high-level athletes. My workhorse is fresh osteochondral allograft transplantation that's reflective of the type of patients that I see, often revision patients, failed prior cartilage restoration, those with malalignment, and those with bipolar defects. And so for me, fresh osteochondral allograft transplantation is really my workhorse for cartilage. It's a precious gift. We have to acknowledge and thank the donors and their families for making the sacrifice to help other patients. And it's an osteochondral solution that treats an osteochondral problem. You can shape this defect to do whatever you need to do for that patient. The outcomes are terrific. We and many other groups have published on this with excellent survivability at five years or longer following fresh osteochondral allograft transplantation. So to sum it all up, this is my algorithm, debridement for in-season athletes and those with mechanical symptoms, and usually that's enough. Marrow stimulation has a limited role, typically only as part of randomized controlled trials where this is the control arm, because there certainly are better options with more durable solutions out there. OATs autograft for those small full thickness defects in high level athletes, cell-based techniques, more so patellofemoral. Although in my practice, I would say 80 to 90% of my cartilage restoration falls on that last category, which is osteochondral allograft transplantation. Thank you all very much. Thank you. Thanks. Thank you, Rachel. Our next speaker is Seth Sherman from Stanford, who's gonna be talking to us about ramp it up, treat unstable ramp lesion. I think Rachel has an osteochondral allograft and she just sprinted out the door. It's pretty good. So I appreciate the opportunity to be here talking about the unstable ramp lesion. Oh. I'll use the PC one. My disclosures are online. When you have this patient with a 3B Lachman, you must think that this is way more than an ACL tear. Similarly, when you have these patients with explosive pivot shifts, we have to think more broadly. This also is way more than an ACL tear. And one of the things that we can think about in our toolbox, and we've heard other things like slope changing osteotomy, is about these medial ramp lesions. So basically these are meniscal capsular tears of the posterior horn on the medial side, as you see there. And they've been out of sight and out of mind for quite some time. They were coined by Strobel over 40 years ago. They were talked about by Gilquist and others and repaired open posteriorly back in the day before I was born. And they've been called the hidden lesion in the knee. And really Bertrand Sonnery-Cate and others have brought this back to the forefront of our attention in their large series. He found in 300 ACLs, 50 ramp lesions. 17% of them were quote unquote hidden until probing. And MRI sensitivity is only about 77%. So we need to understand why. You can see here in flexion, where we don't take MRIs, there's gapping back there. But in extension, those limbs are opposed and they can sometimes be difficult to see and detect. And when we probe from inside the joint from the front, we also may not see these tears. We have to look posterior medially, as I'll show you in a moment. But we can have a higher index of suspicion on our MRIs, looking for this posterior medial tibia edema pattern. So I think this is a critical game changer for me, raising my awareness. We can also look and see this meniscus capsular separation. We can do things like the modified Gilquist. This is our Get Goods video, which is beautiful, showing us a nice chronic ramp lesion. And you can take it through a range of motion arc and you can see the opposition in extension and the gapping in flexion. And then this also is another video from our friend Aaron Critch. And you can see, just putting a spinal needle posterior medial, you can probe and then decide whether you may or may not want to fix that. And so they're not so hidden. The incidence is varied from 9%, 16%, depending on which series and when. We know now there are risk factors for ramps, including male sex, young age, this posterior medial tibia edema pattern on MRI, concomitant lateral meniscus tears, complete tears, and injury chronicity. And interestingly, contact injuries and revision ACLs were not associated specifically with the presence of ramp lesions in that paper. So why is this important? Why are we talking about it? Because in the ACL-deficient knee, these ramp lesions increased our anterior tibial translation, internal rotation, and the pivot shift. And if you just do the ACL and leave these alone, the pivot shift is not restored to your native state. And so these are cases where you may need to do more than just the ACL. As always, Rob LaPod and team, Jorge is here as well, have done some beautiful work elucidating the anatomy posterior medial. I think what we can take from that is knowing that there's menisco-tibial and menisco-capsular ligaments, and that they share a common attachment on the posterior aspect of that medial meniscus. And we can see that histologically as well. And so this gives us an opportunity to understand how and where we might fix this. This is also a recent article from our friends at Wash U. Looking at all inside repairs, either sutured devices from anterior medial or curved suture passers from posterior medial, and those have really become the standard of care for treatment in 2022. So here we're looking from the back. We've established a posterior portal. You can see debriding and shaving the ramp. So the capsule is to the left, and the posterior aspect of the meniscus is to the right. Those who do shoulder surgery know about these suture-type lassos, and you can tie knots, you can use non-absorbable sutures or tapes, and you can get a very nice repair construct by putting in as many sutures as you need to get the job done. This is Al's work showing that you can also do this looking from the front and the back using these other all-inside devices. And so he's putting in vertical mattress-type sutures. The first one passed through the capsule. The second one passed through the meniscus and then the capsule. And again, with this technique, visualizing posterior medial, visualizing from inside the joint, he can do a similar job and get this excellent apposition as you see here. Outcomes when you repair these in large series are quite excellent, as you see in this series, and the failure rates are low. And so I think I'm gonna leave you with this case, which I think is interesting, as I approach when and how and why I might do ramps. So here's a 19-year-old. It's an acute ACL tear. It's a contact injury. We have all the indexes of suspicion that we talked about before, that posterior medial edema pattern, meniscal capsular separation. We go to the operating room, and you look at this tear from the front, and we can't really detect it, but we know we have to look through the notch towards the back. And in fact, even at this early time point, this is healed, and this is not one that we would need to fix. This is not an explosive pivot shift. This is a standard ACL, and I would leave that alone. And so in conclusion, look for more than the ACL in patients with the explosive pivot shift, because the ACL alone will not restore your normal knee kinematics, have a high index of suspicion for the ramp lesions based on MRI confirmed at arthroscopy, and all inside repair of whichever flavor is the current standard of care with excellent reported outcomes in our recent literature. Thank you very much for your attention, and this certainly is a moving space and continues to evolve. Thank you. Thanks, Seth. Next, we have Karen Sutton talking about meniscus root repairs. Thank you. Just to go over