Morning. I want, you know, maybe all the speakers have come up, you know, for this first session and we actually have three papers and then we have a Q&A afterwards over there. First paper will be by Dr. Jacob Fox. The title is Meniscus Repair in the Setting of Revision ACL Reconstruction. Six-year follow-up results from the MARS cohort. Thanks, Jacob. I want to start off by thanking the committee for the opportunity to present on behalf of the MARS group today. This project has involved many people whom have played vital roles in its completion. I have no disclosures and the disclosures from the MARS group can be found on the Academy website. The MARS group, which stands for Multi-Center ACL Revision Study, was formed based on the premise that revision ACL reconstruction consistently demonstrates worse outcomes compared to the primary setting. The group is comprised of 83 IRB approved surgeons at 52 sites across the nation with a 50-50 split of academic and private practice surgeons. Treatment in meniscal pathology has shifted over the past 50 years from removal to repair when feasible. This is because the meniscus has been found to be a critical structure for low transmission, lubrication, and distribution of forces across the knee joint. Meniscal repair has been studied frequently in the ACL intact patient and in the primary ACL reconstruction setting with failure rates between 9 and 24 percent. MARS two-year follow-up data has been published evaluating meniscus repair in the setting of revision ACL reconstruction and that study demonstrated an 8.6 percent failure rate. The purpose of the study was to evaluate six-year follow-up on patients who underwent concurrent revision ACL reconstruction and meniscal repair. Our primary outcome was repair failure, which was defined as reoperation for meniscal pathology. Our secondary outcome was a variety of patient reported outcome measurements including COOS, IKDC, and MARCS activity scores. We hypothesize that meniscal repair failures would increase compared to two-year follow-up. However, we predicted repair would still prove to be a worthwhile endeavor. This is a longitudinal prospective cohort study which enrolled patients between 2006 and 2011. At six-year follow-up, patients were contacted via email and phone to determine if any subsequent surgery had occurred since a revision ACL reconstruction. If surgery had occurred, operative reports were obtained when possible for further information. Wilcoxon rank sum tests were used for continuous variables, Pearson Chi-square tests for categorical variables, and Cox regression analyses were used for survival analysis. 221 subjects were included, comprising 238 meniscal repairs. 60% were males, median age was 21, and time since index ACL reconstruction was 3.3 years. In this study, the overall meniscal repair failure rate was found to be 16%. There were 31 failures, 28 of those being medial, and three lateral. Medial failure rate was 20%, and lateral failure rate was 5.7%, which was statistically significant. The survival analysis pictured to the right demonstrates more rapid deterioration in medial-sided repairs, this is shown by the red line, compared to lateral repairs shown by the blue line. Patients with lower BMI were interestingly found to have a significantly higher failure rate, and this was independent of activity level. And lastly, there was no significant difference on the success of meniscal repair when looking at tear location, tear severity, tear type, ACL graft choice, and method of repair. At six-year follow-up, KOOS and IKDC scores were greater in non-failures compared to the failure group. However, all but one of these were clinically insignificant. The only clinically significant difference at six years was a KOOS quality of life subset, which was 50 points in failures and 69 points in successful repairs, which is significant as a change of greater than 10 would indicate clinical significance. The 16% meniscal failure rate at six years is well within reported failure rates from long-term follow-up on meniscal repair in the setting of primary ACL reconstruction. 16% is an increase from our two-year follow-up failure rate of 8.6%. This was expected, though, as the literature shows that failure rates increase with prolonged follow-up. Our finding of increased medial-sided repair failure is consistent with primary ACL reconstruction in two years MARS data as well. This could be explained by the fact that the medial meniscus is more tightly engaged to the plateau, leading to higher medial-sided biomechanical forces. We also confirmed the notion present in the literature that all inside and inside-out repairs demonstrate no significant difference in failure. Strengths of our study include long-term follow-up of meniscal repair in the revision ACL reconstruction setting, which has not been previously reported. We had a large sample size and we also have a 50-50 split of private and academic practice surgeons. To conclude, meniscal repair in the revision ACL reconstruction setting is indeed a worthwhile endeavor with an 84% success rate over six years. Medial-sided repairs continue to show higher rates of failure compared to lateral-sided repairs in short and long-term follow-up, and the medial repairs also fail earlier. Finally, repair technique, meniscal tear morphology, and ACL graft choice were found to be insignificant in the success of meniscal repair in the revision setting. Thank you everyone for your time. Great. We're going to have the question and answer after our third paper. So, second paper is actually by Dr. Richard Danickiewicz, talking about intra-articular VEGF and MMP1 are the primary drivers of worst baseline coup symptoms and quality of life subscores at time of knee chondroplasty. All right. Good morning everyone. My name is Richard Danickiewicz. I'm one of the sports fellows at Rush. I'll be presenting on behalf of my co-authors. Intra-articular VEGF and MMP1 are the primary drivers of worst baseline coup symptoms and quality of life subscores at the time of knee chondroplasty. These are our disclosures, none of which are mine. A little bit of background here. As we all know, articular cartilage is a complex composition of various zones, each with their own form and function. We also know that there is also a complex interplay of various cells, cytokines, and surrounding structures in the joint that all play a part in the homeostasis of articular cartilage health and then can also be thrown off as well. A number of these cytokines that we've identified in the joint can be more broadly classified into anabolic and catabolic seen here, not necessarily green and red for good or bad, just more so anabolic versus catabolic. Previous literature has shown that synovial fluid makeup can have an effect on outcomes after a knee arthroscopy as shown in this study by Strauss and colleagues where they found IL-6 was correlated with preoperative and postoperative pain and functional deficits. Similarly, they showed a