medial meniscus root repairs, which are getting a lot of attention these days, really trying to save the joint, and hopefully they don't have to go to Rachel and have cartilage procedures. So if we can help them along and prevent arthritis down the road, this is potentially the way to do it. Meniscus root tear is just an overview. They're becoming more recognized as a cause for pain and early onset of knee osteoarthritis, occur in the setting of multiligamentous knee injury or trauma resulting from hyperflexion or squatting. Risk factors include female sex, increased age, higher BMI, greater varus mechanical access, and low sports activity level. Really what we're gonna be talking about today is more of the female sex, increased age, higher BMI patient, as opposed to the trauma patient. The diagnosis is challenging due to low likelihood of common signs and symptoms will manifest with patients. In root tears, it can be very thought of as having just a meniscus, a generic meniscus tear, but patients usually describe a little bit more mechanical symptoms. Not typically associated with a traumatic event, usually minor events like squatting, inability to recall any event. And then again, they can occur in multiligamentous knee injuries or from trauma. The physical exam is usually post-tear knee pain with deflection, joint line tenderness, positive McMurray's, basically the same that we would have for a typical meniscus tear. Overview, there's variable detection in sagittal views. Post-tear medial meniscus root is easily viewed in two consecutive coronal MRI images. Oftentimes you just see a space there where the meniscus root should be and the meniscus is floating on the MRI. Typically the meniscus root is seen as a band of fibrocartilage anchoring the post-tear horn to the tibial plateau. T2 weighted and axial sequences are best for visualizing tears. The presence of meniscus extrusion has a high correlation with presence of a root tear. But again, we see that frequently also in patients with osteoarthritis. Operative versus conservative decision. I think the pendulum now is switching to more operative decision making. At least have that in your armamentarium. Don't just blow these patients off and say, okay, you have a little bit of arthritis, a little bit of a meniscus tear, let's just do steroid viscose supplementation. But just put a little bit more thought into it and consider operative treatment for these patients. Meniscus repair versus meniscectomy versus non-operative treatment. The non-operative patient is the patient who's not a good surgical candidate. Comorbidities, advanced arthritis, elderly patients. Most of these patients, a meniscectomy has historically been performed, but the results are more poor compared to a meniscus root. Usually less stringent post-operative rehabilitation protocol, faster return to activities. These patients do require a lot more information on their consent because they'll be talking to other patients who have had a meniscus surgery or a meniscectomy. However, these patients are obviously gonna be braced and have crutches and you don't wanna have them be surprised at the end. Meniscus repairs and acute traumatic root tears in patients with osteoarthritis. Chronic symptom root tears in young middle-aged patients without significant pre-existing arthritis and usually occurs with a complex tear of the MCL. Recent literature demonstrates more improvement and less osteoarthritis progression for patients with meniscus repair versus meniscectomy. This was an interesting study looking at a 10-year outlook for osteoarthritis and total knee replacements. So looking at all meniscus root repair over 10 years and the rate of getting a knee replacement. Meniscus root repair, there was a 53% rate of osteoarthritis at 10 years and a 33.5% rate of total knee replacement. Meniscectomy, not so hot there, 99.3% rate of osteoarthritis, 51.5% rate of total knee replacement and then not operative treatment about the same going into osteoarthritis, 95.1%, 45.5% for total knee. Case report, this is the typical patient. They may even be a little bit older than this but 47-year-old female that I saw in my office with right knee pain, BMI of 25, reported a POP, inability to weight bear and continued medial sided pain. The POP really puts me over to, it wasn't an ACL mechanism so I thought it potentially is more than just a degenerative meniscus tear. Typical physical exam and then the imaging, you saw the x-rays and then here on the case report just looking at the MRI showing where there is just that space where that meniscus root should be. So you can see that on the sagittal pictures there. And then meniscus root repair, what we look at is going through arthroscopically examining the joint. So first we do see that patient did have some arthritis. That meniscus root is lifted off. It's nice to perform some sort of release of the MCL when you go in there. This was just the lateral side to compare. But you can see that meniscus root is just floating in between the tibial plateau and the femoral condyle. What you want to do is capture that meniscus root. You're also using that device as a guide to put your hardware up there and to be able to bring the sutures down through the tibia. And then those sutures are captured in place with usually using a lateral row of the shoulder anchor. So a type of lateral row anchor usually captures the suture down on the tibia. In general, surgical treatment, meniscus medial root repair, chondroplasty, plaque and limited debridement. So this patient underwent medial meniscus root repair. They do very well. The pain afterwards is pretty minimal. So you actually have to hold these patients back frequently. PT, I do talk to them about a potential gel injection three months, post-op brace, unlock zero to 60. Takeaways, medial meniscus root repair should be favored over meniscectomy for patients with no or mild arthritis. I think the pendulum is shifting to even a little bit more arthritis here. And surgery should be a go-to rather than pursuing non-operative rehabilitation. References. Thank you very much. Thank you, Karen. Next up is Kevin Bonner. Kevin's gonna keep us rolling along and talk to us about more in depth on fresh osteochondral allografts, subchondral bone is key. I'd first like to congratulate the program chairs for a great program and thank you for the invitation. So I'm gonna talk about fresh osteochondral allografts and why that has become my workhorse as well. My, it's not. Should I use the PC instead? There we go. My disclosures, the only thing could be deemed as a disclosure is I'm on the board now for LifeNet, although I've been doing these for over 23 years. So basically, as we know, there's various different options for chondral defects, there's no validated algorithm. And really, it determines, I think, like many other things, what cartilage religion where you're raised tends to be what you do at least in your first five years of practice. And I would just tell you that as time goes on, you should have an open mind. So if you look at trends in cartilage surgery, what is actually trending up the most is fresh osteochondral allografts. Then if we look at, okay, you know, how are we gonna approach these defects? So we have to understand that subchondral marrow edema occurs in 55 to 83% of chondral defects. And really, the question is how much of the pain is coming from the defect versus the bone? And so basically, when you address a lesion with an osteochondral graft, you don't have to worry about the bone. And there are definitely studies showing that with surface treatments, there's controversy whether or not the subchondral bone edema will affect your outcomes. So I will say that these are one of the more satisfying things we do. And really, other than autologous chondral transfers, or sometimes what we call OATs, it's the only way to restore a defect with normal articular cartilage architecture. And you have to think about it as an osteochondral unit. And the bone serves as the fixation component here. However, it also can address pathologic or painful subchondral bone as well. So high and unlike, I would tell you, is just really not the real deal. And I want to apologize to Macy in advance in that I still do Macy. I did one last week in a 13-year-old girl who was undergoing her fourth cartilage procedure for patella. So I do think there is a role. But I will say by far, by far, if I have the opportunity to do a fresh osteochondral graft, that has become my preference. And again, if you look at cartilage biopsies later on, I honestly drank the Kool-Aid 24 years ago. I was involved in the STAR study. And I will tell you that high and unlike is not high and unlike. And with a fresh osteochondral graft, the good news is it is not high and unlike. It is high and unlike cartilage, and it's viable high and unlike cartilage. So osteochondral grafts, whether it be allografts or autografts, are really the most predictable cartilage procedures that we do. And if you look at some of the data quickly, again, I credit Bill Bugbee with a lot of this. 93% survivorship at 10 years, 95% satisfaction. If you look at comparative studies in athletes, autografts are good, but those are smaller lesions. And if you look at ACI versus osteochondral grafts, better results in terms of return to play and bias towards much larger lesions with fresh osteochondral grafts. Again, here, same thing, looking at the results out of RUSH with Brian Cole, as well as more data from Bill Bugbee. Excellent results at 10 years, 93% plus in general. Here's another one, over 2,500 athletes, yes, autograft oats was good. But allografts actually had a great survivorship and return to play. So you can do these in athletes. And again, better than ACI despite the bias towards allografts being used for larger defects. And so Bill Bugbee is about to publish on this. If you look at ideal candidates, 93% satisfaction at 12 years. Now surface treatments have evolved. This is way back when, when we used to do ACIs and the misery of harvesting the periosteum, and we went through that. MACI, clearly a big improvement. However, if you look at some of these very well-done studies, there's really here no difference, again, between ACI and MACI. The results, 51% at 10 years. You can look at this, and everybody can critique these studies, but look at the failures. No difference between the two significantly, but ACI failures, 42%, microfracture, 32%. Look at this, again, well done, and this was done by Eric McCarty. The failure, treatment failures, no difference between ACI and microfracture. So the elephant in the room is the cost comparison. I can basically do four osteochondral grafts for every MACI that I do. So very, very expensive study showing it's the least cost effective. And so MACI is a big improvement. There's certainly reasons that I'll do it. However, it's less reliable with a longer recovery than a fresh osteochondral allograft. And so traditionally, osteochondral grafts are used for larger lesions. There's expanding use due to success. It restores hyaline cartilage architecture. It's more predictable, even in athletes. It's more resilient, and why it's trending up. So if you look at all these comparisons, resilient structural grafts, it's more resilient, immediate secure fixation, you have more confidence with an aggressive rehab, you get bone to bone healing, you address the subchondral bone, which can be questionable, you get normal hyaline cartilage, you can make the economic argument, and you get more predictable clinical results. And that's why I choose osteochondral grafts over surface treatments. Thank you. All right. Thanks, Kevin. Next, we'll have Dave Flanagan talking about autologous contraceptive implantation. And here we go. Well, now I get to tell you the truth, right? Thanks, Kevin. All right. Are we ready? Perfect. My disclosures are in the Academy website. Well, I can pretty much stop at this, just one slide here. So why MACI? Well, we have a long history of success, much longer than OCA's. It's a simplified procedure. Any surface of the knee, simplified, simple to complex lesions, an accelerated rehabilitation program, and it is cost effective. That being said, I'm not a one-shot person. I think it's really critical, as we think of any type of cartilage lesion, just like Rachel said earlier, that we need to have an individualized approach. What's the location? What's the concomitant pathology? What's the size of the lesion? What's the demand of patient? Because it's not, again, one treatment fits all type of patients. So let's talk about this history of ACI, now MACI. It's had over three decades of results. First implanted in 1995, the FDA approved this in 1997. Subsequently, first clinical report of MACI was in 2003, with Europe approving it in 2013, and finally in the United States, being approved in 2016. And so if we want to look at evidence, this was from my friend Seth Sherman here, there's a lot of evidence supporting ACI and MACI within the literature. And when you compare that to osteocounterallograft, there is no contest as far as the amount of level one studies, and really all these in high-impact journals. So we have proven results in focal defects of the knee, especially in the femoral condyle. So the summit pivotal trial in Europe showed that the average size was about four and a half square centimeters, and these were, again, of the mule femoral condyle. The two years had a significant difference in responder rates, so an improvement in both pain and function in the CU scores, where you almost had 90% of people with MACI compared to 70% with microfracture. But more importantly is we see a durability of results over time at their five-year study, again, showing that MACI is continually having excellent results at that time. Well, how about these true long-lasting results? So Tom Minus was really one of our early adopters. He has just a plethora of information and data on ACI. So you can see here the 20-year survivorship of 63%, and nearly 80% of these patients retained their native knees. So this is truly a big win when we're thinking about long-term effects of the cartilage defects on these patients. Well, how about MACI? Again, this is mostly coming from our Australian counterparts, where they adopted this much earlier than here in the United States. We can see that all patient-reported outcomes improved, and there was no significant difference in decline at two to 10 years, with majority of patients able to get back towards sports, and the majority of these patients satisfied with their procedure. So what are the indications when we're looking at ACI or MACI today? Well, have they failed non-operative treatment? I think this is something that Rachel said really well in her earlier talk. Typically, even just a debridement, some people can improve. But now these are people who are truly symptomatic and continue to give you trouble. No significant osteoarthritis. It could be focal or multifocal chondral defects. The size is typically over two square centimeters, and this is not limited by age, like was just quoted with OCAs. The U.S. experience has shown, again, these are typically large lesions over four square centimeters, and these are often of the patella area and solitary defects. What's great now is the very simplified technique. So these cookie cutters allow us to have a fast and reproducible technique. This is actually faster for me than an osteochondrolograft. You can have accurate borders in cutting the