correlation with MMP3 as well, which brings us to the purpose of our study, which is to characterize a synovial environment of patients undergoing arthroscopic chondroplasty alone and also to investigate the relationship of synovial inflammatory cytokines with baseline PRO scores and defect characteristics. So in order to accomplish this, 60 patients undergoing arthroscopic chondroplasty had a synovial fluid aspiration performed at time of surgery. These patients also had preoperative PROs obtained and then intraoperative defect characteristics were recorded. These again were the cytokines that were analyzed as part of the study. A list here of the patient reported outcomes that were collected, primarily COOS subscores, and these are the different patient specific characteristics and intraoperative findings that were analyzed. In terms of results, univariate correlations were seen between number of defects, patient sex, and a number of the cytokines. Similarly, correlations found between a number of the COOS subscores and cytokines except for COOS pain and COOS sports. More specifically, looking at COOS symptoms, VEGF and MMP1 were the drivers from a cytokine standpoint, total defect area, number of defects were also correlated, and COOS quality of life scores, MMP1, IL-1 antagonists, and aggrekin were correlated, and ICRS grade was found not to be. On multivariate regression, we really started to see that cytokines were the driver of these PRO changes more so than the defect characteristics. Again, VEGF being the primary driver and the COOS symptoms and MMP1 being the driver of COOS QOL. So circling back to the Strauss paper, they found that the VAS score and COOS PS had some correlations with IL-6, MMP3, and TMP1 versus our study which had a number of COOS subscores and a different cytokine profile, but it should be noted that in their study they took a number of different procedures in knee arthroscopy including ACL and meniscal procedures, whereas ours was strictly chondroplasty, which could account for some of the variation seen between the two. Also important note to make that we know that the knee is a complex interaction between the cartilage and the meniscus and the synovium, so it's important to know that this isn't done in a vacuum and research has been done and should continue to be performed looking at the joint holistically, specifically looking at how the synovium interacts with this milieu as well. So in conclusion, elevated inflammatory cytokines appear to be the driving force behind worse baseline COOS symptom and QOL subscores. Number of defects and sex were independently correlated with the synovial profile of the patient and there's a number of future areas of study we believe from this, whether it be investigation of inflammatory cytokines on other procedures, including the healing environment after ocealographs, or just ways that orthobiologics or other known injections, medications can help alter this cytokine environment depending on which pathology you're encountering. I want to thank everyone for their time this morning. Thank you. Third paper is by Arjun Khurana. Titles of mosaplasty, osteochondral autograft transfer remains a durable solution for symptomatic chondro defects of the knee, two to ten year follow-up analysis. We will have our Q&A after this paper, so for the questions hold on and just come up to the microphone right after this topic. Great, thank you. Good morning, my name is Arjun Khurana and I'm a research assistant at the Hospital for Special Surgery working with Dr. Riley Williams. Here are disclosures. A little bit of background on this topic. While the deleterious long-term effects of microfracture are well documented, studies examining the long-term clinical outcomes in patients treated with osteochondral autograft transfer are scarce. OATS, also known as mosaoplasty, is a single-stage cartilage repair technique that is characterized by the transfer of viable bone cartilage dowels harvested from the low weight-bearing areas to treat symptomatic chondral and osteochondral defects of the knee condyles. This procedure allows for immediate restoration of osteochondral architecture, the use of autograft tissue, and facilitates predictable bony healing, easier graft accessibility, and lower cost compared to other commonly used cartilage repair methods. In light of the limited long-term published data on patients treated with osteochondral autograft transfer, we sought to establish the likelihood of achieving both the MCID and SCB thresholds in this unique population of primary OATS for symptomatic focal cartilage lesions. The purpose of this study was to assess mid- and long-term clinical outcomes of the primary OAT performed from the treatment of symptomatic articular cartilage lesions of the knee, and our hypothesis was that OATS slash mosaoplasty will demonstrate favorable outcomes and durability through 10-year follow-up. We used a longitudinally maintained prospective institutional registry dedicated to the tracking of patient outcomes following articular cartilage restoration procedures, and we retrospectively queried those patients who underwent OATS from September 1999 through April of 2021. The inclusion criteria included patients who underwent OATs as a primary college procedure, as well as preoperative and postoperative problems at at least two-year follow-up, all completed. However, we excluded any patients that had undergone any prior ipsilateral cartilage repair procedure, as well as any advanced osteoarthritis, inflammatory arthropathy, paratotal meniscectomy, as well as bipolar lesions. Furthermore, our primary outcomes of interest were all patient-reported outcome measures, which have been validated in orthopedic assessment for general well-being, knee function, and knee-related disability, and they're listed here. And then our secondary outcome measures we were interested in were both reoperation rate, as well as total knee arthroplasty conversion rate. And we used paired T-tests to evaluate the differences between time points, and we used p-values of less than 0.05 to deem statistical significance. Our results found 63 total patients who had met the selection criteria with a mean follow-up of 5.7 years, and they were at an age of 27 point years at the time of surgery. The mean lesion size was found to be 2.3 centimeters squared with a deviation of 1.6, and a range of 0.6 to 6.5 centimeters squared, and required a mean of 2.2 autograft plugs with a deviation of 1.3. The medial femoral condyle represented nearly half of all lesions at 47.6%, followed by the lateral femoral condyle, and then the patellar lesions. And donor site backfill with acellular synthetic scaffold plugs was performed in 68.3% of cases. Our primary outcome measure results showed statistical significance improvement was observed from baseline to two, five, and 10 years for all investigated outcome measures. Specifically for the SF-36, we looked at their physical functioning subscores, and so for the physical function subscale, we saw an increase from 58.1 at baseline to 83.3 at two-year, 85.1 at five-year, and 80.3 at 10-year. And similarly for the SF-36 role limitation subscale, we saw an increase from the mean of 53.8 to 88.1 at two-year, 90 at five-year, and 83.3 at the 10-year, and both of those had p-values less than 0.01. Furthermore, patients available at five-year follow-up achieved MCID rates, achieved MCID at rates of 78.2%, and 68.8% for the IKDC and COOS ADL, respectively. Furthermore, these patients also achieved SCB for the IKDC and COOS ADL measures at 60.9% and 68.8%, respectively. We had 15 patients that were available for 10-year follow-up, and they saw statistical improvement in both their IKDC and mean baseline scores. 