scaffolds. This allows a precise defect in scaffold matching. It can be used any area of the knee. So ACI has shown to have similar effects in success in the patella-femoral joint as with the femoral condyle. That being said, there's really important, especially in the patella-femoral joint, that you consider an osteotomy, especially depending on where the lesion is located. But we can have high success even in high-demand patients like the military. Well, how about complex and bipolar lesions? So these are really, I would say, the ugly parts of the cartilage restorative procedures. And you can see for bipolar lesions, the tibial-femoral joint or the patella-femoral joint, we have excellent success based on Tom Minus' studies here at 80 percent at five years, with very little fall-off at that 10 year. Majority of these patients had improvement of patient-reported outcomes with minimal progression of osteoarthritis and high patient satisfaction. But again, in the patella-femoral joint, you need to consider a combined procedure. The accelerated rehabilitation is really what kind of has pushed this forward over the last couple of decades. And this came from a lot of Jay Ebert's work in Australia. And what has been shown is that you can have an early weight-bearing protocol with faster return to function, no impact on failure rates, with maintenance results over time. The rehabilitation now is quite similar to osteochondroallografts, and the expectations and guidelines for these rehabilitations have been well-delineated in literature. And finally, we can see that return to sport criteria is similar for both ACI and osteochondroallograft, especially with this accelerated program. And even though Kevin said this is not cost-effective, this has been shown in multiple studies across the world to be a very cost-effective treatment, especially because of the longevity of this procedure. So cell-based therapies are on the rise. We talked a lot about MACI, but there's a lot of other options that are coming out. But these just don't have the literature support at the time. That being said, I'm not a purist. I think you always need to entertain other alternatives, especially if there's large bony defects. You can use a sandwich technique, but typically an osteochondroallograft is my choice. If you have a compromised subchondral plate, heavy laborers, failed previous procedure, high BMI, and any inability to comply with rehabilitation. But why MACI? Because I think it's easy. It's expedited procedure, accelerated rehabilitation, successful anywhere in the knee, and years of evidence. Thank you. Thanks, Dave. Next, Catherine Logan is going to talk to us about biologic solutions for the degenerative knee. Can we believe the hype? Where are they? Okay. And then where's the advance? Here's the piece. The MAC. I have a MAC. Okay. We're just figuring out PC versus MAC. Okay. Good morning. Thank you, program chairs, for putting together a great program. So these are my disclosures. So I'm going to talk to you a little bit about this population in general, the problem, as well as some therapies that are available, including those that are most researched to this day. So PRP, BMAC, as well as some cell-based therapies, as well as provide my summary recommendations. So we know biologic-based therapies for cartilage pathology have gained some considerable attention over the last decade or so. We like them because they're minimally invasive. They should be simpler to perform, should have a faster recovery time. But we also know that there is out-of-pocket costs, and that we need some further basic science as well as RCTs to really be definitive on these decisions. So this is a big problem globally, as well as in the U.S. Osteoarthritis of the knee is the leading cause of severe long-term pain, and disability affects approximately 10% of our global population. It's the leading cause of extremity disability in older adults. And with our aging population, as well as obesity on the rise, we know that this burden is going to just continue to grow. So what treatment options do we have for knee osteoarthritis? Certainly we're still going to rely on the old and true methods of strengthening, physical therapy, activity modification. We have some oral medications to offer, as well as some of our other injection therapies like the gel-based or cortisone. But today we're going to be focusing on disease-modifying therapies. So PRP, it's certainly not new. It has documented use in multiple aspects of medicine, not just orthopedics. Several studies have demonstrated that intra-articular PRP can help reduce pain and inflammation with osteoarthritis, as well as maybe influence tissue regulation due to the high level of growth factors in these platelets. So starting off with some indications. So McCarty and his colleagues investigated PRP versus hyaluronic acid for knee osteoarthritis. They included 18 level 1 studies. The mean improvement was significantly higher in PRP group for the Womack scores. And of the 11 studies based on VAS, six reported PRP patients to have significantly less pain. Of note, when we talk about which types of PRP, the leukocyte-poor was significantly better, subjective IKDC relative to the leukocyte-rich. Regarding the advanced osteoarthritis, Navarro and colleagues investigated PRP for advanced osteoarthritis. So we're speaking about grade 3 and grade 4. The authors included prospective double-blind RCTs for PRP versus corticosteroids. There was not really significant changes in both groups. But I think really at the end of this, we're not really considering the PRP as advantageous for those severe osteoarthritis population. So this next study reported that patients with early OA, we wanted to look at how many injections are we giving, what's the injection frequency and sequence. They looked at 162 patients with different stages of osteoarthritis. They're randomly divided into four groups. Those four groups were three intra-articular doses of PRP, one dose of PRP, one dose of hyaluronic acid or saline. The knee scores of the patients treated with the three PRP injections were significantly better than those of the other groups. Early OA also fared better. The clinical results of the study suggest that intra-articular PRP and hyaluronic treatments are all beneficial, but the three PRP injections are probably the most useful clinically. So now as far as synergy, PRP and hyaluronic acid, it's been reported that PRP in combination with HA may have synergistic actions. This is a level three study. It's a meta-analysis of randomized and non-randomized comparative trials. Four studies were included. This was comprised of 377 patients. The patients who received PRP combined with HA had significantly greater improvements compared with those injected with hyaluronic acid alone. In terms of EAS, this was at three months, six months, and 12 months. And additionally, with the 12-month WOMAC for physical functioning, as well as the WOMAC for stiffness. There was no difference, however, in the pain score. So is there a downside? There's no significant difference is found in the adverse effects when we're looking at other therapies relative to PRP. This is a systematic review and a meta-analysis of randomized and quasi-randomized controlled trials, level two evidence. 40 studies were included. Over 3,000 patients were also studied. This analysis focused on comparing PRP with hyaluronic acid, corticosteroid, as well as saline injection. So at six-month follow-up, PRP was effective. And in some studies, it was more effective than the other therapies. The current literature, this, you know, the data is really subject to risk of bias, as well as there is great heterogeneity in these studies. So moving on to BMAC, the indications for BMAC are similar to those described for PRP. It's theorized that the progenitor cells from the bone marrow could help improve the regenerative potential of BMAC, and possibly helpful in more significant cases of osteoarthritis. So why and why not BMAC? Generally when we think about BMAC, the harvest technique is very different than PRP in our clinic. This study was a double-blind randomized controlled trial. It compared the clinical improvements, as well as looked at X-ray up to two years, post just one single intra-articular injection of BMAC versus hyaluronic acid. So the IKDC subjective score is improved from baseline with all follow-ups for BMAC, while it was improved at 12 months, and then decreased at 24 months when we're looking at hyaluronic acid alone. So compared to hyaluronic acid, BMAC had some longer, more consistent results over time. So studies have demonstrated good clinical efficacy of BMAC. This is with single injections, solo injections, as well as with common ten procedures. The early clinical data still suggests BMAC may be helpful to stimulate more robust hyaluronic cartilage repair tissue, but there's less studies out there that are really looking at the long-term clinical efficacy relative for knee osteoarthritis. So finally, I'm just going to touch base briefly on cell-based therapy. Stem cells, they're defined as undifferentiated cells. They're capable of proliferation, regeneration, self-maintenance, as well as replication. So we can see why we have interest in them. Due to the accessibility, the MSCs are the most popular stem cell option for articular cartilage repair. This is a study by Jorge, who's on our panel today. He did a systematic review that was published in JBJS to review the studies of Level Evidence 3 and greater. They examined cell therapies delivered inter-articularly into the knee. There was only six studies included. The authors presented some concerns on cell sourcing, cell characterization, adjuvant therapies, basically a lot of inconsistencies with clinical outcome reportings limiting the comparison. Importantly, I think from the study, the takeaway is that there was no significant adverse events, so a good starting point. Finally, systematic review and meta-analysis was also presented more recently, which included 13 studies. These cell-based therapies did not significantly reduce the WOMAX score at the six-month. However, cell-based therapies significantly improved the COUS at 12 months in the follow-up and also reported reduced pain. So the long-term effect, we're still getting better understanding, but the adipose high dose is probably more worthy of study. So finally, my practice summary. So there's an increasing and obviously widespread use of these biologic treatments for good reason. As I stated earlier, they can be done more easily. They have some cost-associated concerns. My practice is still going to be first-line therapy. It's going to be physical therapy, strengthening, activity modification, and then I'm going to start to talk to them about PRP if they've sort of failed those practices. I use leukocyte-poor. I have the Arthrex Angel system in my clinic. My recommendation is three injections separated by a week apart, and then I also speak to them about the synergistic properties associated with hyaluronic acid. For me, BMAC is not showing superior evidence to PRP for knee osteoarthritis, and due to the differences in how we have to harvest this and the logistical aspects of this procedure, it's not taking over PRP. And then finally, cell-based therapies. I think there's more to learn, more to come. It's not currently part of my practice. Thank you. All right. Thank you. So next, we have Jorge Challa talking about it's not PRP, bone marrow, adipose, and other emergency surgical adjuncts in six minutes. Everything about biologics in six minutes. We're just talking with Michael Ai about this, and giving this talk in six minutes is basically the same as getting a six-pack in five, but we'll give it a shot. Let's pull up the talk, please. So thank you, Catherine. That was a great segue for my talk. I think there will be some repetition, but that's how we learn. So hopefully we can bring the MAC presentation up. If not, we're going to continue. Do we have any questions from the audience while we load the talk so far for the speakers? Jorge and Catherine, how do you guys go about billing or getting some of these biologics paid for? And how do you discuss it with patients? So it's all out of pocket. As Catherine was saying, it's not my first line of treatment ever. I usually try physical therapy, cortisone injections most of the times first. And then we build our way up. Some people, we try a gel injection, for example, first. And then if that doesn't work, then we go to more biological options. Billing is out of pocket. We charge, I think it's 2,100 for the series of three injections for PRP. And I think it's 2,500 or 3,000 for BMAC. But we usually use BMAC only in the OR because we have a patient over there. So we use it for osteocoronal allografts and things like that. But it's a hard conversation with a patient if you present it as a first option. So that's why I wouldn't recommend it as the first line of treatment. All right, I think we're ready. So it's not just about PRP. Let's talk about bone marrow, adipose, and others. And why do we need to talk about biologics? Because most of the times, we have a biological problem that we don't address. We usually treat mechanical or biological problems with mechanical solutions. We have a meniscus tear. We have an osteocoronal defect. We treat it with a mechanical solution. And a lot of those times, a biological problem will have a biological solution that can help. There's multiple sources for cell-based therapies, but we're gonna concentrate on the ones that have the most evidence, which are bone marrow, adipose tissue, and synovium. How about bone marrow? This is one of the few forms to deliver progenitor cells. We should stay away from calling them stem cells. That is approved by FDA, and it's relatively easy to obtain. When I say this, we should take into consideration that the progenitor cells are basically on the trabecula of the bone. So there's multiple studies now showing that if you take it from multiple sides, from one side, it's pretty much the same as long as you break the trabecula. When you put your trocher in, you really wanna break that trabecula to get the most progenitor cells. And what are the differences with PRP? This is the main thing that we hear. If you don't move that trocher, I can tell you that most of the things you're gonna get from the bone marrow, it's actually blood. So if you try to get good bone marrow, this is a very elegant study by Cassano and Fortier. They showed that BMAC has more neutrophils. They have more TGF-beta-2 and VGF, which may be potentially more beneficial for muscle healing. But they have more interleukin-1 receptor antagonists that this may be something that we need to look more in the future because it can block chondrocyte apoptosis and inflammation. We looked at how to prepare this. There's a lot of people that ask, how do you prepare this? And the short answer is nobody knows. There's 46 publications, none of the studies that we've seen reporting on every single item that you needed to have external validity. But also, there was no consensus in the number of spins, in the RPMs, the time for centrifugation and activation. If you see this plot, this is each of those studies. There's no two dots on top of each other, which means nobody knows how to do this. How about the literature? This is one of the most important studies that is out there, although it's not a great number of patients, 25 patients from Shane Shapiro at the Mayo Clinic, bilateral knee OA. They injected BMAC, so $3,000 in one knee, versus saline, probably $0.25 on the other knee. The outcomes were exactly the same. Now, they did a follow-up study looking at imaging, because some people say, okay, you didn't have enough time to see the clinical benefits of this. Let's just do T2 quantitative imaging on this knee, same thing, same thing for BMAC, same thing for saline. 