60% achieved MCID, while 33% achieved SCB for the IKDC and for the COOS ADLS, 60% achieved both the MCID and SCB at 10-year follow-up. Furthermore, there was re-operation rates at a rate of 28.6% at an average of 3.76 years after index procedure, the most common types being revision cartilage procedures followed by arthroscopic debridements, as well as license of adhesions and manipulation under anesthesia. And two patients did undergo conversion throughout our study timeline. There were some limitations, including regarding study sample size, as it was relatively small, which would have introduced some form of selection bias. However, OATS does remain a niche procedure that warrants increased use over microfracture, which would in turn provide more patients to externally validate this experience. And we were able to also, and also given the fact that the surgeons used, there was six fellowship-trained surgeons over a 22-year period, so there was some heterogeneity in both the surgical technique as well as the pre-operative and post-operative protocols, and loss to follow-up is obviously an issue that we experience in many research studies. Lastly, our conclusions are, compared to the poor mid and long-term results associated with microfracture, primary OATS remains an effective and durable cartilage restoration procedure for patients with symptomatic cartilage knee defects at long-term follow-up. Furthermore, re-operation was common, however, is consistent with the literature, and results suggest low TKA conversion rate at the 10-year follow-up. Thank you very much. Thank you. Okay, thanks to our speakers. Those were all great talks. If anyone has any questions, please come up and use the microphones in the center of the aisles here. To start things off, I'm gonna do the first question. Dr. Danilkovich, with the sort of commonness of orthobiologics, I was curious if any of those patients had received an orthobiologic injection before you guys did your synovial fluid sample. None of the patients in the study did, but that's kind of the next step, is to see first in the lab what orthobiologics specifically have what impact on the various cytokines, and then the hope would be to start either doing it preoperatively or postoperatively as well, and seeing if first in the PRO changes, and then expanding on to different procedures, because it may be a different cytokine mix depending on how invasive or which structures are being altered. Great. Microphone, too. Thank you. Another question for Richard. How did you decide on which biomarkers to test for? I think a couple of times you mentioned Eric Strauss' work where aisle six seems to be an important player, but it didn't seem to me that you actually tested for that. I think it was actually just the array that our lab used, so it was less of the specific ones that we picked out and more of what was available for that. That's a good question, though. There definitely could be a larger panel used in future studies, but I think this was particularly just the one that our lab was utilizing at the time. Okay, thank you. Microphone three, yeah. Thank you. My first question's for Dr. Elias. So for the, since you tested multiple variables to control for type one error, did you use an adjustment like a Bonifori correction or any other adjustment to reduce type one error? I'm sorry, say that again? So given that you tested multiple variables, multiple different synovial markers, did you adjust the p-value using Bonifori correction or a similar method? Not that I'm aware of, no. Okay. And a second question is for Dr. Corona. What do you think the effect of alignment is on your outcomes? Did you look at alignment or concomitant osteotomies? We didn't look at any sort of concomitant procedures or alignment, but that would be a very interesting follow-up to look at in the future in regards to this procedure. Okay, great, thank you. I'm gonna jump to a question for Aja and Tuli for your OATS procedure. You know, what about a backfill? Because you mentioned about half the patient had backfill, half not. What is the difference in outcome for those patients? That's another thing we didn't specifically investigate, but I do think that that would be a future direction we would like to go in, and whether or not the backfill would be something that we want to look at, whether or not that has an impact on the outcomes. Ben, can I talk? Yeah, so the majority of those mosaic plasty patients were mine. The true fits were the Acellular scaffolds that we used probably for about five or six years in the middle of that series, but it's a 22-year series. Every single patient either had an Acellular scaffold or a lesional bone or cancellous bone chips with fibromyalgia, just a various number of things. And the other thing which we didn't really talk about is most of the plug harvests are from the notch, very seldomly from the superlateral, supermedial trochlea, which has been described. But I think the main take-home message from that study is that there were only 63 patients, but these were clean, well-aligned, no prior surgery, no ligaments, no meniscus work, just straight-up osteochondral lesions of varying etiologies. But I'm very proud of the study because it basically just demonstrates what I've been yelling for 20 years is when you have a cartilage lesion, use autograft, first, not second, not third. It's the best operation, it's durable, it works great. Thank you, yeah. Microphone two, yeah. For the MARS study, those patients that were repaired, were they new tears or were they failed initial repairs? I believe that they were new tears. But I would follow up that to make sure. I believe they're new tears. Great, well, thank you for the first panel over here. Really appreciate, you know, a great discussion. And we want the panelists and also our speaker for the second session to come up to the stage. Thank you. Thank you. Next, we actually have a friend of AOSSM coming to present to us on meniscus-reinforced tears. A technique video, Dr. Bertrand Courir-Cotet. Welcome. Thank you. Thank you very much for your kind invitation. I have an audio for my surgical techniques. This is my disclosure. Since the beginning of 2013, we explore systematically the posterior medial compartment