60 patients, HA versus BMAC, this is a newer study, similar clinical results, but the BMAC had more durable results. We did multiple systematic reviews on the hip, on the knee, on the ankle. Basically, what we found was that the best results are for mild to moderate osteoarthritis. Series of injections seems to do better over the course of one or two months. Now, as Catherine was saying, when you compare BMAC to PRP and what to use, there's 21 randomized clinical trials in PRP, we just completed the clinical practice guidance for AOS, and it's pretty impressive that there's 19 studies that basically say that it's better than their counterparts, including placebo, saline, ozone, and corticosteroids, so I would say PRP probably should be the mainstay as of now, based on the literature that we have. How about adipose tissue? There's some benefits to this, it's more easily isolated. The harvest is greater, so 500 to 2,500 times more cells than you get from bone marrow. They have increased proliferative and differentiation capacity, and they have a lower senescence ratio. We have to be very careful with the new FDA guidance as well, with lipids, because we know that they're supposed to be for homologous use, it's hard to say that fat can be used for homologous use in the knee and the shoulder or any other joints, so that's, I think, something that we should be careful about as we move forward. There's multiple ways to prepare this, by washing, mechanical separation, as well as enzymatic. It's kind of difficult to understand when you start getting into the nitty gritty of this, but if you do the mechanical, the washing technique, you get what we call microfragmented adipose tissue, or MFAT, and then if you do centrifugation, you get the SVF or stromal vascular fraction, which also can be separated, again, into a mechanical SVF and somatic SVF, and if you culture this, you get the culture ASCs. There's not a whole lot of studies on this. This is one, 120 knees, with Kenny Lawrence, two to four osteoarthritic progression, single dose of MFAT injection, KUSA two years, showed that they had improved outcomes in comparison to the control group. You can see they also had the best improvement in people that had less osteoarthritis. So again, you're gonna see that this repeats itself over and over for all the biologics. The least amount of damage that you have, the better that you can do. If you have Kenny Lawrence four, bone-on-bone arthritis, probably nothing's gonna help it besides a new replacement. This is another study, first randomized clinical trial, 30 patients, one injections versus two injections versus control, which was basically just continuing with conservative management, 12 months follow-up. They did say that the adipose giraffe stem cells had better pain scores as well as better patient-reported outcomes. This is the first long-term follow-up study, 18 patients, 96 weeks follow-up, and you can see that they said improved pain, function, and cartilage volume, and that was safe. There's some things coming on the horizon that I think will help us understand, which is, one is that there's seven randomized clinical trials underway. There's one multicenter FDA trial that will be published this year, I hope, which will shed some light into this. Take-home points for ADSEs, 2% of lipoaspirates are mesenchymal stem cells or progenitor cells. Multiple injections seem to be better than one. Improved pain, function, quality of life should be expected, and it's relatively safe, but we still need some more data to be able to understand exactly where this stands. How about synovium? This is one of the things that I think we'll be looking more and more in the future. There's some evidence that Johnny Hewitt has done some studies looking at rats that basically were taking all the synovium and injecting marked stem cells, and compared to rats that had a synovium, and the marked stem cells actually were not the ones healing the chondral defect. It was the synovium cells that were going there, but the ones that were marked were acting as a paracrine kind of source of stem cells for those, so I think we're gonna see more and more of this in the future. They have a very high proliferation potential, and when you looked at different differentiation potential into chondrogenic lineage, you can see that synovia and bone marrow stem cells have the greatest chondrogenic potential. This is the study on synovium-derived stem cells encapsulated in PRP gel for osteochondral defects in rabbits, and they basically looked at four, 12 weeks, 24 weeks after injection, and you can see in this picture, it's pretty interesting to see that the PRP with the synovium-derived stem cells have a very, very nice connection between the graft and the donor, and when you look at this at 24 weeks, there's evidence of hyaline cartilage, and as Flanagan was saying, and Boner was saying, having normal cartilage is there, it's much better than having cartilage-like or hyaline-like type of products there. The evidence is very low. Still, there's no human clinical trials, but there's some limitations to synovium, which are that the harvest yield is very low, and the culture expansion is required for this purpose, but there's new publications. This is one from AGSM looking at an agitating device called the stem device that produce increased stem cells and more chondrogenic results after this. Overall, when we think about stem cells, patients ask us, well, doc, is this gonna be able to regenerate my cartilage? Is my cartilage gonna grow back again? I just saw this picture in a magazine where they showed a patient that had bone-on-bone arthritis, got a gel injection, and now has pretty much a normal knee. So these people published this paper in Nature basically looking at symptomatic relief from all these therapies, which seems to be the case, but are we able to improve structure? So they looked specifically at this, and two of the studies said that you can actually grow or improve the cartilage volume. Six of those said that you can actually improve the cartilage quality. However, when you take a deep dive and analyze those studies, the evidence is very low. There's poor study design, there's a very high risk of bias and large heterogeneity. So there's no way, at least as of now, to say that any sort of cell-based therapies can improve cartilage thickness or volume and or the quality of the cartilage. In conclusion, BMAC is promising for cartilage damage and OA. Other post-derived stem cells have a greater yield and may be a promising cell source as we move forward. High-quality adipose randomized clinical trials will be coming soon, and I think we need to look at those to be able to determine how effective they are. And finally, there's limited evidence on synovial stem cells, but they might be promising moving forward. Thank you. And then, thank you, Jorge. Next, finally, Al Gitgut's gonna wrap it up for us and remind us to respect alignment and talk to us about osteotomy and coronal and sagittal plane. Perfect, thanks, Clay. So deformity correction in six minutes. And as we're running a little bit behind time, we'll try and do it in five. All right, these are my disclosures. So if you think about broad indications for realignment, we can think about sort of, we're in a session talking about joint