during our ACL reconstruction by pushing the scalp transnotch and by probing the capsule to be sure to don't miss the hidden lesion of the medial meniscus. We just published this paper showing almost 40% of concomitant medial meniscus tears in our primary ACL ruptures. Interestingly, you can observe that the rate of medial meniscus increase when the delay between injury to surgery is over 10 to 12 months, but the ramp lesion seems to be stable, which means that it's probably a lesion due to the trauma itself. Based on the more than 6,000 ACL reconstructions since 2013, we found 30% of ramp lesion in our primary ACL, 45% in our revision case, and moreover, over 50% in professional athletes. In terms of injury mechanism, it was described very long time ago by Kaplan the proximity between the semimembranous and the posterior horn of the medial meniscus. We also published this study where we clearly show a direct link between a capsular branch of the semimembranous to the posterior horn of the medial meniscus, and we also described that the meniscal tibial ligament is the inferior surface of the medial meniscus, not at the posterior one. So our hypothesis was that during the trauma with the very important tibial translation due to the ACL ruptures, you have automatic contraction of the semimembranous, which should be probably the cause of this ramp lesion. It's very clear in this soccer player. You see the anterior translation of the tibia and the automatic contraction of the semimembranous which is probably the cause of this ramp lesion. This is my surgical techniques with audio, please. This video presents the arthroscopic repair of medial meniscus ramp lesion. Firstly, anterior probing of the posterior horn of the medial meniscus is performed using an arthroscopic hook. This is followed by a trans notch approach to the posterior medial compartment of the knee. With the arthroscope passing between the medial condyle and the PCL with the knee inflection and slightly in valgus. This allows a perfect posterior medial view of the knee. We recommend starting with the needle palpation of the posterior aspect of the medial meniscus, which as in this case allows the identification of a very fragile scar tissue prompting a posterior medial accessory portal to be performed. The saphenous vein and nerve can be avoided by using trans elimination. Meticulous debridement of the scar tissue is then easily achieved via the accessory portal using a shaver. This will also further promote healing of the lesion. The next step is to remove the scar tissue and begin. Using a posterior medial portal ensures ruptures of the meniscus tibial ligament are identified as this is the most important stabilizing structure of the posterior horn of the medial meniscus. An anterior probing cannot clearly identify this injuries. The repair is performed using a specific 25 degrees curved hook loaded with a restorable suture. It is advisable to firstly grasp the capsular part which includes the meniscus tibial ligament followed by the anterior border. It is important to stay very close to the lesion since it is located in the red red zone with a high healing potential. A sliding knot is performed with half hitches to lock the knot outside of the knee and then pushed into the joint with a knot pusher. This is repeated 2 or 3 times depending on the extent of the lesion. The repaired rump lesion is assessed with a hook to make sure there is appropriate contact between the repaired edges to ensure healing. Final probing of the posterior horn of the medial meniscus is performed with an arthroscopic hook to ensure that there is no anterior translation, which would indicate potential residual instability. In terms of clinical results, we published this important study with almost 100 months follow-up, where we showed that the failure rate with all inside repair for this posterior horn of the medial meniscus was above 30% failure rate. With the hook, we dropped to 15%, but we also demonstrated that when you combine this rump repair with the hook with an extraticular reconstruction, we dropped the failure rate by an average of three. We obtained 7% failure rate, which is a huge improvement when you come from more than 30%. We also have this paper in revision, where we analyzed more than 1,000 rump repairs, and we found less than 5% failure rate with the hook and the extraticular reconstruction compared to 13% when it's isolated ACL reconstruction. So it's clear for us that adding an extraticular reconstruction helped for the healing of this posterior horn of the medial meniscus. We also published a long time ago the complication rate due to the posterior medial portal. We only have two cases of hematosis due to the injury of the saphenous vein, but we do not have any single case of nerve injury. In conclusion, rump, in our experience, is very frequent, and it never heals spontaneously. It's very important. Definitively, the best option to repair the rump and to decrease the secondary meniscectomy is the use of this posterior medial portal with the hook, adding a lateral extraticular reconstruction. For our group, all inside searches for the posterior horn of the medial meniscus should be avoided, and particularly in rump lesions. Thank you for your attention. Thank you, Bertrand. Our next speaker is Aaron Kretsch from Mayo Clinic. We're going to talk about meniscus repair in 2024. Thanks, Aaron. Well, good morning. Thank you, moderators. Thank you, program chairs. So our mission is saving the meniscus. Unfortunately, we still see patients like this. This is a 14-year-old sent to me, had this repairable lateral meniscus tear that, unfortunately, we see not 10 years later, but 10 months later with a destroyed lateral compartment and a knee that will never be the same. We know from Ashish Bedi's work that the most important part of the meniscus is their circumferential fibers, that 20% to 30%. So even if we're able to get that peripheral 20% to 30% to heal, we'll maintain our contact pressures. So I'm going to give you five steps and five minutes of how to repair and make these radial repairs easier. So step number one is you have to make the diagnosis in the office. If you come out of the operating room with a surprise diagnosis for the patient, you're going to lose the trust of that patient and the family. So on the sagittal images, we look for the so-called gap sign. On the coronal images, you might see an absent meniscus, but really start to study your axial images. The gap sign is the most confirmatory and probably our best cut on the MRI for a radial tear. In this case, you can see two radial tears, one in the posterior horn near the root and one in the anterior horn. Step number two is really counsel the patient before surgery and obtain buy-in. If this is with an ACL injury, you have to have that athlete understand that their recovery will be fundamentally different than their teammates. Otherwise, they're going to think they're behind the entire time. They're going to think you're a poor surgeon. So really get that buy-in and counsel them before surgery. Step number three is get to the operating room early. So this is an 18-year-old college running back. At six weeks, you can see this radial tear is already retracted. A very difficult operation at that point to get back. In this case, we're fortunate that we do, and then treating his cartilage. On the medial side, you heard about the meniscotibial ligaments from Bertrand. So they don't tend to retract. But on the lateral side, these radial tears tend to occur through the popliteus hiatus, and then you get retraction of the posterior segment. Step number four is plan your repair constructs. So you really have to bridge that gap. How do we bridge that gap? Well, really using ripstop sutures more and more frequently. Whether you use a tie grip or hashtag configuration, either one is fundamentally important to repair your radial tears. If you look at the biomechanics of the ripstop sutures, they behave as well as tibial tunnels, but they have the advantage of not over-constraining the meniscus. So I would encourage you to use ripstop sutures. And then finally, it comes down to execution on the day of surgery. And we execute by using the principles ABCs. So anatomic reduction, biologic preparation, and circumferential compression. And I'll illustrate these principles in this challenging case where we have a 15-year-old scaly immature patient presents with an ACL injury, but also severe lateral meniscus radial tear two months ago. So again, make that diagnosis, look for the gap sign on your sagittals, look for the absent meniscus on your coronals, and confirm on your axials that you have that radial tear. In this patient, because they presented subacute, now at two months we also got a long leg standing film, and whether this is congenital or acquired, this is now an issue for this lateral meniscus radial tear. So here's the time of arthroscopy. Again, this is two months out. Certainly wish we would have been able to get here six weeks ago. Now you can see this chronically retracted tear. When you look at the mobility, it's very poor. Here there's no releases to do. This tissue is chronically contracted. So in this case, we have to perform our ripstop. It's important to perform a mobile ripstop, so you don't want to tether this to the capsule, or you won't be able to reduce it. Now we're able to perform our anatomic reduction, our A, which then facilitates our biologic preparation and our circumferential compression. So once we get it reduced, then we can apply our ripstop configuration and get a very robust repair. Always remember the biology. If this is an isolated case, we perform marrow venting. You can see those cells and that blood knows where to go. They find the area of repair and form a nice clot. In this patient, we had a very nice follow-up MRI at six months, demonstrating healing. And again, even if we get the 30% circumferential peripheral fibers to heal, we're in good shape. We also performed growth modulation for the valgus malalignment. And here you can see, recently back at five years, we saved the knee of this patient through the principles of meniscus repair. Here's a companion case without a significant gap. So if you have a radial tear like this, then you can just perform inside-out ripstop sutures through the capsule. Once you get your anatomic reduction, you can then apply your full ripstop technique and get circumferential compression. When we look at these clinically, they do very well. They do as well as a bucket handle repair or update at 10 years as an 80% success rate for these patients. So we'll pivot now into the oblique radial tear or the L-mort. These are very common in our hands at the ACL injury. About one in eight knees will have these L-mort type injuries. Why is it unique? Well, it's not really a root tear because it's more than a centimeter away from the root. It always happens with the pivot shift. It does not happen in isolation. And for a long time, we weren't certain what to do because we weren't entirely certain of the biomechanics. We've done the biomechanics work, looking at both incomplete and complete L-mort lesions. And what we found was that they both negatively affect stability. So this highlights the secondary stabilizer concept of the lateral meniscus by both increasing anterior drawer as well as pivot shift. What happens with treatment? If we leave it, if we debride it, if we repair it, how does that behave? When we look at it biomechanically, if you debride it, you're going to lose about two millimeters on your anterior drawer at time zero. When you look at pivot shift, you're going to lose about a millimeter and a half at time zero. And I don't know about you, but I'm not a good enough ACL surgeon to leave two millimeters at time zero in my patients in the operating room. So we want to repair it in order to restore the mechanics. And again, we go back to our ABCs. Oftentimes, we'll see a missing fragment. I call that the kickstand fragment. So you're going to have to go find it up in the notch. Sometimes this is scarred into the ACL stump. Here's a case of mild scarring. Substantial scarring, and I'm sure these have ended up in our shaver tubing over the years without the recognition. The blood supply is really robust in this area, so I would encourage you to rasp liberally. You can really encourage a lot of bleeding at the tear site. When it comes down to fixation, my opinion is that intrameniscal fixation is best. If you avoid tethering to the capsule, you'll avoid stress risers, you'll avoid the chance for neurovascular injury, and you'll avoid the extrusion of that meniscus. So your first, most important stitch is your anatomic reduction. So here, we'll use a self-retrieving device in order to line it up anatomically. And then in this case, I've shown I don't normally put four sutures across, but you can actually place a number of sutures in a very small, limited space with this technique. Again, this does not compromise the mobility because you have meniscus to meniscus compression rather than through the capsule. This is our typical repair, two sutures, very efficient, takes approximately five minutes. Sometimes we over-reduce the meniscus, as you can see here. If you cycle the knee and then take a look, you'll be anatomically reduced. And then the other important factor to point out is that you do get circumferential compression with this technique. So you can see nice tethering of the meniscus there, both superiorly as well as inferiorly. Do they heal? Here's a case of a second look arthroscopy. You can see complete healing and synovialization. When you look in the literature, both by second look arthroscopy and MRI, you see healing rates upwards of 95%. Clinical outcomes, we've recently published. We've looked at 100 of these, compared them to an isolated ACL reconstruction. What we found in almost five years is zero operations or re-operations for this lateral meniscus tear, similar to