preservation, arthritis, meniscus, cartilage. You know, and that's really the workhorse is gonna be your coronal plane corrections. Instability, more on the sagittal, axial plane corrections, I think somewhat outside of the scope of this talk, so I'm not really gonna focus on that. But why is it so important? Well, it really sits right at the top of any joint preservation surgical algorithm. It's right up there. And while David and Kevin can disagree about their procedure of choice, I'm sure both would agree that if they don't address the alignment, that probably either procedure's not gonna do so well. And why did I say that? Well, it's really the question is, can biological tissue, whether that's allograft, whether it's reparative tissue, can it recapitulate normal physiologic state? And this study, I think, is a really nice example of probably not. This is an allograft meniscus transplant in cadaveric knees, showing that even in a neutrally aligned limb, that it does not restore the normal physiologic state, and maybe even a small correction would be beneficial to restore the normal contact stresses. And of course, we also know this clinically. You know, this is pioneering work from the early series of Al Gross in Toronto looking at osteochondral allograft. The best results in these cases was when the alignment was addressed and reduced the failure rates. So when we're thinking about joint preservation procedures, really the workhorse is the medial opening wedge high tibial osteotomy, and the goal here is to reduce a knee adduction moment in stance phase. And of course, on the valgus knee, we're trying to reduce the abduction moment. And why is that? Well, the abduction moment is a great surrogate for medial compartment pressure and medial compartment load, and that's been directly correlated with articular cartilage loss. Now, if you do an osteotomy, what happens to the articular cartilage? Well, actually, a number of studies have shown that you actually even just get some regeneration just by doing the realignment procedure alone. This is an MRI study, as well as a second look arthroscopy study showing restoration of cartilage surface. Whether or not it's a highline cartilage, highline light cartilage, that's debatable. But Dave Flanagan's done some great systematic reviews here showing that really from point of view of survivorship, does additional cartilage repair actually improve survivorship? And it doesn't really. So if you have an opportunity to realign the limb, it's really giving a significant treatment effect. This is some work from our own group in London, Ontario, and really showing that, you know, if we look at our survivorship of osteotomies, 10-year survivorship, 88% in Kellgren-Lawrence, two or less. So again, we're very aggressive in treating these younger patients with more mild to moderate disease, because I do think you get a much better outcome. Now, that being said, this is a medial opening wedge in fairly advanced disease. This is just an example of a medial opening wedge for a correction of that medial OA. And then in the valgus knee, my procedure of choice would be a medial closing wedge, distal femoral osteotomy, which is a very reproducible technique. We can offload the lateral compartment. And then when thinking, when faced with more of an issue with regards to the articular surface, then we can often combine this with an osteochondral allograft or your other procedure of choice. This is a young patient, so I tend to do this in the same sitting, but it's not uncommon, or we'll do an osteotomy first and then only do the cartilage at a later stage if they remain symptomatic. And it's actually quite remarkable just how few patients really require the cartilage procedure as a secondary procedure. So what's hot in 2022? Okay, you're seeing much, much more talk of osteotomy in many of our meetings. And what are we all talking about? Well, the big thing really at the moment is deformity analysis and planning. So this is more of an example of looking at medial or mechanical axis deviation and then planning, either using a Miniaci or a Dugdale method. What we're really moving more towards is digital planning and 3D analysis and being able to simulate our osteotomies and really looking to see, number one, where the deformity is and correcting where the deformity lies. So it's not uncommon where a varus knee, actually the deformity's on the femur, which really requires a femoral correction rather than a tibial correction. But the other issue, of course, is the issue of joint line and joint line obliquity. And we don't want to create deformity. So this is an example of a guy who's really significant varus and required a double-level osteotomy to try and improve his joint line obliquity. Now, that being said, you can see that I still wasn't able to achieve an absolutely perfect result. And so that's where we're really starting to see the advent of patient-specific instrumentation and implants coming to the fore. And I think if we're in a position where maybe less experienced surgeons doing osteotomy, I think these types of techniques where we have really good planning software, opportunities for implants, or sorry, instrumentation, to help get that ideal correction, I think that's something that we should definitely be looking at. So in summary, joint preservation, always look to do an osteotomy where it's indicated. The realignment improves in mechanical and biological environment. Don't forget about it. There's a significant treatment effect that comes from realignment alone. And look for osteotomy courses to really learn the latest techniques and get into a much more in-depth view. And if you do fancy a trip to Lyon, France, come and join us for this master's course on osteotomy. Thank you very much for your attention. Great, thanks, Al. So we're gonna invite any questions from the audience. In the meantime, I'd like to also invite up Christian Latterman, who will be moderating the next case discussion. Yes, I'd like to ask Irish Alan Gitgood. As a proponent of osteotomies, one question I have, like you weigh in on, is the patella. Because many people think that opening wedge potentiates patella-femoral arthrosis. So when do you not pull the trigger? When do you worry about making their arthritis worse? Yeah, actually the data from our clinic would suggest that patella-femoral arthrosis, particularly low grades, really has no impact on patient-reported outcomes. So I actually tend to ignore it. And when doing a medial opening wedge, it really has limited effect on patella height, unless you're doing corrections greater than 12 millimeters, in which case we do a biplanar osteotomy distal to the tubercle, which will maintain your patella height. I told you he was smart. So I have a question for Kevin and for Dave. What do you do if it fails? You got great results, but what if it fragments, it fails? What do you think then? Well, that's one advantage I think of Macy, because you don't burn bridges. So then if it fails, I move to an osteochondroallograft. I think it's a little bit harder the other way. You can redo an osteochondroallograft. Again, when they fail, they fail at the bone. They typically, their cartilage can wear away, don't get me wrong, but they often will fail at the bone in that first few years when they fail. But I have had to revise them and re-revise them. I know Bill Bugbee and I have talked about it. He's had multiple, multiple cases where he has re-revised and they can do very well. So you can re-revise an osteochondroallograft. Clearly, revising a Macy is easier than revising an osteochondroallograft, but it's not that difficult as long as the lesion itself doesn't expand significantly. All right, Emily. I'd like to query James. I just wanted to add, I think with