what you've heard with the MARS data earlier. And when you look at their clinical outcome, they did as well as patients who had never had a lateral meniscus tear. What about double radial tears? So sometimes you get failure in both the root or the elmort and the midbody. In these cases, again, don't throw this meniscus away in a young patient. These can be technically challenging, but we can just break them down into their principal components and repair one at a time. So here we do a ripstop configuration for the radial tear of the body and then our standard two suture technique for the lateral meniscus oblique radial tear. When you look at these clinical outcomes, they're also excellent, 95% success at almost three years follow-up. So in conclusion, I think it's important to make the diagnosis early, obtain and counsel the patient to get buy-in, repair all radial tears in young knees with intact cartilage. You really have nothing to lose. Plan and execute your ripstop repair and then finally, when we look at clinical results, they are very favorable. So thank you very much. Thank you. Thank you. Well, thank you. Outstanding talk earlier. We're going to switch gears a little bit and talk about cartilage in the next 15 minutes, right, Robin? So I want to introduce my co-moderator, Robin West from Inova and I'm Ben Maher from San Francisco. We're going to talk about a few cases in college. We have an outstanding panel that's going to talk to us today about cartilage in an injury. We have Riley Williams from HSS, Vulcan Basal from the University of Pittsburgh, Tom Cronin from UCLA and Dave Flanagan from Ohio State. So thank you guys. Without further ado, I'm going to start with the first case here. Jeff Bear from University of Wisconsin over there. So thank you. I think Dave is actually blogging right now at the end of the podium over there. So thanks. Sorry about that, Jeff. So first case, 22-year-old basketball player, swelling in the knee, difficult with playing. He can still play but don't have power. Want to continue with basketball after college. And these are some of the physical examination, full range of motion, mild effusion, swells up after every game. There's some crepitus with knee extension. The patella examination otherwise are fairly nonspecific. No instability, no apprehension but do have some pain with knee extension. These are the plain x-rays done on this patient. I would say it's pretty good alignment and the Katon to Sean ratio is actually fairly normal. These are some of the imaging findings. Let me see if I can kind of turn the videos forward. So I'm going to put my mentor Riley Williams on the spot first. Riley, what do you think? Basketball player, want to play for the New York basketball team over there and what do you think about this patient here? Well I like the use of the fat suppression images because in a basketball player early patella femoral wear is very common. I'd say it's in over half of the MRIs you're going to see at the combine. NBA combine. So I don't see a lot of bone edema which makes me happy. Although the persistence of this trochlear lesion may lead to some mechanical symptoms. So I'm already in a better mood when I see this MRI mainly because I think the overall metabolic process in and around this lesion is not that high. That's what I think. And what do you think about the effusion? Obviously there's not a lot of bony changes but clearly the player's feeling it, right? The ball is reacting to it. Does that worry you about diagnosis and how aggressive would you discuss with this player about treatment? Ben, if I got uptight with an effusion of that size I would be uptight all day. This is what I see all day every day. Listen, clearly there's some reactivity there but my level of concern quite frankly in the scope of what I see is I'm interested but not overly worried. Okay. Tom, what would you do if you saw a player over here maybe had some rehab, not recovering, still not getting the medicine you want and not playing as well try some injections and not really responsive? What are you thinking right now? I think if he's tried all the non-operative measures and you're sort of moving down more of a surgical pathway, that's certainly an option. 22 hasn't had a procedure before, like Dr. Williams was saying, the bone health looks pretty good, probably has a good subchondral plate, maybe a little flap there on the trochlea, on the other image. I think you would probably talk to him about trying something like a chondroplasty and maybe taking a biopsy when you're in there for a little backup option if you need it. Okay, to Brinkman first, maybe a biopsy. Jeff, what do you think here? Yeah, I mean, this one I think depends, a lot of things you're weighing into it is what year is he in, where are you at in the season, is he able to play, is he not able to play, and what level, I think those factors weigh in. But I think for this defect, I think for a first-line therapy, I think chondroplasty, potential abrasion chondroplasty can do fairly well for these athletes. So he's a senior, it's actually February, and team's not gonna make it, Cal's horrible over there, they're not gonna make it. So he wants to try out, he doesn't want to get ready, so he got one shot. He said, I really want to get one shot, have surgery done, and then get ready. Any changes in terms of your treatment, in terms of try to be more definitive, or kind of see how it works, what are your thought process? To me? Yeah. That's a tough one, because if you're in February, if you do anything more than a chondroplasty, he's not gonna be ready just from the rehab time afterwards. I mean, you can let him bear full weight, you can start doing some stim and so forth, but to get to a level to be at the combine, they're not gonna be ready at that point. So really, to give him the one shot, I think you have to do something a little bit more limited, rather than a definitive. I did an OATs on it, or do a Macy on it, they're not gonna be ready to come back by the time you combine it. So, all right, so let me actually move on over here. So, let's see. And so, full thickness lesion over there is jumping athlete. We talk about the concern, the time of the injury also. So he did fail non-operative treatment. These are some of the arthroscopic pictures. And let's see, let me see if we can get the display here. We actually, you know, debrided lesion is about a centimeter and a half, and we talk about options for him. We actually debrided lesion. Actually, we actually did a particular college, you know, juvenile particular college implant for him. Try to get him to hopefully have one, you know, procedure and get him back, you know, and see whether he can kind of continue with activities. Dave, what do you think? You think I'm kind of too aggressive, or this is okay? You know, his career is over? What do you think? Yeah. I think this is definitely an option for your patient. I think it's all that preoperative discussion and their goals and timeline as far as when you can get him back towards sport. So I think this is definitely reasonable, especially if he had more time that he can rehabilitate. I agree with the option, especially with this small, more limited focal lesion, not doing any type of osteotomy for this type of case in the patellofemoral joint. I think it's gonna give him the best chance to get back. Volker, any other concerns in terms of durability of this technique? And also, like, you know, what's rehab like in terms of like a mosaic plasty type osteochondrial allograft versus like a, you know, cell-based type treatment? And do it change your rehab at all? Yeah. So I like, you know, oats very, very much, except in this particular case, you're at a centimeter and a half. You're probably looking at two plucks, maybe three. So a technique like this with the cells, or if this is a minced allograft, I think all of the techniques will work. The problem is that in the rehab, if they go too early, you'll see problem again and again. So if they go before four months and get too aggressive, you will see relapses. So I think managing the expectations is the most important thing, and just taking your time. So it's a one-time deal. Yeah, I think that's the most important, kind of setting the right expectation about a recovery. And this particular, you know, our athlete actually did pretty well. We actually let him kind of go back to the, doing court work at about four and a half months. He was able to kind of, you know, go to the next level in Europe. And this actually, he came back and see me in two years over here, and these are some of his pictures. He's still playing overseas. And this is kind of a nice little follow-up in terms of with the lesion. There's a little bit of bony overgrowth, but that actually certainly have good college coverage. You can see the knee is quiet, no effusion. He's playing, you know, right now. So just gonna share a slightly different technique in terms of, you know, dealing with these, just slightly different from a completely cell-based type treatment versus osteochondral autograft or allograft over here. So, well, thank you for the panel over here. So I'm gonna turn to Robin for the second case. Yeah. Thanks, Ben. Hey, Ben. Sorry. I just wanna make a comment. Sorry, Robin. We just did a meta-analysis looking at modern cartilage repair and the OATs. Clearly, when you compare OATs, microfracture, osteochondral allograft, and MACE, the quickest return to sport is always with the OATs. There's no real longitudinal analysis of PJAQ, which I agree. I think it's certainly a reasonable option. The concern I have is you're asking the body to synthesize new articular cartilage repair tissue in an overloaded environment, which kind of goes counter to what we teach. Just, I'm not saying don't do it. I'm just saying be understanding of what you're trying to do. That case is fantastic. But my thought is if you're gonna do something and you're speaking to an athlete and you wanna have a predictable return to sport, OATs, and you can tell them with a straight face it's gonna be five to six months, provided you can maintain fitness. Great point over there. But I think, you know, for this technique, it does not burn the bridge, you know, and hopefully we can get a little bit quicker. But another alternative I think people should discuss with the athletes. So thank you, yeah. All right, our next case is a little more complex. This is a 14-year-old softball player who came to see me. And she was having this right anterior knee pain and instability, a really tough girl. She's been playing all season. A year ago, she underwent a microfracture of her patella and an MPFL reconstruction by another surgeon. On exam, she had bilateral valgus alignment. She had a three to four quadrant lateral patellar glide in full extension and 30 degrees of flexion. She had apprehension. She had a fixed minus 20 degree patellar tilt on her right involved knee and severe patellofemoral crepitation. These are her radiographs. We won't go through all of them, but you can see she had pretty significant osteopenia. These are her lateral views. Her CD ratio was 1.6 on the involved side and 1.5 on the uninvolved side. You can see her standing alignment. She was eight degrees of valgus alignment on the involved side. These are her images. Her CD ratio is 23. Riley, you were talking about bone marrow edema. You know, it's interesting because, we can look at her femoral tunnel placement as well, but you can look at the bone marrow edema. Bone marrow edema is really not a lot. She's got very significant symptoms and crepitation. So based on this, Riley, what are you thinking? Okay, I'm concerned. If you look at the axials, obviously she's massively laterally displaced in the valgus knee. So I'm already thinking that the symptoms are mechanical due to multiple planes of poor alignment. Eight degrees of valgus is a problem. So I'm already thinking that that's probably gonna have to be addressed and trying to get that patella centered. I haven't even really begun to contemplate what I would do with the articular cartilage on the patella but I am trying to get her back in a better alignment. Can I see some more? Can I see some more data? Yeah, and Jeff, would you get any more imaging? Is there anything else you'd wanna do here? Before making a decision on how to move forward? Do you have her images from her last scope or how long ago was that? I don't have her images from the scope. This is a kid, as Riley said, you're gonna be doing a lot on this kid. You have valgus you have to deal with. You have a high patella, you have overload. You're really not sure how significant the cartilage damage is and how large it is. And then you have an MPFL that's not anatomic. So you're gonna have to do everything. If I don't have images, if I haven't had a scope on her, I would wanna do a diagnostic arthroscopy. If I'm in there and I think this is a case that I would consider Macy, I'd go ahead and get cartilage harvested at that point. You consider what, I'm sorry? What was that? What was that? I would wanna do a diagnostic scope to see what her patella cartilages look like. And I'd tell her this is really a diagnostic procedure. So I know what my next step is. And then if I thought it was a case I would consider doing a Macy type procedure. I would go ahead and collect cartilage at that point. So I had options for her. Yeah. Volker, is there anything else you would add? Or would you wanna diagnostic arthroscopy as well? Or would you get a CT scan? Is there anything else to do beforehand? Yeah, I mean, certainly a rotational profile as well. I would get a CT scanogram and the long cassette radiograph and having eight degrees, okay, that I would not rely on the fact that this is an accurate test. You may need to repeat the long cassette and get a very different result. So CT is probably the better way to go. And then in the end, you have five big issues, rotation, coronal alignment, patella, entrochial dysplasia