that, it's kind of like approaching the failed ACL, because I do a fair number of revision allografts as well. And you have to see why did they fail. If they failed due to a mechanical overload, that's an easy fix. You could totally fix that. If they failed due to bad biology, you can maybe try to attempt that. And if they failed just because it was unlucky, perfect surgery, perfect recovery, perfect patient, there are some strategies for revision you can use. In those cases, I always use metal headless compression screws to get more compression. Even if it's a perfect press fit on the revision, I still use the screws. So I think there's a lot of things you can do to address it, but I think the key take-home is making sure you understand why they failed. Because if it's an easy fix, just like if it's a bad tunnel for an ACL, you can easily fix that. All right, I think that we are gonna go straight into some cases. And we are gonna do this a little bit more like a rapid fire thing. We have a couple of minutes to do this. First situation, degenerative meniscus tears. We've heard from Katherine Logan how she approaches degenerative tears or degenerative situations in the knee with OA. Now, question to Kevin. You know, we have PT, intraocular cortisone injections, orthobiologics, scope debridement. How do you approach somebody who comes in with a degenerative tear in the setting of mild OA? I will certainly try to treat them conservatively. I think various things will determine the success of conservative treatment. So I try to, you know, most of them have an MRI, so I'll try to look at the meniscus tear pattern, how bad it is, their articular cartilage, their subchondral bone, just to try to get an assessment of success. But virtually, unless somebody has a locked knee or for some reason has to get into surgery right away for some reason, which is less common, but there are situations where sometimes surgery is better sooner than later. But in most situations, I'll try conservative treatment with, number one, giving it time with physical therapy. Often have them try to see a therapist. Sometimes it's home directed. I'll try anti-inflammatories. I'll very, very commonly do an intra-articular steroid shot for these patients. And that's typically how I'll start. And then I'll see them back in four to six weeks. And I'll tell you probably two thirds, similar to the literature, probably two thirds of them can often do well with non-operative treatment. But it's a spectrum. There are some people who have really bad tears that are locking and catching who cross over and they do get surgery. But I'll start with conservative treatment most of the time unless there's a reason, a good reason not to. Okay, thank you. Very quick question to Jorge. So we've heard all the things that you can do. Hand on your heart. When do you do orthobiologics? Do you do it before cortisone injections, before PT? Do you do it after? How aggressive are you there? Not very aggressive to be quite frank. I usually try physical therapy first. If that fails, I get them to the second level, which is a cortisone injection. If they had good relief from that, but it was not durable, then I would offer the other two options, maybe HA and PRP. And in an attempt to try to make it more durable, but I'm not aggressive at all. All right, thank you. So next topic, root repair. This is a question for Seth. When do you not do a root repair? It's a great question. I'd say, you know, I'm always prepared to do a root in an ACL and it's mostly a lateral root in that case. I'm less apt or I have to know before I go for the medial side. So I'll get mechanical axis views and then we'll think about obviously alignment, BMI, chondrosis, KL grade, and I'm more guarded treating those isolated medials unless they fit right in the middle of the group with the, you know, they have the low energy pop and their parameters check out. All right, the question to Catherine Logan. If you have significant OA with it, do you do a root repair or not? I think, you know, kind of as Seth was saying, I'll look at a lot of different things as far as their alignment, their activity level, their BMI, also access. In Colorado, we tend to have a low BMI active, high demand type population, so I'm probably more on the repair side of the spectrum. Okay, thank you. Next topic, meniscus transplant. So I'm asking Al, do you have an age limit on when you do and still consider meniscus transplants? I'm less likely to do it in someone over the age of 50, but, you know, at the end of the day, it's more physiologic state rather than chronologic state, and I think if you've got a good joint in an active patient, then I think I wouldn't have such a hard cutoff. Okay, thank you. Next question, and this is a question to David Flanagan. If you're comparing medial and lateral meniscus transplants, on which one do you pull the trigger earlier? Lateral for sure. I think that that joint is at much greater risk, and so if I am at all questioning if they're having recurrent effusions, that's going to be someone I'm going to be moving towards a meniscal transplant. Okay, question for Kevin Bonner. You know, how aggressive are you with piecrusting the MCL when you're doing wood repairs or meniscus transplants? Do you open it all the way up, or do you not do that? I do it virtually on every one. So, I mean, as long as I can get my instruments in, that's what I want to achieve. So, usually I'll start, and once the joint is distracted enough where I'm not going to cause what I call iatromalacia by the procedure, then I'll stop there, but I do it on virtually every one. Okay, I think this is a really important point because you shouldn't be struggling getting into that medial space, right? So, osteochondral defects. So, let me ask Cassandra, actually, while we have you here. You know, when do you do osteochondral defect, for osteochondral defects, when do you use osteochondral allografts versus MACI? Do you have an algorithm? What's the number one determining factor for you? That's a great question. I think my algorithm is evolving. I would say if it's purely a surface-type lesion, I will be more aggressive about MACI, and the nice part about MACI is you can do it anywhere within the joint. I think within the patella. My practice tends to be more patellofemoral, so I tend to use more MACI. If there's any evidence of subchondral edema, then I tend to be, right now, my pendulum is swung very much more towards osteochondral grafting for that. Okay, and Clayton, are they kind of sort of equal techniques for you? You just adjust them according to certain criteria, or do you believe that one is truly better than the other? I think similar to Cassandra, you know, more surface lesions, maybe lean a little bit towards MACI, and then if I'm really worried about structural integrity, then certainly the osteochondral allograft. I think on the condyles, I lean a little bit more towards an osteochondral allograft, and I feel a little bit better about maybe early weight-bearing with that, with a nice structural unit versus the patellofemoral joint where you maybe, there's less weight-bearing issues as much, and it's not as much of a weight-bearing joint, so I feel a little bit better about a surface procedure in the patellofemoral joint. Okay, so I think a take-home message, we have great technical options available. We just need to make sure that we use them appropriately, and I think we are out of time. Thank you very much, everybody.

knee osteoarthritis

treatment options

conservative approaches

physical therapy

cortisone injections

platelet-rich plasma

bone marrow aspirate concentrate

adipose tissue-derived stem cells

joint preservation surgeries

patient-specific instrumentation

cartilage repair