and soft tissue issues. I think the cartilage is the least, I mean, it's the innocent bystander. So you just need to figure out how many of these items you need to reconstruct on her. And again, sit with her, explain how difficult of a situation this is. And she may need much more than just a little cartilage procedure. And she's 14 as well, which is, she's young. And her growth plates were almost closed at this point. So obviously these were the considerations. We only have about 50 seconds left, so I'm gonna move quickly here. But here's some interoperative findings. Unfortunately, I didn't have the video. Oh, we have five minutes? Okay, sorry. So anyway, we went through the arthroscopic pictures and this is an old operation, so I didn't have any of the videos, but she had diffuse articular cartilage wear across her entire patella. And I had ordered an osteohondral graft actually for her. So at the time I performed an arthroscopy, distal femoral osteotomy, lateral retinacular release, TTO and NPFL. So I did it all at once. Again, kind of planning on it, but scoping her initially and ordering the graft. So here we are, we replaced her whole patella, did the DFO. And then I wound up doing both sides actually, because she was symptomatic on both sides. The other one was not a revision, it was a primary. And she's now about four years out and she's playing softball in college now. And so these are her post-operative x-rays. Ben, do you wanna go this one or do you wanna do the next? With this discussion. Just go ahead. Any discussion, obviously big case, the last one over there, I think a lot of learning points on that over there. And what do you people think about, I think any time when we have these carcia injury, what happened to the original surgery, right? The original injury, we talked about the femoral tunnel that maybe when the kids was grow place, not close and actually change position. Would a better surgery, the first time gonna change the outcome with the second one? But obviously this is a big surgery reconstruction. Waiting time, yeah. There's a laundry list of problems that probably the first procedure was not gonna address. I think that's probably, probably this person's yet signed up for more than one procedure in her lifetime at some point, but could have done a little more in the beginning maybe. Yeah, maybe the first one you could do, address some issue, hopefully avoid this one that Robin had to take care of. She's done really well with it. Thanks Robin. Yeah, I agree. I think she dislocated her patella initially when she was like 10 and she never had that address. You start getting this chronic instability and that patella articular cartilage wear. This is another girl. She came to see me. She was a collegiate soccer player, but she was 24 years old, had just graduated. And she presented to me with lateral, sorry, with medial-sided knee pain and anterior knee pain. But mostly her pain was medial. She had undergone a 16 millimeter osteochondral allograft plug five years prior and she had been doing really well, had played actually all throughout college and then presented to me with six months of pain. And so at this point, she had tried an unloaded brace, activity modification and was symptomatic. Go here. So Tom, she had pretty neutral alignment. Is there anything else you would try at this point? We'll look at the images. So again, she had tried the unloaded brace already. She had modified her activities. It was painful and really localized the medial pain, but had some anterior knee pain with stair climbing as well. What did she have done medially? Sorry, I missed that. She had a 16 millimeter OATS, an osteochondral allograft plug. And now it's symptomatic and- Now it's medial-sided knee pain. No mechanical symptoms, it's just pain. Yeah, I mean, it looks like there's some bone marrow edema there. So I think you're probably looking at some kind of osteochondral type procedure if she's failed non-operative management and kind of on board with moving in that direction. She probably knows what she's getting into at this point after being through a previous procedure, but that's what I'm thinking about. And David, is there anything else you would want, any other imaging you'd want? Or is this good enough? Would you go ahead and schedule surgery or is there something else you would recommend at this point? You can definitely get a CT as well to look at some of the cystic changes and how the bone looks. Obviously, I'd be concerned with this graph that it's on its way to potential failure. You're seeing too much edema around the previous graft and cystic changes underneath. So I think a CT scan can be useful as well. And again, neutral alignment, is that correct? To a neutral alignment. Riley, anything else to add? I mean, this is the reason why my utilization of osteochondral allografts is probably 10% of what it was 10 years ago, right? This is the story. You relieve their pain, they're a young athlete, they go back and play. It inhibits graft incorporation. At five years, they're back in your office with this dead bone spacer and you're with very limited options. So what would you consider now at this point? If she's failed this and what would be your next step? So what I've done, which is a little out of the box is I'm like, okay, she's 24 years old. What is my responsibility to this patient? It's more for life and maintenance of the knee. I take out the graft and I do, it's just a bone graft procedure, maybe with a guy-slitch patch to hold it in, fiber and glue. It typically works very well. I get a CT scan at two months to reaffirm reestablishing the bony stock. And each time I've done that, I haven't done it, I've probably done it 20 times. Every time I think I'm gonna need to go back and do a cartilage procedure, it forms a nice little fibro cartilage cap over the reparate and we typically are done. That has worked in my hand. So it just basically made me realize that I'm not doing these young athletes any favors by putting these osteocondal allografts in these weight-bearing spaces because inevitably at that five to seven year time point, they go badly. That's a good point. So her exam, again, she had some patellofemoral crepitation, limited motion. These are her arthroscopic findings. You can see she had a little trochlear wear. She had some mild diffuse wear, some great two to three changes on her patella at zero. But I'm just gonna show you what I did. There's her lesion. You can see it's a calcified OATS and you can see it was failing. So I did an osteocondal allograft, unlike what you recommended, Riley, but we went ahead with that. And she's now about three years out as well. And so far she's doing well, but again, she's only three years, so. Thank you. Thank you. Thank you, everybody.

cartilage injuries

young athletes

patellar injury

diagnostic arthroscopy

patellar restoration

less invasive procedure

chronic instability

valgus alignment

surgical complications

tailored treatment approach